Here’s another article that I shared on National Eczema Association website which is a great resource. Read my 8 survival tips for caring for eczema baby, and the many more by other eczema friends around the world.
For those of you who like to read the journeys of other eczema sufferers, do check out the National Eczema Association website which is a great resource. My journey “Getting through the Darkest Moments..” has been published on NEA’s website, and there are several other journeys shared. Do read them!
Scientists from the National Institute of Allergy and Infectious Diseases (NIAID) have identified a gene mutation called CARD11 that led to atopic dermatitis/ eczema. Their findings were recently published in Nature Genetics (June 2017)1. Gene sequencing was performed for 8 individuals from 4 families, and the researchers found that although each family had a distinct mutation affecting a different region of the CARD11 protein, each mutation disrupted its normal function in T cells – an essential type of white blood cell.
The potential of this study was that glutamine may correct the defective signally mechanism of the mutated CARD11. Glutamine is available as a supplement, and the researches intend to study the effects of glutamine consumption on individuals with CARD11 mutations/ severe eczema. If the future study proved conclusive, it would open an easy therapeutics method for treating eczema!
Germline hypomorphic CARD11 mutations in severe atopic disease
Chi A Ma, Jeffrey R Stinson, Yuan Zhang, Jordan K Abbott, Michael A Weinreich, Pia J Hauk
Nature Genetics; Jun 19, 2017
Science Daily New genetic mutations linked to eczema
An eczema study1 published in April 2017 showed that there was
little evidence of clinical or economic benefit of using silk garments in addition to standard care, compared with standard care alone, in children with moderate to severe eczema.
As always, the team of researchers from the University of Nottingham in the U.K had taken on clinical studies that address questions raised by doctors and patients, with the view of having a direct impact on clinical practice. They had conducted very practical studies like softened water eczema trial and compared the efficacy of a short burst of potent topical corticosteroids versus prolonged period of mild corticosteroids. Their website also maps out the systematic reviews on eczema and list their ongoing studies (also found at the bottom of this post).
For this study, the key points are below:
Nature of study: Parallel-group, randomised, controlled, observer-blind trial
Participants: Children aged 1 to 15 year old with moderate to severe eczema; 300 children were included: 42% girls, 79% white, mean age 5 year old
Randomized groups: Participants were randomised to receive standard eczema care plus silk clothing (100% sericin-free silk garments; DermaSilk or DreamSkin) or standard care alone.
Measurement: At baseline, 2, 4 and 6 months against the Eczema Area and Severity Index (“EASI”)
Outcome: No evidence of a difference between the groups in eczema severity (EASI score) assessed by research nurses
Purpose of the study: Silk clothing is available on prescription (and online) but the randomized controlled trials previously done were for small group of participants. To provide direction for clinical practice as to whether to recommend silk clothing, this study was taken on. Silk garment claimed beneficial for eczema as they are smooth, helped regulate humidity and temperature, reduce scratching damage and have anti-microbial properties. These are important qualities that would benefit eczema to reduce scratching (versus a ‘scratchy’ fabric like wool), keep the skin cool and reduce likelihood of flucuating temperature triggering eczema flareups and reduce bacteria load as eczema skin is prone to staph bacteria colonization. However, from the outcome of this study, it would appear that standard eczema care such as regular emollient use and topical corticosteroids (or topical calcineurin inhibitors) for controlling inflammation would be adequate.
In my view, this study would really get parents who are spending a lot of money on silk clothing/ bedding to question if such money needs to be spent. These silk garments are not cheap but parents pay for them due to positive testimonies, anti-inflammatory/ anti-microbial properties of silk and that these clothing are soft, free of dye and will not irritate the skin (interviewed Dermasilk here). However, a lower-cost alternative of cotton may work as well, with standard care for eczema.
I’ve also contacted Professor Kim Thomas who is part of the research team for this study and she kindly shared this video on University of Nottingham’s website
Please refer to the CLOTHES Trial page here for information sheets for children of various age group.
My personal take is if you’re seeing benefits for your child with silk clothing and can afford it, there is no reason to stop using the clothing. However, if it hasn’t seemed to make much difference and you feel confident that the eczema therapeutics measures that you use for your child are sufficient, then it makes sense not to spend that money. See this post for the review of various eczema therapeutics and also the review study that Nottingham University had done.
Silk garments plus standard care compared with standard care for treating eczema in children: A randomised, controlled, observer-blind, pragmatic trial (CLOTHES Trial) Thomas KS, Bradshaw LE, Sach TH, Batchelor JM, Lawton S, et al. (2017) Silk garments plus standard care compared with standard care for treating eczema in children: A randomised, controlled, observer-blind, pragmatic trial (CLOTHES Trial). PLOS Medicine 14(4): e1002280. https://doi.org/10.1371/journal.pmed.1002280
Ongoing studies at Centre of Evidence Based Dermatology at Nottingham University:
We’re still at the letter A and the last one was on the confusing nomenclature of Eczema versus Atopic Dermatitis. This week (pardon last week’s absence, can’t promise it won’t happen again though as I’m so tied up with work, family and doing other things I enjoy) we’re onto Atopic March. Sometime last year, DrFelix.co.uk (a registered online UK doctor and pharmacy service) contributed a write-up on Atopic Triad, which covers eczema, asthma and allergic rhinitis (hay fever).
Atopy is a genetic tendency to develop certain allergies. Most commonly, Eczema, Asthma and Hay Fever. In fact, if either parent has at least one of the three, there is a high chance that their child will also develop the condition. In these three ailments, the body areas become inflamed and produce excess immunoglobulin E (IgE) in response to harmless stimuli such as dust or pollen.
It is very common for people who experience eczema to also have asthma and hay fever. The connection between these conditions can be summarised by one word: hypersensitivity.
The body including the skin and respiratory system are over sensitive towards certain substances and they overreact when exposed. Rashes on the skin and a congested nose are all ways in which the body is trying to protect itself from something that it deems to be harmful. Unfortunately, this overreaction can be very uncomfortable and unnecessary.
There are also other connections between the Eczema and the development of Asthma. 50-70% of children with Eczema go on to develop Asthma. Recent research undertaken by Washington University School of Medicine has discovered that Eczema damaged skin produces a protein called thymic stromal lymphopoietin (TSLP). TSLP has also been found to directly cause asthma symptoms. This research is still in its early stages and this mechanism has not yet been fully confirmed in humans, but it shows a promising new direction for pharmaceutical research that may be able to stop the development of secondary conditions in their tracks.
Byline: Dr Samuel Malloy, Medical Director at DrFelix.
We understand that atopic conditions are related, in the sense one’s hypersensitivity may manifest in other than skin. But what about the term Atopic March? Does one condition literally marches your child off to another?
While it is more commonly noted that Atopic Dermatitis (Eczema) progresses to asthma and hay fever, the progression is not the same for every child.
Some recent research on this:
Skin Barrier Dysfunction and Atopic March 1 – It was noted in the study that the atopic conditions should be viewed as causally related, as they are conditions related to the lack of filaggrin gene. Recent studies on skin barrier dysfunction suggest that if we can treat the skin defects early, there is a chance of stopping the progression to other atopic conditions.
The Atopic March: Progression from Atopic Dermatitis to Allergic Rhinitis and Asthma 2 – It was noted that the “concept of the atopic march has been supported by cross-sectional and longitudinal studies“; however, “whether AD in the march is necessary for progression to other atopic disorders remains to be defined”. The conclusion was that it is important to identify infants at risk as it presents a critical window of opportunity for therapeutic intervention.
Increasing Comorbidities Suggest that Atopic Dermatitis Is a Systemic Disorder 3 – The associations (even though causality is not proven) showed that AD is linked to the whole body, not just the skin.
Thus, while we see a progression of atopic conditions in a majority of children with eczema, it may not be a “march” of one onto another – not all children undergo the progression, and a few conditions may co-exist. What looks certain (and practical) is that there is urgency to treat the skin during infants as untreated eczema increases risks in many ways > scratching resulting in infection, dry and ‘porous’ skin to more opportunities for sensitization. Extract from WorldAllergy.org below:
Atopic March is frequently misunderstood as the development from minor symptoms over a mild disease expression towards more severe chronic manifestations. It also has been misinterpreted as the exclusive development from atopic dermatitis in infancy to airway disease, particularly asthma in school-age. These interpretations have been shown to underestimate the variations and heterogeneity of atopy development during the first decade of life.
Clausen, ML., Agner, T. & Thomsen, S.F. Curr Treat Options Allergy (2015) 2: 218. doi:10.1007/s40521-015-0056-y
Zheng T, Yu J, Oh MH, Zhu Z. The Atopic March: Progression from Atopic Dermatitis to Allergic Rhinitis and Asthma. Allergy Asthma Immunol Res. 2011 Apr;3(2):67-73. https://doi.org/10.4168/aair.2011.3.2.67
Increasing Comorbidities Suggest that Atopic Dermatitis Is a Systemic Disorder Brunner, Patrick M.Bagot, Martine et al. Journal of Investigative Dermatology , Volume 137 , Issue 1 , 18 – 25
Well, the first step of recovery is acknowledging the problem. Borrowing from Alcoholics Anonymous, their 1st of the 12 steps is We admitted we were powerless over alcohol – that our lives had become unmanageable.
In our case, it is difficult to fully acknowledge the problem when we don’t know what the problem is. The irony is that there is difficulty defining the problem – in fact, the very term “atopic dermatitis” seems to be somewhat a matter of contention.
Mostly, we understand atopic dermatitis to refer to a chronic skin condition characterized by itch (pruritus), dry skin and inflammation, which waxes and wanes (with flare-ups). It is a multi-factorial condition, with causes and triggers linked to autoimmune and genetic factors, defective skin barrier, staph aureus bacteria colonization and hypersensitivity to allergens (including environmental ones like inhaled allergens, food allergens and contact allergens).
The difficulty is that there are many forms of dermatitis, and there are overlaps in symptoms and treatment. Broadly speaking, we want a way to differentiate whether we get the skin inflammation/ rashes because it is linked to immunoglobulin E (IgE) (antibodies produced by the immune system which defend the body but our immune system can wrongly recognize harmless substances as something to fight against, thus leading to allergic reaction). For instance, there are other forms of dermatitis where IgE is not involved, notably irritant contact dermatitis (where your skin develops rashes because it is in contact with a substance over a prolonged period).
There was an article published1 in European Journal of Allergy and Clinical Immunology in August 2016 which suggested the use of the term atopic dermatitis in literature, to differentiate from eczema which is commonly used to cover all forms of inflammatory rashes. Quoting from the article that reviews the existing literature:
Atopic dermatitis is the most commonly used term and appears to be increasing in popularity. Given that eczema is a nonspecific term that describes the morphological appearance of several forms of dermatitis, we strongly suggest the use of a more specific term, AD, in publications, healthcare clinician training, and patient education.
On the other hand, another article2 published in the Acta Dermatovenerol Croat highlighted that the Nomenclature Review Committee Of The World Allergy Organization recommended the term “eczema”. As extracted from World Allergy Organization website,
The umbrella term for a local inflammation of the skin should be dermatitis. What is generally known as “atopic eczema/dermatitis” is not one, single disease but rather an aggregation of several diseases with certain characteristics in common. A more appropriate term is eczema.
…eczema in a person of the atopic constitution, should be called atopic eczema.
The non-allergic variety can also be described by terms like irritant/toxic contact dermatitis.
I wonder why it seemed to be difficult to agree on whether it ought to be atopic dermatitis or atopic eczema, but inserting atopic does help to clarify that the skin condition should be rooted in IgE. Atopy as defined by the World Allergy Organization is:
Atopy is a personal and/or familial tendency, usually in childhood or adolescence, to become sensitized and produce IgE antibodies in response to ordinary exposure to allergens, usually proteins. As a consequence, such individuals can develop typical symptoms of asthma, rhinoconjunctivitis, or eczema. The terms ‘atopy’ and ‘atopic’ should be reserved to describe the genetic predisposition to become IgE-sensitized to allergens commonly occurring in the environment and to which everyone is exposed but to which the majority do not produce a prolonged IgE antibody response.
The “good news” is no matter what you call it, the way to treat it is the same – finding out the triggers, avoidance, moisturizing, steroidal and non-steroidal options, and lifestyle changes to reduce inflammation and staph bacteria colonization. The bad news is we will continue to wonder at the back of our mind whether we are contributing to misleading literature if we fail to clearly define what we’re writing about – well, at least for an eczema/ atopic dermatitis blogger like me, I certainly struggle. A cartoon for it:
Kantor R, Thyssen JP, Paller AS, Silverberg JI. Atopic dermatitis, atopic eczema, or eczema? A systematic review, meta-analysis, and recommendation for uniform use of ‘atopic dermatitis’. Allergy 2016; 71: 1480–1485.
Zbigniew Samochocki, Rożalski M, Rudnicka L, Atopic and Non-atopic Eczema. Acta Dermatovenerol Croat 2016 Jun;24(2):110-5.
This year’s series is Atopic Dermatitis ABC – a lighthearted, be-there-with-you companion where the ABCs will act as your eczema survival guide. In just 5 minutes, I came up with 15 words that start with A that are related to atopic dermatitis (AD). I disregarded all of them (not because they’re wrong since we’d get to what is atopic dermatitis, autoimmune, allergies and avoidance), but because I remembered when I first learnt of my baby’s eczema, it’s not the medical terms that come to mind. It’s ANXIETY, and it comes from the heart. Your heart, my heart, the hearts of all parents who suddenly find themselves in a challenging situation. Something like this.
It is normal to feel anxious when something has gone wrong, when something is happening to your baby, and when you’re not sure what that something is (didn’t the delivery hospital say rashes are to be expected? and ok?) and when even when you know what that something is, you can’t cure it and you’re never sure when it would come back? If your heart has started beating faster like mine, it may be that all these feelings and thoughts are anxious ones that come when we’re not in control. And the most paradoxical part is atopic dermatitis is about controlling the eczema, since you can’t quite cure it.
Wait, do you agree with me?
IS THIS ANXIETY EVEN REAL?
Fortunately, we’re not self-deluded. In an October 2016 study published in the Asia Pacific Allergy1 by researchers at Inha University Hospital, South Korea, 78 children with their parents took part in a study to examine the family quality of life (QoL). The mean age of parents was 37 years old (majority 87% mothers), and the mean age of their children was 5+ years old, having atopic dermatitis for about 2 years. The tests included questionnaires (including Satisfaction with Life Scale survey) and using score card to measure eczema severity (SCORAD index).
It was found that a low family quality of life was related to the eczema severity, when the children with atopic dermatitis were girls and the negative emotionality of parents. Parents of children with AD is known to be associated with depression and stress in previous studies.
In another study2 more than a decade earlier, published in British Journal of Dermatology in Feb 2004, researchers examined the psychosocial well-being of parents caring for a young child with AD. Out of 187 parents, it was observed that parents of children with a higher severity of atopic dermatitis reported a significantly higher impact on family functioning and a greater financial burden. The results showed the need to focus on parental well-being and ability to cope with stress and social strain.
The latest study3 on this was published in Acta Derm Venereol in February 2017 which concluded that quality of life was affected mothers more as moms spent more time caring for the eczema child and carried out more household duties.
NOW THAT YOU KNOW THE ANXIETY IS REAL, HOW DO YOU THINK YOU WOULD FARE ON THE SATISFACTION WITH LIFE SCALE?
Here’s the test4 that you can take:
Below are five statements that you may agree or disagree with. Using the 1 – 7 scale below, indicate your agreement with each item by placing the appropriate number on the line preceding that item. Please be open and honest in your responding.
7 – Strongly agree
6 – Agree
5 – Slightly agree
4 – Neither agree nor disagree
3 – Slightly disagree
2 – Disagree
1 – Strongly disagree
____ In most ways my life is close to my ideal.
____ The conditions of my life are excellent.
____ I am satisfied with my life.
____ So far I have gotten the important things I want in life.
____ If I could live my life over, I would change almost nothing.
31 – 35 Extremely satisfied
26 – 30 Satisfied
21 – 25 Slightly satisfied
15 – 19 Slightly dissatisfied
10 – 14 Dissatisfied
5 – 9 Extremely dissatisfied
I hope you end up on the satisfied end of the scale, but if not, don’t be anxious – 5 questions are not going to determine your life’s happiness. Your child’s eczema condition is. (One question, in this eczema context).
Jang HJ, Hwang S, Ahn Y, Lim DH, Sohn M, Kim JH. Family quality of life among families of children with atopic dermatitis. Asia Pacific Allergy. 2016;6(4):213-219. doi:10.5415/apallergy.2016.6.4.213.
Warschburger, P., Buchholz, H.TH. and Petermann, F. (2004), Psychological adjustment in parents of young children with atopic dermatitis: which factors predict parental quality of life?. British Journal of Dermatology, 150: 304–311. doi: 10.1111/j.1365-2133.2004.05743.x
Acta Derm Venereol. 2017 Feb 16. doi: 10.2340/00015555-2633
Ed Diener, Robert A. Emmons, Randy J. Larsen and Sharon Griffin as noted in the 1985 article in the Journal of Personality Assessment
Atopic dermatitis, well it starts with “A” – how uncanny to start this year’s blog series on Atopic Dermatitis ABC! I’ve got the inspiration to work on a ABC series from reading the book “The Middle Class ABC – a
toilet loo book” which shared funny facts about the British middle class – I love its hand lettering and cartoons, and would love this year’s blog posts to be filled with more lighthearted moments. And even more disturbingly coincidental, the first page of the book is on A for Allergies!
I’d be working on my blogging calendar over this weekend, and hope to bring you regular blog posts from next week. Have a lovely weekend, and anyone has a fave letter to work on, leave a comment!
Today, it felt like coming home – sharing on this blog again after taking a year break from regular posting. I took a break when Marcie started grade school last year and I didn’t feel that it would help you by posting for the sake of posting. As such, for the past year:
On this blog:
On other pursuits:
I took an interest in hand lettering and visual notes, and you’d see more of these for this year’s posting.
In 2017, I’d post twice a week, a lighter posting schedule compared to three times a week in the past. I feel that this feels a little like coming home, returning to what this blog is about, i.e. turning blues to bliss.
Sharing verses from a poem Coming Home by American poet, Vern Rutsala (from January 1985 Poetry Magazine)
We thought we knew these
sidewalk cracks by heart
but even they have altered
in our absence, branching out
on their own. The yard too
has a new identity -some
plants dead, others new.
Inside, the knives and forks
don’t seem the same and feel
wrong in our hands. The design
is more extreme than we remember and there has been
some subtle change in scale
too. The touch of familiar
things is strange, surfaces
feel foreign as if we had
brought back some art
of foreignness. Even the old
companions – tables and chairs,
the light through a window –
seem alien. We are back
but not back all the way.
I came across this study “IL-1 beta-induced protection of keratinocytes against Staphylococcus aureus-secreted proteases is mediated by human beta defensin 21” where the researchers studied how the skin protected itself against staphylococcus aureus (“staph bacteria”). This research is important because staph bacteria is known to colonize atopic dermatitis skin, and in doing so, have resulted in worsened control of atopic dermatitis. (Note to readers: Due to many types of eczema, it is recommended to use atopic dermatitis to avoid confusion with other types of eczema like contact dermatitis).
I’m privileged to interview the lead researcher for the study, Dr Donald J Davidson MBChB PhD. Dr Davidson is the MRC Senior Research Fellow and University of Edinburgh Senior Lecturer. The Davidson Group within the MRC Centre for Inflammation Research focuses on understanding the physiological importance of cationic host defence peptides (CHDP) to host defences against bacterial and viral infections. Dr Davidson is a medical graduate of the University of Edinburgh who chose to pursue a scientific research career. He completed a PhD at the MRC Human Genetics Unit, studying the pathogenesis of cystic fibrosis lung disease, then was awarded a Wellcome Trust Travelling Research Fellowship to undertake post-doctoral training in innate immunity research at the University of British Columbia, Vancouver. You can read more of his research interests here.
MarcieMom: Thank you Dr Davidson for taking the time to help with the questions. The questions will be based on the study, but more focused on its practical implications.
Staphylococcus aureus is a resilient bacteria found on the skin that can survive in dry condition and on dry skin with little oxygen. It tends to involve areas that are warm and moist especially such as skin near mucous membranes such as the nose, mouth, genitals and anal area. It is found in less than 30% of healthy adults and generally does not cause an infection in those with healthy skin. However, as pointed out in the study, 75% to 100% of atopic dermatitis patients have staph bacteria on their lesional skin and 30% to 100% of atopic dermatitis patients have staph bacteria on their non-lesional skin (Breuer et al., 2002; Gong et al., 2006; Park et al., 2013). The problem with staph bacteria is that it secretes toxins and proteases that can worsen atopic dermatitis.
MarcieMom: From your study, protease V8 was of interest which showed it led to skin barrier dysfunction. Can you explain what you learnt about staphylococcus aureus’ interaction with atopic dermatitis skin/ normal skin and how does it damage skin integrity?
Dr Davidson: In our study we did not use the whole live bacteria, but concentrated instead on its harmful proteases. Using skin cells grown in the laboratory and collecting the substances made by the bacteria Staphylococcus aureus, we were able to show that the bacterial protease V8 was the most powerful product when it came to breaking down and damaging the skin barrier. Together with studies from other research groups, this suggested that one of the main ways these bacteria can damage skin is by producing V8, and that finding ways to block this damage may help to maintain and/or restore the skin integrity in atopic dermatitis.
Natural Skin Defence
In your study, it was mentioned that human beta defensin 2 (hBD2) is a substance on our skin that have antimicrobial properties and able to protect against skin integrity damage caused by staph bacteria protease V8. It was further noted that the level of hBD2 on atopic dermatitis skin was significantly lower than normal skin, therefore atopic dermatitis skin may be more prone to infection and unable to defend itself against staph bacteria.
MarcieMom: I hope I have understood hBD2’s role correctly; can you explain more about what you have found out about hBD2, for instance, how important is its role in maintaining skin integrity, fighting infection and the effects of protease V8?
Dr Davidson: Our bodies can make quite a wide range of substances we call antimicrobial host defence peptides (HDP). The skin is one site that produces these. These HDP have a lot of different roles in protecting us from infection and disease. hBD2 is an HDP from the defensin family. hBD2 was already known to be capable of killing bacteria in the laboratory. It is less clear if it definitely does this in normal functioning on our skin. However, it has been suggested by other researchers that the failure of atopic dermatitis skin to make as much hBD2 as one would expect (for the amount of skin inflammation or damage), could be one reason that atopic dermatitis skin lesions are prone to infection. What our new MRC-funded research discovered was that hBD2 can also stop V8 from damaging laboratory-grown skin. This worked both when we instructed the skin to make extra hBD2 (using genetic modification) and when we added hBD2 in the style of a treatment. Just how important this is in a living human remains to be seen, but it has obvious potential and shows that hBD2 can protect the skin barrier as well as kill bacteria.
MarcieMom: The interesting part of your study was its demonstration that application of hBD2 was found to be protective, and therefore a possible future eczema therapeutic. How does the application of hBD2 work? What are its protective effects?
Dr Davidson: At this point we don’t know how hBD2 protects this skin barrier integrity and we are currently applying for more funding so that we can start to work this out. It may act directly on the V8 to block the damaging effects of this bacterial protease, but we’ve found that it can also help to speed up repair where damage has occurred. So hBD2 may work in more than one way.
Is this something you foresee that can be easily added into a moisturizer or would it be more likely to be a non-steroidal topical prescription?
Dr Davidson: At this stage we are still in the discovery science phase of the research, so it is too early to predict how, and even whether, it will turn out to be a useful treatment. However, in the best case scenario for the outcome of our research, I would envisage adding hBD2 (or drugs made to mimic some of its functions) into prescription moisturizer-type creams or ointments.
How would the application of hBD2 be compared with the existing eczema measures such as bleach bath to kill staph bacteria?
Dr Davidson: I’m afraid it is too early to be able to make comparisons of that kind, until we have a better understanding of exactly how hBD2 functions to protect the skin barrier.
MarcieMom: Thank you Dr Davidson once again for your time and will certainly look forward to further breakthroughs and more studies done in this area.
Wang B, McHugh BJ, Qureshi A, Campopiano DJ, Clarke DJ, Fitzgerald JR, Dorin JR, Weller R, Davidson DJ, IL-1beta-induced protection of keratinocytes against Staphylococcus aureus-secreted proteases is mediated by human beta defensin 2, The Journal of Investigative Dermatology (2016), doi: 10.1016/j.jid.2016.08.025.
Breuer K, S HA, Kapp A, Werfel T (2002) Staphylococcus aureus: colonizing features and influence of an antibacterial treatment in adults with atopic dermatitis. Br J Dermatol 147:55-61.
Gong JQ, Lin L, Lin T, Hao F, Zeng FQ, Bi ZG, et al. (2006) Skin colonization by Staphylococcus aureus in patients with eczema and atopic dermatitis and relevant combined topical therapy: a double-blind multicentre randomized controlled trial. Br J Dermatol 155:680-7.
Park HY, Kim CR, Huh IS, Jung MY, Seo EY, Park JH, et al. (2013) Staphylococcus aureus Colonization in Acute and Chronic Skin Lesions of Patients with Atopic Dermatitis. Ann Dermatol 25:410-6.