Blog on hold

Have to take a break for a while to work out some NEW back problems. Isn't getting older fun? Best wishes to everyone.

"Me no like carrots"/Protein fragment could be target for treatment of eczema itch

Saturday--double swimming lessons again. We're getting dried off afterward, me and the two kids, and in the men's changing room they're getting some lessons in anatomy as a number of hirsute and moderately obese men shower. One of them lathers himself head to toe with soap. I kid you not, I have never seen someone so completely covered with suds, as if he'd been dipped like a sheep. What must it be like to be able to use soap like that without consequences? For me and Voov soap is something to be used sparingly if at all.

Voov, as you may know, has been on a restricted diet. For about a year or so she has eaten about eight things (others are allowed but not always available as organic produce--e.g. asparagus). So three weeks ago we were given the green light to start trying a small roster of new foods. The first candidate was carrots, which we chose for their nutritional punch. We were excited as we placed the first plate of chopped, boiled carrots in front of Voov. She picked up a piece and stuck it in her mouth.

"Me no like them. Me not eat them," she said.

And so it proved, after we offered them every day for two weeks: she doesn't like carrots. Fortunately she liked the next two items, apple and pork; we are on week two of pork and next week on to something else.

Hidden B went away last week to a veterinary conference and chose the opportunity to wean Voov off breastfeeding. That's two and a quarter years Voov has been breastfed (Hidden B is ecstatic to be able to eat dairy again) and I hope that her eczema and potential asthma are less severe because of it. I myself was fed on formula pretty much from birth. My mother says that that was what mothers were told to do in those days. I suspect but cannot prove that my food-related eczema has been nastier because of the formula--Hidden B tells me the opinion of doctors at her vet practice (now there's authority for you) is that it's better for kids to be exposed to tiny amounts of allergens through their mothers' milk, rather than be completely deprived of exposure and then hit all at once when they eat real food.

* * * 

I thought I would write a bit about a recent paper in the Journal of Neuroscience. Scientists at Yale and Johns Hopkins have found, in experiments with human volunteers, that BAM8-22, a common protein fragment found in the body can produce itch by a neural pathway independent of histamine.

Histamine is a small molecule that some foods (pickles, aged cheese, red wine) contain a lot of; it is also stored in white blood cells called mast cells that release it in response to food allergies. There are neurons with receptors for histamine, and these neurons send itch impulses to the central nervous system. This is why I scratch like a demented monkey after I eat Parmigiano-Reggiano.

But it is also known that there are other neural pathways for itch; researchers don't know many details yet. For this new paper, the scientists showed that when they poked volunteers' forearms with little plant spines coated with BAM8-22, the forearms got itchy, even if they had been rubbed with antihistamine cream beforehand.

The plant spines are called "cowhage spicules." Cowhage is famous for making people itchy, and it has tiny spines covered with an enzyme that triggers itch. A group of scientists has decided that cowhage spicules are the perfect instruments for applying chemicals that induce itch. Is that weird or what? Apparently if you autoclave (treat at high temperature & pressure) the spicules for an hour, the original enzyme is destroyed and the spicules don't make you itchy.

So the upshot of this new research is that BAM8-22 and the receptor it interacts with (its identity is known too) could be a major pathway by which chronic itch signals, like those that operate in eczema, are sent to the central nervous system. It's possible that pharmacologists may now search for drugs that inactivate the BAM8-22 receptor, and conduct clinical trials to find out whether the drugs relieve chronic itch. My guess is that such drugs could emerge in a decade or so, if a pharma company--or startup--decides that the pathway could be profitable.

Baring it at the pool--or on Facebook

So Hidden B did something evil. Not only did she go away for a five-day-four-night trip to a conference in Denver (thus leaving me to deal with the kids) but she signed them up for swimming lessons AT THE SAME TIME on Saturday mornings, which means (because she works Sats) I have to take them both. Oh boy what chaos. No parking at the pool so we have to park in the neighborhood and schlep over; then the changing room is full and there's no place to put anything down; Shmoop ends up in the wrong class, and Voov is in tears because her new flipflops are pinching her toes.

Of course neither of them is actually going to learn to swim. (Voov is only two, so I have to get in the pool with her and try to convince her to blow bubbles. That would count as an achievement.)

And afterward--moisturizing Voov or myself? In that situation, with Shmoop tearing around investigating the urinals and lying on the floor and pulling all the lockers open? Forget it.

One benefit of the chaos is that I could care less whether people notice that I have eczema. I just want to get out of there with both kids alive and all the crap we came in with, and they don't know me anyway.

I've never been keen on the water. Maybe it's because I was born on the prairies. It took me forever to learn to swim. These days I would like to swim because it's great exercise but, ironically, I found out that swimming is bad for my back. Should have done it while I had the chance!

And then there's the eczema. Ever since high school I've avoided letting other people see me anything but fully clothed. Most of my friends and coworkers probably don't know I have eczema, although they must have noticed that I'm twitchy and scratchy. I would prefer that they not find out, because there's no benefit to me. Their reaction would range somewhere from "so what" to "that's disgusting."

That too is a shame, because I would like to connect with people like myself--on Facebook for example. I know the NEA has a Facebook page and I check it out every once in a while. I see that people have problems like my own and children like my own. (Some of them ALSO TYPE IN ALL CAPS FOR SOME REASON and some of them are selling quack remedies, but fortunately not all.) But, because most of my Facebook friends don't know I have eczema--I have about 175 "friends" and apart from my wife and brother and sister none of them are clued in--I am not about to participate on the NEA page, because I don't want my Facebook friends to see comments that I write on the NEA page. That would be too much information for them. Just as it would be for me if someone was writing comments about their inflammatory bowel disease.

So I wonder whether there's a social-media way for the NEA to connect with patients and to enable them to support each other. I can't be the only one who feels uncomfortable writing openly about my eczema under my real name in a world where everybody can see everything all the time. It's like being naked in a public place like a swimming pool.

An immune link between the gut and the skin in eczema

New research led by Raif Geha at Children's Hospital Boston has revealed how the immune system connects the gut to the skin, and thus how food allergies may affect the skin.

The connection is made by helper T cells. Geha and his team were investigating, in mice, how it is that an allergic reaction that the body has to a food--and we all know that the usual way that food enters the body is when we eat it--can manifest as an eczema-type reaction when the food is rubbed on the skin. Not eaten; rubbed on the skin.

The authors of the paper claim that this is a common occurrence but I beg to differ. I've never heard of it. But they put a lot of work (and taxpayers' money) into their experiments, and their results are intriguing.

Helper T cells are white blood cells whose job it is to detect foreign material in the body, and when it's detected, to stimulate B cells to produce antibodies. What I didn't know was that there are distinct populations of T cells, determined by molecules embedded in their outer membranes, which home in on different regions of the body. Some go to the gut; some to the skin; presumably, some to the lungs, etc. What happens is that the molecules in their membranes will bind specifically to "adhesion molecules" that are found in these different regions. A T cell that homes to the gut will stick to the adhesion molecules in the gut but not the skin.

And Geha and colleagues find that T cells that originally home to the gut can be reprogrammed to head to the skin instead. They immunized mice with the egg protein ovalbumin, and then later observed what happened when ovalbumin was applied to the skin of the mice. Normal mice developed eczema-like inflammation at that spot. Mice that had been genetically engineered with T cells that did not have the skin-homing surface molecule CCR4 did not show signs of eczema. In a truly gruelling series of experiments carried out late at night by grad student slaves, the authors showed that the initial immunization generated a bunch of gut T cells specifically programmed to hunt down ovalbumin; the body then modified these T cells to head to the skin. The reprogramming takes place in the lymph nodes.

I find this fascinating; I didn't know there was such a pathway. It could be that (in the way distant future) someone will develop a way to treat eczema patients with well-defined food allergies, and in these patients prevent the food-antigen-specific T cells from homing to the skin.

The research raises one huge question for me, though. Most eczema related to food allergy does not occur because we rub food on our skin. (At least, I know that I'm allergic to parmesan, but I sure as hell don't go rubbing it on the backs of my knees.) So what is going on to connect the gut to the skin and cause inflammation in the majority of eczema patients?

Scientists: We want you to stop the itch

On Twitter I heard about this survey that the University of Nottingham is doing. You can do it too!...it's not exactly a big investment of effort. They ask you what you would like to learn from eczema research. I'd assume that they are hoping to get some interesting questions, like "how do food allergies develop in children aged 1-3" or "what are the genetic defects in structural proteins in the skin that are most strongly linked to adult eczema."

As a relatively well-educated guy with an interest in eczema, I was interested to step outside my skin, so to speak, and watch as I entered in my questions in the survey--I didn't think too hard, so they were my knee-jerk reactions, what I want to know at a primal level:

1. how can I stop scratching?
2. how can I stop scratching at night?
3. how can I stop my scratched skin from getting infected?

Not exactly PhD material, eh?

But I think this illustrates what patients want from researchers. We are not interested in the science. We want results. And there's basically one thing we want: we want the itch to stop. If the itch stops, the scratching stops, and then there's much less risk of infection. So our challenge to researchers is "figure out what's causing the itch in eczema. Then figure out how to stop it."

I do have to say that eczema is a fascinating condition, though, when you start to read the scientific literature. I just wish my interest in it was purely intellectual.

Julie Block at the NEA asked me to write a brief research summary for the next e-newsletter, about a new discovery in itch pathways. When the newsletter comes out I'll comment on it.

Here comes the asthma

So it happened, a few weeks ago: Voov showed the first signs of developing asthma. We were always aware that she might, because eczema runs in the family and my sister has eczema and asthma, and asthma is the final part of the famous Atopic Triad. Still, it is a bummer to see your two-year-old with a rubber mask over her face taking her twice-daily dose of an inhaler.

Voov had had a cold, and was in for a checkup, and the doctor noted that she had a slight wheeze; her blood oxygenation was at 95%. So, with her history, the doctor tentatively diagnosed asthma and sent her home with the inhaler and a special mask. Voov was initially pretty excited about the attention, but after a few days, applying the inhaler took two adults, one to straitjacket the kid and the other to handle the inhaler.

Then she got better or at least well enough that she didn't have a wheeze. For now, the inhaler's packed away. Voov is healthy and upbeat and I think she'll cruise right through childhood just fine even if she has to carry an inhaler with her.

* * * 

I thought I'd mention this great review I read recently titled "Epidermal Barrier Dysfunction in Atopic Dermatitis." It's from 2009 and provides an encyclopedic view of how known genetic factors are related to the breakdown of the skin barrier, and how many factors such as pH and enzymes and antimicrobial peptides are involved. It also has an interesting section toward the end featuring this graphic

with an accompanying explanation of how it is that many more kids than adults have eczema, and how the condition improves with age for the lucky majority. Basically, when we're newborn, our skin barrier is terrible, the worst it'll ever be. In the first few years of childhood, the quality of our skin improves. In those people who have minor genetic defects that affect the skin barrier, eczema develops early on but fades away as the skin improves past some threshold. People with serious genetic defects like major filaggrin mutations never see their skin improve past the threshold, so they never escape eczema.

At least that's how the authors put it. It's a pretty hand-waving theory. For one thing, many scientists think that a poor skin barrier lets in pathogens and allergens that trigger a heavy immune response early on, and that this response imprints a permanent memory in the body (in the form of antibodies) that powers reactions to certain foods. So if this "memory" is made early on in the 20% of kids who have eczema, why does it go away for most of them after the skin barrier improves?

* * *

One final item: Anacor Pharmaceuticals has begun phase 2 clinical trials of two novel anti-inflammatory ointments for treatment of eczema. The two compounds are boron-based (this is unusual) and have shown promise for treating psoriasis in more advanced clinical trials. For a thorough comparison of psoriasis and eczema, see the most recent JACI Journal Club, which discusses a two-part review paper on the topic.

Math nerds identify possible cause of persistent inflammation in eczema

Researchers in London have developed a mathematical model of a molecular feedback loop thought to cause persistent inflammation in eczema patients.

Normal skin is maintained in a steady state in which old skin cells slough off and are continually replaced by new ones pushing from beneath. Flattened skin cells called keratinocytes are initially held together with bonds that are digested by enzymes called "kallikreins," according to a recent paper in the journal PLoS One. Kallikreins also cleave a receptor called PAR2 that, in normal skin, controls the skin steady state but, in eczematous skin, turns on a type of autoimmune response.

The authors of the PLoS One paper observe that, in eczema, inflammation that can start with a mild or short-lived stimulus (such as scratchy clothing) persists far longer than it does in healthy skin. They make the hypothesis that this is the result of a feedback loop between PAR2 and kallikreins. Even when the initial stimulus is gone, this feedback loop--like a screaming speaker connected to a microphone in front of it--keeps eczematous skin inflamed.

The authors ran their model on a computer (actually, they probably ran many models thousands of times on different computers, and tweaked tens or hundreds of parameters until they got the answers they wanted) and showed that it behaved consistently with data from real patients. So it's consistent with reality that there may be a positive feedback between PAR2 and kallikreins, or a negative feedback between PAR2 and a molecule called LEKTI that inhibits kallikreins.

They don't say this right out, but a potential benefit of this work--way, way, way down the line--is that if further modelling and experiments show that this feedback loop is real, then we may be able to break the loop with a custom-designed or -discovered drug, and stop inflammation quickly in eczema.

NEA eczema research grants too small. Philanthropist needs to step up

Julie Block at the National Eczema Association recently announced that the NEA offers research grants of $10-25k/year. I am all for supporting eczema research, both basic investigations into the causes of eczema and applied projects to help treat it. That’s why, as a patient and parent, although I applaud the NEA’s program--who else is doing this for us?--but I think it’s way too small. Someone needs to give it a boost.

Now, I know that the NEA’s primary purpose is patient support, and I know that sometimes these tiny grants can be used as leverage on bigger grant applications. Martin Steinhoff, I think, told me that NIH “study groups” that decide who gets federal money give great weight to grants from patient advocacy groups like NEA. They're a seal of approval.

Nevertheless, let me give a bit of perspective. Modern biology is expensive. The salary alone of a single graduate student is $50k/yr (counting overhead). The last time I looked at NIH research grants, the median grant was $250k. And, from what I’ve seen, the budget for a single lab at the University of California is at least $1M/year. Bigger labs, $2.5M/yr, a hundred times as much as an NEA grant.

Plus, here’s another issue: I don’t think leading scientists are going to bother applying for $10-25k grants. They’re not worth the time of a Kevan Shokat or a Carolyn Bertozzi: an innovator who could make radical discoveries that would transform a research field.

So we need to think bigger. How can the NEA get more money for its grant programs? We can’t rely on the NIH alone to fund eczema research. They don’t even include eczema as a condition worth listing in their public accounts.

The NEA is not going to get money from the government. And at their current annual subscription fee, they’re not going to get it from you or me. They might get it from one or more wealthy philanthropists who either themselves suffer from eczema or who have close family members who do.

And these philanthropists are going to want to know that they are not throwing their money away, giving it to scientists to buy expensive toys. They are going to want to know there is good management in place, with a plan that includes milestones. Would we be ready to convince such a philanthropist that we merit their money?

Or, possibly, someone would be interested in offering a prize, like an X Prize (an Ecz Prize?) of a million dollars or more for the first research group to, say, provide an effective pH-balanced filaggrin-based scalp moisturizer. Big prizes, so the scuttlebutt goes, offer a factor of ten leverage. You pay a prize of $1 million, but you get $10 million worth of research done by competing groups. Plus, a prize draws attention to a challenge.

The question is: what goal would a prize be offered for? Eczema is such a complex problem, and we’re far from a complete understanding of it. So what realistic, inspirational goals could a prize committee set? I’d be happy to learn of parallels where this approach has worked for other conditions.

Managing eczema on your scalp

Scalp eczema doesn’t get much press, but a lot of us live with the problem every day. Me, for example: I own virtually no dark-colored tops, because a snow of skin flakes shows up within seconds. I comb my hair, or what’s left of it (hey, I’m a 40-year-old man) not to straighten tangles, but to clear up any rogue scabs. And I’ve had to develop my own regimen for scalp care because nobody ever handed me a pamphlet.

Eczema on your scalp is the same as it is everywhere else, except for two complications.

1. most people have hair on their heads, which makes it difficult and unsightly to apply thick creams and ointments
2. it’s right out in the open where everyone can see. You can hide it only with long hair, and long hair makes it difficult to treat the scalp.

So how should we treat it? Pretty much as we do “normal” eczema. You have to clear up infection with antiseptics; reduce the inflammation; and moisturize as much as possible. And any concerns about how your hair looks are secondary. You’re not Fabio or Catherine Zeta-Jones, so get over it.

I keep my hair very short. I use a #2 buzzer on my head. I can get away with this because I’m a man in a job where hairstyle doesn’t matter. The #2 keeps my hair short enough that I can apply steroid creams or ointments but long enough that other people can’t see my sores or scabs easily.

Steroid ointments (say, fluocinonide 0.05%, my “strong” option) come with warnings about folliculitis. You’d think this would be a problem on the scalp, but I haven’t found it to be. I try to use it sparingly, though.

Many shampoos and conditioners brag about their moisturizing properties, but they refer to what they do for your hair, not your scalp. In my experience, both shampoos and conditioners have detergents that dry out my scalp to a painful degree, and fragrances that irritate it. What to do?

Go fragrance-free, for a start. Or as fragrance-free as you can; medicated shampoos seem all to come with masking fragrances to hide their smell. Options that I’m aware of are coal tar (say, T-Gel, Zetar, Polytar); zinc pyrithione (e.g. Head and Shoulders, Selsun Blue); and iodine (Betadine). I spent several years in the UK where Betadine is available as a shampoo. I haven’t seen it as a shampoo in North America, but Hidden B, who’s a veterinarian, has a bottle of it that she uses on dogs.

Let’s tackle these one at a time, and ignore any qualms about weird smells.

Zinc pyrithione (http://en.wikipedia.org/wiki/Zinc_pyrithione) is an antimicrobial that kills bacteria and fungi. It doesn’t work for me. This is probably because my primary problem is in the skin barrier, not a secondary infection. I may also have infections that it does or doesn’t clear up.

I remember Betadine being relatively pleasant, and leaving terrible brown stains on everything. I think it worked well because it didn’t have a very strong detergent component, and was much more a medical than a cosmetic product. I’m all in favor of this. Hey, maybe I should borrow some from Hidden B. Again, the active ingredient in Betadine is iodine, because it’s a broad-spectrum antimicrobial.

Coal tar works for me, but only in the strongest formulation. I use T-Gel Extra Strength and Polytar. In the past these have been difficult to find where I live in California, and I have bought them online from a Canadian source, but recently I’ve seen tar shampoos on the shelf in pharmacies here.

Coal tar’s a bit of an oddity. It is not a pure substance that can be easily quantified. It is a mixture of apparently up to 20,000 organic compounds, and it’s a traditional treatment for scaling skin diseases that reduces inflammation and itch and kills microbes. Which of the 20,000 compounds are doing what is anyone’s guess, and there have occasionally been claims that coal tar causes cancer. I don’t take these seriously because there has never been a conclusive study and if there were a large risk we’d know about it by now. (See a recent study here.) I think that it matters very much which brand of coal tar you use, because different brands are probably from different sources and contain different stuff.

What I DO take seriously is the increased sensitivity to UV that comes with using tar shampoo. The days I use it, I often find I get lightly sunburned on my face. Sunburn = cancer risk. So if I were going to spend a day outside, I’d be careful not to use tar shampoo that morning.

The more I learn about eczema, though, the more I understand that we might not want to use a strong antiseptic on our head too much. We probably have a flora of beneficial bacteria and fungi living on our scalps, and we ought to keep them healthy while killing off the S. aureus etc. that cause us so much grief.

Lastly, for moisturizing: every morning, and after I shower (which I do not do every day), I rub jojoba oil into my scalp. Jojoba’s a very light oil, and it doesn’t make my head too greasy. I think grapeseed or walnut oil would also do the job, but olive oil would be too heavy. Sometimes, when I have really dry skin, I have resorted to rubbing Eucerin into my scalp, but this is a bit gross.

What are your solutions to cooling itch and moisturizing on your scalp? I’d be interested to hear them.

Gil Yosipovitch on alternative therapies for itch

The basic problem with treating chronic itch is that there is no cure for most conditions, including eczema. But several approaches reduce the severity by a significant amount. Some of these approaches are “Western” medicine, which I take to mean they are based on refined drugs manufactured by a pharma company. Some are “alternative,” which includes acupuncture, probiotics, “Chinese medicine” (that is, herbs that probably contain active ingredients that have not been isolated and refined into “Western” drugs), and others. Gil Yosipovitch, a world expert on itch, combines both in his approach, without overt prejudice--as long as the alternative component is not patently ridiculous.

Psychology plays a large part in Y’s method. “There are a lot of issues involved in the suffering that are beyond dermatology,” he says. “We use a lot of meds that come from psychology.”

He works with an acupuncturist. He collaborates with a practitioner of healing touch.

Here’s an aside: my own mother practices healing touch, and in past years I have mocked her for it, because there is no way that waving your hands over someone’s body is going to cause physiological changes through the medium of some imaginary “energy field” that has no connection with the laws of physics. But here’s the rub: if the patient believes there is such a connection, then I acknowledge that it is possible that undergoing healing touch could relax the patient and, via psychological paths, relieve itch or pain. Won’t work for me, though; I don’t believe in it!

“I’m a physician--I’m OK with the placebo effect,” Y says. Y doesn’t care, as long as the patient feels better. He found out that his acupuncturist has expertise in itch, and his patients who undergo acupuncture see their symptoms relieved by 20-30%. That’s better than he sees with most drugs. “Why should I prescribe drugs with side effects?” he asks. “We don’t know everything.” One of his patients was taking “enough meds for an elephant,” but they didn’t do much, and it was healing touch that appeared to improve his condition.

This holds, he says, only for chronic itch. Acute itch, that is caused by something like poison ivy or insect bite, likely has a well-defined treatment. And in any case, why worry about acute itch? It will go away. (That’s my opinion, not his.)

Probiotics: he’s not super-keen on them, but he sees a lot of people asking about them. “We have to address the issue,” he says. Again, if it works, it works, so why not try eating yogurt if it seems like a good idea.

But sometimes he sees ads for less legitimate treatments such as garlic pills or suppositories. “That’s not what I want my patients to try,” he says.

I’m confused. It seems hard to draw any sort of boundary between valid and invalid therapies, if you’re OK with healing touch. Perhaps with healing touch, or yoga, if you are “treated” or practice it regularly, there is a rhythmic relaxation effect, whereas garlic pills or their ilk are unlikely to produce anything but a weak, transitory placebo effect. However, Y knows what he sees, and he sees that healing touch has a practical, beneficial outcome.

Also, it could be that genuine caring human contact reduces anxiety. A theory occurs to me: maybe the apparent increase in incidence of eczema in developed countries is partly related to social alienation in modern life. We spend so much time dealing with machines instead of people, and so much time with strangers instead of friends and family. Can we improve our eczema symptoms by spending more time with family?

I doubt it, unfortunately. Ask any mother of a young child with eczema. It’s not that the mother doesn’t care, or isn’t doing her best to try to calm her child.

In this blog I intend mostly to pursue Western therapy as a means of treating eczema or relieving itch. I’m open-minded, though, and I hope not to bad-mouth any therapies without good reason. So, within reason, I’ll try anything myself and see if it works. That includes vitamin D. In the near future I will try a course of 4000 IU vitamin D per day, and we’ll see what happens.

With itch medicine, Y says, “large studies are a problem” because itch has so many potential causes and pathways that it’s hard to find a large identical test population. “You can’t give just one antibody for itch. That’s a simplistic approach.” And so personalized medicine, a customized approach for each of us, is our future. The responsibility lies with us. But we already knew that.

Thinking about a comeback

Hey all.

I have been thinking about returning to this blog--I miss keeping up with the latest research, and sharing ideas with people.

But as you might have read below, I am struggling with some neck and back trouble probably caused by computer use or poor ergonomics. My job involves sitting in front of a computer, and it doesn't feel good toward the end of the day, and I sure don't feel like aggravating it with more computer time after I get home and help feed the kids and put them to bed and do my prescribed physiotherapy. Plus I don't have much spare time anyway.

So bear with me--maybe I can write shorter posts during the odd lunch time; maybe I can do some video posts.

At least I feel like I owe you the second half of my interview with Gil Yosipovitch.

One new thing for now: did anyone notice this link, part of the NIH's campaign for public accountability? It's a list of all the NIH's research expenditures--I think their annual budget is $20 billion, but I haven't taken the time to add up the totals. The list shows money spent per disease, and there are a lot of diseases in the list. But there's one that seems to be missing: eczema. Is it really not there? Not under atopic dermatitis or some other name? Apparently not. Maybe it comes under psoriasis? Does anybody know?

Surely they can't not be funding eczema research. (I KNOW they are at least funding Donald Leung's multisite project.)

Yosipovitch on itch clinics

Last Thursday I spoke to Gil Yosipovitch, an eminent dermatologist and itch expert at Wake Forest University. I called him because Martin Steinhoff said Yosipovitch ran the only itch clinic in the United States, and I wanted to learn how such a clinic operates.

The only problem: Yosipovitch does not run an itch clinic. There are NO itch clinics in the United States. "I very much believe it's the future and there should be many of them," he says. He's happy that Steinhoff is establishing one. The centers in Germany are the model; apparently a colleague is also starting one in Singapore.

Y believes there are a couple barriers to itch clinics getting started in the US. The major one is insurance companies and the current system for reimbursement; doctors have much more incentive to do basic treatment like wart removal than they do to care for patients with chronic conditions who require regular monitoring. Also, he says, to establish a clinic, a department chair (at a hospital or university) has to put money into it. That means leadership, and no-one except for Steinhoff has shown that leadership.

Y says that he likes Steinhoff's plan of directing a clinic with a number of resident doctors and a nurse practitioner who keeps in touch with patients through an online forum. In fact, Y himself once ran such a forum, called "Living with Itch" (if I understand correctly, it got folded into the International Forum for the Study of Itch website, but I can't find a link to old postings). The problem was that the site, on which patients shared their "anguish, frustration, and practical ideas," was quickly "hacked," in Y's words--possibly not hacked, but overwhelmed with spam from quacks advertising miracle cures like some garlic diet. So the forum became useless and was abandoned. Y thinks an online patient forum could work if someone was dedicated to the web technology side, and ensuring that only authorized patients could use it. (Also, there are "HIPAA," or medical privacy, issues, he says; presumably his former site managed to solve them.)

A point Y insisted on making was that itch should be treated as a disease, not a symptom. It's a major issue. He sees many parallels between itch and pain; itch is now where chronic pain was thirty years ago.

Y also thinks that eczema patients should look to psoriasis as a disease whose patients have been successful in setting up support groups and activism for funding. "But [itch clinics] needsencouragement from the upper levels," he says, meaning the NIH and legislators who have the power to make insurance companies change the incentive model.

Y is a fan of the National Eczema Association. "They're providing a lot of support to atopics," he says. He was able to leverage a small NEA grant into a large NIH one (that's how science funding works--a granting agency will only give you money if someone else has already given you money). I suppose I should be happy that he likes the NEA. He said he only decided to talk to me because I was raising money for them.

In my next post I'll talk about Y's position on alternative medicine. My next post, by the way, may be my last for some time. I need to resolve this trouble I've been having with my neck, and the less time I spend at a computer the better, for the moment.

Up next, Gil Yosipovitch

Today I spoke with Gil Yosipovitch on the phone--he was at his home in North Carolina. It was a good conversation and I learned quite a bit that I will share with you in the near future. I'll be considering it in two parts: one about traditional Western medicine and one about Gil's opinion of alternative methods, which might surprise you. He is concerned that I not misrepresent his views on that subject so I'll be running his quotes by him first.

I wish I could write more today but recently I have been short of time. (My physiotherapist has given me home exercises to do that take the time I'd set aside for blogging.) Best regards to all.

The "itch receptor"

Another thing for me to be excited about: this Thursday, I get to talk to Gil Yosipovitch, the "Godfather of Itch," who runs a clinic at Wake Forest University and founded the International Forum for the Study of Itch. (I made him an offer he couldn't refuse.) If you have any questions for him, please ask and I will pass them along. Myself, I just want to get an idea of how his clinic operates, and find out why there aren't more of them.

Also, whether he envisions any pharmaceutical cures for itch appearing soon. Martin Steinhoff scribbled a list of possible targets in the itch pathway that one might like to shut down to reduce or eliminate itch. Here's what he wrote down, before I distracted him with another question:

• GABA
• GRP
• Proteases

The "GRP" rang a bell in my memory so I looked it up. It stands for "gastrin-releasing peptide," whatever that is. What's important is that in 2007, two scientists at Washington University in St. Louis discovered that a receptor for GRP is a major gate for itch nerve impulses in the spinal cord, at least in mice. (And basic neurology isn't different in mice and humans.) I could be wrong, but I think that GRP receptor is still the prime suspect.

The scientists were able to do their experiments because they had developed a strain of mice without GRP receptors. These mice were much less likely to scratch themselves when their skin was injected with substances known to induce itch. And in normal mice, a compound that inhibits GRP receptors greatly reduced scratching behavior.

This isn't exactly breaking news, but it is good for me to know as I explore "itch centers" in the US and around the world.

* * * 

A wee  bit of business news: a small company in Seattle, recently acquired by Bristol-Myers Squibb, is developing an anti-IL-31 antibody which is now in preclinical trials for atopic dermatitis. (Now, what does IL-31 do? I always get confused by these IL-X things. It is apparently produced by Th2 cells and has something to do with inflammation.

How an "itch center" (or clinic, really) would work

After I wrote the last post, I realized that I should clarify what I mean by "itch center." If you search for the term on Google, you don't turn up much, but I did find one indirect listing for the "Center for the Study of Itch" at Washington University in St. Louis, Missouri. It has something to do with the Washington University Pain Center. Anyway, what I mean by "itch center" is a place that primarily serves patients, rather than a pure research lab. As far as I know there is currently only one such entity in the U.S., Gil Yosipovitch's at Wake Forest University in Winston-Salem, North Carolina. And you can't find a webpage for it. How is a patient supposed to get help?

Martin Steinhoff told me that he plans to establish an itch center at UCSF--a clinic to help patients. He also mentioned, in conjunction with that clinic, that he's putting together a research center. You might be interested to know how these things get planned.

For his clinic, to begin with, Steinhoff would serve as the lead doctor with three residents working under his direction, plus one nurse. In Germany, he says, with such a setup he was able to see 50 patients in a day. At UCSF, he says he wants to think on a bigger scale, so eventually there may be several senior doctors and many residents and nurses.

As I mentioned in the previous post, Steinhoff says that at his Muenster clinic the most important feature was that patients would arrive for diagnosis and spend the next one or two weeks under close supervision so that their treatment could be adjusted according to need. In the US system this can't happen (barring unusual philanthropy)--doctors usually see ambulatory patients only for very short times, and then send them away for 4-6 weeks.

Steinhoff says that he's thought about this--the limitation is frustrating, but he thinks that he could achieve some sort of active modulated treatment by having patients join a self-help group, moderated by the clinic's nurse. The patients could check in to a website or wiki online where the nurse would be available several hours a day to check how people were doing, and in off-hours they could converse with each other in forums. I'm extrapolating here, but I expect his idea is that the patients would lend each other moral support as well as practical advice. It'd be interesting to see this in operation--how much of the forums would consist of comments like "OMG I'm so itchy" or "Just scratched, feels so goooood"? Probably knowing that the conversation was moderated by the nurse would improve the tone.

In Steinhoff's proposed itch research center, he'd again be the director, with, to begin with, two assistant professors in his laboratory. (He's an active research scientist and in fact got his PhD in biology before his MD.) I'd like to visit his laboratory sometime to see how one carries out itch experiments, but I've used up my quota of his valuable time for several months.

* * *

You may have noticed that I am posting less often at the moment. My current target is twice per week. I've been having some back trouble that may have been brought on by my enthusiastic start to blogging--until recently the ergonomics of my home computer setup were terrible, and I'm now at about 75 posts, so that makes about two days' straight worth of typing with bad posture. My physiotherapist has advised me to make several changes to my lifestyle, and seeing as I already spend 8 hours a day in front of a computer at work, it doesn't make sense to overdo it at home.

Martin Steinhoff plans largest itch center in the world

Today I met with Martin Steinhoff, a professor of dermatology at the University of California, San Francisco (UCSF). (He's listed as a "professor in residence," but assures me he's here to stay.)

Steinhoff plans over the next 25 years to build the biggest "itch center" in the world at UCSF. Previously he led the itch clinic at Muenster, which he believes is the largest such center in Germany. An itch center is a special clinic with dedicated residents and staff, at which patients are diagnosed, treated, and observed intensively over a period of one to two weeks, and their treatment modulated to get the itch under control.

Steinhoff came to UCSF because he was impressed with the research being done in neuroscience. UCSF is a purely medical and research campus with no undergraduates--it used to be the medical school of UC Berkeley, and although not well known to the public, it is the second largest recipient of NIH funds (presumably after Johns Hopkins in Baltimore). However, he says he is the only itch specialist currently at UCSF, although he works closely with four scientists who study pain, which shares neural pathways with itch.

Steinhoff has been impressed with the can-do, entrepreneurial spirit in California. "Here you have the possibility to build a computer company like Apple in your garage," he says. "In Germany, people expect everything from the government."

However, he prefaced those remarks with ones less likely to be repeated by American politicians. He is frustrated and unimpressed with what passes for a fragmented health care "system" in the US. Because of the power wielded by insurance companies, itch patients in particular receive substandard care. "In Germany, when a patient visits [the itch clinic], they come for one week, get a diagnosis, and we get it under control," he says. Here, you are seen for two minutes--maybe 15, at a university--you get a quick diagnosis and you're told to come back in 6 weeks. There is no time. And because of money, you cannot prescribe the optimal treatment, because of insurance." [This is true for me, actually: my own insurance wouldn't pay for me to attend Steinhoff's proposed clinic.] "

"In the US, insurance wants to prescribe the cheapest topical or systemic steroid," he says, even if the best treatment would be a large dose of (admittedly expensive) nonsedative antihistamines. [A surprise to me, this; I'm not the expert, but I thought antihistamines were not effective. Maybe just the ones I've taken.] His conclusion: "You cannot help patients because of the insurance."

Whatever your political views, you'd have to agree that the point of health care is to help the patient, and from that perspective, the current "system" is broken.

I'll give a few details of Steinhoff's proposed clinic in the next post, and how he plans to work around the limitations. I'd just like to add that he's a little mystified why eczema has such a low profile in the US, while conditions such as psoriasis that, according to him, "have much less effect on quality of life," are well-known. Once he gets his clinic off the ground, it will be only one of two such centers in the US, the other one being Gil Yosipovitch's at Wake Forest University. Two centers for 240 million people in the richest country in the world.

Most definitely no definite answer for vitamin D and eczema

As with most of the posts on this blog, I wrote the last one in a hurry--there's only so much free time if you've got a job and a commute and two kids. Being in a rush makes blogging unsatisfying as a writing exercise, both for the strength of argument and the quality of prose. A blog is nothing more than a series of first drafts, and the expression "shitty first drafts" (Google it) exists for a reason.

So I thought perhaps I'd been too quick to diss vitamin D as potentially having benefit for patients with eczema. A PubMed search turned up this review paper, which I am inclined to trust as credible for several reasons:

1. one of the two authors is Donald Leung, head of pediatric allergy and immunology at National Jewish Health Center in Denver; editor-in-chief of the Journal of Allergy and Clinical Immunology; and principal investigator for the Atopic Dermatitis Research Network
2. the authors cite 73 papers instead of just one or two selected to support their cause; they present a balanced view with opposing data
3. they don't use scary headings like "Is This Nutritional Deficiency Ruining Your Heart?" or provide a convenient link to an online store with products such as krill oil, vitamin spray, and bidets.

Anyway, I learned quite a bit. In short, vitamin D deficiency is a real phenomenon in the US population. There are a number of molecular mechanisms in which a lack of vitamin D might increase the severity of eczema. And a few trials have been done with small numbers of people that show that a short course of increased vitamin D improves symptoms.

That's not enough to make me rush out and buy barrels of vitamin D though, especially since there are multiple side effects of an overdose, including kidney damage. As Caroline commented after my last post, the issue is really whether you're deficient or not, not that it's a good idea to take an excessive dose. (I sent her a copy of the paper so we can look forward to learning her perspective.)

A reading of the paper turns up a bewildering number of studies in cells and mice that produced conflicting results. E.g. mice deficient in vitamin D had helper T cell responses greatly slanted toward type 1 instead of type 2; but it's known that, in humans, eczema patients have overactive type 2 helper T cells. If you were to take that one paper as gospel, you'd try to deprive yourself of vitamin D to cure your eczema.

Another paper shows that adults who received vitamin D supplements as infants were more likely to develop atopy and allergy. But then opposing papers balance this out. Dosage and timing could be crucial.

So, as with most science, the conclusion is the familiar "more research needed."

Vitamin D isn't the answer

In a recent conversation with Caroline over at Fighting Eczema, she mentioned that she wanted to look into whether having low levels of vitamin D might be correlated with risk of developing eczema. The theory was her own, but she mentioned "a strong advocate for the benefits of vitamin D on the internet, Dr. Mercola." I thought I'd check the man out, since I'd seen another article or two by Mercola in the general health news.

I was seriously unimpressed. Joseph Mercola is a self-appointed "expert" on "natural health" who, in short, is a scaremonger peddling fears of modern technology and the drug industry. Natural cures are best, he says; and just in case you were wondering where to get them, you need only visit his extensively stocked online store.

He's big on vitamin D, for sure; has an entire section devoted to it. According to him, it cures just about everything. Count me a skeptic. Every doctor I've asked, and a few I haven't, has told me that anyone eating a balanced diet has no need of any vitamin supplements at all. Vitamin C, and perhaps a few others, are flushed out of your body in your urine, but the rest accumulate in your tissues. Too much of a vitamin or mineral is a bad thing, just like too little. No way would I take an excessive dose of one particular substance unless I'd been diagnosed with a severe deficiency.

(Amusing aside: in my 20s, for a short while, I took several multivitamins a day, in the belief they would make me super-healthy. I developed a remarkable case of hemorrhoids that cleared up when I stopped taking the pills.)

Caroline, I mean no offense--in the search to cure eczema for our children and ourselves, we ought to explore every avenue. But vitamin D isn't going to be the answer.

If you're interested--I recommend it--the blog Science-Based Medicine has a comprehensive and entertaining takedown of Mercola. Here's one segment. The FDA has served Mercola with two warning letters concerning unwarranted claims for seven of his products.

Steinhoff's 2006 itch review fascinating, useful

So in advance of meeting Martin Steinhoff, I've been reading a couple of his review papers on itch research. I am well used to reading scientific papers--the slog through the jargon and hard-to-grasp concepts. It's liberating to read a paper about a subject that touches you personally, instead of one about some anonymous molecule with an acronym like ADF46-PGL (I made that up) that is somehow linked to something that might be useful to someone someday. With Steinhoff's itch reviews, there's a fair amount of jargon, yes, but I can relate to virtually every paragraph, and I pay attention because I hope to learn tips that I can apply to my daily life. For example:

Recent results suggest that noxious heat stimuli and scratching produce a stronger itch inhibition than do noxious cold stimuli.

I've always found that a cold pack from the freezer helped kill an itch, at least for a while. Maybe I'll try a hot pack next time.

The main point I take away from the review I've just finished is that itch research is unfortunately far from being able to produce a good target for anti-itch drugs. Decades, maybe--although that review is from 2006, so the current state-of-the-art may be much further ahead; you never know. There's always the hope that an already-approved drug might turn out to have a beneficial side effect against itch. Certainly, one thing that's been discovered is that pain inhibits itch--this was discovered partly because painkiller drugs tend to make people itchy.

A major recent development is that scientists have identified specific neurons that carry itch from the skin to the spinal cord and then to the thalamus in the brain. Some of these neurons are called "histamine-sensitive itch fibers," or "pruriceptors," although there must be other itch fibers because there are many more molecules besides histamine that have been shown to induce itch.

This diversity of primary afferent "itch fibers" would nicely fit to the different submodalities of pruritis ("itch quality") observed in patients.

Exactly! Um...that is, I know I experience different kinds of itch. There's the tickly kind, like when an ant is crawling on my neck; there's a distinct itch I get from a small, active patch of eczema, on my foot, say; and there's the full-on-paroxysm that I occasionally wake up with after I've had the poor judgement to drink eggnog or eat something laced with cayenne pepper. And there are others.

As I just mentioned, there are many more itch-inducing molecules besides histamine. Steinhoff thinks that researchers have focused too much on histamine. Table 1 lists 16 different types of molecules (he calls it the "itching army") that represent the major culprits. In eczema, acetylcholine and mu-opioids appear to be more significant than the other molecules.

On to the next review, which has more gems, I'm sure.

Zema, the Warrior Princess

Voov has reached a new stage. Like HAL in Stanley Kubrick's 2001, she has become self-aware. Hidden B informs me that earlier today, Voov raised her arm, pointed at her wrist (which is always red and inflamed, because we can't put steroids anywhere near her hands) with the forefinger of the other hand, and, for the first time, spoke the word "Zema."

Zema, the Warrior Princess.

* * *

Yesterday, Caroline at Fighting Eczema posted about her son's recent scratching attack and how she has begun to suspect that dust mites might be partly responsible for his eczema. (Specifically, it's the dust mite droppings that are the allergen.) I have always been aware of the dust mite issue, but because  eczema is maddeningly inconsistent and hard to connect to any causes, even though at times it seems certain that some foods or allergens trigger flares--and because it would take a lot of time, effort, and money to attempt to control dust mites in our house, I have never done anything about them.

Vacuum? Sure, we do that once in a while. But vacuuming probably stirs up dust mite droppings and blows them into the air. Read Caroline's blog for details on what you'd have to do to begin to control dust mites.

And so it occurred to me that dust mites--and grass pollen, another thing it's virtually impossible to control exposure to--are the two most important targets for immunotherapy for eczema patients.

Three papers (here, here, and here) from the current issue of JACI show that we could expect these therapies to make it to the clinic. The grass pollen treatments are tablets, taken for about 6 months, and improved symptoms in both kids and adults by about 20% on some qualitative scale of hay fever misery. The dust mite treatments may have been injections (I don't have access to the full paper right now) and were taken over 3 years (hoo boy) but the researchers found improvements of about 45% in hay fever and 80% in asthma, so they were definitely more effective.

I'd say that the NEA should consider funding some of this research (they may already be doing so) to translate these findings into FDA-approved therapies, at least in the case of dust mites. Are the scientists considering founding a company, or patenting and licensing their discovery?

* * *

It's taken a while, but I have made an appointment to speak to Martin Steinhoff, a visiting professor of dermatology at UCSF, about the German itch center model. I'll be talking to him on January 25th. (He's visiting from the University of Muenster.) In advance of our meeting, he's given me a couple references to his papers, and I'm reading one at the moment: a review of how the skin, nervous system, and brain work together to create the sensation of itch. It's eye-opening stuff and I'll share some key points with you when I understand them! Let me give you just one quote:

"...the impression that one's skin itches is nothing but a sensory illusion created by the brain."

So, you'd think, you don't necessarily have to treat itchy skin to control itch. You could take something that acts directly on the brain. Pop a tablet, instead of smearing yourself with steroids.

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).

The itch roundtable

When I heard back in December about the NIAMS (division of the NIH) itch roundtable--a discussion that involved the NEA's CEO Julie Block, a number of NIAMS directors, and a larger number of active itch researchers--I was excited that the meeting summary would be made public. I don't know why it is, but in the media you hear about eczema much more from the allergy perspective, or as if it's a cosmetic issue with dry skin, rather than the reality for a lot of us: chronic itch. If we could control the itch, we'd be less at risk of infection, we wouldn't prolong our flares, and possibly most importantly, we'd have more self-respect.

It's hard to feel like you're a grown-up when your self-control in this one dimension is no better than a three-year-old's.

The summary of the itch roundtable was recently put online (at the link above). I got there by following a link in the email the NEA sent all its members. At the end of the summary there's a long list of the participants. I plan to check out what research they're all doing.

Two things jumped out at me from the summary. The first thing is that itch research is building on the much more established field of pain research. It appears well-known that certain types of pain can inhibit itch. (And, in fact, that the same type of neuron carries both impulses.) As an eczema patient I know this very well first-hand. In fact, sometimes scratching feels good precisely because it hurts, and seems to spread a cool blanket of pain over the burning itch.

I've got a rather silly story to relate about this. When I was a teenager I discovered this pain-itch connection, and I happened to have an itchy scalp at the time. I found that a good way to relieve the itch was to pull out small clumps of hair. Ouch! you say. Ouch is right. Felt great. I did this for about a week.

The problem was that I then developed an extremely nasty case of something like eczema herpeticum--little fluid-filled blisters that spread all over my body and threatened to leave me looking sandblasted for life. Fortunately my parents took me to a doctor who prescribed some magical cream that completely reversed the infection. I have no idea what the cream was, only that it worked, and that my parents said it was "very strong." It must have been an antibiotic of some kind.

Dr. Sib, if she still reads this blog--will remember this episode. During the recovery period, I drove her crazy by picking at my scabs.

So don't try that at home.

The second thing that jumped out at me from the summary was that, although mice are the standard laboratory model animal for many human diseases, there are several key reasons why itch in mice and humans is substantially different at the molecular level and at the level of the skin as an organ. Therefore, it's unlikely that a mouse model will be developed for human itch. To quote NIAMS:

• Itch- and pain-specific neurons and receptors identified in mouse models may not have the same distinct functions in humans.
• Structural differences in mouse and human epidermis may create differences in itch transduction, and downstream cellular activity (e.g., protease production).
• Overexpression of many cytokines in mice will induce non-specific itch, whereas the itch mechanisms in humans appear to be more complex.
• Current mouse models correspond to acute itch, whereas clinical itch tends to be chronic.
• Linking itch mechanisms from animal models to the spectrum of itch descriptions in human patient populations can be challenging, because some behaviors in animal models, such as scratching, licking, and biting that are attributed to the condition may be unrelated to it.

These complications with animal models will slow itch research. But pain research has faced similar hurdles, and is more advanced as a field, so we can hope the scientists can piggyback their work on existing pain research.

A close-up look at immunotherapy

January's issue of the Journal of Allergy and Clinical Immunology is dedicated to immunotherapy. To be honest, the first time I heard of immunotherapy, I thought it was a quack treatment (it didn't help that what I'd heard of was sublingual immunotherapy, and the point of the author was that because the FDA hadn't yet approved it in the US, it must be too effective). But the more I learn about it the more I find that it is a long-established therapy with proven results. You should read the issue's editorial, which summarizes immunotherapy over the past 100 years.

What did I learn from this issue? (Not: what is news to everyone; what was news to me.) First, it seems that immunotherapy is largely directed at allergic rhinitis, or hay fever, caused by grass pollen; that, in the US, the standard method is repeated injections over a long period, from four months to three years; that sublingual immunotherapy is widely practiced in Europe, and appears safe and effective; and that trials of therapies for other allergens such as cat dander and dust mite droppings are being conducted and show promise.

For now let's leave aside the issue that doctors don't seem to be prescribing immunotherapy for eczema patients. Say it were available. What then?

The problem for me is that I don't know for sure what allergens cause my eczema. I know that my skin prick test, 10 years ago, showed that I reacted to a bunch of things including cat (at least, one cat allergen), egg white, and rye grass. But does that guarantee that, say, rye grass pollen is a major factor in my eczema during the period that rye grass pollen is in the air? Everything I've read regarding food allergies says that skin prick tests are not diagnostic, and that the gold standard is to lay off the offending food and see if the problem goes away. There's no good way to try an avoidance diet with pollen or dust mites.

An aside: the reaction I get in the spring and summer, which I attribute to pollen, is quite different from the eczema I experience on my hands, arms, scalp, etc. In the summer, on both east and west coasts, I get red, inflamed skin on my face in a butterfly pattern. It's distinctive, and out there in the open for everyone to see. I saw the same pattern once on someone else's face.

One thing I am sure of: Claritin and Allegra, the over-the-counter antihistamines marketed for hay fever, do absolutely nothing for me.

Would I undergo injection immunotherapy, a long, arduous, and (in the US) expensive procedure, in the hope that 1) the thing I'm getting injected with is a major contributor to my eczema and 2) the therapy works for me? No, I wouldn't. And I do suspect that at least one form of pollen gives me trouble.

But I would take a course of immunotherapy tablets orally (or sublingually). That would not seem like a waste of time, nor would it be hard to get a kid to take them. One good thing is that grass pollens are, apparently, "cross-reactive," which I read as meaning their allergens are similar enough that if you induce tolerance to one, you induce tolerance to the rest of them. So you don't have to take more than one type of allergen as immunotherapy.

Reading the editorial, I did learn that grass pollen tablets are not effective if you take them as only one component of a mix of allergens in immunotherapy. Here's another difference between the US and Europe: in the US, a multiallergen mix is a common approach, while in Europe, immunotherapy for a single allergen at a time is the norm. (Any experts or Europeans are free to correct me on this.) So, it does appear that the US is lagging Europe in easy, effective immunotherapy.

When will we see immunotherapy applied to eczema? Is there anywhere in the world where it already is?

A day at the geneticist

Cindy posts that her family's been having a hard week. I do admit I've wondered how it goes in larger families; once one child comes home with a flu or something, does that inevitably means it goes around and everyone gets it? Even in our family of four, often just because a kid has a cold doesn't mean that the parents will get it, but it's almost guaranteed that the other kid will pick it up. Voov acquired a viral fever from her cousin at Xmas, and then had some congestion, so we had to have the humidifier on every night. We were going to put the humidifier away, but then Shmoop started getting congested too. And now he most likely has an ear infection. (And a rare, for him, incidence of eczema behind his knees.) The fun never stops!

Voov's eczema has been moderate for a while, so that's why I haven't mentioned it. Some on her scalp though. Whenever she gets stressed about anything, even momentarily, her hands shoot up to her head and she starts scratching away. I have to laugh because I do the same thing, even though I'm all grown up. It's a reflex.

Eczema isn't the only nonstandard feature Voov came equipped with. She's also had a few weird things with her eyes; she took a long time to learn how to walk and talk; and her face looks a little odd--her forehead's kinda bulgy, and her eyes look far apart. Taking everything together, her pediatrician advised us to get a genetic consult to determine whether she might be suffering from some syndrome. So that's what we did today-- went in for the consult.

We saw an MD and a genetic advisor, who asked us all kinds of questions about medical conditions in our families (we had also come with a stack of photos of family members so the docs could compare Voov's face with the photos) and took measurements of length ratios of her fingers to palms; torso to legs; pupil-to-pupil vs. width of the bridge of the nose, etc. At the start, the docs were almost too caring and friendly--it was unnerving, like they were preparing for us to freak out if they found something was wrong. But in the end their initial conclusion was that Voov had no obvious syndrome (although the bridge of her nose is very wide). Which was a huge relief, of course. However, they did suggest that we get done a procedure called "array comparative genomic hybridization," which I'd never heard of, and which consists of comparing stretches of Voov's genome to standardized DNA from "normal" people and looking for deletions and insertions.

Since there's no pressing need to get this done, I'm actually not keen on it. I could imagine that the test might turn up some deletion or insertion that might be associated with a fractionally increased risk for some condition, and then we'd just have something new to worry about. Hidden B wants to get it done, though. She says she wants to know, and that we might find out that (for example) we should get Voov's heart checked out, or at the very least, we'd be contributing her genetic information to a databank that would help other parents.

I can't really argue otherwise-- if there's something definite we could act on, we need to know. The thing is, what's more likely is that there won't be anything definite, or there might be something definite that we can't do anything about. I know that much is true about genetic information.

Ain't he cute?

Not too much to post tonight-- I'll note that the current issue of the Journal of Allergy and Clinical Immunology is dedicated to immunotherapy, and there's an interesting review of what the future may hold, as well as a number of articles about clinical trials of immunotherapy for allergens important to eczema, including timothy grass and cat dander. Can't wait to read the papers! --but haven't had the time.

Check this photo out. Who's this handsome fella? Yours truly, Spanish Key, Christmas 1972. My mom sent it to me recently. For me it's particularly interesting because it's really hard to see any traces of eczema on the exposed skin. There's some healing scabs on my left foot. Maybe the photographer airbrushed the shot!

There's no denying that I've had eczema as long as I can remember, so I'm interested to see a baby photo of me that looks so...normal. 

A Canadian sister of the NEA

Yesterday I was talking about how so many "news" articles about eczema are of the "eczema is..." variety. Here's one such: "Winter brings itchy, scratchy woes to sufferers of eczema," courtesy of www.canada.com. Now, being Canadian (as well as American) and having spent eleven years in Saskatchewan, I can attest that Canadians know winter, and that winter indeed brings on the misery. There are two reasons, I think: once everything freezes, the air becomes very dry and sucks moisture out of your skin; and inside, the air from central heating dries you out too. Try that for five or six months of every year.

The article isn't really news, and the author isn't well-informed ("An allergen-- and there are many, including harsh soaps, perfumed items, fabric softeners, dust mites and certain foods...") but it did contain a nugget that was news to me. It introduced me (and, hence, you) to the Eczema Society of Canada, a nonprofit sister of the National Eczema Association. You have to check out the ESC's website. It's very well done. Their mission is to educate sufferers and to increase public awareness of the disease, and they're clearly doing both.

Another interesting point: the ESC website has a section devoted exclusively to hand eczema. I don't know why this is-- is hand eczema of particular interest to the society's board? I have eczema on my hands, but I also have it virtually everywhere. I guess certain people must subject their hands to stresses while doing their jobs-- maybe they have to wear rubber gloves-- I know a former dentist of mine had trouble with his latex gloves.

In the past few years a specific treatment for hand eczema has been developed by the Swiss company Basilea. The drug is aliretinoin and the trade name is Toctino. A business news item of note, from Bloomberg: apparently the stock of Basilea, which is a midsize company, just took a big jump because an investment research firm decided Basilea was undervalued and ripe for a takeover. Part of Basilea's value stems from $130 million it won in a suit against Johnson & Johnson because J&J mismanaged clinical trials of another Basilea drug. J&J, you may know, owns Aveeno.

Why should we care about these details of the business world? Well, I like to know stuff, and while I generally find business news boring, somehow it's more interesting when it involves companies that make products that I use. Also, if you want to know about emerging eczema treatments, the business section is where you should look. Any treatments that qualify as eczema "cures" are going to have to be made by companies for a profit.

And the companies that innovate the cures will be small ones-- that is how innovation happens in pharma-- and then big pharma, like J&J, is going to buy the small companies. So I like to know what's going on both at the small and big ends of the eczema therapy market.

Cryptic children

So I read all of the backlogged eczema news from the holidays. Quite remarkable: there wasn't anything worth talking about. A trawl of the internet at any given time turns up a host of hits for eczema, 50% of which are "eczema is..." explanations for the lucky people who don't know what eczema is; 45% of which are miracle cures; and 5% of which are Yahoo Answers postings along the lines of "OMG i have exsema on my face so gross what can i do about it." Every few days, you see something interesting. But not over the past two weeks, apparently.

And so today I muse: One of the more difficult things about having a very young child with eczema is that they can't explain what they're feeling. Voov is about 18 months and she's just learning to talk, and a lot of the things she says come out garbled. We think she understands most of what we say-- but her answer to any question is usually "yes." What are we to make of it, then, when she starts writhing and crying when we put CeraVe (unscented moisturizer) on her, and she can't tell us why? We ask "is it cold?" "Yes." "Does it sting?" "Yes." Of course, you get the same answer if you ask if it's warm, or if it smells like roses.

I put the CeraVe on myself, and didn't feel anything. But is her skin the same as mine? It must be much more sensitive. As far as we know, CeraVe is the best thing we could be putting on her, and it doesn't raise any irritation.

Lately, she's been learning how to manipulate us, especially where her brother is concerned. She likes to yell "Shmoop!" in a loud, anguished voice, and enjoys bringing her parents' wrath down like artillery on the competition. Perhaps she likes the attention she gets when she complains about CeraVe. It's hard to tell.

New Year's resolutions? Ditch the coffee and candy

How are you all? Anyone make any New Year's resolutions?

I didn't. Forgot to, actually. New Year's isn't as exciting as it once was. Since we had our first kid, we've been in bed well before midnight every Dec 31.

In past years, I made a number of resolutions. Most of them had to do with eczema. They were along the lines of "won't scratch so much." I was no more successful than people who resolve to lose weight and take out gym memberships. My father-in-law has a great cartoon from the New Yorker-- a bunch of blobs of fat out for a jog (they may have some label like "Your Lost Weight") and one turns to another and says "It's about time to head back."

One thing I do have to do, though, is kick the addiction to sugar and caffeine I reacquired over Christmas. We got a new coffeemaker--Hidden B likes it every day, and I indulge on Sundays normally, but had several cups a day over the last week--and because I ate so many chocolates, I developed a craving that would hit me every afternoon around 3. I know neither sugar nor caffeine are good for eczema. So: away with ye, coffee and candy!

The first work week after the holidays has been busy and we've had a series of minor crises in the house (both kids are sick; car trouble; Hidden B working out bugs on her new Android phone) so I'm not up to the minute on eczema news. Let me get back to you when I am. I'm also hoping in the near future to talk to a philanthropist about fundraising strategy, and to have a conversation with UCSF's Martin Steinhoff about itch centers in Germany.