Something I've wanted to do for a long time is create a world map of all the major centers or points of interest for eczema patients, doctors and scientists.
Why? Because
I feel that we're all largely isolated, even in the internet age. Especially with a disease that makes you want to stay away from other people. We can get on our computers and search for blogs or advice or therapies, but there's very little sense of belonging to a greater community. We don't know what's going on in the big picture.
And so I would like to introduce to you the Eczema Map Project, a work in progress. It is a map of the world marking the locations of key researchers, therapy centers, and patient associations.
I've decided to make the map a permanent tab on this blog, so I can update it continually when I learn about new people or developments.
The items on this map are those that I consider significant--game-changers, not just good dermatologists. But please feel free to write a comment about your dermatologist if you think he or she is above average!
You can see that at present the map is a bit USA and UK-centric. This could be for a few reasons. I largely operate in English, and I live in California, so I tend to hear about developments in the USA more than anywhere else. But it is true that the USA is a very large and well-developed country with some of the best medical care in the world (for those who can afford it--an issue I have strong opinions on, but which I am not going to get into right now). So it may turn out that more of the most important sites are indeed here.
But please tell me what is missing from this map. Is there a major therapy center or a patient association I don't know about? Leading scientists not there? Tell me, and I'll add them. Or, if you think an item doesn't merit being listed, let me know. Nothing is set in stone.
And have fun exploring the world map from an eczema perspective.
View The Eczema Map Project in a full screen map
Showing posts with label therapy. Show all posts
Showing posts with label therapy. Show all posts
Thursday, May 2, 2013
Wednesday, April 11, 2012
Oral treatment of infants appears to reduce risk of developing eczema
Treating infants orally with extracts from bacteria apparently reduces the risk that they will develop eczema--but the treatment doesn't work if both parents have a history of atopy, a group of scientists from Germany and the Netherlands recently found.
It's been known for a while that exposure to certain microbes, particularly on farms, seems to protect children against eczema to some degree. The microbes must contain, or be coated in, some active compounds that cause the immune system to develop tolerance; researchers have identified a number of classes of compounds, including those called lipopolysaccharides and peptidoglycans. In this recent trial, involving over 600 subjects, the scientists used whole-cell extracts from heat-inactivated Escherichia coli and Enterococcus faecalis. They asked parents to dose their kids three times daily from the age of 5 weeks to 7 months.
Parents were selected for the trial if one or both had a history of eczema, asthma, or allergic rhinitis. Overall, the treatment had no effect on whether or not the children developed eczema. However, when the scientists considered children who only had one parent with atopy, the treatment reduced the kids' chances of developing eczema from 19% to 10% (measured right at the end of the trial; the improvement was lasting, up to three years out). The effect was even more pronounced if it was the dad, rather than the mom, who was atopic; the risk dropped from 32% to 11%.
Now I'd like to know why the children of atopic dads had a 32% chance of getting eczema, versus 19% for children who had either an atopic mom or dad. I can't find an explanation in the paper.
Instead, the authors focus on why the improvement was weaker in the atopic either-mom-or-dad group. They suggest that this is because a fetus's immune system depends not just on its genetics but also a heavy imprint that the fetus receives from the mother during pregnancy. If the mom is atopic, dosing the infant with bacteria after birth has less influence on whether he or she develops eczema. If the dad is atopic, the medicine has a stronger effect.
This seems contradictory to me; if the maternal imprint has a major effect, the children of parents of whom only the mom is atopic should be more likely to develop eczema than the children of parents of whom only the dad is atopic. The authors say that this is indeed the fact, but their own paper has it the other way around.
The inactivated-bacteria therapy is well-documented as safe, the authors say; it has been used to treat irritable bowel syndrome. In this trial they saw very few adverse reactions.
Do you think that parents of newborns would be likely to use this treatment on their kids? I wonder. Only if you've lived with severe eczema, or already had a child with it, or seen it close up, would you be motivated at the very difficult early months to try to give your kid medicine. And you could say it roughly halves the chances of developing eczema, but in truth, it reduces it from 20% to 10%. If this study is true, that's what you get for six months of giving your kid medicine three times a day. Would you do that if only one parent had hayfever?
It's been known for a while that exposure to certain microbes, particularly on farms, seems to protect children against eczema to some degree. The microbes must contain, or be coated in, some active compounds that cause the immune system to develop tolerance; researchers have identified a number of classes of compounds, including those called lipopolysaccharides and peptidoglycans. In this recent trial, involving over 600 subjects, the scientists used whole-cell extracts from heat-inactivated Escherichia coli and Enterococcus faecalis. They asked parents to dose their kids three times daily from the age of 5 weeks to 7 months.
Parents were selected for the trial if one or both had a history of eczema, asthma, or allergic rhinitis. Overall, the treatment had no effect on whether or not the children developed eczema. However, when the scientists considered children who only had one parent with atopy, the treatment reduced the kids' chances of developing eczema from 19% to 10% (measured right at the end of the trial; the improvement was lasting, up to three years out). The effect was even more pronounced if it was the dad, rather than the mom, who was atopic; the risk dropped from 32% to 11%.
Now I'd like to know why the children of atopic dads had a 32% chance of getting eczema, versus 19% for children who had either an atopic mom or dad. I can't find an explanation in the paper.
Instead, the authors focus on why the improvement was weaker in the atopic either-mom-or-dad group. They suggest that this is because a fetus's immune system depends not just on its genetics but also a heavy imprint that the fetus receives from the mother during pregnancy. If the mom is atopic, dosing the infant with bacteria after birth has less influence on whether he or she develops eczema. If the dad is atopic, the medicine has a stronger effect.
This seems contradictory to me; if the maternal imprint has a major effect, the children of parents of whom only the mom is atopic should be more likely to develop eczema than the children of parents of whom only the dad is atopic. The authors say that this is indeed the fact, but their own paper has it the other way around.
The inactivated-bacteria therapy is well-documented as safe, the authors say; it has been used to treat irritable bowel syndrome. In this trial they saw very few adverse reactions.
Do you think that parents of newborns would be likely to use this treatment on their kids? I wonder. Only if you've lived with severe eczema, or already had a child with it, or seen it close up, would you be motivated at the very difficult early months to try to give your kid medicine. And you could say it roughly halves the chances of developing eczema, but in truth, it reduces it from 20% to 10%. If this study is true, that's what you get for six months of giving your kid medicine three times a day. Would you do that if only one parent had hayfever?
Thursday, January 13, 2011
Dogs: eczema patients' best friend in more than one way
And now for something completely different...
Dog eczema!
Quite frequently I see items in my news feed about canine eczema. I haven't paid them any attention. But today I saw something worth commenting on. Imulan, a company based in Arizona, announced that it had developed a biomarker for canine eczema.
Who cares? was my first thought. But I was intrigued, because in reading the NIAMS roundtable summary the other day, I'd seen that dogs are considered a potential experimental model for human eczema. So any research done using dogs as models might not only benefit dogs, but also humans.
I wondered why it was worth anyone's time to develop a biomarker for eczema in dogs. (A biomarker is any protein or metabolite in your body whose level is correlated with your risk of developing a disease-- or the chance that you have it already. Biomarkers are emerging as a biomedical field--for example, Tethys Bioscience in Emeryville, CA is developing biomarkers for diabetes.) If you have eczema, it shows. Why do you need a biomarker?
Then I understood. Dogs scratch all the time. They get fleas, etc. They roll in their own feces and other stuff. So it's harder for a veterinarian to diagnose eczema for a dog than for a human doctor to diagnose it for a patient. A biomarker would enable the vet to make a quick, definitive diagnosis.
Imulan says that its canine eczema biomarker is based on its "T cell receptor therapeutic peptide vaccine." This opened my eyes. They're claiming to have a vaccine for eczema! Bold. I have no idea what data this is based on. Nor do I know exactly what a "TCR peptide vaccine" is.
I did a Google search and it seems that there have been a number of papers published on TCR peptide vaccines, although the ones I checked out concerned vaccines against lymphocytic cancer in mice. And those were EXTREMELY preliminary.
The idea, Imulan says, is that a messed-up T cell balance (type 1 helper vs. type 2) is at the root of eczema (this, of course, is not established in humans; the imbalance is likely a symptom, not the original cause) and so you need to cancel out, or mute, the type 2 T cells. In short, as I understand it, you vaccinate so that your body produces a lot of antibodies against YOUR OWN T cells, thus shutting them down.
This seems nutty to me, and if tried in humans, likely to lead to something like the "cytokine storm" that nearly killed the six volunteers in a 2006 trial of an experimental T cell-stimulating antibody. But Imulan claims their vaccines have shown promise in dogs.
I'll have to ferret out their data (pun intended).
Dog eczema!
Quite frequently I see items in my news feed about canine eczema. I haven't paid them any attention. But today I saw something worth commenting on. Imulan, a company based in Arizona, announced that it had developed a biomarker for canine eczema.
Who cares? was my first thought. But I was intrigued, because in reading the NIAMS roundtable summary the other day, I'd seen that dogs are considered a potential experimental model for human eczema. So any research done using dogs as models might not only benefit dogs, but also humans.
I wondered why it was worth anyone's time to develop a biomarker for eczema in dogs. (A biomarker is any protein or metabolite in your body whose level is correlated with your risk of developing a disease-- or the chance that you have it already. Biomarkers are emerging as a biomedical field--for example, Tethys Bioscience in Emeryville, CA is developing biomarkers for diabetes.) If you have eczema, it shows. Why do you need a biomarker?
Then I understood. Dogs scratch all the time. They get fleas, etc. They roll in their own feces and other stuff. So it's harder for a veterinarian to diagnose eczema for a dog than for a human doctor to diagnose it for a patient. A biomarker would enable the vet to make a quick, definitive diagnosis.
Imulan says that its canine eczema biomarker is based on its "T cell receptor therapeutic peptide vaccine." This opened my eyes. They're claiming to have a vaccine for eczema! Bold. I have no idea what data this is based on. Nor do I know exactly what a "TCR peptide vaccine" is.
I did a Google search and it seems that there have been a number of papers published on TCR peptide vaccines, although the ones I checked out concerned vaccines against lymphocytic cancer in mice. And those were EXTREMELY preliminary.
The idea, Imulan says, is that a messed-up T cell balance (type 1 helper vs. type 2) is at the root of eczema (this, of course, is not established in humans; the imbalance is likely a symptom, not the original cause) and so you need to cancel out, or mute, the type 2 T cells. In short, as I understand it, you vaccinate so that your body produces a lot of antibodies against YOUR OWN T cells, thus shutting them down.
This seems nutty to me, and if tried in humans, likely to lead to something like the "cytokine storm" that nearly killed the six volunteers in a 2006 trial of an experimental T cell-stimulating antibody. But Imulan claims their vaccines have shown promise in dogs.
I'll have to ferret out their data (pun intended).
Saturday, November 6, 2010
A tale of two itches
As SK is cavorting across the continent, I will take the opportunity to introduce myself as a guest blogger on End Eczema. You can call me Dr Sib.
As mentioned in previous posts, I share in approximately half of SK's genetic pool, being his sister. Unfortunately for me, our genetic overlap appears to include a faulty filaggrin gene that has been the root cause of much unhappy scratching by us both. And, while I've certainly spent my fair share of time shredding my own skin with my 10 digits, I have to confess that this particular organ is fairly intact at the moment, my atopy manifesting itself more at the asthma end of the allergy spectrum.
I attribute this happy state of affairs, based on a sample size of 1 (myself), in part to my geographic locale. My eczema has never been as flared as it was for the 12 months I spent on Vancouver Island on Canada's western coast. There, I spent the entire time bleeding into my sheets at night, tossing and turning with the torment, and avoiding showers because the chlorine in the water burned too much to bear on a daily basis. No dietary measure had any effect. Nor did the usual routine of steroids and emollients that I had come to rely on in the past.
Musing back, I realize (quite ironically for reasons that will become clear in a moment) that I never consulted a physician during this time, nor did it even occur to me to do so. Essentially, anything I had learned about managing my eczema up to this point had been from personal experience and the advice of fellow sufferers. It was well known amongst this same cohort, that our family doctors had proven to be pretty useless when it came to treating our dysfunctional skin. At the same time, I had never been referred to a dermatologist, so I assumed I was stuck with things as they were, bad as they were.
Now, as a first year resident in family medicine, what do I do with this memory? I admit I do feel it reveals a certain incompetence on the part of the family doctors I've had in the past in managing atopic dermatitis. The time I've spent with dermatologists thus far in my training has suggested that family doctors have a tendency to be far too cautious when it comes to the use of topical steroids, particularly in children and adolescents. I seek to rectify the problem in myself by taking a special interest in the dermatological complaints of my patients. And, I hope I have a well-developed capacity to empathize fully with the impact a symptom as 'harmless' as ITCH can have on an individual's life. Finally, I feel the drive to be competent in diagnosing, counseling, and managing this problem in my own patients. For me, this will mean an extra rotation in dermatology during my residency training.
My story brightened when I moved back east, first to central Canada (Ontario), and then to the Maritimes. My skin healed of its own accord. While I used to attribute my temporary misery to some quality of the water to which I was exposed, I've come around to assuming there must have been an environmental allergen triggering me, be it mould in the basement apartment I was inhabiting, or some type of noxious pollen circulating in the botanical breezes of the west coast. Either way, I'm left a number of habits/superstitions that I use to ward off a recurrence: I never miss a full-body moisturizing after a shower/bath. I don't expose my skin to long, hot soaks. And, I'm aware that every coffee, every alcoholic beverage, and every spicy meal exacts a toll that may tip me over the edge into a flare.
As mentioned in previous posts, I share in approximately half of SK's genetic pool, being his sister. Unfortunately for me, our genetic overlap appears to include a faulty filaggrin gene that has been the root cause of much unhappy scratching by us both. And, while I've certainly spent my fair share of time shredding my own skin with my 10 digits, I have to confess that this particular organ is fairly intact at the moment, my atopy manifesting itself more at the asthma end of the allergy spectrum.
I attribute this happy state of affairs, based on a sample size of 1 (myself), in part to my geographic locale. My eczema has never been as flared as it was for the 12 months I spent on Vancouver Island on Canada's western coast. There, I spent the entire time bleeding into my sheets at night, tossing and turning with the torment, and avoiding showers because the chlorine in the water burned too much to bear on a daily basis. No dietary measure had any effect. Nor did the usual routine of steroids and emollients that I had come to rely on in the past.
Musing back, I realize (quite ironically for reasons that will become clear in a moment) that I never consulted a physician during this time, nor did it even occur to me to do so. Essentially, anything I had learned about managing my eczema up to this point had been from personal experience and the advice of fellow sufferers. It was well known amongst this same cohort, that our family doctors had proven to be pretty useless when it came to treating our dysfunctional skin. At the same time, I had never been referred to a dermatologist, so I assumed I was stuck with things as they were, bad as they were.
Now, as a first year resident in family medicine, what do I do with this memory? I admit I do feel it reveals a certain incompetence on the part of the family doctors I've had in the past in managing atopic dermatitis. The time I've spent with dermatologists thus far in my training has suggested that family doctors have a tendency to be far too cautious when it comes to the use of topical steroids, particularly in children and adolescents. I seek to rectify the problem in myself by taking a special interest in the dermatological complaints of my patients. And, I hope I have a well-developed capacity to empathize fully with the impact a symptom as 'harmless' as ITCH can have on an individual's life. Finally, I feel the drive to be competent in diagnosing, counseling, and managing this problem in my own patients. For me, this will mean an extra rotation in dermatology during my residency training.
My story brightened when I moved back east, first to central Canada (Ontario), and then to the Maritimes. My skin healed of its own accord. While I used to attribute my temporary misery to some quality of the water to which I was exposed, I've come around to assuming there must have been an environmental allergen triggering me, be it mould in the basement apartment I was inhabiting, or some type of noxious pollen circulating in the botanical breezes of the west coast. Either way, I'm left a number of habits/superstitions that I use to ward off a recurrence: I never miss a full-body moisturizing after a shower/bath. I don't expose my skin to long, hot soaks. And, I'm aware that every coffee, every alcoholic beverage, and every spicy meal exacts a toll that may tip me over the edge into a flare.
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