Etiology

Dyshidrotic dermatitis is of unknown etiology. A number of risk factors and potential contributing factors have been investigated. There is conflicting evidence about whether atopy confers increased risk.[6][7] Some investigators have found that contact allergy (especially to metals) is correlated with dyshidrotic dermatitis, while others have not.[8][9] Nickel-sensitive patients may have flares of dyshidrotic dermatitis following dietary exposure or systemic administration of the metal.[10][11] The high eccrine duct density on the palms and soles may lead to concentration of metal on these surfaces when sweating leading to flares in nickel-sensitive patients.[12] Hyperhidrosis appears to be an aggravating condition for a subset of people with dyshidrotic dermatitis.[6][13] Common irritants such as water, detergents, and solvents may also have a role in exacerbating the condition in some patients.[14][15]​ One study demonstrated a correlation between dyshidrosis and smoking, oral contraceptives, and acetylsalicylic acid.[7] Emotional stress can also trigger outbreaks of dyshidrotic dermatitis, but the condition is not linked to sex or age.[3][4][6][8][16]​​

Pathophysiology

Dyshidrotic dermatitis is not related to an alteration in eccrine ducts as is suggested by its name. On histopathology, it is simply spongiotic dermatitis in the setting of acral skin. It is the thickened stratum corneum that causes the classic "tapioca" appearance of dyshidrotic dermatitis by its impedance to vesicular rupture.[17] The intra-epidermal portion of eccrine ducts is unaffected by this process.[17]

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