Abstract
Two major physiological events in eczema include transepidermal water loss owing to the loss of the stratum corneum, and occlusion of the sweat ducts, which leads to decreased sweat on the skin surface. Sulzberger noted occluded sweat ducts in atopic eczema in 1947. The observations that people with atopy do not sweat normally and that they will then suffer the effects of heat prostration combine with the clinical observation (and patient historical data) that sweating makes eczema worse. We propose that atopic dermatitis results from subclinical miliaria, which involves occlusion of sweat ducts. The difference in miliaria and eczema is found within the genetic part of the double-hit phenomenon. Once a patient begins scratching a genetically deficient stratum corneum, the disease process becomes ongoing.
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References
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Sulzberger MB, Hermann F, Zak FG. Studies of sweating. I. Preliminary report with particular emphasis on a sweat retention syndrome. J Invest Dermatol. 1947;9(5):221–42. Dr. Sulzberger and his colleagues sought to prove that plugging of the sweat-gland orifices played an important role in the pathogenesis of atopic dermatitis, ichthyosis, atypical seborrheic dermatitis, and patchy prickly heat. They present cases in which they exposed patients, presumably with these diseases, to transient heat and found that the patients had typical clinical and histologic findings. Sulzberger found that these patients immediately developed pruritus and malaise and had decreased sweating as evidenced by starch iodine tests and increased pH on the skin surface. Subjects also developed new or more pronounced papulovesicles that had the low pH of sweat. On pathology, numerous sweat glands showed plugging. Biopsies after heat exposure showed increased vesicle formation and exocytosis.
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Allen, H.B. (2015). Physiology. In: The Etiology of Atopic Dermatitis. Springer, London. https://doi.org/10.1007/978-1-4471-6545-3_6
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DOI: https://doi.org/10.1007/978-1-4471-6545-3_6
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