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Atopic dermatitis: Up in smoke!


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By Warren R. Heymann, MD
Feb. 8, 2017


The etiology of atopic dermatitis (AD) is multifactorial, with genetic mutations of the filaggrin mutations affecting barrier function, immunodysregulation of the TH2 pathway, and environmental triggers being of primary importance. AD has long been associated with autoimmune diseases such as vitiligo and alopecia areata. Andersen et al examined the co-occurrence of selected autoimmune diseases in 8112 adult patients (at least 18 years old) with AD using national health registries in Denmark compared to 40,560 matched controls. AD was significantly associated with 11 of 22 examined autoimmune diseases. (Interestingly, there were no significant associations with type I diabetes or autoimmune thyroid diseases. In Table II, however, while there was no significant association with Graves disease, the association was statistically significant for Hashimoto thyroiditis.) Patients with a history of smoking had a significantly higher occurrence of autoimmune comorbidities compared to nonsmokers. The authors suggest that there is a susceptibility of autoimmune diseases in adult patients with AD, especially in smokers (1).

What role does smoking play in AD? Does secondary smoke affect children with AD? What about perinatal exposure?

Kantor et al performed a systematic review and meta-analysis of observational studies addressing these questions. They found that a diagnosis of AD was associated with higher odds of active smoking and exposure to passive smoke, but not maternal smoking during pregnancy. Passive smoke was associated with AD in children and adults (2). In a study of 1081 newborns, of whom 222 (28%) had AD by age 12 months, there was no correlation with parental smoking in the perinatal period (3). Other studies, however, suggest that prenatal smoke exposure may increase the risk of AD, possibly via epigenetic regulation (i.e., DNA methylation, histone modification, and non-coding RNAs) (4).There is conflicting data regarding whether or not there is a dose-response relationship between active smoking and AD. In Kantor et al (2) there was no correlation; a dose-response association was observed by Graif et al for active smoking, but not environmental tobacco smoke (5).

The pathomechanisms of smoke aggravating AD may include free radicals inducing oxidative stress, causing an increase of pro-inflammatory cytokines (e.g., TNF-alpha and IL-1-beta) with a concomitant reduction of anti-inflammatory cytokines such as IL-10. The healing process may also be hindered by diminished tissue oxygenation. Interestingly, smoking has also been associated with nickel sensitization (6).

I always ask about smoking habits with certain diseases such as hidradenitis suppurativa and palmoplantar pustulosis. My curiosity has been piqued — I’ll be asking about smoking or secondary smoke exposure in my atopic patients. It’s always worthwhile finding another reason to kick the habit!

1. Andersen YMF, et al. Autoimmune diseases in adults with atopic dermatitis. J Am Acad Dermatol 2017; 76: 274-80.
2. Kantor R, et al. Association of atopic dermatitis with smoking: A systematic review and meta-analysis. J Am Acad Dermatol 2016; 75: 1110-25.
3. Parazzini F, et al. Perinatal factors and the risk of atopic dermatitis: A cohort study. Pediatr Allergy Immunol 2014; 25(1):43-50.
4. Wang IJ, et al. Prenatal smoke exposure, DNA methylation, and childhood atopic dermatitis. Clin Exp Allergy 2013; 43: 535-43.
5. Graif Y, et al. Dose-response association between smoking and atopic eczema: Results for a large cross-sectional study in adolescents. Dermatology 2013; 226: 195-9.
6. Lai YC, Yew YW. Smoking and hand dermatitis in the United States adult population. Ann Dermatol 2016; 28: 164-71.


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