Alcohol and Skin Disorders
Cutaneous abnormalities have been associated with alcoholism and are either caused indirectly through impaired functioning of other organ systems or directly from the toxic effects of alcohol on the skin.
Skin Changes Indirectly Caused by Alcohol
The majority of cutaneous manifestations associated with excess alcohol use are indirectly mediated through the impairment of various organ systems.
Hepatic dysfunction impairs estrogen and bile salt metabolism, resulting in characteristic findings of spider angiomata, palmar erythema, and pruritis.[2,3,5] Male alcoholics are consequently hyperestrogenic.[2] In addition to high estrogen levels, testosterone production is also inhibited, further exacerbating the problem. Direct inhibition of testosterone production leads to gynecomastia, which presents as a disappearance and redistribution of body and pubic hair and female pattern fat redistribution.[2] Caput medusae and hemorrhoids are the result of hepatofugal blood flow caused by portal hypertension from liver cirrhosis.
Systemic and superficial skin infections, including bacterial and fungal infections, represent another health problem found to be more prevalent in alcoholics.[2–4] The higher incidence of infections is likely attributable to multiple factors, including alcohol associated nutritional deficiencies in combination with immunodeficiency. Most notably, zinc and vitamin C deficiencies lead to poor wound healing, weakened mucosal barriers, and altered immune defenses with increased risk for infections. Group A streptococci, Corynebacterium, and Staphylococcus aureus are common bacterial culprits,[2] as are fungal infections with various tinea and Candida species.[2,3]
Malabsorption associated with alcoholism is another mode by which alcohol can produce cutaneous abnormalities. Angular stomatitis, glossitis, perifollicular hemorrhages, pellagra, petechia, and ecchymosis are just a few such cutaneous manifestations.
Skin Changes Directly Caused by Alcohol
Porphyria Cutanea Tarda (PCT) is a metabolic disorder with cutaneous manifestations resulting from an aberration in hepatic heme biosynthesis. Whether acquired or inherited, PCT results from a deficiency in one of the hepatic enzymes involved in porphyrin metabolism, specifically uroporphyrinogen decarboxylase.[2,3,6] The resultant upstream accumulation of photoreactive porphyrin precursors renders the skin extremely photosensitive.[2] Alcohol is a potent inducer of the hepatic enzymes and the heme metabolic pathway, leading to an accumulation of photoreactive porphyrin compounds proximal to the enzymatic defect and, thus, precipitating PCT flare-ups.[3,6] The cutaneous characteristics of an acute PCT attack include skin blistering and erosions on sun exposed areas[2,3] that resolve leaving residual scarring and milia.
Alcohol impairs the vasomotor center of the brain, inducing peripheral vasodilatation.[2,3] Hence, it has been suggested that this resultant cutaneous vasodilatation may exacerbate rosacea,[2,3] contributing to the hallmark redness and flushing. Alcohol can also promote facial erythema in people without rosacea through a genetic deficiency involving an alcohol metabolism enzyme. This phenomenon is most commonly recognized in Asians, as studies have shown that 50% lack the ability to make aldehyde dehydrogenase, leading to an accumulation of acetaldehyde after alcohol consumption.[2]
Skin Therapy Letter. 2011;16(4) © 2011 SkinCareGuide.com
Cite this: Alcohol and Skin Disorders - Medscape - Apr 01, 2011.
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