What is the pathophysiology of miliaria?

Updated: Mar 27, 2020
  • Author: Nikki A Levin, MD, PhD; Chief Editor: Dirk M Elston, MD  more...
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Answer

The primary stimuli for the development of miliaria are conditions of high heat and humidity that lead to excessive sweating. Occlusion of the skin due to clothing, bandages, transdermal medication patches, [3] or plastic sheets (in an experimental setting) can further contribute to pooling of sweat on the skin surface and overhydration of the stratum corneum. In susceptible persons, including infants, who have relatively immature eccrine glands, overhydration of the stratum corneum is thought to be sufficient to cause transient blockage of the acrosyringium. Foxc1 knockout in mice produces miliaria, suggesting a genetic predisposition may exist. [4]

If hot humid conditions persist, the individual continues to produce excessive sweat, but he or she is unable to secrete the sweat onto the skin surface because of ductal blockage. This blockage results in the leakage of sweat en route to the skin surface, either in the dermis or epidermis, with relative anhidrosis.

When the point of leakage is in the stratum corneum or just below it, as in miliaria crystallina, little accompanying inflammation is present, and the lesions are asymptomatic. In contrast, in miliaria rubra, the leakage of sweat into the subcorneal layers produces spongiotic vesicles and a chronic periductal inflammatory cell infiltrate in the papillary dermis and lower epidermis. In miliaria profunda, the escape of sweat into the papillary dermis generates a substantial, periductal lymphocytic infiltrate and spongiosis of the intra-epidermal duct.

Resident skin bacteria, such as Staphylococcus epidermidis and Staphylococcus aureus, are thought to play a role in the pathogenesis of miliaria, possibly through formation of biofilms. [5, 6]  Patients with miliaria have three times as many bacteria per unit area of skin as healthy control subjects. Antimicrobial agents are effective in suppressing experimentally induced miliaria. Periodic acid-Schiff-positive diastase-resistant material has been found in the intraductal plug that is consistent with staphylococcal extracellular polysaccharide substance (EPS). In an experimental setting, only the strains of S epidermidis that produce EPS can induce miliaria. [7]

In late-stage miliaria, hyperkeratosis and parakeratosis of the acrosyringium are observed. A hyperkeratotic plug may appear to obstruct the eccrine duct, but this is now believed to be a late change and not the precipitating cause of the sweat blockage.


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