COMMENTARY

Atopic Dermatitis: A Personal Journey

Gary J. Stadtmauer, MD

Disclosures

September 01, 2021

Atopic dermatitis (AD) is a uniquely challenging condition for the treating allergist and patient. I say this as a doctor who treats AD and as someone who has lived with it nearly my entire life. The following points reflect both my own experience and those of my many AD patients who have entrusted me with their care.

AD is known as the itch that rashes. But it doesn't just itch, it hurts — and why wouldn't it? The active lesions are open wounds. Eczematous hands are often fissured at the joints, leading to pain with typical hand motions. In general, eczema occurs at the intertriginous zones, potentially causing discomfort with every flexion and contraction. An ocean swim for an eczema patient is likely to be unbearably painful (not salt in one wound but salt in a few hundred microscopic wounds).

AD pain is not just physical but causes a fair amount of psychological distress. From my own experience and from discussions with patients, bullying and teasing due to AD is common and seldom forgotten. Patients with facial — and particularly perioral — flares are self-conscious, have scaling and erythema extending beyond the vermilion border, and can't kiss a romantic partner without discomfort.

AD patients, awake or asleep, scratch unconsciously which makes them appear fidgety. Per AD studies, up to 15% of sleep is spent scratching, leading to sleep fragmentation, nocturnal arousals, and disrupted spousal sleep. Of note, certain altered levels of cytokines in AD are associated with impaired circadian rhythm in AD and perhaps melatonin production. Whatever the mechanism, a vicious cycle may ensue, with AD triggering sleep impairment. The stress of this disrupted sleep stresses patients, leading to more scratching and worsening AD. The nocturnal scratching may also impair the sleep of the bed partner, resulting in a difficult decision: Sleep apart or suffer the same sleep issues?

The pattern of eczema flares is the inverse of seasonal allergy in colder climates. As opposed to the spring and fall pollen seasons, eczema patients flare in winter and summer. The one exception I have noted is that patients with seasonal atopic conjunctivitis rub their eyes, aggravating periocular eczema. In general, though, the dryness of winter and excessive humidity and heat of summer are far worse than seasonal pollen. Summertime is particularly difficult for many reasons:

  • Heat and humidity lead to sweating, further irritating the skin.

  • Sunscreen compounds the problem (dryer sunscreens are better).

  • So does swimming in chlorinated pools.

Medication use in AD. Avoiding tachyphylaxis with topical steroids requires a drug holiday which, in my experience, is best managed with a topical calcineurin inhibitor. Other topical therapies are not nearly as effective. Dupilumab is in a class by itself, but its expense is only justified in the extremely compliant patient.

Immunotherapy and AD. There are conflicting data on the efficacy of allergy immunotherapy (AIT) in AD. In fact, AIT caused an eczema recurrence in one of my patients treated for severe AD with Odactra (HDM allergy tablet), and Dr Tom Platts-Mills warned of aggravation of AD during AIT(public communication, AAAAI Annual meeting, many years ago).

Comorbidities. The excoriated eczematous skin puts AD patients at risk for infection (eczema herpeticum, Staphylococcus aureus). Of note, although AD is not an autoimmune disease it is associated with two of the more common ones (alopecia areata and vitiligo). It remains to be seen whether dupilumab affects these associated autoimmune conditions.

My eczema saga is the story of eczema management in the past 50-plus years. As a child, I had widespread painful and pruritic eczema. I was teased and my confidence was undermined due to my delayed growth, short stature, open wounds, and constant fidgety scratching. Teachers also criticized me for not sitting still, and I could not focus in the classroom. Biting my nails made me seem more nervous, but scratching with longer nails traumatized the skin more. Treatments were more limited then; topical calcineurin inhibitors were not yet available and the "Saran Wrap treatment" (wrapping areas after steroid application, usually before bed) just made me scratch more.

Things improved a bit but then worsened as I developed an intolerance of powdered gloves at the height of the AIDS epidemic. In my residency in the late 1980s to early '90s, the only available gloves were both powdered and made of highly allergenic latex. In this pre-antiretroviral era I had to choose between the consequences of powdered glove use or skipping gloves entirely and risking exposure to AIDS-infected blood teeming with millions of viral particles. I drew blood and inserted central lines gloveless while still occasionally biting my nails and with yet unhealed hand excoriations. It's a miracle that I did not contract HIV.

I entered an allergy fellowship in part to have a more mellow, office-based specialty in order to escape the fatigue of more grueling fields. Then, as a fellow, I realized that the intense latex-induced severe rhinitis and eczema were the source of my exhaustion. Over the ensuing years I lectured and conducted clinical research on latex allergy. I also developed the autoimmune conditions linked to AD: vitiligo and alopecia areata. I'm in my 50s now and things are better, but I habitually and unconsciously scratch (including during sleep, to my dear and tolerant wife's chagrin), flare in winter and summer, and sometimes take a few days of prednisone to get back to baseline.

It was especially tough as a child, but I can now see my AD experience as a mixed blessing. I empathize with my AD patients with whom I have a strong connection. This article is dedicated to them and their families.

Gary J. Stadtmauer, MD, is an allergist-immunologist in New York City. His areas of clinical interest include asthma, eczema, chronic cough, and sinusitis. He has been a Medscape contributor since 2014.

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