Sometimes life can cramp your style. Ten days ago I fractured my right shoulder in a bicycle accident, courtesy of some streetcar tracks downtown. (I am not alone in doing this; it is entertaining, if a bit gruesome, to Google "streetcar tracks bicycle accident San Francisco". At least I still have my legs.)
Anyway, it's not particularly painful, and as you can see I am able to type--but the arm isn't useful at the moment and everything takes a lot longer to do. My commute is now twenty minutes longer each way. That's about the margin of time in which I have been operating this blog. I won't have the time to post until my arm is functioning again, which will be in about a month and a half.
In the meantime I'll be collecting ideas for future blog topics and I'll be happy to respond to any comments made on existing posts. Enjoy your holiday season and I'll see you again in 2013.
Sunday, December 2, 2012
Sunday, November 25, 2012
Eczema Q&A with Zimbabwean immunologist Elopy Sibanda
When developing countries appear in news stories about eczema, they mostly serve as contrast with industrialized countries, where allergic disease is on the rise. We also tend to hear only from scientists in the US, the UK, Europe, and Japan. That is why I was fascinated to read a recent story about eczema in The Herald, a government newspaper published in Harare, Zimbabwe.
The story focuses on the physical and social costs of eczema that we are so familiar with. It quotes Odwell Gwengo, founder of the Eczema Association of Zimbabwe Trust:
The story focuses on the physical and social costs of eczema that we are so familiar with. It quotes Odwell Gwengo, founder of the Eczema Association of Zimbabwe Trust:
"Judging by the numerous cases attended to, eczema is common in our communities than we had anticipated."
Which makes you think that perhaps Western scientists have not got a complete handle on the statistics of allergic disease in the developing world. This is understandable, when HIV/AIDS, malaria, Ebola, cholera, etc., claim priority.
The story also quoted Dr. Elopy Sibanda, a professor of clinical immunology and allergy at the University of Zimbabwe. I wrote to Dr. Sibanda with a few questions--I am well aware of my own first-wold slant--and he graciously responded to the cold call. Here's the Q&A:
Spanish Key: In the USA and elsewhere there is a perception that our societies are too clean--this is the "hygiene hypothesis"-- and that infants are not exposed to enough microbes in their early years, so that their immune systems tend toward an allergic response, and we develop eczema and asthma as a result. What is your perspective on the hygiene hypothesis?
Elopy Sibanda: I am familiar with the hygiene hypothesis but I am unsure about the extent to which it applies to our population. In immunological parlance this boils down to a Th1 to Th2 lymphocyte shift. We have seen no evidence of such a shift. The hypothesis is not an adequate explanation for the the increase in allergic diseases. [SK comment: I'd guess in the end we will find that antibiotic overuse is to blame.]
Elopy Sibanda: I am familiar with the hygiene hypothesis but I am unsure about the extent to which it applies to our population. In immunological parlance this boils down to a Th1 to Th2 lymphocyte shift. We have seen no evidence of such a shift. The hypothesis is not an adequate explanation for the the increase in allergic diseases. [SK comment: I'd guess in the end we will find that antibiotic overuse is to blame.]
Spanish Key: There is also a small, but vocal, anti-vaccine movement that claims that the relatively large number of vaccines given to children predisposes them to develop allergic diseases and even autism. As a result quite a few people, some of whom I have met personally, do not vaccinate their children. What is your perspective on this phenomenon?
Elopy Sibanda: There are pockets of religious sects that are against the immunization of children for various reasons. Immunization rates in Zimbabwe are quite high. I have not seen any convincing evidence of immunization influencing allergic trends. The anti-vaccine advocates just have to provide us with the evidence. [SK comment: I would love to see Dr. Sibanda in conversation with a Marin County anti-vaccine advocate.]
Spanish Key: I have read that eczema may be an evolutionary development to protect the body against helminthic worms. What is your opinion?
Elopy Sibanda: My experience is that people with eczema are at no lesser risk of helminthic infections than those without. If it was developed for that purpose it is failing in its role. [SK comment: very interesting. I wonder why eczema has persisted in our DNA despite being so debilitating in some cases, if it does not have some hidden benefit. But then look at all the other hereditary diseases we are passing along to our children--diabetes, Tay-Sachs, Huntington's, multiple sclerosis, etc.]
Spanish Key: What do you think are the most important therapies that African children and adults with eczema lack?
Elopy Sibanda: Before we can address the issue of therapies, the challenge we face is patient education and disease awareness. Once the people understand the disease, they will begin to appreciate the interventions and establish treatment options and priorities. Like everywhere in the world medical interventions aim to stop the itch (anti-histamines), reduce the dryness (mosturisers and ointments) and prevent infection. [SK comment: very similar to the NEA's outlook here in the US. Although antihistamines generally not considered useful for treating itch of chronic eczema, as I have discussed in earlier blog posts.]
I am grateful to Dr Sibanda for replying and I hope to add other voices to this blog to build a truly global perspective on eczema.
Tuesday, November 20, 2012
Filaggrin mutations cause distinct pattern of eczema in children
The giant protein filaggrin has several vital functions in skin. People with mutated copies of the filaggrin gene (FLG) are at risk of developing eczema that begins earlier and is more severe than usual. A new population study by Danish scientists (published in the journal PLoS ONE) now shows that children with FLG mutations develop a distinct variety of eczema, with emphasis on exposed areas such as the cheeks and the backs of the hands.
The research, led by Hans Bisgaard at the University of Copenhagen, could in the future help doctors diagnose children at risk of developing eczema and design personalized treatment for them—including therapy that could change the course of the disease.
The researchers analyzed data from the Copenhagen Study on Asthma in Childhood, which comprised 411 children born to mothers with asthma and followed them over the course of seven years, with checkups every six months (or more often, if eczema flares warranted). The scientists tested DNA from the children, checking to see if they had one of the two most common FLG mutations, known as R501X and 2282del4.
The results were not as cleancut as one might like. Roughly 15% of the 170 children who developed eczema had FLG mutations. But so did 7% of the 212 children who did not develop eczema. So clearly having mutated FLG does not guarantee eczema, and there are other factors at work to compensate for the mutation or cause disease to develop even if you have good filaggrin.
The researchers found that, in general, short- and long-term symptoms of eczema were worse in children with mutated FLG; and the disease set in earlier and flares tended to cluster in certain areas, most importantly the cheeks and backs of the hands.
What is your child’s eczema like? Or what was yours like as a child? Does it fit this pattern? I seem to remember it concentrated on the backs of my knees and the insides of my elbows. But over the years it has moved around a lot. Maybe we will see scientists develop a catalog of eczema subtypes caused by known mutations.
The research, led by Hans Bisgaard at the University of Copenhagen, could in the future help doctors diagnose children at risk of developing eczema and design personalized treatment for them—including therapy that could change the course of the disease.
The researchers analyzed data from the Copenhagen Study on Asthma in Childhood, which comprised 411 children born to mothers with asthma and followed them over the course of seven years, with checkups every six months (or more often, if eczema flares warranted). The scientists tested DNA from the children, checking to see if they had one of the two most common FLG mutations, known as R501X and 2282del4.
The results were not as cleancut as one might like. Roughly 15% of the 170 children who developed eczema had FLG mutations. But so did 7% of the 212 children who did not develop eczema. So clearly having mutated FLG does not guarantee eczema, and there are other factors at work to compensate for the mutation or cause disease to develop even if you have good filaggrin.
The researchers found that, in general, short- and long-term symptoms of eczema were worse in children with mutated FLG; and the disease set in earlier and flares tended to cluster in certain areas, most importantly the cheeks and backs of the hands.
What is your child’s eczema like? Or what was yours like as a child? Does it fit this pattern? I seem to remember it concentrated on the backs of my knees and the insides of my elbows. But over the years it has moved around a lot. Maybe we will see scientists develop a catalog of eczema subtypes caused by known mutations.
Thursday, November 15, 2012
Contact dermatitis, delayed allergies, and eczema
Contact dermatitis is a more important and complex factor than I thought for patients with atopic dermatitis, I learned from reading a presentation given by Dr. Luz Fonacier at the annual meeting of the American College of Allergy, Asthma and Immunology, held this year in Anaheim, CA. (I was not present at the meeting.)
Fonacier is head of the allergy section of the Division of Rheumatology, Allergy & Immunology at Winthrop University Hospital in Mineola, NY. Her talk, titled “Food Allergy and Atopic Dermatitis: Generating a Common Approach with the Dermatologist,” covered many well-known techniques to diagnose food allergy. She also devoted a large section to a controversial test: the atopy patch test.
What stood out for me was the role of contact dermatitis in atopic dermatitis. According to Fonacier, contact dermatitis, a specific type of allergic reaction to substances such as certain metals and fragrances, affects roughly two-thirds of young (infant to teenage) patients with chronic eczema. Rash and inflammation from contact dermatitis can intensify AD and change the long-term course of the disease, presumably for the worse--by exposing you to more allergens and pathogens.
While contact dermatitis often affects the hands, arms, and face, a systemic exposure to an allergen to which a person has a contact allergy can affect skin over the entire body. Metals, fragrances, and other substances that cause contact dermatitis are often present in foods. When a person eats a food containing a substance to which he or she has a contact allergy, it can manifest as a body-wide skin inflammation.
So how is this different from “classic” food allergy?
The differences lie in the timing and pathway of the reaction. “Type I” allergens such as wheat, soy, milk, and the usual culprits provoke a specific type of allergy, initiated by IgE-class antibodies, that appears over 30 minutes to two hours.
“Type IV” allergens—and I am not even sure I am using the correct term for these substances—cause a “delayed-type hypersensitivity” reaction driven by T cells that manifests hours or days later.
Fonacier lists several allergens in food that can cause systemic contact dermatitis: the most common are nickel sulfate and something called “balsam of Peru,” a natural resin that contains a mixture of oils and chemicals and is used in many processed products.
Nickel is overwhelmingly found in soy and a small number of other foods, according to Fonacier’s slides. (That means that you can have a type IV allergy to soy but not necessarily test positive on a skin prick test or IgE assay.) Balsam of Peru, in contrast, is found in a wide variety of foods. Check out slide 15 of the presentation—see spices, citrus, tomatoes? I have no idea how balsam of Peru ends up in citrus peel or tomatoes; maybe it's an agriculture or food industry thing [update: Fonacier says that tomatoes contain chemicals similar to those in balsam of Peru].
Now, how to diagnose contact dermatitis? Patch testing, in which a nurse applies an array of patches containing potential allergens to a patient’s back. About two days later, an allergist looks for inflamed spots, and the corresponding patches indicate which items you should avoid.
Fonacier does explain patch testing in her slides, probably because it’s so obvious to an allergist. Instead, she devotes a large section of the presentation to the “atopy patch test,” or APT, which is a patch test in which the allergens are dairy, wheat, soy, and so on--those commonly assessed for type I allergies by skin prick tests and specific IgE measurements. But an APT tests for type IV hypersensitivity reactions, the delayed ones.
The advantages of the APT are that it apparently can predict type IV allergies to cow’s milk, egg, and wheat pretty well. The disadvantages are that it takes a long time and the person observing the results has to be well-trained. According to one slide, an NIAID expert panel recommends that the APT not be routinely used in the clinic because it is not as reliable as oral food challenges.
So when does Fonacier recommend using the APT? If a patient has a history of severe and persistent AD, and skin prick and IgE tests have been done, and no trigger has been identified—or if there are multiple instances of IgE reactions that have no apparent connection to AD—then it's time to try the APT.
Fonacier is head of the allergy section of the Division of Rheumatology, Allergy & Immunology at Winthrop University Hospital in Mineola, NY. Her talk, titled “Food Allergy and Atopic Dermatitis: Generating a Common Approach with the Dermatologist,” covered many well-known techniques to diagnose food allergy. She also devoted a large section to a controversial test: the atopy patch test.
What stood out for me was the role of contact dermatitis in atopic dermatitis. According to Fonacier, contact dermatitis, a specific type of allergic reaction to substances such as certain metals and fragrances, affects roughly two-thirds of young (infant to teenage) patients with chronic eczema. Rash and inflammation from contact dermatitis can intensify AD and change the long-term course of the disease, presumably for the worse--by exposing you to more allergens and pathogens.
While contact dermatitis often affects the hands, arms, and face, a systemic exposure to an allergen to which a person has a contact allergy can affect skin over the entire body. Metals, fragrances, and other substances that cause contact dermatitis are often present in foods. When a person eats a food containing a substance to which he or she has a contact allergy, it can manifest as a body-wide skin inflammation.
So how is this different from “classic” food allergy?
The differences lie in the timing and pathway of the reaction. “Type I” allergens such as wheat, soy, milk, and the usual culprits provoke a specific type of allergy, initiated by IgE-class antibodies, that appears over 30 minutes to two hours.
“Type IV” allergens—and I am not even sure I am using the correct term for these substances—cause a “delayed-type hypersensitivity” reaction driven by T cells that manifests hours or days later.
 |
| Nickel. You probably don't want to eat this stuff. But it's in your cutlery and tofu. |
Nickel is overwhelmingly found in soy and a small number of other foods, according to Fonacier’s slides. (That means that you can have a type IV allergy to soy but not necessarily test positive on a skin prick test or IgE assay.) Balsam of Peru, in contrast, is found in a wide variety of foods. Check out slide 15 of the presentation—see spices, citrus, tomatoes? I have no idea how balsam of Peru ends up in citrus peel or tomatoes; maybe it's an agriculture or food industry thing [update: Fonacier says that tomatoes contain chemicals similar to those in balsam of Peru].
Now, how to diagnose contact dermatitis? Patch testing, in which a nurse applies an array of patches containing potential allergens to a patient’s back. About two days later, an allergist looks for inflamed spots, and the corresponding patches indicate which items you should avoid.
 |
| Balsam of Peru. Appearing soon in toothpaste near you. (And spices, and citrus, and tomatoes, and fragrances...) |
The advantages of the APT are that it apparently can predict type IV allergies to cow’s milk, egg, and wheat pretty well. The disadvantages are that it takes a long time and the person observing the results has to be well-trained. According to one slide, an NIAID expert panel recommends that the APT not be routinely used in the clinic because it is not as reliable as oral food challenges.
So when does Fonacier recommend using the APT? If a patient has a history of severe and persistent AD, and skin prick and IgE tests have been done, and no trigger has been identified—or if there are multiple instances of IgE reactions that have no apparent connection to AD—then it's time to try the APT.
Friday, November 9, 2012
"Do not scratch your itch. Ever."
When characters like Donald Trump set the standard on Twitter it's hard to get worked up about any single tweet in particular.
Nonetheless, yesterday a tweet in my feed got me riled.
Claudia Aguirre is scientific communications manager at Dermalogica, a skincare/cosmetics company headquartered in California.
The tweet apparently came from an audience member in a talk Aguirre was giving in Antwerp, Belgium. [update: via Twitter, Aguirre implied that I took her words out of context, since she says the talk was not about eczema.]
Aguirre has tweeted the "don't scratch"/eczema message a couple times that I've seen, so my conclusion is that she believes it.
For the record, Aguirre does understand that eczema is a complex problem with many causes and treatments. If you like 17-minute YouTube videos, she's got one for you.
But “don't scratch”? That would be nice. I've spent my whole life trying to pull that off.
With my customary tact, I made my opinion known. Aguirre replied. My man Gary beat me to the punch.
The problem: you can TELL someone not to scratch, but it doesn't work. It’s not that you won’t stop, it’s that you can’t stop. Google "eczema don't scratch" and the results fall into two main categories: pages advising you not to scratch your eczema, and pages from outraged eczema patients and parents saying that this is bullshit. (See this recent discussion on the NEA forum.)
Not only does it not work, telling people to stop scratching makes them feel bad. They already suffer from the itch, sores, and shame of eczema; now you’re telling them they don’t have any self-control. They then believe it’s their fault they look and feel the way they do.
The urge to itch in cases of extreme eczema is so intense that willpower is no defense. Not to mention that willpower is irrelevant while you're asleep, which is when many patients scratch.The intensity of eczema itch is hard to believe. I know, because I and my daughter have eczema, and when she’s itchy and I’m not, I can hardly understand what she’s going through. But when I’m itchy, it’s like a demon has possessed me, like Linda Blair’s character in The Exorcist.
So is it possible to exorcise the demon?
Nonetheless, yesterday a tweet in my feed got me riled.
Claudia Aguirre is scientific communications manager at Dermalogica, a skincare/cosmetics company headquartered in California.
The tweet apparently came from an audience member in a talk Aguirre was giving in Antwerp, Belgium. [update: via Twitter, Aguirre implied that I took her words out of context, since she says the talk was not about eczema.]
Aguirre has tweeted the "don't scratch"/eczema message a couple times that I've seen, so my conclusion is that she believes it.
For the record, Aguirre does understand that eczema is a complex problem with many causes and treatments. If you like 17-minute YouTube videos, she's got one for you.
But “don't scratch”? That would be nice. I've spent my whole life trying to pull that off.
With my customary tact, I made my opinion known. Aguirre replied. My man Gary beat me to the punch.
The problem: you can TELL someone not to scratch, but it doesn't work. It’s not that you won’t stop, it’s that you can’t stop. Google "eczema don't scratch" and the results fall into two main categories: pages advising you not to scratch your eczema, and pages from outraged eczema patients and parents saying that this is bullshit. (See this recent discussion on the NEA forum.)
Not only does it not work, telling people to stop scratching makes them feel bad. They already suffer from the itch, sores, and shame of eczema; now you’re telling them they don’t have any self-control. They then believe it’s their fault they look and feel the way they do.
The urge to itch in cases of extreme eczema is so intense that willpower is no defense. Not to mention that willpower is irrelevant while you're asleep, which is when many patients scratch.The intensity of eczema itch is hard to believe. I know, because I and my daughter have eczema, and when she’s itchy and I’m not, I can hardly understand what she’s going through. But when I’m itchy, it’s like a demon has possessed me, like Linda Blair’s character in The Exorcist.
So is it possible to exorcise the demon?
- Topical steroids give you some control, but not many people would claim they are the answer.
- Yoga and meditation: meh.
- Keeping your hands busy with art or a musical instrument might work as long as you keep doing that activity. Once you stop, the itch starts.
- I am aware of a handful of psychiatric techniques, including habit reversal, made popular by Christopher Bridgett in the UK. I like habit reversal, and believe that it works to reduce habitual, nervous scratching—and thereby calm the itch/scratch cycle and bring overall relief to a degree. But it’s not a solution for everyone. It takes work, and commitment, and for some people, habitual scratching is not the dominant factor in their eczema. (E.g. I get eczema on my face which is caused by pollen. I get outbreaks caused by weather, exercise, food triggers, dust mites, animal dander and stress.)
Thursday, November 1, 2012
Antibody therapy for extreme eczema
I just wrote a short post on the NEA website about the use of omalizumab, an anti-IgE antibody, as an experimental therapy for patients with refractory (hard-to-treat) eczema. Omalizumab is currently approved in the US for treating extreme asthma--it knocks IgE levels down and thereby reduces the immune system's tendency to flare up. It appears to work for around 20% of eczema patients, but the current evidence is pretty slim so I'd wait a few years before calling it a real therapy.
Monday, October 29, 2012
Upcoming eczema information sessions in Montreal, Toronto, and Calgary
Canadians who have eczema or who are parents of affected children can get cutting-edge information about eczema therapies at upcoming sessions in Montreal (Nov. 8), Toronto (Nov. 12), and Calgary (Nov. 22) put on by the Eczema Society of Canada.
At each session a local dermatologist will speak and an expert panel will take questions.
Tristan Joseph at Atopic Girl told me about the events and advised me to talk to Amanda Cresswell-Melville, president of the ESC. Amanda took time from organizing the sessions to answer my questions by e-mail.
SK: Is this the first time you've had this kind of event?
AC-M: We host these free education sessions each November for our Awareness Month. It is a great opportunity for eczema sufferers to hear from an expert dermatologist in the area of eczema, as well as hear from patients. Perhaps the most dynamic portion of the events is when the expert panel takes questions from the audience.
What are they modeled on?
These are common in the Canadian health care community, and conditions from Parkinson’s disease to Anaphylaxis host similar events throughout the year to reach out to patients. These types of events are a great opportunity to bring people together. With all of the great exchanges in a virtual setting today, such as through Facebook, Twitter, and email, we still get overwhelming responses from people who want to come to live events, and have a chance to ask questions face to face. I think we will do them as long as people want to attend them!
Who will the dermatologists be, and do you have an idea what they'll talk about?
We have a different dermatologist in each city, as we like to use a local dermatologist. The focus lately has been barrier function related to eczema, and how medical management, coupled with self care strategies, can help to control the condition. Eczema was often thought of as an “inside out” condition, and now we are focused on an “outside in” approach – maintaining and repairing the skin barrier, for less flare ups.
Who will be on the panels? What questions do you envision the audience will ask?
The expert panel is different in every city; however, it consists of the dermatologist speaker, the patient speakers, and typically a dermatology nurse who has expertise in the skin care counselling area of eczema management.
The Q&A session is perhaps the most anticipated portion, as some of the questions that seem to fly out of your mind when you are sitting in front of your own dermatologist can be addressed. I was surprised at one event when most of the questions came to a very dynamic young woman who spoke about her battle with eczema. Everyone wanted advice from her!
The questions usually centre on the common concerns: safety of medication, bathing and moisturizing questions, and the relationship between eczema, allergies, and asthma. Of course, if questions get too specific to the individual, they are advised to seek that advice from their own dermatologist or health care provider. Our intention is never to diagnose or create a treatment plan for individuals.
Who do you want to show up? What is/do you expect to be the ratio, among attendees, of parents of children with eczema to adults who have eczema?
While every year, and every city is different, there is usually a balance between parents of pediatric patients and adult patients of all ages. There is a great inclusive environment created, as the adult patients can relate to, and remember the struggles of the parents, as they have been there themselves, and the parents of little ones with eczema often express feeling of hope seeing the adult patients, because they know their children will be able to get through it.
Eczema is not a condition that one wants to advertise--and I myself feel weird about socializing with others when I have a flareup. And it would feel doubly weird to hang out with others in the same situation. What is the best way to reach adults such as myself?
We are very sensitive to maintaining dignity and privacy surrounding these events. We don’t allow any photography or video taping of the events, and we ensure that our language is always respectful. Most of our volunteers, and I, live with eczema on a daily basis, so these events try to respect what that experience is.
We also offer an online and telephone support component for those individuals who either don’t feel comfortable attending an event, or who cannot attend, for geographic or other reasons.
The main goal of these events it to provide information about the condition and its management, and to provide hope. Eczema can be as emotionally draining as it is physically, and we are just trying to support those living in through it, and show stories of people and families who have lived it, are living it, and are getting through it.
At each session a local dermatologist will speak and an expert panel will take questions.
Tristan Joseph at Atopic Girl told me about the events and advised me to talk to Amanda Cresswell-Melville, president of the ESC. Amanda took time from organizing the sessions to answer my questions by e-mail.
SK: Is this the first time you've had this kind of event?
AC-M: We host these free education sessions each November for our Awareness Month. It is a great opportunity for eczema sufferers to hear from an expert dermatologist in the area of eczema, as well as hear from patients. Perhaps the most dynamic portion of the events is when the expert panel takes questions from the audience.
What are they modeled on?
These are common in the Canadian health care community, and conditions from Parkinson’s disease to Anaphylaxis host similar events throughout the year to reach out to patients. These types of events are a great opportunity to bring people together. With all of the great exchanges in a virtual setting today, such as through Facebook, Twitter, and email, we still get overwhelming responses from people who want to come to live events, and have a chance to ask questions face to face. I think we will do them as long as people want to attend them!
Who will the dermatologists be, and do you have an idea what they'll talk about?
We have a different dermatologist in each city, as we like to use a local dermatologist. The focus lately has been barrier function related to eczema, and how medical management, coupled with self care strategies, can help to control the condition. Eczema was often thought of as an “inside out” condition, and now we are focused on an “outside in” approach – maintaining and repairing the skin barrier, for less flare ups.
Who will be on the panels? What questions do you envision the audience will ask?
The expert panel is different in every city; however, it consists of the dermatologist speaker, the patient speakers, and typically a dermatology nurse who has expertise in the skin care counselling area of eczema management.
The Q&A session is perhaps the most anticipated portion, as some of the questions that seem to fly out of your mind when you are sitting in front of your own dermatologist can be addressed. I was surprised at one event when most of the questions came to a very dynamic young woman who spoke about her battle with eczema. Everyone wanted advice from her!
The questions usually centre on the common concerns: safety of medication, bathing and moisturizing questions, and the relationship between eczema, allergies, and asthma. Of course, if questions get too specific to the individual, they are advised to seek that advice from their own dermatologist or health care provider. Our intention is never to diagnose or create a treatment plan for individuals.
Who do you want to show up? What is/do you expect to be the ratio, among attendees, of parents of children with eczema to adults who have eczema?
While every year, and every city is different, there is usually a balance between parents of pediatric patients and adult patients of all ages. There is a great inclusive environment created, as the adult patients can relate to, and remember the struggles of the parents, as they have been there themselves, and the parents of little ones with eczema often express feeling of hope seeing the adult patients, because they know their children will be able to get through it.
Eczema is not a condition that one wants to advertise--and I myself feel weird about socializing with others when I have a flareup. And it would feel doubly weird to hang out with others in the same situation. What is the best way to reach adults such as myself?
We are very sensitive to maintaining dignity and privacy surrounding these events. We don’t allow any photography or video taping of the events, and we ensure that our language is always respectful. Most of our volunteers, and I, live with eczema on a daily basis, so these events try to respect what that experience is.
We also offer an online and telephone support component for those individuals who either don’t feel comfortable attending an event, or who cannot attend, for geographic or other reasons.
The main goal of these events it to provide information about the condition and its management, and to provide hope. Eczema can be as emotionally draining as it is physically, and we are just trying to support those living in through it, and show stories of people and families who have lived it, are living it, and are getting through it.
Wednesday, October 24, 2012
Kimchi on trial as eczema therapy. Not convinced
Those of you who are fans of probiotics, especially kimchi, will be thrilled to know that scientists recently reported the results of a trial testing kimchi-extracted bacteria as a treatment for eczema.
The researchers, led by Jihyun Kim at Sungkyunkwan University School of Medicine in Seoul, conducted a randomized, double-blind, placebo-controlled test of a strain of Lactobacillus plantarum in 118 eczema patients. L. plantarum is apparently a major species of bacteria found in Korean pickled cabbage, or kimchi, and a previous study showed that it had promise in a mouse model of eczema.
The idea behind probiotics is the hygiene hypothesis: in short, that being dirty is good for you (I'm pretty sure that most research shows that, if this is true, it holds only for kids during the first few years when their immune systems are developing). Proper balance of gut flora might tilt your immune system more toward a type 1 helper T cell-run operation rather than one dominated by type 2 Th cells, which are possibly over-represented in eczema patients. So: eat friendly bugs and reduce your chances of developing allergic disease.
The scientists split their subjects into a test group and a control group. From what I can tell they did as good a job as anyone could to make sure the results were not biased by expectation.
However, while they present their data openly in the paper, they claim it shows that L. plantarum clearly reduced symptoms of eczema, as measured by self-assessed quality of life as well as lab-quantified levels of immune cells and signaling molecules.
When I look at their data it says no such thing. In fact, it says that within experimental bounds, L. plantarum does nothing at all. I am surprised the journal editors allowed them to make those claims--but as always, maybe I'm missing something.
The trial was published in the journal Pediatric Allergy and Immunology, and paid for by the CJ Cheiljedang Corporation, which manufactures probiotic capsules of L. plantarum.
Thanks to reader K.M.O. for the tip.
The researchers, led by Jihyun Kim at Sungkyunkwan University School of Medicine in Seoul, conducted a randomized, double-blind, placebo-controlled test of a strain of Lactobacillus plantarum in 118 eczema patients. L. plantarum is apparently a major species of bacteria found in Korean pickled cabbage, or kimchi, and a previous study showed that it had promise in a mouse model of eczema.
The idea behind probiotics is the hygiene hypothesis: in short, that being dirty is good for you (I'm pretty sure that most research shows that, if this is true, it holds only for kids during the first few years when their immune systems are developing). Proper balance of gut flora might tilt your immune system more toward a type 1 helper T cell-run operation rather than one dominated by type 2 Th cells, which are possibly over-represented in eczema patients. So: eat friendly bugs and reduce your chances of developing allergic disease.
The scientists split their subjects into a test group and a control group. From what I can tell they did as good a job as anyone could to make sure the results were not biased by expectation.
However, while they present their data openly in the paper, they claim it shows that L. plantarum clearly reduced symptoms of eczema, as measured by self-assessed quality of life as well as lab-quantified levels of immune cells and signaling molecules.
When I look at their data it says no such thing. In fact, it says that within experimental bounds, L. plantarum does nothing at all. I am surprised the journal editors allowed them to make those claims--but as always, maybe I'm missing something.
The trial was published in the journal Pediatric Allergy and Immunology, and paid for by the CJ Cheiljedang Corporation, which manufactures probiotic capsules of L. plantarum.
Thanks to reader K.M.O. for the tip.
Monday, October 22, 2012
Product review: CLn Bodywash, the "bleach bath in a can"
A PR firm retained by TopMD Skin Care, a Dallas-based startup company, approached me about reviewing the company's first product: CLn Bodywash, which has been described as a bleach bath in a can.
CLn Bodywash, the company says, was designed to treat bacterial infections of the skin, such as acne and the staph infections that often accompany eczema. The product comes in a small can like shaving cream--when you squeeze it out, it's a gel that you're supposed to rub into a lather and apply in the shower. It contains sodium hypochlorite (bleach) plus some unspecified surfactants, which essentially means detergent.
The idea of bleach baths makes sense to me. That's why I took them up on their offer.
They sent me two bottles in the mail. I like getting free stuff, so this was cool. The thing is, when you get something designed to treat a staph infection, you have to sit around and wait until you get one.
But I have eczema, so that didn't take long. This was the first time in my life I welcomed an outbreak of folliculitis. (Sorry, TopMD, I know you wanted me to test this on my three-year-old daughter, but that ain't gonna happen!)
CLn Bodywash foams up to a less-exciting degree than shaving foam. For me, it was a little bit stringy, like mucus, at first. But you can get it to lather. Then you leave the lather on for 1-2 minutes and rinse.
I used it on some mild folliculitis which appeared first on my left leg. Then, a couple days later, I got it on my right leg too. My first instinct was to use my right leg as an untreated control of sorts. But I hate folliculitis and want it to go away, so I used CLn on both legs.
And my folliculitis went away within a few days. It has not yet returned.
Was this because of CLn? Maybe. In the past, my folliculitis has always gone away. What goes up usually comes down.
On the plus side: CLn didn't make things worse; it didn't dry my skin out unduly; and it didn't smell all perfumy, as so many skin products do.
The obvious place to look for "proof" of whether CLn works is a clinical trial. TopMD claims that CLn has been subject to "extensive clinical testing." I found no evidence of this on the web, and asked the PR firm to send me the link. They kindly sent me a poster that had been presented earlier this year at a conference. The poster describes how the authors tested CLn on 11 subjects (all kids--this is clearly meant for kids) and appears to show that their skin infections largely cleared up.
The thing is--unless I am reading this wrong--the authors were about as scientific as I was. There is no control group, which is one of the most basic requirements for a clinical trial. There is nothing to compare the results to.
The PR rep tells me that there is another clinical trial of CLn just getting started in Houston. [updated 10/30/12]
Until the results of this presumably larger and more rigorous trial come out, I hesitate to recommend CLn Bodywash. I like the idea behind it, but I am not convinced it is any better than a decent soap.
CLn Bodywash, the company says, was designed to treat bacterial infections of the skin, such as acne and the staph infections that often accompany eczema. The product comes in a small can like shaving cream--when you squeeze it out, it's a gel that you're supposed to rub into a lather and apply in the shower. It contains sodium hypochlorite (bleach) plus some unspecified surfactants, which essentially means detergent.
The idea of bleach baths makes sense to me. That's why I took them up on their offer.
They sent me two bottles in the mail. I like getting free stuff, so this was cool. The thing is, when you get something designed to treat a staph infection, you have to sit around and wait until you get one.
But I have eczema, so that didn't take long. This was the first time in my life I welcomed an outbreak of folliculitis. (Sorry, TopMD, I know you wanted me to test this on my three-year-old daughter, but that ain't gonna happen!)
CLn Bodywash foams up to a less-exciting degree than shaving foam. For me, it was a little bit stringy, like mucus, at first. But you can get it to lather. Then you leave the lather on for 1-2 minutes and rinse.
I used it on some mild folliculitis which appeared first on my left leg. Then, a couple days later, I got it on my right leg too. My first instinct was to use my right leg as an untreated control of sorts. But I hate folliculitis and want it to go away, so I used CLn on both legs.
And my folliculitis went away within a few days. It has not yet returned.
Was this because of CLn? Maybe. In the past, my folliculitis has always gone away. What goes up usually comes down.
On the plus side: CLn didn't make things worse; it didn't dry my skin out unduly; and it didn't smell all perfumy, as so many skin products do.
The obvious place to look for "proof" of whether CLn works is a clinical trial. TopMD claims that CLn has been subject to "extensive clinical testing." I found no evidence of this on the web, and asked the PR firm to send me the link. They kindly sent me a poster that had been presented earlier this year at a conference. The poster describes how the authors tested CLn on 11 subjects (all kids--this is clearly meant for kids) and appears to show that their skin infections largely cleared up.
The thing is--unless I am reading this wrong--the authors were about as scientific as I was. There is no control group, which is one of the most basic requirements for a clinical trial. There is nothing to compare the results to.
The PR rep tells me that there is another clinical trial of CLn just getting started in Houston. [updated 10/30/12]
Until the results of this presumably larger and more rigorous trial come out, I hesitate to recommend CLn Bodywash. I like the idea behind it, but I am not convinced it is any better than a decent soap.
Wednesday, October 17, 2012
Scientists find a molecule that recruits white blood cells to site of allergic itch
A type of white blood cells called neutrophils combines with helper T cells to create inflammation due to skin contact with allergen, a group of scientists led by Raif Geha at Harvard Medical School has shown in a mouse model of eczema.
The researchers showed that by blocking the neutrophils' ability to produce a signaling molecule called leukotriene B4 (LTB4), they could prevent the accumulation of both neutrophils and T cells, and hence inflammation, in skin that had been mildly irritated and exposed to a model antigen.
The research was published in the journal Immunity. [paper] [media summary]
The scientists were investigating the role of neutrophils, which are attracted to the site of scratching. They suggest that blocking LTB4's interaction with its receptor (not necessarily by the drug they used, bestatin) could prevent sudden eczema flares in patients that were exposed to something they were allergic to.
The research doesn't sound immediately useful to me, as the real problem with eczema--or atopic dermatitis--is that in general we don't know the cause, and flares aren't usually triggered by direct exposure to something you're allergic to. But it is interesting to learn that neutrophils are flooding scratched skin, and that they are recruiting other neutrophils and T cells--I would like to see whether a drug reducing this phenomenon might calm down itch. As always, the details are in the drug discovery process: finding something that works, isn't toxic and doesn't have weird side effects.
The researchers showed that by blocking the neutrophils' ability to produce a signaling molecule called leukotriene B4 (LTB4), they could prevent the accumulation of both neutrophils and T cells, and hence inflammation, in skin that had been mildly irritated and exposed to a model antigen.
The research was published in the journal Immunity. [paper] [media summary]
The scientists were investigating the role of neutrophils, which are attracted to the site of scratching. They suggest that blocking LTB4's interaction with its receptor (not necessarily by the drug they used, bestatin) could prevent sudden eczema flares in patients that were exposed to something they were allergic to.
The research doesn't sound immediately useful to me, as the real problem with eczema--or atopic dermatitis--is that in general we don't know the cause, and flares aren't usually triggered by direct exposure to something you're allergic to. But it is interesting to learn that neutrophils are flooding scratched skin, and that they are recruiting other neutrophils and T cells--I would like to see whether a drug reducing this phenomenon might calm down itch. As always, the details are in the drug discovery process: finding something that works, isn't toxic and doesn't have weird side effects.
Thursday, October 11, 2012
Sperm for sale cheap. Only one small problem
Last night I was watching the first episode of the TV series "Parenthood" on Netflix. There's a scene where one of the male characters gets out of bed, where he's just had sex with his girlfriend, and opens the fridge to find a vial of frozen sperm--not his--from a sperm bank. "It's very high-quality," she says (or something like that). "It's from an Olympic athlete who was also a Rhodes Scholar."
Why this successful stallion was selling his baby batter for $50 a pop (I admit ignorance of the going rate) is not discussed, but the scene did make me think.
The prurient aspects of sperm donation disappear into the background when a single woman decides to have a baby. She's concerned only with quality. And from my experience with mothers, they want nothing but the best for their babies, whether it's a stroller, a crib, a nanny...or their DNA.
But what is quality? And, relevant to this blog, if I hypothetically donated to a sperm bank, would any woman want to buy it?
Here are the selling points: I'm a decent-looking guy, in shape, highly educated. No major health problems run in my family.
Or do they? Does eczema count as a major health problem? I think it probably would, for a prospective mother shopping for sperm. There's almost no cash discount that would make any of the yuppie moms I know choose my vial if they knew I was likely to pass on the genes for eczema.
Evidently my wife made the calculation at some level. She wasn't buying it like shoes on Zappos though. Things would have gone differently.
I bet sperm shopping is like a high school dance, but worse. Everyone wants a hot partner, but the reality is that there are only so many to go around. Nevertheless most people find someone to go to the dance with. That's not the case with sperm; the "best" vials are probably in high demand, while the others sit on the shelf. Dog and horse breeders know that you get fine animals only if you start with the best material.
I don't know what point I want to make, only that I would surely correct the errors in my own DNA if I could and if it would do any good; and that this thought experiment makes it clear that all human lives are valuable--especially to the people like me who are living them. Chance and environment play major roles in how a human being turns out.
By saying this, I do not mean that I am in the "pro-life" camp when it comes to abortion or euthanasia, but just that the vast majority of people have something unique and worthwhile to offer, and that in the big picture, eczema doesn't make that much of a difference.
Why this successful stallion was selling his baby batter for $50 a pop (I admit ignorance of the going rate) is not discussed, but the scene did make me think.
The prurient aspects of sperm donation disappear into the background when a single woman decides to have a baby. She's concerned only with quality. And from my experience with mothers, they want nothing but the best for their babies, whether it's a stroller, a crib, a nanny...or their DNA.
But what is quality? And, relevant to this blog, if I hypothetically donated to a sperm bank, would any woman want to buy it?
Here are the selling points: I'm a decent-looking guy, in shape, highly educated. No major health problems run in my family.
Or do they? Does eczema count as a major health problem? I think it probably would, for a prospective mother shopping for sperm. There's almost no cash discount that would make any of the yuppie moms I know choose my vial if they knew I was likely to pass on the genes for eczema.
Evidently my wife made the calculation at some level. She wasn't buying it like shoes on Zappos though. Things would have gone differently.
I bet sperm shopping is like a high school dance, but worse. Everyone wants a hot partner, but the reality is that there are only so many to go around. Nevertheless most people find someone to go to the dance with. That's not the case with sperm; the "best" vials are probably in high demand, while the others sit on the shelf. Dog and horse breeders know that you get fine animals only if you start with the best material.
I don't know what point I want to make, only that I would surely correct the errors in my own DNA if I could and if it would do any good; and that this thought experiment makes it clear that all human lives are valuable--especially to the people like me who are living them. Chance and environment play major roles in how a human being turns out.
By saying this, I do not mean that I am in the "pro-life" camp when it comes to abortion or euthanasia, but just that the vast majority of people have something unique and worthwhile to offer, and that in the big picture, eczema doesn't make that much of a difference.
Tuesday, October 9, 2012
Eight new genetic targets for eczema treatment
A group of scientists has found eight new genetic locations linked to eczema in the Japanese population.
Eczema is a disease on which genetics has a strong influence. New data of this type could highlight previously unknown genetic causes for which it might be possible to develop treatments.
The scientists, led by Mayumi Tamari at RIKEN in Yokohama, conducted a genome-wide association study, or GWAS, on a group of about 1500 eczema patients and 8000 controls, and validated their results on a similar group. They published their results in the journal Nature Genetics.
DNA is built of two strands, each of which is a string of molecular fragments called "bases"--A, C, G, and T--paired with its complementary base (the two complementary pairs are A/T and C/G) In a GWAS, researchers select a number of bases (in this study, 600,000) that are known to vary in the human population, and identify which locations, if any, contain bases that are more common in people with a certain trait (in this case, eczema).
The Japanese scientists conducted their study to identify new locations in addition to seven other candidates, including filaggrin, that had previously been found in Caucasian and Chinese patients. The eight new locations were found in or near genes important in skin barrier function; adaptive immunity (white blood cells and antibodies); the inflammatory response; and vitamin D processing.
My own take on this is that GWAS studies in eczema patients continue to highlight the mysterious nature of the disease and how far we are from anything approaching a cure. If there are 15 known, quite different, genetic locations associated with eczema, exactly which ones should scientists focus on to try to develop treatments? The disease is remarkably complex and the best hope for new treatments would seem to be an unanticipated discovery of a new or repurposed drug.
Eczema is a disease on which genetics has a strong influence. New data of this type could highlight previously unknown genetic causes for which it might be possible to develop treatments.
The scientists, led by Mayumi Tamari at RIKEN in Yokohama, conducted a genome-wide association study, or GWAS, on a group of about 1500 eczema patients and 8000 controls, and validated their results on a similar group. They published their results in the journal Nature Genetics.
DNA is built of two strands, each of which is a string of molecular fragments called "bases"--A, C, G, and T--paired with its complementary base (the two complementary pairs are A/T and C/G) In a GWAS, researchers select a number of bases (in this study, 600,000) that are known to vary in the human population, and identify which locations, if any, contain bases that are more common in people with a certain trait (in this case, eczema).
The Japanese scientists conducted their study to identify new locations in addition to seven other candidates, including filaggrin, that had previously been found in Caucasian and Chinese patients. The eight new locations were found in or near genes important in skin barrier function; adaptive immunity (white blood cells and antibodies); the inflammatory response; and vitamin D processing.
My own take on this is that GWAS studies in eczema patients continue to highlight the mysterious nature of the disease and how far we are from anything approaching a cure. If there are 15 known, quite different, genetic locations associated with eczema, exactly which ones should scientists focus on to try to develop treatments? The disease is remarkably complex and the best hope for new treatments would seem to be an unanticipated discovery of a new or repurposed drug.
Friday, October 5, 2012
Vitamin D receptor mutation found in severe eczema cases
A set of mutations in the gene for the vitamin D receptor are more common in patients with severe eczema than they are in controls or patients with moderate eczema, a group of German researchers has found.
In a paper in press at the British Journal of Dermatology, the scientists explain that this set of mutations, or "haplotype," likely does not cause eczema but combines with other factors to make the disease more severe.
Vitamin D is widely touted on the internet as a miracle cure for many conditions including eczema. Clinical data on links between eczema and vitamin D is spotty. However, it's known that vitamin D plays an important role in inflammation--and eczema is nothing if not an inflammatory disease.
The mutations of interest occur not in the coding region of the gene, but in an upstream regulatory region, which means that the structure of the vitamin D receptor is not changed, but the amount of the receptor that the body produces is probably reduced. That would indicate to me that consuming excessive vitamin D could be of little help in treating severe eczema, since the body would simply not have the receptors present to react to the supplements
The scientists, led by Margitta Worm at Charité - Universitätsmedizin Berlin, sampled DNA from two groups of adults: a control group of 259, and a group of 265 eczema patients, 142 of whom were classified as severe cases. The scientists found that the odds of the severe group having any one of three particular mutations was about 50% higher than for the control group.
In a paper in press at the British Journal of Dermatology, the scientists explain that this set of mutations, or "haplotype," likely does not cause eczema but combines with other factors to make the disease more severe.
Vitamin D is widely touted on the internet as a miracle cure for many conditions including eczema. Clinical data on links between eczema and vitamin D is spotty. However, it's known that vitamin D plays an important role in inflammation--and eczema is nothing if not an inflammatory disease.
The mutations of interest occur not in the coding region of the gene, but in an upstream regulatory region, which means that the structure of the vitamin D receptor is not changed, but the amount of the receptor that the body produces is probably reduced. That would indicate to me that consuming excessive vitamin D could be of little help in treating severe eczema, since the body would simply not have the receptors present to react to the supplements
The scientists, led by Margitta Worm at Charité - Universitätsmedizin Berlin, sampled DNA from two groups of adults: a control group of 259, and a group of 265 eczema patients, 142 of whom were classified as severe cases. The scientists found that the odds of the severe group having any one of three particular mutations was about 50% higher than for the control group.
Wednesday, October 3, 2012
Three years of immunotherapy enough for dust mite allergy
Dust mite allergies are a common trigger of eczema flares for many. Dust mites--tiny relatives of spiders--thrive in bedding because they eat flakes of skin. And with the amount of skin that flakes off when you have eczema, it's a catch-22 problem.
From what I can find out, dust mite feces is the major source of their allergens. Eww!
One solution is to get allergy shots: regular injections of allergens at low doses that cause your immune system to develop a tolerance over time. I don't know what the regimen is--how many shots, and when you have to get them--but it is undoubtedly a hassle. Certainly it goes on for years. Doctors have debated how many years, some saying that five were required. A new study concludes that three years is enough. (Not a regime you're going to start on a whim.)
I asked the study's author, Iwona Stelmach, a professor at the Medical University of Lodz in Poland, for a copy of the paper, but haven't got one yet, so all I know is what I've read in the press release and the paper's abstract. It seems that the researchers worked with a three-part study group, totaling 90 asthmatic children, 30 each of whom had either had no immunotherapy, three years of immunotherapy, or five. While immediately after therapy, the five-year group needed less steroid to control a reaction to dust mite allergen, by the time three years had passed, the three- and five-year groups were essentially the same.
If you've got a severe dust mite allergy (and congratulations on figuring that out), it must be a relief to know you only need three years of allergy shots instead of five.
From what I can find out, dust mite feces is the major source of their allergens. Eww!
One solution is to get allergy shots: regular injections of allergens at low doses that cause your immune system to develop a tolerance over time. I don't know what the regimen is--how many shots, and when you have to get them--but it is undoubtedly a hassle. Certainly it goes on for years. Doctors have debated how many years, some saying that five were required. A new study concludes that three years is enough. (Not a regime you're going to start on a whim.)
I asked the study's author, Iwona Stelmach, a professor at the Medical University of Lodz in Poland, for a copy of the paper, but haven't got one yet, so all I know is what I've read in the press release and the paper's abstract. It seems that the researchers worked with a three-part study group, totaling 90 asthmatic children, 30 each of whom had either had no immunotherapy, three years of immunotherapy, or five. While immediately after therapy, the five-year group needed less steroid to control a reaction to dust mite allergen, by the time three years had passed, the three- and five-year groups were essentially the same.
If you've got a severe dust mite allergy (and congratulations on figuring that out), it must be a relief to know you only need three years of allergy shots instead of five.
Friday, September 28, 2012
Small study suggests anti-itch "hydrogel" effective
A small study of an anti-itch "hydrogel" conducted in North Carolina showed promising results, according to a report in the dermatology journal Cutis.
The hydrogel would be an alternative to topical steroids.
I couldn't find any information online about the active ingredient in the hydrogel, "Atapro" or R047-26 in the NIH database. Atapro is a product of Oculus Innovative Sciences, Inc. It would seem to make sense for a company to keep the active ingredient confidential in the early stages--maybe they will need to modify its chemical structure and they don't want their competitors to know what they're working with. But on the other hand, I was easily able to find out the structure of some of Anacor's compounds which are in phase 2 trials.
More than anything, this report reveals how little I know about clinical trials. The study only included 17 subjects, and I'd expect half of them to be controls, so only 8 people were using the product. About seven of the subjects experienced a decrease in itchiness over the trial period. The study would seem to be on the small end of "phase 1," in which the main point is to screen for safety. But there was no explicit mention of what phase the trial might be.
The study details are behind a paywall so I can't find out whether the author had any conflicts of interest. All in all, rather mysterious!
The hydrogel would be an alternative to topical steroids.
I couldn't find any information online about the active ingredient in the hydrogel, "Atapro" or R047-26 in the NIH database. Atapro is a product of Oculus Innovative Sciences, Inc. It would seem to make sense for a company to keep the active ingredient confidential in the early stages--maybe they will need to modify its chemical structure and they don't want their competitors to know what they're working with. But on the other hand, I was easily able to find out the structure of some of Anacor's compounds which are in phase 2 trials.
More than anything, this report reveals how little I know about clinical trials. The study only included 17 subjects, and I'd expect half of them to be controls, so only 8 people were using the product. About seven of the subjects experienced a decrease in itchiness over the trial period. The study would seem to be on the small end of "phase 1," in which the main point is to screen for safety. But there was no explicit mention of what phase the trial might be.
The study details are behind a paywall so I can't find out whether the author had any conflicts of interest. All in all, rather mysterious!
Tuesday, September 25, 2012
Stress makes asthma, hay fever, eczema more likely
Higher stress levels make it more likely that an adult will develop asthma and hay fever, and are correlated with the presence of eczema, Danish scientists reported recently in the journal Allergy.
Stress has been shown to make the body's airways more sensitive to allergens, and intensify asthma symptoms. Similarly, it is generally known that stress can cause eczema flares--but the authors of this study wanted to show statistically that there was a link between stress and onset of atopic diseases in adults.
They drew on data from the Copenhagen City Heart Study, following 5648 adults in two assessments in 1981-83 and 1991-93 to see whether their self-reported stress levels at the first timepoint were correlated with the subjects developing asthma or hay fever in the interim.
Unfortunately the study's planners had neglected to have the subjects self-report eczema in 1981-83, so they just had information on eczema from 1991-93.
They found that subjects with "high," as compared to "low," self-reported stress had roughly doubled odds of developing asthma or hay fever.
Subjects with high stress had odds 75% higher of reporting eczema--although the authors do not mention that perhaps if you have eczema you are likely to feel more stressed.
However, the "atopic triad" of asthma, hay fever, and eczema tend to occur together in many people, so these findings are intriguing, and suggest that if you can reduce your stress by any means, you could also decrease your eczema symptoms--or never get it in the first place, if you are an adult who has risk factors such as relatives with eczema. I certainly know that if I am less stressed, my skin tends to be clear.
Stress has been shown to make the body's airways more sensitive to allergens, and intensify asthma symptoms. Similarly, it is generally known that stress can cause eczema flares--but the authors of this study wanted to show statistically that there was a link between stress and onset of atopic diseases in adults.
They drew on data from the Copenhagen City Heart Study, following 5648 adults in two assessments in 1981-83 and 1991-93 to see whether their self-reported stress levels at the first timepoint were correlated with the subjects developing asthma or hay fever in the interim.
Unfortunately the study's planners had neglected to have the subjects self-report eczema in 1981-83, so they just had information on eczema from 1991-93.
They found that subjects with "high," as compared to "low," self-reported stress had roughly doubled odds of developing asthma or hay fever.
Subjects with high stress had odds 75% higher of reporting eczema--although the authors do not mention that perhaps if you have eczema you are likely to feel more stressed.
However, the "atopic triad" of asthma, hay fever, and eczema tend to occur together in many people, so these findings are intriguing, and suggest that if you can reduce your stress by any means, you could also decrease your eczema symptoms--or never get it in the first place, if you are an adult who has risk factors such as relatives with eczema. I certainly know that if I am less stressed, my skin tends to be clear.
Friday, September 21, 2012
Hot pepper: the devil incarnate
After I eat food containing hot pepper, sweat beads my brow. Then, for a period lasting 30 minutes to a few hours later, I feel intensely itchy. I find cayenne is the worst--if I accidentally eat some during the day, I wake up scratching at night. But why?
In a recent post on the National Eczema Association website I explored allergy testing for eczema. Although onset is rapid, I wouldn't classify my reaction to hot pepper as an allergy. My symptoms are typical, except for the itchiness. And there is a well-known molecular explanation for how hot pepper gives you a burning, painful sensation, especially when you get some on your skin.
The active ingredient in pepper is a molecule called capsaicin. According to Wikipedia,
But there's no explicit documentation of this in the scientific literature. When I searched for research connecting capsaicin and eczema on PubMed, the NIH archive, I found virtually nothing.
Instead, I was intrigued to discover on Wikipedia, PubMed, and the internet in general that capsaicin, far from being fingered as an evil trigger of eczema, is often touted as a TREATMENT for eczema. There are capsaicin-containing creams that you are supposed to rub on your skin to relieve itch. The theory, I guess, is that the burning pain overwhelms the itch neurons. I get that.
Unfortunately you're not supposed to rub capsaicin on open wounds. And with eczema, your skin always has open wounds. Even worse, the one clinical study I found showed that capsaicin cream relieved itch only for people who did not suffer from atopic dermatitis. Capsaicin appears to control itch that is caused by histamine; but chronic eczema itch is not caused by histamine, and so topical capsaicin does nothing for it.
In short, if you have eczema, hot pepper is not your friend, in any form. I love my hot sauce, but I can only look on it as a vice, not a virtue.
In a recent post on the National Eczema Association website I explored allergy testing for eczema. Although onset is rapid, I wouldn't classify my reaction to hot pepper as an allergy. My symptoms are typical, except for the itchiness. And there is a well-known molecular explanation for how hot pepper gives you a burning, painful sensation, especially when you get some on your skin.
The active ingredient in pepper is a molecule called capsaicin. According to Wikipedia,
The burning and painful sensations associated with capsaicin result from its chemical interaction with sensory neurons. Capsaicin, as a member of the vanilloid family, binds to a receptor called the vanilloid receptor subtype 1 (VR1)... By binding to the VR1 receptor, the capsaicin molecule produces the same sensation that excessive heat or abrasive damage would cause, explaining why the spiciness of capsaicin is described as a burning sensation.I'd assume that when you eat hot pepper, you don't break down capsaicin; instead, most of it gets distributed all over your body, where it makes you feel hot, and triggers symptoms of inflammation. Great! The pepper-induced inflammation is likely generating signals in neurons that carry itch sensation to the brain.
...Essentially, the body inflames tissues as if it has undergone a burn or abrasion and the resulting inflammation can cause tissue damage in cases of extreme exposure, as is the case for many substances that cause the body to trigger an inflammatory response.
But there's no explicit documentation of this in the scientific literature. When I searched for research connecting capsaicin and eczema on PubMed, the NIH archive, I found virtually nothing.
Instead, I was intrigued to discover on Wikipedia, PubMed, and the internet in general that capsaicin, far from being fingered as an evil trigger of eczema, is often touted as a TREATMENT for eczema. There are capsaicin-containing creams that you are supposed to rub on your skin to relieve itch. The theory, I guess, is that the burning pain overwhelms the itch neurons. I get that.
Unfortunately you're not supposed to rub capsaicin on open wounds. And with eczema, your skin always has open wounds. Even worse, the one clinical study I found showed that capsaicin cream relieved itch only for people who did not suffer from atopic dermatitis. Capsaicin appears to control itch that is caused by histamine; but chronic eczema itch is not caused by histamine, and so topical capsaicin does nothing for it.
In short, if you have eczema, hot pepper is not your friend, in any form. I love my hot sauce, but I can only look on it as a vice, not a virtue.
Monday, September 17, 2012
Go swimming. You can do it
I find that, even though I have eczema, I can go swimming regularly. Swimming is good for my back problems. But I can’t be as casual about it as I could if I didn’t have eczema.
First, I have to consider whether my skin is in good enough shape. Eczema, of course, can leave your skin open in many places. Perhaps you’ve seen those signs that say that people who have open sores are not allowed in the pool. Why not? Really, the main reason is that nobody else in the pool wants to get infected by a blood-borne disease such as hepatitis or AIDS. You can’t blame them—neither do I. And even though I am pretty sure I don’t have any such disease, I am not absolutely sure. But I am sure enough that it doesn’t bother me morally to get in the pool.
However, am I sure that nobody else who has swum in that pool over the last month, say, has hepatitis or AIDS? That is a sobering thought, especially in San Francisco, where AIDS first broke the news in the 1980s. It is to kill the microbes that cause such diseases that public pools are chlorinated. I believe I am not putting myself at great risk, but again, I am not absolutely sure. It doesn’t matter which day it is, I’m going to have some cracks in my skin. I get in the pool anyway.
But before I get in the pool, I cover my dry and torn patches with Aquaphor ointment. (Vaseline would do just as well.)
I’ve found that chlorine, and possibly the pH of the pool (slightly alkaline), can irritate my skin. Afterward, for at least half a day, my skin is subject to an intense itch that I don’t get if I don’t go swimming. To try to prevent this, I make sure to shower well. I do a particularly thorough rinsing of my eyes, which can become puffy and red otherwise.
Of course, once you shower, you have to moisturize. I find Aveeno Daily Moisturizing lotion from a pump bottle best for this. It’s a bit embarrassing to be slathering on moisturizer when you’re sitting on a bench in the locker room with two or three other guys dressing or undressing a few feet away. There’s some macho thing that makes you want to pretend that you don’t need any girly moisturizing—but, I suppose, this is where it’s a blessing to be in San Francisco, where a man can be as girly as he wants.
The strange thing is that I’ve found that swimming doesn’t seem to make my eczema worse. It could be that the chlorine, although it irritates, also kills off bad bacteria on my skin. In effect I am giving myself regular bleach baths, which doctors often recommend for eczema.
As far as being embarrassed about my skin goes--when you're swimming, you're underwater, so nobody can see you! The locker room can be a trial, but the facility I use is popular with a lot of wrinkly, hairy old men who, on the whole, make me look like Brad Pitt. Who, as I read in a gossip mag, happens to have eczema.
First, I have to consider whether my skin is in good enough shape. Eczema, of course, can leave your skin open in many places. Perhaps you’ve seen those signs that say that people who have open sores are not allowed in the pool. Why not? Really, the main reason is that nobody else in the pool wants to get infected by a blood-borne disease such as hepatitis or AIDS. You can’t blame them—neither do I. And even though I am pretty sure I don’t have any such disease, I am not absolutely sure. But I am sure enough that it doesn’t bother me morally to get in the pool.
However, am I sure that nobody else who has swum in that pool over the last month, say, has hepatitis or AIDS? That is a sobering thought, especially in San Francisco, where AIDS first broke the news in the 1980s. It is to kill the microbes that cause such diseases that public pools are chlorinated. I believe I am not putting myself at great risk, but again, I am not absolutely sure. It doesn’t matter which day it is, I’m going to have some cracks in my skin. I get in the pool anyway.
But before I get in the pool, I cover my dry and torn patches with Aquaphor ointment. (Vaseline would do just as well.)
I’ve found that chlorine, and possibly the pH of the pool (slightly alkaline), can irritate my skin. Afterward, for at least half a day, my skin is subject to an intense itch that I don’t get if I don’t go swimming. To try to prevent this, I make sure to shower well. I do a particularly thorough rinsing of my eyes, which can become puffy and red otherwise.
Of course, once you shower, you have to moisturize. I find Aveeno Daily Moisturizing lotion from a pump bottle best for this. It’s a bit embarrassing to be slathering on moisturizer when you’re sitting on a bench in the locker room with two or three other guys dressing or undressing a few feet away. There’s some macho thing that makes you want to pretend that you don’t need any girly moisturizing—but, I suppose, this is where it’s a blessing to be in San Francisco, where a man can be as girly as he wants.
The strange thing is that I’ve found that swimming doesn’t seem to make my eczema worse. It could be that the chlorine, although it irritates, also kills off bad bacteria on my skin. In effect I am giving myself regular bleach baths, which doctors often recommend for eczema.
As far as being embarrassed about my skin goes--when you're swimming, you're underwater, so nobody can see you! The locker room can be a trial, but the facility I use is popular with a lot of wrinkly, hairy old men who, on the whole, make me look like Brad Pitt. Who, as I read in a gossip mag, happens to have eczema.
Tuesday, September 4, 2012
New NEA blog post on allergy tests for eczema
I just wrote a new post on the NEA blog, about food allergy tests for eczema. I interviewed Jon Hanifin, a professor at Oregon Health Sciences University and one of the giants in the field of eczema research and practice. (Eczema is commonly diagnosed using the "Hanifin and Rajka" criteria.) Read the post if you are wondering how useful allergy tests are for food triggers of eczema.
The last few weeks my family has been under a lot of stress because my five-year-old son just started kindergarten. He has been unhappy about moving to a new school--where he's in a class of 28 (his preschool had 14 kids) and about 500 students attend total. He cries when we drop him off, when we mention school, and at night when he protests that he doesn't want to go. Plus there's homework--four pages a day, for a kindergartner! and Dad's Club and PTA. So you can understand why my posts have been a bit sparse. The pace will pick up again, I'm sure.
The last few weeks my family has been under a lot of stress because my five-year-old son just started kindergarten. He has been unhappy about moving to a new school--where he's in a class of 28 (his preschool had 14 kids) and about 500 students attend total. He cries when we drop him off, when we mention school, and at night when he protests that he doesn't want to go. Plus there's homework--four pages a day, for a kindergartner! and Dad's Club and PTA. So you can understand why my posts have been a bit sparse. The pace will pick up again, I'm sure.
Friday, August 31, 2012
Filaggrin mutation means more persistent eczema
The super-protein filaggrin helps skin cells take their proper shape as they develop into the upper, outer layer of skin; in its last step, it disintegrates into molecules that help the skin lock in moisture. Back in 2006 a landmark discovery showed that mutations in the filaggrin gene made it likely that the gene’s owner would develop eczema. But even though filaggrin is the poster child for eczema genetics, not that many eczema patients—only about 15%—have mutated copies of the gene.
Now researchers led by David Margolis, a professor of dermatology at the University of Pennsylvania, have shown that, among children with eczema, those who have filaggrin mutations are more likely to experience persistent eczema symptoms than those who do not.
The scientists analyzed data from the Pediatric Eczema Elective Registry (PEER), an ongoing 10-year registry maintained by Novartis to monitor the long-term safety of using pimecrolimus 1% cream. The new results are in press at the Journal of Allergy and Clinical Immunology.
The difference is subtle: at any time up to about four years of follow up (the period covered by the study), a child with a filaggrin mutation and a history of eczema is roughly 50% less likely to have clear skin than a child with two good copies of filaggrin. [Thanks to Margolis for helping me understand odds ratio.]
Interestingly, the authors noted that although all the mutations they studied were “null” mutations—that is, if you have one of these mutations, that copy of filaggrin doesn’t get produced at all—children with different mutations responded differently to treatment with topical steroids. Kids with the most common mutation, R501X, were most likely to need to use steroids to clear their skin. The authors don’t have an answer why this might be so.
Now researchers led by David Margolis, a professor of dermatology at the University of Pennsylvania, have shown that, among children with eczema, those who have filaggrin mutations are more likely to experience persistent eczema symptoms than those who do not.
The scientists analyzed data from the Pediatric Eczema Elective Registry (PEER), an ongoing 10-year registry maintained by Novartis to monitor the long-term safety of using pimecrolimus 1% cream. The new results are in press at the Journal of Allergy and Clinical Immunology.
The difference is subtle: at any time up to about four years of follow up (the period covered by the study), a child with a filaggrin mutation and a history of eczema is roughly 50% less likely to have clear skin than a child with two good copies of filaggrin. [Thanks to Margolis for helping me understand odds ratio.]
Interestingly, the authors noted that although all the mutations they studied were “null” mutations—that is, if you have one of these mutations, that copy of filaggrin doesn’t get produced at all—children with different mutations responded differently to treatment with topical steroids. Kids with the most common mutation, R501X, were most likely to need to use steroids to clear their skin. The authors don’t have an answer why this might be so.
Thursday, August 30, 2012
Bizarre flareup goin' on
It’s rare that my own skin deviates from its usual dryness and sporadic eczema flares. But right now, if I look at things from a detached perspective, things are interesting.
By any measure my skin’s been terrible since I left for vacation with the family. The return trip, which involved a 17-hour moisturizer-free delay in Newark, did me no favors. My scalp is a disaster. And since I got back I have had two weird episodes where my face and torso have gotten all puffy, tight, and red.
Last weekend we spent Saturday night on my kids’ preschool campout. I woke up Sunday with a red face and a weird crusty oozing above both eyelids.
Maybe I brought this on by standing next to the campfire. Maybe it's a reaction to pollen. All I know is that I had to grit my teeth and get through the morning until I could have a shower and moisturize at home. I took an Allegra. I felt pretty shitty.
I even thought I was going to miss work on Monday. But Monday morning my skin had calmed down enough for me to go in.
Then, after I went swimming on Wednesday, a co-worker asked if anything was wrong. “Your face is all red,” she said. It was starting up again. Even my wife, who is quite the diplomat, was looking at me strangely in the evening.
So today I had an appointment with the doctor. He doesn’t know what’s going on, and I don’t think he even expects to find out, but he mumbled something about oedemic urticaria and gave me a shot of prednisone in the butt. Also at some point soon I need to go in for a blood test to see if I have a “complement deficiency"—something wrong with a particular arm of my immune system. But, as with most aspects of eczema, I expect it will remain a mystery.
By any measure my skin’s been terrible since I left for vacation with the family. The return trip, which involved a 17-hour moisturizer-free delay in Newark, did me no favors. My scalp is a disaster. And since I got back I have had two weird episodes where my face and torso have gotten all puffy, tight, and red.
Last weekend we spent Saturday night on my kids’ preschool campout. I woke up Sunday with a red face and a weird crusty oozing above both eyelids.
Maybe I brought this on by standing next to the campfire. Maybe it's a reaction to pollen. All I know is that I had to grit my teeth and get through the morning until I could have a shower and moisturize at home. I took an Allegra. I felt pretty shitty.
I even thought I was going to miss work on Monday. But Monday morning my skin had calmed down enough for me to go in.
Then, after I went swimming on Wednesday, a co-worker asked if anything was wrong. “Your face is all red,” she said. It was starting up again. Even my wife, who is quite the diplomat, was looking at me strangely in the evening.
So today I had an appointment with the doctor. He doesn’t know what’s going on, and I don’t think he even expects to find out, but he mumbled something about oedemic urticaria and gave me a shot of prednisone in the butt. Also at some point soon I need to go in for a blood test to see if I have a “complement deficiency"—something wrong with a particular arm of my immune system. But, as with most aspects of eczema, I expect it will remain a mystery.
Wednesday, August 22, 2012
Airport eczema hell
Nobody likes flying these days. The bag fees, the lines, the security, the delays. But flying is a special hell for those of us with eczema. Each of us has his or her personal pharmacy at home, containing moisturizers, various grades of steroids, and special soaps, shampoos, and shaving creams that cost a lot of money and are difficult to find in stores. When you travel, first of all you have to select what to take with you. Airlines lose bags, so you want to put your vitals in your carryon—but regulations now say that everything has to fit into a quart-size Ziploc, so you have to fill small plastic containers with a few days’ worth of this or that. And if you’re not careful—as happened to me recently—a zealous airline employee can “gate-check” your carryon because the plane’s already full of other passengers’ necessities. You last see your precious mini-pharmacy sitting forlornly on the jet way as you board Untied Airlines 1234 for Topeka.
Untied Airlines. (I don’t want to embarrass the airline, so I’ve given them a pseudonym.)
I’ll never fly Untied again. They made my trip back from my summer family vacation a personal indignity. The worst thing is that it wasn’t the Untied staff, who were almost all truly helpful and pleasant. It was the airline’s system, which was clearly to blame for all the problems. So no free vouchers or drinks will convince me to fly with them again, because the experience would surely be no better next time.
Our trips out and back were two-stage: San Francisco to Chicago to Halifax, and Halifax to Newark to San Francisco. On the way out, both flights were delayed by two hours—but the delays were of the rolling variety, in which the airline tells you the plane’s going to take off in half an hour, but it doesn’t; then they announce it will take off in another half hour, but it doesn’t; etc.
But these delays were peanuts. The real trouble started on the second leg of our return, as you will see.
My mistake was in bringing along on the trip only just enough moisturizers and steroids to last the planned duration. Because the vacation was stressful (my extended family, ten of us, in a small house for two weeks) and heavily air-conditioned, my skin had been especially dry and inflamed—so much so that my dad assumed the redness was sunburn. I ran out of Eucerin two days before our return, and bought a cheap substitute that didn’t really do the job. I squeezed the last microgram of steroids out of a flattened tube, and willed myself not to scratch. You can imagine how that worked out.
I packed my pathetic remaining moisturizer into a small Tupperware container and shoved it into my carryon. As we left Halifax for San Francisco, where my eczema stash awaited, I felt like a nomad in the desert making his way back to a beloved oasis.
We barely made a tight connection in Newark. An Untied employee gate-checked my bag, and I watched my moisturizer disappear into the distance. Untied gave us seats in four different locations throughout the plane, so we had to beg random strangers to let us sit next to our kids. It was 2:00 in the afternoon.
Two hours pass on the tarmac. Then the pilot tells us the flight has been canceled because of mechanical difficulties.
We disembark in confusion. Eventually we get booked on a flight leaving at 8:00 pm. We get food vouchers and search the airport for something that my daughter, who has dairy and nut allergies, can eat. We find essentially nothing. (She doesn’t have known anaphylactic problems, but who wants to gamble?) She's eaten all her snacks already. This is going to be a hungry day for her. We board at 8:00 and, because we have seats in four different locations, beg random strangers to take our cramped middle seats so that we can sit next to our kids.
Three hours pass on the tarmac. The kids fall asleep. Then the pilot tells us the flight has been canceled because of mechanical difficulties.
Someone in the back of the plane yells “Goddamn!”
We all get free drink vouchers and coupons for 10% off our next flight on Untied.
And we get to stay overnight at the Newark Ramada. “Overnight” in this case means four hours, since it’s now midnight and we have to be back at the airport to go through security again for our new 7:00 am flight.
By the morning, my skin is so dry it makes the Dead Sea Scrolls look supple. I introduce myself to my seatmate, but can’t shake hands with her because it would be too painful and disgusting. I look at myself in the mirror of the airplane bathroom. My face is falling off.
Eighteen hours after we were supposed to arrive, we land in San Francisco. The final farce: our bags aren’t on the plane and we have to go searching for them. My wife finds them in a special long-term holding location.
The first thing I do at home is to take a long shower with Dove soap and tar shampoo and cover myself in a thick layer of Eucerin. The second thing: rip all the Untied tags off our baggage.
The moral to this story, I guess, is that you have to plan for the worst when you fly. And I will next time. You have to go into survival mode, and make absolutely sure that you have small containers of your eczema essentials on your person where you can’t possibly lose them. Otherwise, you run the risk of a hellish experience.
Untied Airlines. (I don’t want to embarrass the airline, so I’ve given them a pseudonym.)
I’ll never fly Untied again. They made my trip back from my summer family vacation a personal indignity. The worst thing is that it wasn’t the Untied staff, who were almost all truly helpful and pleasant. It was the airline’s system, which was clearly to blame for all the problems. So no free vouchers or drinks will convince me to fly with them again, because the experience would surely be no better next time.
Our trips out and back were two-stage: San Francisco to Chicago to Halifax, and Halifax to Newark to San Francisco. On the way out, both flights were delayed by two hours—but the delays were of the rolling variety, in which the airline tells you the plane’s going to take off in half an hour, but it doesn’t; then they announce it will take off in another half hour, but it doesn’t; etc.
But these delays were peanuts. The real trouble started on the second leg of our return, as you will see.
My mistake was in bringing along on the trip only just enough moisturizers and steroids to last the planned duration. Because the vacation was stressful (my extended family, ten of us, in a small house for two weeks) and heavily air-conditioned, my skin had been especially dry and inflamed—so much so that my dad assumed the redness was sunburn. I ran out of Eucerin two days before our return, and bought a cheap substitute that didn’t really do the job. I squeezed the last microgram of steroids out of a flattened tube, and willed myself not to scratch. You can imagine how that worked out.
I packed my pathetic remaining moisturizer into a small Tupperware container and shoved it into my carryon. As we left Halifax for San Francisco, where my eczema stash awaited, I felt like a nomad in the desert making his way back to a beloved oasis.
We barely made a tight connection in Newark. An Untied employee gate-checked my bag, and I watched my moisturizer disappear into the distance. Untied gave us seats in four different locations throughout the plane, so we had to beg random strangers to let us sit next to our kids. It was 2:00 in the afternoon.
Two hours pass on the tarmac. Then the pilot tells us the flight has been canceled because of mechanical difficulties.
We disembark in confusion. Eventually we get booked on a flight leaving at 8:00 pm. We get food vouchers and search the airport for something that my daughter, who has dairy and nut allergies, can eat. We find essentially nothing. (She doesn’t have known anaphylactic problems, but who wants to gamble?) She's eaten all her snacks already. This is going to be a hungry day for her. We board at 8:00 and, because we have seats in four different locations, beg random strangers to take our cramped middle seats so that we can sit next to our kids.
Three hours pass on the tarmac. The kids fall asleep. Then the pilot tells us the flight has been canceled because of mechanical difficulties.
Someone in the back of the plane yells “Goddamn!”
We all get free drink vouchers and coupons for 10% off our next flight on Untied.
And we get to stay overnight at the Newark Ramada. “Overnight” in this case means four hours, since it’s now midnight and we have to be back at the airport to go through security again for our new 7:00 am flight.
By the morning, my skin is so dry it makes the Dead Sea Scrolls look supple. I introduce myself to my seatmate, but can’t shake hands with her because it would be too painful and disgusting. I look at myself in the mirror of the airplane bathroom. My face is falling off.
Eighteen hours after we were supposed to arrive, we land in San Francisco. The final farce: our bags aren’t on the plane and we have to go searching for them. My wife finds them in a special long-term holding location.
The first thing I do at home is to take a long shower with Dove soap and tar shampoo and cover myself in a thick layer of Eucerin. The second thing: rip all the Untied tags off our baggage.
The moral to this story, I guess, is that you have to plan for the worst when you fly. And I will next time. You have to go into survival mode, and make absolutely sure that you have small containers of your eczema essentials on your person where you can’t possibly lose them. Otherwise, you run the risk of a hellish experience.
Friday, August 3, 2012
Consumer Reports advises caution with vitamins and supplements
In its current issue, Consumer Reports has a story titled “10 surprising dangers of vitamins and supplements” with the subheading “Don't assume they're safe because they're 'all natural'.” Good reading--I know a lot of people take various supplements in the belief that they will help with eczema.
If you’re a reasonable person, there’s nothing to worry about. A few points jumped out at me though.
If you’re a reasonable person, there’s nothing to worry about. A few points jumped out at me though.
- Dietary supplements can be “spiked with prescription drugs” which can cause side effects and interactions that many people are buying supplements to avoid.
- You need to be careful when buying herbal therapies—CR’s reporter went to a number of traditional Hispanic herbaries and “none [of the “healers”] volunteered relevant facts about possible side effects or the risky interactions that can occur when an herb is taken with a medication.” This would also be true for traditional Chinese medicine, I expect.
- And it’s possible to overdose on vitamins. For patients with eczema, vitamin D is the current fad, and I have heard of people taking regular megadoses—way over the recommended limit. The thing is, just because the recommended limit is 4000 IU (whatever an IU is) doesn’t mean that you can take a supplement of 4000 IU. You have to consider all the sources you’re getting vitamin D from, including fortified dairy and sunlight. CR describes, for calcium, how it’s surprisingly easy to go over the limit.
Tuesday, July 31, 2012
Benign bacteria help T cells signal skin infection
Benign bacteria on our skin partner with T cells to alert the immune system to the presence of dangerous pathogens, according to research recently published online in the journal Science.
The NIH press release explains the science very well, probably better than I could, so I have copied their text below.
The most relevant point that I can see is that this work shows that microbes living on healthy skin have an important role in our immune system. It's a philosophical question whether the microbes are separate from us--or are part of us, even though they don't share our DNA. If you overuse antibiotic ointments (that is, apply them for periods longer than required to treat an infection), you are killing off helpful microbes and weakening your immune response.
The NIH press release explains the science very well, probably better than I could, so I have copied their text below.
The most relevant point that I can see is that this work shows that microbes living on healthy skin have an important role in our immune system. It's a philosophical question whether the microbes are separate from us--or are part of us, even though they don't share our DNA. If you overuse antibiotic ointments (that is, apply them for periods longer than required to treat an infection), you are killing off helpful microbes and weakening your immune response.
NIH team describes protective role of skin microbiota
Commensal bacteria and immune cells work together to fight harmful microbes
WHAT: A research team at the National Institutes of Health has found that bacteria that normally live in the skin may help protect the body from infection. As the largest organ of the body, the skin represents a major site of interaction with microbes in the environment.
Although immune cells in the skin protect against harmful organisms, until now, it has not been known if the millions of naturally occurring commensal bacteria in the skin—collectively known as the skin microbiota—also have a beneficial role. Using mouse models, the NIH team observed that commensals contribute to protective immunity by interacting with the immune cells in the skin. Their findings appear online on July 26th in Science.
The investigators colonized germ-free mice (mice bred with no naturally occurring microbes in the gut or skin) with the human skin commensal Staphylococcus epidermidis. The team observed that colonizing the mice with this one species of good bacteria enabled an immune cell in the mouse skin to produce a cell-signaling molecule needed to protect against harmful microbes. The researchers subsequently infected both colonized and non-colonized germ-free mice with a parasite. Mice that were not colonized with the bacteria did not mount an effective immune response to the parasite; mice that were colonized did.
In separate experiments, the team sought to determine if the presence or absence of commensals in the gut played a role in skin immunity. They observed that adding or eliminating beneficial bacteria in the gut did not affect the immune response at the skin. These findings indicate that microbiota found in different tissues—skin, gut, lung—have unique roles at each site and that maintaining good health requires the presence of several different sets of commensal communities.
This study provides new insights into the protective role of skin commensals, and demonstrates that skin health relies on the interaction of commensals and immune cells. Further research is needed, say the authors, to determine whether skin disorders such as eczema and psoriasis may be caused or exacerbated by an imbalance of skin commensals and potentially harmful microbes that influence the skin and its immune cells.
Tuesday, July 24, 2012
"Red skin syndrome" hyped, but real
A while ago I got a news alert linking to a disturbing press release claiming that topical steroids, commonly prescribed to treat eczema, were in some cases intensifying disease symptoms.
From the release:
It's not news that strong steroids are bad for you. But I hadn’t heard of the phenomenon described by ITSAN before. As I always do when I hear of unfamiliar scientific or medical concepts, I turned to PubMed, the NIH’s database of published papers. I performed searches for "topical steroid addiction," "corticosteroid addiction," and "steroid addiction." In my experience, well-established concepts leap out of PubMed with thousands of hits.
Topical steroid addiction just barely surfaced above the noise at first. It’s hard to find, but it’s there—in three papers by Rapaport.
But then, as I dug around, more results began to appear. The problem is that the papers all use different words to describe the central condition, which (on the face at least) is most precisely labeled “steroid-induced rosacealike dermatitis,” commonly called “red skin syndrome.” A review for practicing physicians can be found here.
The first case of red skin syndrome was reported in 1957. So “topical steroid addiction,” as described by ITSAN, is a real, if not new, condition. I don’t know how many patients it affects, but according to some PubMed results I found, it is well-known in India and China, where it may be emerging because stronger steroids are now being more widely prescribed--and perhaps more casually used.
In my opinion ITSAN’s site is garish and alarmist (do they really need that banner image of a crying girl?) and their focus on Rapaport comes across as promotional. In the "About Us" section, they ask:
From the release:
Using mild over-the-counter hydro-cortisone creams to a range of prescription steroid creams, one's skin can become addicted in less than two weeks of usage and develop worsening symptoms that appear to the [sic] be simply spreading Eczema. However the problem is worsening from the medication.Press releases usually contain news. So what is news here? The release was published by a 501 (c) (3) nonprofit called “The International Topical Steroid Addiction Network,” founded by a dermatologist, Marvin Rapaport, and Kelly Palace, a former patient of Rapaport's. Rapaport practices in Beverly Hills, California.
It's not news that strong steroids are bad for you. But I hadn’t heard of the phenomenon described by ITSAN before. As I always do when I hear of unfamiliar scientific or medical concepts, I turned to PubMed, the NIH’s database of published papers. I performed searches for "topical steroid addiction," "corticosteroid addiction," and "steroid addiction." In my experience, well-established concepts leap out of PubMed with thousands of hits.
Topical steroid addiction just barely surfaced above the noise at first. It’s hard to find, but it’s there—in three papers by Rapaport.
But then, as I dug around, more results began to appear. The problem is that the papers all use different words to describe the central condition, which (on the face at least) is most precisely labeled “steroid-induced rosacealike dermatitis,” commonly called “red skin syndrome.” A review for practicing physicians can be found here.
The first case of red skin syndrome was reported in 1957. So “topical steroid addiction,” as described by ITSAN, is a real, if not new, condition. I don’t know how many patients it affects, but according to some PubMed results I found, it is well-known in India and China, where it may be emerging because stronger steroids are now being more widely prescribed--and perhaps more casually used.
In my opinion ITSAN’s site is garish and alarmist (do they really need that banner image of a crying girl?) and their focus on Rapaport comes across as promotional. In the "About Us" section, they ask:
Could the reason for this huge increase [in the incidence of eczema in the West over the past 30 years] be the use of topical steroids causing Steroid Induced (spreading) Eczema, an iatrogenic (adj.where a medical treatment causes a condition) skin disease?In a word: no. But the information on the FAQ section of their site looks useful. If you think topical steroids are your biggest problem, then why not stop cold turkey and see if you experience the flareup and cooldown that seem to be typical of addiction?
Friday, July 20, 2012
Will we see gene therapy for eczema?
The European Commission is close to approving the first gene therapy in the Western world, according to the New York Times.
The treatment, called Glybera and developed by the Dutch company uniQure, treats a rare condition in which people are unable to break down fat-carrying molecules.
Gene therapy is one way that I imagine patients of the future might be cured of eczema. Glybera gives us a peek into how that might happen.
In gene therapy, doctors replace a patient’s faulty gene with a good one. The large protein filaggrin is currently the best candidate for eczema gene therapy. Several studies have linked filaggrin mutations to a higher risk of developing eczema.
Filaggrin gene therapy would have to be applied early in life. This is because in our current understanding, eczema is caused by a skin barrier defect that allows allergies to develop after a critical time window. Filaggrin mutations cause a faulty skin barrier. So you’d have to fix filaggrin early, because waiting too long would allow allergies to develop, after which fixing filaggrin solves only half the problem.
Glybera is a biotherapeutic, a gene (length of DNA) that is attached to a well-characterized and benign virus. Doctors will inject Glybera into leg muscles, where the virus infects cells and incorporates itself and the therapeutic gene into the patient's DNA—but only in leg muscle cells, presumably because Glybera gets absorbed locally. Then the patients will be able to break down the fat-carrying molecules, and their blood will no longer be overloaded with fat.
A biotherapeutic for eczema would likely be an intact filaggrin gene incorporated into a similar virus.
Gene therapy for the skin would have to be restricted to skin cells. You could accomplish this with a topical cream or ointment applied in the clinic. I'm guessing you would want to treat your whole skin, not just spots that were flaring up at the time.
How long will it last? The effects of Glybera apparently last for years, probably because muscle cells live a long time. Skin cells are a different matter—they are turning over continually. This could turn out to make gene therapy for skin conditions near-impossible.
But perhaps you could take regular doses—pills or injections—of a gene therapy that includes a genetic switch that turns on only in skin cells.
The critical early window for developing allergies in eczema patients could turn out to be a bonus in disguise. Maybe filaggrin gene therapy would only be required during a window of a few years, after which it could be discontinued and allergies would never develop.
Obviously extensive clinical trials for safety would be necessary. I could imagine this type of therapy becoming available within two decades. My grandchildren could be among the first to benefit.
The treatment, called Glybera and developed by the Dutch company uniQure, treats a rare condition in which people are unable to break down fat-carrying molecules.
Gene therapy is one way that I imagine patients of the future might be cured of eczema. Glybera gives us a peek into how that might happen.
In gene therapy, doctors replace a patient’s faulty gene with a good one. The large protein filaggrin is currently the best candidate for eczema gene therapy. Several studies have linked filaggrin mutations to a higher risk of developing eczema.
Filaggrin gene therapy would have to be applied early in life. This is because in our current understanding, eczema is caused by a skin barrier defect that allows allergies to develop after a critical time window. Filaggrin mutations cause a faulty skin barrier. So you’d have to fix filaggrin early, because waiting too long would allow allergies to develop, after which fixing filaggrin solves only half the problem.
Glybera is a biotherapeutic, a gene (length of DNA) that is attached to a well-characterized and benign virus. Doctors will inject Glybera into leg muscles, where the virus infects cells and incorporates itself and the therapeutic gene into the patient's DNA—but only in leg muscle cells, presumably because Glybera gets absorbed locally. Then the patients will be able to break down the fat-carrying molecules, and their blood will no longer be overloaded with fat.
A biotherapeutic for eczema would likely be an intact filaggrin gene incorporated into a similar virus.
Gene therapy for the skin would have to be restricted to skin cells. You could accomplish this with a topical cream or ointment applied in the clinic. I'm guessing you would want to treat your whole skin, not just spots that were flaring up at the time.
How long will it last? The effects of Glybera apparently last for years, probably because muscle cells live a long time. Skin cells are a different matter—they are turning over continually. This could turn out to make gene therapy for skin conditions near-impossible.
But perhaps you could take regular doses—pills or injections—of a gene therapy that includes a genetic switch that turns on only in skin cells.
The critical early window for developing allergies in eczema patients could turn out to be a bonus in disguise. Maybe filaggrin gene therapy would only be required during a window of a few years, after which it could be discontinued and allergies would never develop.
Obviously extensive clinical trials for safety would be necessary. I could imagine this type of therapy becoming available within two decades. My grandchildren could be among the first to benefit.
Thursday, July 19, 2012
The NEA should join Faster Cures nonprofit group
Unless you live under a rock, you’ve probably heard of the Michael J. Fox Foundation for Parkinson’s Research. Fox, the "Back to the Future" etc. megastar who developed early onset Parkinson’s disease, created the foundation to back research leading to a cure.
The Michael J. Fox Foundation is only one of many members of The Research Acceleration and Innovation Network (TRAIN). TRAIN is a child of Faster Cures, the nonprofit patient advocacy organization based in Washington, DC.
Look at the list of TRAIN member organizations. Isn’t it amazing how many diseases there are for which we need scientists and entrepreneurs to develop cures? But I don’t see the National Eczema Association on the list. I think the NEA should join TRAIN.
Although most of the diseases represented on the member list are terminal or degenerative, and eczema is neither, those of us who suffer from it can attest that it seriously affects, and in the worst cases ruins, our quality of life.
According to the Faster Cures website,
I read Fox’s biographical book “Always Looking Up,” published in 2009. His optimism is infectious. Read that book. You won’t regret it!
The Michael J. Fox Foundation is only one of many members of The Research Acceleration and Innovation Network (TRAIN). TRAIN is a child of Faster Cures, the nonprofit patient advocacy organization based in Washington, DC.
Look at the list of TRAIN member organizations. Isn’t it amazing how many diseases there are for which we need scientists and entrepreneurs to develop cures? But I don’t see the National Eczema Association on the list. I think the NEA should join TRAIN.
Although most of the diseases represented on the member list are terminal or degenerative, and eczema is neither, those of us who suffer from it can attest that it seriously affects, and in the worst cases ruins, our quality of life.
According to the Faster Cures website,
[TRAIN] was established to create opportunities for medical research innovators to discuss and tackle the challenges that cut across diseases. It is a group of unique nonprofit foundations that fund medical research across a spectrum of diseases, from breast cancer to Parkinson's disease. In many cases TRAIN's member foundations have been created by patients and their families who are frustrated by the slow pace of change in the traditional medical research system. They represent the kind of organizations that are fast becoming the engine behind innovation in disease research--collaborative, mission-driven, strategic in their allocation of resources, and results-oriented. They are organizations that have a singular focus on, and a significant stake in, getting promising therapies from the laboratory bench to the patient's bedside as rapidly as possible.There’s no reason that I can see that the NEA shouldn’t be part of TRAIN. It looks easy to join. What would it get us? From what I can see, TRAIN provides good models for how to set up sponsored research programs, preclinical and clinical trial templates, agreements for how to share biological samples, etc. I don’t run a patient advocacy organization, so I don’t know firsthand how useful this sort of thing could be, but I imagine that it would be a lot easier to grab a template for a clinical trial than to write one from scratch.
I read Fox’s biographical book “Always Looking Up,” published in 2009. His optimism is infectious. Read that book. You won’t regret it!
Tuesday, July 17, 2012
Do you have a tattoo?
Last Sunday, people-watching at a park with the family, I remarked to my wife how some people like to get tattoos on their necks or arms. You just can't miss a neck tattoo. It conveys a certain je ne sais quoi. Actually, in California, it conveys that you belong to a gang.
"Why would you get a tattoo?" I asked.
"Well, my sister has a giant eagle tattooed on her back," she said.
I didn't know that. My sister-in-law is a bit of a daredevil, and as she nears 40 with two kids, still enjoys the flying trapeze.
"Yes, she did it in her 20s."
And here I must admit that I did, briefly, in my 20s, consider getting a tattoo. It was during my summer in the Canadian military reserves, at Camp Gagetown, New Brunswick. A bunch of mates and I were off-duty at the Canadian equivalent of the Px, as it was too early to start drinking. One guy pointed out a tattoo parlor. "Hey, let's all get tattoos," he said. There was a folder with art samples you could ask to have permanently inked into your skin. I examined the catalog. It seemed to consist exclusively of logos of heavy-metal bands. Jazz being more my thing, I excused myself to get an icecream cone, while my mate rolled up his sleeve, indicating his preference to display an image of Mötley Crüe's "Dr Feelgood" on his bicep until the day he died.
I wonder whether he still feels good about that decision.
That summer was remarkable for me. My eczema completely cleared up. I suspect it was because, being a trooper, I was ordered around the whole time and never had to make a decision for myself. (I kid you not--on the first day, we spent hours learning how to take one step forward.) No decisions, no stress. The warrant officer could singe my ears blue with profanities, informing me that the way I was shouldering my rifle was far from ideal. It didn't matter. I just marched where I was told.
But even then, with perfect skin, I knew that getting a tattoo would be a bad idea. I think I've had eczema on every square inch of my skin since then. Every square inch. What does eczema do to a tattoo? If you scratch, does the ink get torn up and the picture blotched? I'd think so.
Have you gotten a tattoo?
"Why would you get a tattoo?" I asked.
"Well, my sister has a giant eagle tattooed on her back," she said.
I didn't know that. My sister-in-law is a bit of a daredevil, and as she nears 40 with two kids, still enjoys the flying trapeze.
"Yes, she did it in her 20s."
And here I must admit that I did, briefly, in my 20s, consider getting a tattoo. It was during my summer in the Canadian military reserves, at Camp Gagetown, New Brunswick. A bunch of mates and I were off-duty at the Canadian equivalent of the Px, as it was too early to start drinking. One guy pointed out a tattoo parlor. "Hey, let's all get tattoos," he said. There was a folder with art samples you could ask to have permanently inked into your skin. I examined the catalog. It seemed to consist exclusively of logos of heavy-metal bands. Jazz being more my thing, I excused myself to get an icecream cone, while my mate rolled up his sleeve, indicating his preference to display an image of Mötley Crüe's "Dr Feelgood" on his bicep until the day he died.
I wonder whether he still feels good about that decision.
That summer was remarkable for me. My eczema completely cleared up. I suspect it was because, being a trooper, I was ordered around the whole time and never had to make a decision for myself. (I kid you not--on the first day, we spent hours learning how to take one step forward.) No decisions, no stress. The warrant officer could singe my ears blue with profanities, informing me that the way I was shouldering my rifle was far from ideal. It didn't matter. I just marched where I was told.
But even then, with perfect skin, I knew that getting a tattoo would be a bad idea. I think I've had eczema on every square inch of my skin since then. Every square inch. What does eczema do to a tattoo? If you scratch, does the ink get torn up and the picture blotched? I'd think so.
Have you gotten a tattoo?
Wednesday, July 11, 2012
New smallpox vaccine safe for eczema patients
A Danish company will be supplying the US government with 20 million doses of a smallpox vaccine that is safe for eczema patients--unlike the existing vaccine, which can cause rampant and life-threatening infection in rare cases. I blog briefly about it on the National Eczema Association website.
Monday, July 9, 2012
Wheat opens up a whole new universe of food
For the first year of my daughter Voov's life, her face and hands were a red mess of eczema. Blood laced her stool. The combination of symptoms led us and her doctor to think that some allergen was to blame. Skin prick tests registered positive for almost everything--which wasn't much help! Voov was breastfed, so my wife began to cut out foods in her own diet for two weeks at a time to see if anything changed. Removing dairy improved things; so that was it for cow-based milk and ice cream for my wife for a long time.
Then we started Voov on solid foods. At first she had only 12 options, several of which she refused outright. And so most of the atoms now composing her body lived previous lives as chicken, tofu, rice, apple, peas, and banana.
After three years, we redid the skin prick test, and while the technician made a hash of reading the results, we took the apparent improvement as a license to start trying a host of new things. We began with high-value, low-risk items like carrots, potato, chard, and quinoa. It was marvelous: Voov had no reaction to any of them. Eggs, even.
The problem was that she didn't like to eat any of them. She was set in her ways. It seems that three years is precisely the wrong age to start introducing a kid to new foods. However, there was one notable exception: ketchup. We ran trials of tomato and onion, and then Heinz--and bingo, we'd found something she liked and didn't react to.
I immediately realized that I could cover any food in ketchup and there'd be a good chance she'd eat it.
This past week, though, has seen a revolution.
Still standing as major potential villains were the big four: fish, dairy, nuts, and wheat. My wife is a fish-phobe so it's not worth worrying about fish because I can never cook it for the family. We know Voov is allergic to milk, because she threw up shortly after she drank some by accident (her skin test showed major allergy to milk and beef). And we're leaving nuts as something to try in the doctor's office when we have an epi-pen handy. That left one thing to try: wheat.
One week ago, we began giving Voov slices of wheat bread (after carefully checking the ingredient list; it's amazing how many breads contain milk products). She loves it, and she loves wheat noodles, and so far she hasn't had the slightest apparent reaction. Awesome! It has opened up a whole new universe of food.
In the space of a few weeks, we've completely inverted our food restrictions. Instead of Voov only being able to eat a few things, she's suddenly able to eat all BUT a few things. We'll be reading ingredient labels for years to come, but our lives have gotten much simpler and easier.
Coincidentally, Selena over at Amazing & Atopic started her daughter on wheat this week. Things didn't go so well for her, unfortunately.
Then we started Voov on solid foods. At first she had only 12 options, several of which she refused outright. And so most of the atoms now composing her body lived previous lives as chicken, tofu, rice, apple, peas, and banana.
After three years, we redid the skin prick test, and while the technician made a hash of reading the results, we took the apparent improvement as a license to start trying a host of new things. We began with high-value, low-risk items like carrots, potato, chard, and quinoa. It was marvelous: Voov had no reaction to any of them. Eggs, even.
The problem was that she didn't like to eat any of them. She was set in her ways. It seems that three years is precisely the wrong age to start introducing a kid to new foods. However, there was one notable exception: ketchup. We ran trials of tomato and onion, and then Heinz--and bingo, we'd found something she liked and didn't react to.
I immediately realized that I could cover any food in ketchup and there'd be a good chance she'd eat it.
This past week, though, has seen a revolution.
Still standing as major potential villains were the big four: fish, dairy, nuts, and wheat. My wife is a fish-phobe so it's not worth worrying about fish because I can never cook it for the family. We know Voov is allergic to milk, because she threw up shortly after she drank some by accident (her skin test showed major allergy to milk and beef). And we're leaving nuts as something to try in the doctor's office when we have an epi-pen handy. That left one thing to try: wheat.
One week ago, we began giving Voov slices of wheat bread (after carefully checking the ingredient list; it's amazing how many breads contain milk products). She loves it, and she loves wheat noodles, and so far she hasn't had the slightest apparent reaction. Awesome! It has opened up a whole new universe of food.
In the space of a few weeks, we've completely inverted our food restrictions. Instead of Voov only being able to eat a few things, she's suddenly able to eat all BUT a few things. We'll be reading ingredient labels for years to come, but our lives have gotten much simpler and easier.
Coincidentally, Selena over at Amazing & Atopic started her daughter on wheat this week. Things didn't go so well for her, unfortunately.
Thursday, July 5, 2012
Antibody therapy appears powerful against psoriasis
A biotechnology therapeutic for psoriasis appears to clear most of the symptoms in many patients, according to recently published results of clinical trials.
The therapeutic is “ixekizumab,” an antibody that inactivates a “cytokine” or signaling molecule produced by a subset of white blood cells called type 17 helper T cells.* Researchers at the pharmaceutical company Eli Lilly and university colleagues published the Phase 2 results in the New England Journal of Medicine in March. I learned about ixekizumab from a JACI paper published last week, reporting on aspects of the earlier Phase 1 trial.
Th17 are thought to be overactive in psoriasis patients. That is not the case in patients with atopic dermatitis, for whom helper T cells of types 2 and 22 generally exist in higher numbers and are more active than they are in the average person. The authors of the JACI paper speculate that tailored antibody therapy could prove as effective in controlling eczema as ixekizumab has for psoriasis.
In the Phase 2 trial, researchers injected 142 patients with various doses of ixekizumab at regular intervals over a 16-week period. They found that, for all but the lowest dosage, the antibody mostly cleared up psoriasis—as measured by a standard set of measures—for more than 75% of the patients in the trial.
The authors did not present data showing how long the effects lasted. But they did note that hardly anyone dropped out of the trial because of adverse effects. (From what I can tell, those who dropped out came from the lowest dosage group.)
Nor was there any indication how expensive ixekizumab might be. I imagine that, compared to drugs such as steroids, custom-produced antibodies would be extremely expensive for patients and insurers.
Nevertheless, the results are unusually positive. A blog post on the JACI website called the results “near-astonishing.” Keeping in mind that all trials and papers published on them are bankrolled by pharma companies (who else can pay for clinical trials?) this area of antibodies against T cell cytokines seems worth watching closely.
* I am pretty sure that Th17 cells are not the seventeenth type of helper T cells. The only ones I've ever heard of are Th1, Th2, Th17, and Th22. I don't know why the last two are numbered 17 and 22 instead of 3 and 4. This sort of thing is why I got out of immunology.
The therapeutic is “ixekizumab,” an antibody that inactivates a “cytokine” or signaling molecule produced by a subset of white blood cells called type 17 helper T cells.* Researchers at the pharmaceutical company Eli Lilly and university colleagues published the Phase 2 results in the New England Journal of Medicine in March. I learned about ixekizumab from a JACI paper published last week, reporting on aspects of the earlier Phase 1 trial.
Th17 are thought to be overactive in psoriasis patients. That is not the case in patients with atopic dermatitis, for whom helper T cells of types 2 and 22 generally exist in higher numbers and are more active than they are in the average person. The authors of the JACI paper speculate that tailored antibody therapy could prove as effective in controlling eczema as ixekizumab has for psoriasis.
In the Phase 2 trial, researchers injected 142 patients with various doses of ixekizumab at regular intervals over a 16-week period. They found that, for all but the lowest dosage, the antibody mostly cleared up psoriasis—as measured by a standard set of measures—for more than 75% of the patients in the trial.
The authors did not present data showing how long the effects lasted. But they did note that hardly anyone dropped out of the trial because of adverse effects. (From what I can tell, those who dropped out came from the lowest dosage group.)
Nor was there any indication how expensive ixekizumab might be. I imagine that, compared to drugs such as steroids, custom-produced antibodies would be extremely expensive for patients and insurers.
Nevertheless, the results are unusually positive. A blog post on the JACI website called the results “near-astonishing.” Keeping in mind that all trials and papers published on them are bankrolled by pharma companies (who else can pay for clinical trials?) this area of antibodies against T cell cytokines seems worth watching closely.
* I am pretty sure that Th17 cells are not the seventeenth type of helper T cells. The only ones I've ever heard of are Th1, Th2, Th17, and Th22. I don't know why the last two are numbered 17 and 22 instead of 3 and 4. This sort of thing is why I got out of immunology.
Monday, July 2, 2012
Rochester group to focus on skin barrier
Alice Pentland, chair of the Department of Dermatology at the University of Rochester Medical Center, whom I interviewed recently for a post on the NEA website, also directs the newly-formed Skin Barrier Research Consortium, a subunit of her department. The group, as its name suggests, brings together scientists studying the skin barrier--in particular, its permeability, which is thought to be a key factor in allergic eczema, and which could in normal skin be temporarily increased to administer needle-free vaccines.
I learned about the consortium from a Rochester press release. According to Pentland there is no special funding. They aren't applying for any large NIH grants. So the group's formation is symbolic. But it might give the department a mission, and could make it a more formidable applicant for future grants.
Pentland detailed the roles of the researchers in the consortium for me. Of particular interest to eczema patients:
I learned about the consortium from a Rochester press release. According to Pentland there is no special funding. They aren't applying for any large NIH grants. So the group's formation is symbolic. But it might give the department a mission, and could make it a more formidable applicant for future grants.
Pentland detailed the roles of the researchers in the consortium for me. Of particular interest to eczema patients:
- Lisa Beck, who is conducting a pilot-stage clinical trial of Actos, a drug originally developed for diabetics but also found to increase the integrity of the skin. Beck is also building a registry of patients (apparently more than 200 now) who have "classic" (and I'd assume that means "allergic") atopic dermatitis, partly characterized by high levels of IgE antibodies in the blood. A major problem for dermatologists, Pentland said, is that several conditions look like AD on the surface but aren't. A vetted registry of patients will help researchers study causes of AD.
- Anna De Benedetto, a doctor who is studying how the electrical resistance of skin is correlated with its permeability
- Ben Miller, a chemist who is synthesizing small drug molecules aimed at targets identified by others in the group
- Lisa DeLouise, a material scientist looking at how a changed skin barrier, caused by AD or sunburn, may make nanoparticles toxic when they normally wouldn't be
- and Elaine Gilmore, who studies the molecular mechanisms of itch.
Wednesday, June 27, 2012
Plastic chemical linked to eczema in young children
Researchers at Columbia University in New York City have released a study showing a connection between a chemical commonly used in plastic household products and the risk that a young child will develop eczema. [press release] [paper] The work was widely covered in the media, including Fox News, which used a rather odd photo.
No, it's not BPA. It's benzylbutylphthalate (BBzP)--good luck pronouncing that--a component that seems to be found mostly in vinyl flooring, but which makes its way into dust, and thence into the body. However, the dominant source of BBzP is food, say the authors of the study, which was led by Allan Just at the Columbia Center for Children's Environmental Health.
BBzP is one of a class of compounds used to make plastics flexible. Scientists have little idea how it might interact with the skin and immune system.
For this study, the scientists took urine samples from pregnant women in the third trimester. Then, after the children were born, the mothers filled out questionnaires at regular intervals, noting whether their kids had had recurrent rashes or had a medical diagnosis of eczema.
The results, from a cohort of 407 women, showed that the chances of children developing eczema were positively correlated with the mother's prenatal BBzP concentration in the urine. The data makes it hard to give a simple number, but higher BBzP clearly means greater risk.
The pattern was similar for African-Americans and Dominicans, the two main ethnic groups represented in the study.
The scientists originally thought BBzP might increase the incidence or strength of allergies, but did not find that to be true in this work.
It's unclear what one can do about the issue, if the science is true. You don't have much control over your environment, especially if you live in an urban apartment, as virtually everyone does in NYC. And BBzP is only one of many factors, including genetics, gut flora, geographic location, diet, and parental smoking, thought to increase the risk of eczema.
Also, it seems that this problem, at least increasingly in the future, will be limited to the United States, since, as with BPA, Europe and Canada have recognized the toxic properties of BBzP and limited its use. The American Chemistry Council has most likely lobbied for BBzP’s continued use.
No, it's not BPA. It's benzylbutylphthalate (BBzP)--good luck pronouncing that--a component that seems to be found mostly in vinyl flooring, but which makes its way into dust, and thence into the body. However, the dominant source of BBzP is food, say the authors of the study, which was led by Allan Just at the Columbia Center for Children's Environmental Health.
BBzP is one of a class of compounds used to make plastics flexible. Scientists have little idea how it might interact with the skin and immune system.
For this study, the scientists took urine samples from pregnant women in the third trimester. Then, after the children were born, the mothers filled out questionnaires at regular intervals, noting whether their kids had had recurrent rashes or had a medical diagnosis of eczema.
The results, from a cohort of 407 women, showed that the chances of children developing eczema were positively correlated with the mother's prenatal BBzP concentration in the urine. The data makes it hard to give a simple number, but higher BBzP clearly means greater risk.
The pattern was similar for African-Americans and Dominicans, the two main ethnic groups represented in the study.
The scientists originally thought BBzP might increase the incidence or strength of allergies, but did not find that to be true in this work.
It's unclear what one can do about the issue, if the science is true. You don't have much control over your environment, especially if you live in an urban apartment, as virtually everyone does in NYC. And BBzP is only one of many factors, including genetics, gut flora, geographic location, diet, and parental smoking, thought to increase the risk of eczema.
Also, it seems that this problem, at least increasingly in the future, will be limited to the United States, since, as with BPA, Europe and Canada have recognized the toxic properties of BBzP and limited its use. The American Chemistry Council has most likely lobbied for BBzP’s continued use.
Tuesday, June 26, 2012
New NEA blog post, on repurposed skin barrier drug for eczema
See my new post on the website of the National Eczema Association. It's about researchers at the University of Rochester who are conducting a clinical trial of Actos, a drug originally developed to treat diabetes but which looks like it could also repair the skin barrier and help eczema patients.
I learned about Actos when I spoke to Alice Pentland, who directs the new Skin Barrier Research Consortium at Rochester. I was going to write about the consortium but got too excited about Actos instead. I'll have to cover the research group in a second post.
I learned about Actos when I spoke to Alice Pentland, who directs the new Skin Barrier Research Consortium at Rochester. I was going to write about the consortium but got too excited about Actos instead. I'll have to cover the research group in a second post.
Friday, June 15, 2012
Going beyond probiotics: will pathogenic bacteria help us fight eczema in the future?
The human microbiome was the star of this week's science news. In seventeen papers in the journals Nature and PLoS, the Human Microbiome Consortium published the genetic sequences for virtually all the microbes that live in or on the human body. I can't be alone in feeling overwhelmed by the volume of data and analysis. It's clear that the coming years will bring much research into how our body partners with, benefits from, and combats our microbial tenants--which outnumber our cells by a factor of ten.
In a Wall Street Journal story, Michael Fischbach, a professor at the University of California, San Francisco, was quoted as saying "It's likely this work will lead to new treatments for [the inflammatory bowel disorder] Crohn's disease, new treatments for diabetes and metabolic diseases, new treatments for even other diseases, like eczema."
Considering the various locations in the body, the gut and intestines contain the majority of microbes, as you can see in this graphic. A lot of recent work has shown connection between gut flora & systemic inflammation, particularly that involved in asthma and eczema.
A graduate student who reads this blog told me about one of these microbes: Helicobacter pylori. H. pylori has long lived in the human gut--until the twentieth century, it was apparently the most numerous microbe in the stomach. But it seems that antibiotics have since largely killed it off.
A lot of people would say this was a good thing: only about a decade ago, scientists discovered that H. pylori was the cause of stomach ulcers. But Martin Blaser, a prominent researcher at NYU who made a career out of studying H. pylori, has controversially claimed that it's not just a pathogen but can also do some good. Blaser says H. pylori used to protect us from developing allergic disease. The reason that allergic, atopic diseases are increasing in Western society, Blaser says, is that H. pylori isn't around any more.
The graduate student who wrote me gave me a link to a recent paper in which scientists prevent asthma from developing in lab mice by infecting newborn pups with H. pylori. They show that the way H. pylori is most likely working is that it stimulates the body to produce more regulatory T cells--a class of T cells that put a damper on the activity of other T cells.
In a 2008 story in the Economist, Blaser is portrayed as envisioning a future in which doctors colonize babies' digestive tracts with (presumably) non-pathogenic strains of H. pylori to protect the infants against atopic disease. Certainly a more aggressive form of probiotics than kimchi or yogurt! (Am I allowed to say "probiotics on steroids"?)
I could imagine, also, that there may be no need to use H. pylori at all. If you could arrange things so that a patient grew more Treg cells, that might have the same effect as a H. pylori infection, but a reduced risk of disease caused by the bacteria. Perhaps it will be possible to take a drug that increases the number of Treg cells. Or a patient could donate blood so that Treg cells could be extracted and grown in culture before being reinjected.
I'm excited about this area--admittedly only as speculation about what medicine may hold for us in the distant future. Whenever you're talking about altering the developing immune system, you have to be very careful. Of course, what do antihistamines and steroids do but alter the immune response?
In a Wall Street Journal story, Michael Fischbach, a professor at the University of California, San Francisco, was quoted as saying "It's likely this work will lead to new treatments for [the inflammatory bowel disorder] Crohn's disease, new treatments for diabetes and metabolic diseases, new treatments for even other diseases, like eczema."
Considering the various locations in the body, the gut and intestines contain the majority of microbes, as you can see in this graphic. A lot of recent work has shown connection between gut flora & systemic inflammation, particularly that involved in asthma and eczema.
A graduate student who reads this blog told me about one of these microbes: Helicobacter pylori. H. pylori has long lived in the human gut--until the twentieth century, it was apparently the most numerous microbe in the stomach. But it seems that antibiotics have since largely killed it off.
A lot of people would say this was a good thing: only about a decade ago, scientists discovered that H. pylori was the cause of stomach ulcers. But Martin Blaser, a prominent researcher at NYU who made a career out of studying H. pylori, has controversially claimed that it's not just a pathogen but can also do some good. Blaser says H. pylori used to protect us from developing allergic disease. The reason that allergic, atopic diseases are increasing in Western society, Blaser says, is that H. pylori isn't around any more.
The graduate student who wrote me gave me a link to a recent paper in which scientists prevent asthma from developing in lab mice by infecting newborn pups with H. pylori. They show that the way H. pylori is most likely working is that it stimulates the body to produce more regulatory T cells--a class of T cells that put a damper on the activity of other T cells.
In a 2008 story in the Economist, Blaser is portrayed as envisioning a future in which doctors colonize babies' digestive tracts with (presumably) non-pathogenic strains of H. pylori to protect the infants against atopic disease. Certainly a more aggressive form of probiotics than kimchi or yogurt! (Am I allowed to say "probiotics on steroids"?)
I could imagine, also, that there may be no need to use H. pylori at all. If you could arrange things so that a patient grew more Treg cells, that might have the same effect as a H. pylori infection, but a reduced risk of disease caused by the bacteria. Perhaps it will be possible to take a drug that increases the number of Treg cells. Or a patient could donate blood so that Treg cells could be extracted and grown in culture before being reinjected.
I'm excited about this area--admittedly only as speculation about what medicine may hold for us in the distant future. Whenever you're talking about altering the developing immune system, you have to be very careful. Of course, what do antihistamines and steroids do but alter the immune response?
Tuesday, June 12, 2012
"Natural" does not necessarily mean "good for you"
You can generally separate eczema bloggers and tweeters into three groups. In increasing size of their representation on the web:
This is utterly wrong.
So, I found this cluster of healthy, clean-looking weeds outside my back gate. It looked like Italian parsley. It smelled like parsley. Did it taste like parsley? Whoa--let's not taste it right now, I thought.
And I'm a fan of wild mushrooms. I pick them and taste them raw. There is no mushroom that will kill you if you spit it out. Something just told me not to taste this plant.
I called my father-in-law, a biologist and naturalist, and he brought over a pile of books to help identify my weed. We narrowed it down to a few candidates that grow in our region.
It also said that since so many plants in the parsley family are extremely poisonous, you shouldn't eat them unless you have absolutely, positively, identified them.
I don't know what this stuff is, but even though it's all-natural, I won't be using it to garnish my pasta.
And, by contrast, the same night I quite happily popped a few pills of ibuprofen to reduce my back pain. They worked just fine, like they always do. I don't mind paying big pharma for ibuprofen.
I know the comparison between poison hemlock and ibuprofen is hardly a fair one, and that most practitioners of Chinese medicine know what they're handling, but it did starkly illustrate the point that "natural" plants can produce some of the most evil toxins we know.
- Those (e.g., me) who believe that Western science and medicine have good solutions to offer
- People who believe that Western medicine is a conspiracy designed solely to funnel money into the pockets of big pharma (generally, wackos, although they may have a point)
- Those who won't go as far as the second group, but who favor "natural" products and therapies instead of refined, "artificial' pharmaceuticals
This is utterly wrong.
So, I found this cluster of healthy, clean-looking weeds outside my back gate. It looked like Italian parsley. It smelled like parsley. Did it taste like parsley? Whoa--let's not taste it right now, I thought.
And I'm a fan of wild mushrooms. I pick them and taste them raw. There is no mushroom that will kill you if you spit it out. Something just told me not to taste this plant.
I called my father-in-law, a biologist and naturalist, and he brought over a pile of books to help identify my weed. We narrowed it down to a few candidates that grow in our region.
- Actual feral parsley
- Water hemlock
- Poison hemlock
It also said that since so many plants in the parsley family are extremely poisonous, you shouldn't eat them unless you have absolutely, positively, identified them.
I don't know what this stuff is, but even though it's all-natural, I won't be using it to garnish my pasta.
And, by contrast, the same night I quite happily popped a few pills of ibuprofen to reduce my back pain. They worked just fine, like they always do. I don't mind paying big pharma for ibuprofen.
I know the comparison between poison hemlock and ibuprofen is hardly a fair one, and that most practitioners of Chinese medicine know what they're handling, but it did starkly illustrate the point that "natural" plants can produce some of the most evil toxins we know.
Friday, June 8, 2012
Scots could benefit from vitamin D in the winter
A moderate dose of ultraviolet light during the winter months increases the levels of vitamin D in the blood and appears to put a brake on the T-cell arm of the immune system--which could reduce the severity of autoimmune disease, a new small-scale study on a group of Scottish patients has shown.
The research was led by Mark Vickers and Anthony Ormerod, a professor and clinical reader in dermatology, respectively, at the University of Aberdeen. It was reported in the Journal of Allergy and Clinical Immunology.
The trial was conducted between December and March, 2012. Before and after exposing 24 subjects repeatedly to the equivalent of a quarter of a day's worth of summer sunlight, the scientists measured blood levels of vitamin D; the fraction of white blood cells comprised of "regulatory" T cells; and the degree to which T cells expanded their numbers when stimulated.
Regulatory T cells are a subset of T cells known to suppress the activity of other T cells. According to Wikipedia, "Mouse models have suggested that modulation of Tregs can treat autoimmune disease and cancer, and facilitate organ transplantation." Eczema with an allergic component qualifies as an autoimmune disease.
The scientists found that, after two weeks' exposure to UV, vitamin D levels increased by 50%; after four weeks, by 100%. The fraction of regulatory T cells increased threefold, and other classes of T cells reacted less vigorously to stimulation.
While I am always interested in the connection between vitamin D, T cells, and eczema--I wonder whether this study really tells us anything new. The American Academy of Dermatology says there is no safe recommended level of exposure to UV (because of the risk of skin cancer).
The connection between vitamin D and regulatory T cells appears to be well-established, according to a PubMed search I just did. And everyone knows that regulatory T cells suppress other T cells.
Having spent several years in the north of Scotland myself, I well know how little sunlight the Scots get in the winter. Were the subjects' vitamin D levels low to begin with? I bet they were. Could they benefit from supplements? Almost certainly.
Especially since, as I recall, the Scottish diet consists largely of chips, lager, and cigarettes!
The research was led by Mark Vickers and Anthony Ormerod, a professor and clinical reader in dermatology, respectively, at the University of Aberdeen. It was reported in the Journal of Allergy and Clinical Immunology.
The trial was conducted between December and March, 2012. Before and after exposing 24 subjects repeatedly to the equivalent of a quarter of a day's worth of summer sunlight, the scientists measured blood levels of vitamin D; the fraction of white blood cells comprised of "regulatory" T cells; and the degree to which T cells expanded their numbers when stimulated.
Regulatory T cells are a subset of T cells known to suppress the activity of other T cells. According to Wikipedia, "Mouse models have suggested that modulation of Tregs can treat autoimmune disease and cancer, and facilitate organ transplantation." Eczema with an allergic component qualifies as an autoimmune disease.
The scientists found that, after two weeks' exposure to UV, vitamin D levels increased by 50%; after four weeks, by 100%. The fraction of regulatory T cells increased threefold, and other classes of T cells reacted less vigorously to stimulation.
While I am always interested in the connection between vitamin D, T cells, and eczema--I wonder whether this study really tells us anything new. The American Academy of Dermatology says there is no safe recommended level of exposure to UV (because of the risk of skin cancer).
The connection between vitamin D and regulatory T cells appears to be well-established, according to a PubMed search I just did. And everyone knows that regulatory T cells suppress other T cells.
Having spent several years in the north of Scotland myself, I well know how little sunlight the Scots get in the winter. Were the subjects' vitamin D levels low to begin with? I bet they were. Could they benefit from supplements? Almost certainly.
Especially since, as I recall, the Scottish diet consists largely of chips, lager, and cigarettes!
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