Psoriasis and alcohol: is cutaneous ethanol one of the missing links?

Abstract

Many exogenous factors including excessive alcohol consumption have been associated with psoriasis, but the underlying mechanisms still remain elusive. Drinking worsens therapeutic compliance, and decreases the efficacy and increases the toxicity of systemic antipsoriatic treatments. Excess alcohol intake results in compromised immunity and increased risk of infections, but alcohol can induce proinflammatory cytokine production in various cell types and can increase mitogen-derived lymphocyte proliferation and lymphocyte activation. As we have previously reported, alcohol and one of its metabolites, acetone, induce keratinocyte proliferation and increase the mRNA levels of genes characteristic for proliferating keratinocytes, such as alpha5 integrin, cyclin D1 and keratinocyte growth factor receptor. Recently the correlation between blood and skin ethanol levels in humans was determined by a transdermal alcohol monitoring device, against the 'gold standard' breath alcohol readings. Based on transdermal alcohol measurements it can be concluded that cutaneous alcohol concentrations can reach levels that induce proinflammatory cytokine production and lymphocyte and keratinocyte proliferation in vitro. It is expected that the development of methodologies measuring transdermal ethanol will provide additional tools to evaluate how alcohol influences skin physiology and different dermatological conditions including psoriasis. Our review focuses on the possible link between alcohol misuse and psoriasis, particularly on the possible role of cutaneous ethanol in precipitating the disease.

Psoriasis: epidemiology, natural history, and differential diagnosis

“…16,20,32 Several mechanisms by which alcohol may induce psoriasis have been proposed, including upregulation of pro-inflammatory cytokines in various cell types, proliferation and activation of lymphocytes, hyperproliferation of keratinocytes as well as an increased risk of infection which can precipitate psoriasis. 31,[33][34][35] Acute bacterial and viral infections have been associated with the onset or exacerbation of psoriasis. 36,37 Streptococcal infections are often triggers of guttate psoriasis, especially in children and young adults.…”

Alcohol, Liver, Systemic Inflammation and Skin: A Focus on Patients with Psoriasis

“…Heavy drinkers are more susceptible to infections, have innate and acquired immunity deregulation and have skin barrier function alterations. Moreover, ethanol can directly and indirectly increase pro-inflammatory cytokine production of many cell types leading to persistent systemic inflammation and can enhance lymphocyte and keratinocyte proliferation [12]. In this review, we will focus on the effects of alcohol on the liver, on systemic inflammatory responses and on the role of skin ethanol and its metabolites in triggering psoriasis.…”

A psoriasis és az oxidatív stressz

“…A fentieken kívül a klasszikus rizikófaktorokkal (alkoholfogyasztás, dohányzás, elhí-zás) rendelkező betegek esetében is nagyobb a psoriasis incidenciája. A túlzott alkoholfogyasztás és a dohányzás által okozott oxidatív stressz és immunmoduláció króni-kus gyulladáshoz vezet, amely a psoriasis kiváltója és fenntartója lehet [13,14]. Egy több mint 130 ezer beteget involváló összefoglaló közlemény szerint pozitív összefüggés van a BMI és a psoriasis súlyossága között.…”