This week you'll find me blogging over at the National Eczema Association website. I interviewed Donald Leung of National Jewish Health about the Atopic Dermatitis Research Network. Three years in to a $42M program to investigate the links between genetics and our susceptibility to skin infections, the ADRN is registering patients with the NIH before proceeding with clinical trials.
They still need black and Hispanic patients to sign up--eczema, genetics, and skin pathogens are different for different ethnic groups. The better your demographic is represented in the trials, the more that scientists will learn that applies to you.
The ADRN has centers in Boston, Chicago, Denver, Los Angeles, Portland OR, and Rochester NY.
If you're interested in participating, email Judy Lairsmith at National Jewish or call 1-888-413-5852.
Showing posts with label clinical trials. Show all posts
Showing posts with label clinical trials. Show all posts
Wednesday, July 17, 2013
Thursday, June 20, 2013
Three years in: what has the $42M Atopic Dermatitis Research Network produced?
In July it will be three years since the NIH awarded National Jewish Health in Denver, CO $31 million to create and administer the Atopic Dermatitis Research Network, a consortium of five academic sites across the US. A contractor, Rho Federal Systems of Chapel Hill, NC, won an $11 million contract to operate a center to coordinate statistics and clinical trials for the project.
That makes $42 million—spread over five years—which puts the project on the large end of NIH funding for individual biomedical efforts. The typical NIH research grant ranges from $100 thousand to $2 million, and anything bigger is fodder for university news releases. Which raises the question: what have US taxpayers gotten in return?
I ask this as a patient who is grateful that these scientists are working to understand a disease that affects me, my family, and millions in the US and worldwide.
The answer is not obvious, since the publications page on the ADRN website hasn’t been updated since July 2011.
According to the website:
The ADRN’s NIH contract number is HHSN272201000020C. A search in the NIH’s PubMed database returns 12 papers that acknowledge funding by that contract number. Three of those are review papers (which did not involve new research).
So that makes two clinical trials and nine research papers, three years into a five-year $42 million project.
Should US taxpayers expect more; be satisfied; or be impressed?
The answer is probably that we will have to wait to find out.
In each year, a typical top university research lab operates on about $2-3M a year and publishes somewhere around ten papers. That’s roughly $200k a paper.
Three of the five years in the ADRN contract are up; three-fifths of $42M is around $24M. We might therefore naively estimate that we should have seen upwards of 100 papers produced so far.
Most likely the reasons there are only 12 at the moment are that you don't start publishing papers right at the outset of a project. The research must be done first and then written up; and the process of getting accepted to a journal takes months. And the ADRN appears largely to rely on clinical trials--which take time to set up.
So why do we only see two trials listed on clinicaltrials.gov?
I've never had anything to do with a clinical trial, but when I was a researcher, I conducted animal experiments, and there were formidable administrative hurdles to get over before I could start work. I imagine that trials with human subjects are heavily regulated by the government, and for good reason. So the apparently small output of the ADRN to date is, I'm guessing, because it takes a long time to plan trials, get approval, and conduct them, before you can begin analyzing data and reporting it.
Looking at the titles of the published papers, I can't immediately judge which are the most important. So I emailed Donald Leung, the principal investigator for the ADRN (he's a professor and head of the Division of Pediatric Allergy and Immunology at National Jewish Health), and asked him whether he could summarize the consortium’s findings so far and highlight key points. I hope to hear back from him soon and perhaps to interview him on the phone.
I’d like to know what ADRN scientists have found that surprises them. What have they learned that is truly new?
And what is going to be truly useful to patients in the end? Publishing papers should not be the be-all and end-all of scientific research. What about patents? I’d like to know whether anyone in the ADRN has thought about controlling intellectual property and commercialization. While it’s true that clinical studies may highlight the ideal dosing amount or schedule for existing therapies, and this does not involve creating a new commercial enterprise, most medical technology must pass through the marketplace before it can benefit the consumer/patient.
Someone has to do the dirty work of developing scientific discovery into therapy, and it’s not academic scientists.
More to come.
That makes $42 million—spread over five years—which puts the project on the large end of NIH funding for individual biomedical efforts. The typical NIH research grant ranges from $100 thousand to $2 million, and anything bigger is fodder for university news releases. Which raises the question: what have US taxpayers gotten in return?
I ask this as a patient who is grateful that these scientists are working to understand a disease that affects me, my family, and millions in the US and worldwide.
The answer is not obvious, since the publications page on the ADRN website hasn’t been updated since July 2011.
According to the website:
The Atopic Dermatitis Research Network (ADRN) is a consortium of academic medical centers that will conduct clinical research studies in an attempt to learn more about skin infections associated with atopic dermatitis (AD). The studies will focus on antibiotic-resistant Staphylococcus aureus infections and widespread viral infections of the skin, both of which are more prevalent among AD patients. The ADRN will build on the work of the Atopic Dermatitis and Vaccinia Network (ADVN) which conducted clinical studies focused on making smallpox vaccinations safer for people with AD.
This research will lead to a greater understanding of the immune system in AD patients and may lead to novel therapeutic strategies to manage or prevent infectious complications associated with this disease.
The ADRN will conduct a number of clinical studies over the next five years and will be enrolling large numbers of people with AD.A search on clinicaltrials.gov returns two entries for the ADRN: one (open) to create a database of patients for the study of genetic markers connected to susceptibility to infections, and one (completed) to look into how AD patients respond to a new flu vaccine.
The ADRN’s NIH contract number is HHSN272201000020C. A search in the NIH’s PubMed database returns 12 papers that acknowledge funding by that contract number. Three of those are review papers (which did not involve new research).
So that makes two clinical trials and nine research papers, three years into a five-year $42 million project.
Should US taxpayers expect more; be satisfied; or be impressed?
The answer is probably that we will have to wait to find out.
In each year, a typical top university research lab operates on about $2-3M a year and publishes somewhere around ten papers. That’s roughly $200k a paper.
Three of the five years in the ADRN contract are up; three-fifths of $42M is around $24M. We might therefore naively estimate that we should have seen upwards of 100 papers produced so far.
Most likely the reasons there are only 12 at the moment are that you don't start publishing papers right at the outset of a project. The research must be done first and then written up; and the process of getting accepted to a journal takes months. And the ADRN appears largely to rely on clinical trials--which take time to set up.
So why do we only see two trials listed on clinicaltrials.gov?
I've never had anything to do with a clinical trial, but when I was a researcher, I conducted animal experiments, and there were formidable administrative hurdles to get over before I could start work. I imagine that trials with human subjects are heavily regulated by the government, and for good reason. So the apparently small output of the ADRN to date is, I'm guessing, because it takes a long time to plan trials, get approval, and conduct them, before you can begin analyzing data and reporting it.
Looking at the titles of the published papers, I can't immediately judge which are the most important. So I emailed Donald Leung, the principal investigator for the ADRN (he's a professor and head of the Division of Pediatric Allergy and Immunology at National Jewish Health), and asked him whether he could summarize the consortium’s findings so far and highlight key points. I hope to hear back from him soon and perhaps to interview him on the phone.
I’d like to know what ADRN scientists have found that surprises them. What have they learned that is truly new?
And what is going to be truly useful to patients in the end? Publishing papers should not be the be-all and end-all of scientific research. What about patents? I’d like to know whether anyone in the ADRN has thought about controlling intellectual property and commercialization. While it’s true that clinical studies may highlight the ideal dosing amount or schedule for existing therapies, and this does not involve creating a new commercial enterprise, most medical technology must pass through the marketplace before it can benefit the consumer/patient.
Someone has to do the dirty work of developing scientific discovery into therapy, and it’s not academic scientists.
More to come.
Thursday, May 23, 2013
TopMD conducts clinical trial of CLn Bodywash for marketing purposes
CLn Bodywash, the “bleach bath in a can,” sounds like a product that we all need—a quick and easy way to cleanse your skin of Staphylococcus aureus and other nasty bacteria associated with eczema. But the marketing campaign arranged by CLn’s maker, Dallas-based TopMD, could be better.
For a start, they could arrange a decent clinical trial.
CLn must be classified as a cosmetic and not a medical product, because the FDA didn’t require tests before CLn hit the stores.
You would think the usual way to proceed with a medical product would be:
1) clinical trial to prove safe and effective
2) manufacturing and marketing
But TopMD scientists recently published the results of a clinical trial for CLn in the journal Pediatric Dermatology, about nine months after I first heard the product was for sale.
Of course dilute bleach baths are a known household treatment to manage skin bacteria. CLn is a portable bleach bath and isn't going to be any more hazardous than what thousands of people are already doing in their bathtubs. But is it any better? Is it worth paying money for?
I think that some marketing analyst decided that doctors around the US were reluctant to buy or recommend CLn because it hadn’t undergone a clinical trial. Now it has—with the shiny label “peer-reviewed,” although the journal it was published in is low-impact, and the “peer” who deemed the study worthy of publication could well have been a single graduate student.
The study might possibly qualify as a “phase 0” trial. It’s conducted on 18 subjects all of whom are given the product. There’s no control group that receives a placebo.
This is a problem, because both the doctors conducting the trial and the patients both want the product to work. So the reported results are bound to look better than they really are. Scientifically, this study is far from the final word on whether CLn is truly effective.
The way to avoid this problem is to have a double-blind randomized control trial where, at the very least, half of the patients get CLn and half get something that looks like it but isn’t, and nobody knows which is which until the results have been recorded.
For an example of how this might be done, at least in a way that looks good from a marketing perspective, you can see that the makers of DermaSilk clothing appear to get it right in their studies, the most recent of which was published online this week.
That the recent CLn study was motivated by marketing is clear from one of its measures. Participants were asked “Would you recommend CLn to a friend?” This is not a data point you see in too many scientific papers.
The company’s press release quotes UC San Diego’s Dr. Larry Eichenfield, chief of pediatric and adolescent dermatology at Children's Hospital, San Diego—a world leader in the field. Eichenfield says “I am excited to read the study by Dr. Ryan et al showing the benefits of TopMD's sodium hypochlorite-based body wash.”
The release doesn’t mention that Eichenfield sits on TopMD’s medical board.
I like the idea of CLn, and I think it’s probably a valuable product. I’m happy they sent me a free bottle to review back in October, and I’m keeping it in case I need it. But I wish they could present some more convincing evidence that it works. Are they afraid that it doesn’t? If not, why not use a control group in the study?
For a start, they could arrange a decent clinical trial.
CLn must be classified as a cosmetic and not a medical product, because the FDA didn’t require tests before CLn hit the stores.
You would think the usual way to proceed with a medical product would be:
1) clinical trial to prove safe and effective
2) manufacturing and marketing
But TopMD scientists recently published the results of a clinical trial for CLn in the journal Pediatric Dermatology, about nine months after I first heard the product was for sale.
Of course dilute bleach baths are a known household treatment to manage skin bacteria. CLn is a portable bleach bath and isn't going to be any more hazardous than what thousands of people are already doing in their bathtubs. But is it any better? Is it worth paying money for?
I think that some marketing analyst decided that doctors around the US were reluctant to buy or recommend CLn because it hadn’t undergone a clinical trial. Now it has—with the shiny label “peer-reviewed,” although the journal it was published in is low-impact, and the “peer” who deemed the study worthy of publication could well have been a single graduate student.
The study might possibly qualify as a “phase 0” trial. It’s conducted on 18 subjects all of whom are given the product. There’s no control group that receives a placebo.
This is a problem, because both the doctors conducting the trial and the patients both want the product to work. So the reported results are bound to look better than they really are. Scientifically, this study is far from the final word on whether CLn is truly effective.
The way to avoid this problem is to have a double-blind randomized control trial where, at the very least, half of the patients get CLn and half get something that looks like it but isn’t, and nobody knows which is which until the results have been recorded.
For an example of how this might be done, at least in a way that looks good from a marketing perspective, you can see that the makers of DermaSilk clothing appear to get it right in their studies, the most recent of which was published online this week.
That the recent CLn study was motivated by marketing is clear from one of its measures. Participants were asked “Would you recommend CLn to a friend?” This is not a data point you see in too many scientific papers.
The company’s press release quotes UC San Diego’s Dr. Larry Eichenfield, chief of pediatric and adolescent dermatology at Children's Hospital, San Diego—a world leader in the field. Eichenfield says “I am excited to read the study by Dr. Ryan et al showing the benefits of TopMD's sodium hypochlorite-based body wash.”
The release doesn’t mention that Eichenfield sits on TopMD’s medical board.
I like the idea of CLn, and I think it’s probably a valuable product. I’m happy they sent me a free bottle to review back in October, and I’m keeping it in case I need it. But I wish they could present some more convincing evidence that it works. Are they afraid that it doesn’t? If not, why not use a control group in the study?
Tuesday, April 9, 2013
San Diego eczema meeting: an intense experience
After you’ve been tormented by eczema your entire life, and always avoided talking about your embarrassing condition, and dealt with doctors whose solution is to prescribe more steroids and expect you to go away happy, what is it like to spend two days in the company of some of the world’s leading eczema experts, talking about nothing else?
It’s pretty intense, I found out last weekend at the HOME (Harmonising Outcome Measures for Eczema) meeting in San Diego, California, where I and four other patient representatives helped clinicians and pharma reps from the US, UK, Germany, Japan, Brazil and other countries define how eczema severity should be characterized in clinical trials.
I’ll cover the technical details in a later post. Right now I just want to describe the experience.
I had been invited by Julie Block of the National Eczema Association. She introduced me to Gil Yosipovitch, Jon Hanifin and others. My initial feeling was one of awe. Many years ago I realized that scientists were actually studying itch and eczema when I read a New York Times article about Yosipovitch’s work. Now here I was on Saturday sitting with him and Block, eating fish tacos and getting my balding head sunburned.
And then Hanifin walked by. He developed the original criteria, now used worldwide, for diagnosing eczema in the clinic. In the conference room, was that Eric Simpson of Oregon Health Sciences University? And Hywel Williams of the University of Nottingham, the UK leader in eczema research? It was surreal—the equivalent for a tennis fan, say, would be being in the same room as Roger Federer, Rafael Nadal, Andy Murray and the Williams sisters.
Also present along with me were several other patient representatives, three of whom either had eczema themselves and one who was the father of two affected children. Among them were Stephanie Merhand, founder of l’Assocation Francaise de l’Eczema (from Toulouse, France) and Rosemary Humphreys from the National Eczema Society (in the UK).
At first, it was a bit strange to meet people with whom you have nothing in common but a medical condition, but over the course of the two days I came to realize that it was not so much the eczema we shared but similar life experiences: the days and nights of itch, the social anguish.
During a short car ride, Tim Burton (a UK patient) and I traded stories about the various pharmaceuticals we’d inflicted on ourselves. It was hilarious. I’d given up on Protopic because it burned so badly. Tim uses it on his face. “It’s like holding your face to a three-burner fire for a couple weeks, but it eventually stops,” he said. Sounds like fun! I informed him that the best way to take prednisone was as an injection in the buttock.
In the working sessions I had cognitive dissonance hearing my condition discussed openly and unemotionally. I’ve spent nights tearing with my nails at scalp, my arms, my feet. I’ve endured, as anyone with chronic eczema does, the social pain of high school and university, the outings and activities missed, the relationships that never happened. Eczema is something that makes me want to hide in the basement. And here were people calmly displaying Powerpoint slides and droning on like it was a graduate seminar in statistics or comparative literature.
The jargon really was incredible. In casual conversation you were supposed to know what “xerosis,” “oedema,” “erythema,” and other words meant. You were supposed to be familiar with the acronyms for what seemed like fifty different clinical techniques. You were supposed to know the difference between “signs” and “symptoms,” which turned out not to be so clear-cut.
At one point I was asked what I thought about a topic they’d been discussing for fifteen minutes. I had to admit I hadn’t understood a word. It felt a bit like being a laboratory rat listening to scientists describe experiments they’d done on you.
That is why we patients were invited—to humanize things. “You might not realize it, but you are changing the tone of the session just by being here,” Roberto Takaoka, a dermatologist from Brazil, told me. Several of the presenters opened their talks by showing pictures of children or adult patients and reminding everyone that we were doing this for the patients. Apparently many doctors tend to “treat the disease, not the patient” and meetings without patients can become even more abstract and academic. Rosemary Humphreys told me that it she was on a crusade to get scientists to use the word “patient” instead of “subject”—“I’m a linguist and I know what the difference means,” she said.
At the same time, I remarked that we patients were treated as equals by the academics at this meeting. And everyone was committed and attentive and sincere. If anyone was checking their iPhone it was me. That says something.
As time went on, I realized that I was surrounded by some of the world’s top dermatologists and could get free consultations for myself and my kids just by asking. For example, if your daughter says that Cerave (a ceramide cream) is burning her cracked hands, you can get the clinical benefit of the cream by first rubbing her hands with olive or safflower oil, than applying Cerave, and then putting Vaseline on the cracks. And apparently 3M has a great new surgical tape that sticks to anything but doesn’t hurt the skin when you peel it off. You can use it like a Band-Aid on greasy skin.
It was sobering to know that after having gone to this meeting I now know as much as most people on Earth about the state of eczema therapy at the moment and in the near future. There are no miracle cures in the offing. But there are many intelligent, motivated doctors and scientists working on our behalf to make things better. Not as many as there should be, and they are not funded nearly well enough. We need to get involved to let them know how important this work is and to make sure they get the support they need.
It’s pretty intense, I found out last weekend at the HOME (Harmonising Outcome Measures for Eczema) meeting in San Diego, California, where I and four other patient representatives helped clinicians and pharma reps from the US, UK, Germany, Japan, Brazil and other countries define how eczema severity should be characterized in clinical trials.
I’ll cover the technical details in a later post. Right now I just want to describe the experience.
I had been invited by Julie Block of the National Eczema Association. She introduced me to Gil Yosipovitch, Jon Hanifin and others. My initial feeling was one of awe. Many years ago I realized that scientists were actually studying itch and eczema when I read a New York Times article about Yosipovitch’s work. Now here I was on Saturday sitting with him and Block, eating fish tacos and getting my balding head sunburned.
And then Hanifin walked by. He developed the original criteria, now used worldwide, for diagnosing eczema in the clinic. In the conference room, was that Eric Simpson of Oregon Health Sciences University? And Hywel Williams of the University of Nottingham, the UK leader in eczema research? It was surreal—the equivalent for a tennis fan, say, would be being in the same room as Roger Federer, Rafael Nadal, Andy Murray and the Williams sisters.
Also present along with me were several other patient representatives, three of whom either had eczema themselves and one who was the father of two affected children. Among them were Stephanie Merhand, founder of l’Assocation Francaise de l’Eczema (from Toulouse, France) and Rosemary Humphreys from the National Eczema Society (in the UK).
At first, it was a bit strange to meet people with whom you have nothing in common but a medical condition, but over the course of the two days I came to realize that it was not so much the eczema we shared but similar life experiences: the days and nights of itch, the social anguish.
During a short car ride, Tim Burton (a UK patient) and I traded stories about the various pharmaceuticals we’d inflicted on ourselves. It was hilarious. I’d given up on Protopic because it burned so badly. Tim uses it on his face. “It’s like holding your face to a three-burner fire for a couple weeks, but it eventually stops,” he said. Sounds like fun! I informed him that the best way to take prednisone was as an injection in the buttock.
In the working sessions I had cognitive dissonance hearing my condition discussed openly and unemotionally. I’ve spent nights tearing with my nails at scalp, my arms, my feet. I’ve endured, as anyone with chronic eczema does, the social pain of high school and university, the outings and activities missed, the relationships that never happened. Eczema is something that makes me want to hide in the basement. And here were people calmly displaying Powerpoint slides and droning on like it was a graduate seminar in statistics or comparative literature.
The jargon really was incredible. In casual conversation you were supposed to know what “xerosis,” “oedema,” “erythema,” and other words meant. You were supposed to be familiar with the acronyms for what seemed like fifty different clinical techniques. You were supposed to know the difference between “signs” and “symptoms,” which turned out not to be so clear-cut.
At one point I was asked what I thought about a topic they’d been discussing for fifteen minutes. I had to admit I hadn’t understood a word. It felt a bit like being a laboratory rat listening to scientists describe experiments they’d done on you.
That is why we patients were invited—to humanize things. “You might not realize it, but you are changing the tone of the session just by being here,” Roberto Takaoka, a dermatologist from Brazil, told me. Several of the presenters opened their talks by showing pictures of children or adult patients and reminding everyone that we were doing this for the patients. Apparently many doctors tend to “treat the disease, not the patient” and meetings without patients can become even more abstract and academic. Rosemary Humphreys told me that it she was on a crusade to get scientists to use the word “patient” instead of “subject”—“I’m a linguist and I know what the difference means,” she said.
At the same time, I remarked that we patients were treated as equals by the academics at this meeting. And everyone was committed and attentive and sincere. If anyone was checking their iPhone it was me. That says something.
As time went on, I realized that I was surrounded by some of the world’s top dermatologists and could get free consultations for myself and my kids just by asking. For example, if your daughter says that Cerave (a ceramide cream) is burning her cracked hands, you can get the clinical benefit of the cream by first rubbing her hands with olive or safflower oil, than applying Cerave, and then putting Vaseline on the cracks. And apparently 3M has a great new surgical tape that sticks to anything but doesn’t hurt the skin when you peel it off. You can use it like a Band-Aid on greasy skin.
It was sobering to know that after having gone to this meeting I now know as much as most people on Earth about the state of eczema therapy at the moment and in the near future. There are no miracle cures in the offing. But there are many intelligent, motivated doctors and scientists working on our behalf to make things better. Not as many as there should be, and they are not funded nearly well enough. We need to get involved to let them know how important this work is and to make sure they get the support they need.
Thursday, July 5, 2012
Antibody therapy appears powerful against psoriasis
A biotechnology therapeutic for psoriasis appears to clear most of the symptoms in many patients, according to recently published results of clinical trials.
The therapeutic is “ixekizumab,” an antibody that inactivates a “cytokine” or signaling molecule produced by a subset of white blood cells called type 17 helper T cells.* Researchers at the pharmaceutical company Eli Lilly and university colleagues published the Phase 2 results in the New England Journal of Medicine in March. I learned about ixekizumab from a JACI paper published last week, reporting on aspects of the earlier Phase 1 trial.
Th17 are thought to be overactive in psoriasis patients. That is not the case in patients with atopic dermatitis, for whom helper T cells of types 2 and 22 generally exist in higher numbers and are more active than they are in the average person. The authors of the JACI paper speculate that tailored antibody therapy could prove as effective in controlling eczema as ixekizumab has for psoriasis.
In the Phase 2 trial, researchers injected 142 patients with various doses of ixekizumab at regular intervals over a 16-week period. They found that, for all but the lowest dosage, the antibody mostly cleared up psoriasis—as measured by a standard set of measures—for more than 75% of the patients in the trial.
The authors did not present data showing how long the effects lasted. But they did note that hardly anyone dropped out of the trial because of adverse effects. (From what I can tell, those who dropped out came from the lowest dosage group.)
Nor was there any indication how expensive ixekizumab might be. I imagine that, compared to drugs such as steroids, custom-produced antibodies would be extremely expensive for patients and insurers.
Nevertheless, the results are unusually positive. A blog post on the JACI website called the results “near-astonishing.” Keeping in mind that all trials and papers published on them are bankrolled by pharma companies (who else can pay for clinical trials?) this area of antibodies against T cell cytokines seems worth watching closely.
* I am pretty sure that Th17 cells are not the seventeenth type of helper T cells. The only ones I've ever heard of are Th1, Th2, Th17, and Th22. I don't know why the last two are numbered 17 and 22 instead of 3 and 4. This sort of thing is why I got out of immunology.
The therapeutic is “ixekizumab,” an antibody that inactivates a “cytokine” or signaling molecule produced by a subset of white blood cells called type 17 helper T cells.* Researchers at the pharmaceutical company Eli Lilly and university colleagues published the Phase 2 results in the New England Journal of Medicine in March. I learned about ixekizumab from a JACI paper published last week, reporting on aspects of the earlier Phase 1 trial.
Th17 are thought to be overactive in psoriasis patients. That is not the case in patients with atopic dermatitis, for whom helper T cells of types 2 and 22 generally exist in higher numbers and are more active than they are in the average person. The authors of the JACI paper speculate that tailored antibody therapy could prove as effective in controlling eczema as ixekizumab has for psoriasis.
In the Phase 2 trial, researchers injected 142 patients with various doses of ixekizumab at regular intervals over a 16-week period. They found that, for all but the lowest dosage, the antibody mostly cleared up psoriasis—as measured by a standard set of measures—for more than 75% of the patients in the trial.
The authors did not present data showing how long the effects lasted. But they did note that hardly anyone dropped out of the trial because of adverse effects. (From what I can tell, those who dropped out came from the lowest dosage group.)
Nor was there any indication how expensive ixekizumab might be. I imagine that, compared to drugs such as steroids, custom-produced antibodies would be extremely expensive for patients and insurers.
Nevertheless, the results are unusually positive. A blog post on the JACI website called the results “near-astonishing.” Keeping in mind that all trials and papers published on them are bankrolled by pharma companies (who else can pay for clinical trials?) this area of antibodies against T cell cytokines seems worth watching closely.
* I am pretty sure that Th17 cells are not the seventeenth type of helper T cells. The only ones I've ever heard of are Th1, Th2, Th17, and Th22. I don't know why the last two are numbered 17 and 22 instead of 3 and 4. This sort of thing is why I got out of immunology.
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?
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