Effects of Occlusion on the Skin of Atopic Dermatitis Patients

Kristen Kobaly; Ally-Khan Somani; Thomas McCormick; Susan T. Nedorost

Disclosures

Dermatitis. 2010;21(5):255-261. 

In This Article

Discussion

We showed that polyethylene occlusion of AD skin induced an inflammatory immune response that was visible in some cases and detectable with RNA isolated from tape-stripped areas of skin. We were able to replicate previous studies that used tape stripping to measure mRNA produced by the skin.[9–12] However, these studies did not include patients with AD. We showed that occlusion with polyethylene wrap induced mRNA for 1L- 8, 1L-1a, and 1L-1RA in our subjects. Occlusion induced significantly more mRNA for IL-8 (a proinflammatory chemokine) than did SLS and induced significantly less IL- 1RA mRNA (an antiinflammatory cytokine) than did SLS. Similar amounts of IL-1α mRNA were induced by occlusion and SLS. Our results thus show that with AD patients, occlusion with polyethylene can cause irritation to the skin similar to that caused by SLS, a known irritant.

Keratinocytes manufacture cytokines; the most common constitutively expressed cytokine is the proinflammatory cytokine IL-1α. In normal mouse skin, latex occlusion for 24 to 48 hours significantly reduces IL-1α.[18] However, after acute barrier disruption with acetone or tape stripping, occlusion does not lessen either IL-1α or other inflammatory cytokines.[18]

Clinically, occlusion is known to be poorly tolerated by AD patients; however, supporting literature investigating the mechanism of action for this observation is sparse. Evidence in normal subjects suggests that occlusion may obstruct skin ventilation and compromise skin barrier function, which may exacerbate dermatitis.[19,20] In a study comparing the unaffected skin of atopic, psoriatic, and normal individuals in response to plastic occlusion of the forearm for 2 days, the water-retention capacity of AD patients was shown to be significantly less than that of normal or psoriatic patients, whereas TEWL was significantly increased.[21]

In psoriasis cases, occlusion is a well-established treatment that has been shown to improve outcomes.[22–24] In hairless mice, occlusion appears to prevent increases in DNA synthesis that may contribute to epidermal hyperplasia.[25] Rapid drying after occlusion is removed may explain the observation that low humidity contributes to the seasonal exacerbation of some inflammatory dermatoses. In a study of 10 nonatopic patients, TEWL was increased 10 minutes after the removal of occlusive polyethylene wrap worn for 3 days.[26]

Leow and Maibach cite examples of improved wound healing in normal skin with occlusion but also review data showing that water-impermeable materials delay the repair of barrier damage in mice.[27] AD is linked to a defect in the filaggrin gene, which causes impaired barrier function.[28]

Filaggrin defects have been found in both European and Japanese AD patients.[29] The decreased integrity of the epidermis due to defects in adhesion molecules may make AD skin more likely to fissure during rapid drying. Frequent wet-to-dry cycles (from high-humidity occluded skin rapidly drying when occlusive gloves are removed in low-humidity air) are a common cause of wintertime occupational hand dermatitis in patients who do "wet work." TEWL increases transiently after occlusive gloves are worn for 4 hours and TEWL is measured 20 minutes after the gloves are removed.[30] Upon the removal of occlusion, atopic skin may be more likely to fissure and become inflamed due to filaggrin defects. Juvenile plantar dermatosis is another clinical model for the detrimental effects of occlusion combined with moisture from perspiration in atopic children.

Adhesion defects such as those due to filaggrin may also allow protein antigens to penetrate past the stratum corneum; AD patients are particularly likely to have an allergic response to protein allergens. Occlusion causes the proliferation of commensal yeast such as Malassezia sympodialis.[26] In AD patients, the yeast causes delayed-type hypersensitivity that manifests as dermatitis of the skin on the head, neck, and upper torso where sebaceous activity is sufficient to support yeast growth. Adult patients with dermatitis of the neck and upper torso in areas of maximal contact with clothing often react to patch tests with this yeast.[31]

Another possible explanation for our findings may be related to microbial overgrowth under the occlusive material. IL-1α levels have been shown to increase in the skin of mice during Staphylococcus aureus infection.[32] Patients with AD are known to be markedly susceptible to cutaneous infection with bacteria, fungi, and viruses,[32] and cutaneous superinfection with S. aureus is elevated even in healthy-appearing skin of AD patients when compared to unaffected controls.[33] Microbes can invade the skin after skin barrier disruption, and the innate immune system responds to these pathogens. One mechanism of innate immunity includes antimicrobial peptides (such as human b-defensin 2 and LL-37, a cathelicidin), which are induced by injury or inflammation of the skin.[33,34] Patients with AD have been shown to be deficient in these peptides, which are effective against bacteria, viruses, and fungi. Specifically, the quantities of these peptides found in AD patients were insufficient to be effective in killing S. aureus.[35]

Shin guard dermatitis is observed in athletes who wear shin guards, and patch-testing with all components of the shin guards often yields negative results.[36] This condition is more common among patients with AD.[37] Occlusion plays a role in this condition, which may be partly due to irritation from sweating under the shin guard, microbial proliferation, and barrier damage from drying after shin guard removal.

Limitations

The limitations of the current study include the small number of subjects; thus, the analyses cannot be regarded as definitive. Additionally, no nonatopic controls were analyzed; further investigation is therefore needed to discern whether the induction of inflammatory cytokines by occlusion is truly limited to atopic patients. The cytokine profile we selected to evaluate was limited to very specific markers known to be associated with inflammation. Additional cytokine and chemokine mRNA profiles would be desirable and necessary to demonstrate more definitively the extent of mRNA changes associated with occlusion of the skin of AD patients. Further, differences in the time course of mRNA expression may have existed between occlusion and SLS, and it is possible we did not do our tape stripping at the time of peak mRNA expression. It also would be worthwhile in future studies to do cultures to see if additional microbes are present in occluded versus non-occluded skin. Nonphysiologic bacterial flora are increased under synthetic fibers when compared to less occlusive cellulose fibers.[38]

Finally, it is not known whether these findings extend to other types of occlusion.

Treatment Implications

Our results show that occlusion with polyethylene disrupts AD skin, a finding that we have observed clinically as well. Although the specific mechanism whereby occlusion worsens barrier function in AD remains to be elucidated, this finding has many clinical implications. Filament polyester and nylon fabrics are occlusive. Polyester has been shown to be irritating to the skin. Yao and colleagues compared subjects wearing cotton or polyester pajamas for 3 weeks and found that mean stratum corneum water content was significantly higher in those wearing cotton pajamas. There was a significant improvement in stratum corneum water content when subjects changed from polyester to cotton, coupled with a significant decline when subjects changed from cotton to polyester.[39] Nylon clothing was also recently found to cause flares of eczema in children.[40] Nonfilamentous cellulosic fibers such as cotton or lyocell are preferable for AD patients.

Occlusion remains a popular treatment for inflammatory skin diseases in general, most likely due to the evidence supporting its efficacy in treating psoriasis. Our data suggest that occlusive treatments such as sauna suits or plastic dressings should be reconsidered and further studied in AD patients. The penetration of antiinflammatory topical medications is enhanced by occlusion such as plastic tape and may outweigh the inflammatory effects of occlusion itself in some circumstances (such as on lichenified skin). However, transdermal medication delivery may cause irritation in AD patients.[41] Occlusive ointment therapy was not addressed in our studies; we speculate that gradual change in the humidity gradient as ointments are gradually removed from the skin surface may be less damaging than the abrupt removal of occlusive dressings, clothing, or athletic gear. We also did not study more-complex occlusive systems such as diapers, which include absorptive layers and retain urine, which may alter the regional microbiome.

Additional investigation of the mechanism of occlusion and its effects on AD is warranted to improve quality of life for AD patients and to refine recommendations for protective equipment, apparel, and topical vehicles for these patients.

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