Psoriasis vulgaris and digestive system disorders: is there a linkage?

Abstract

Psoriasis is well-known immune-mediated skin disease often associated with co-morbidities, including dyslipidaemia and obesity. Few reports imply that the disease might be also related to pathology of mucosal surfaces, especially that of the digestive system. The authors present a case of psoriasis and concurrent digestive system abnormalities, and review the literature regarding the topic. A 40-year-old man suffered from an exacerbation of exudative psoriasis for about 6 months. Topical antipsoriatics proved ineffective and the disease gradually progressed to a severe disseminated form. Subsequent detailed examinations revealed persistent gastroduodenitis due to H. pylori infection, pancreatic dysfunction and fatty change of the liver, although the patient denied any gastrointestinal symptoms. As a result appropriate treatment of the diagnosed digestive system disorders was added to topical antipsoriatic therapy. Within 2 weeks of treatment clinical symptoms and laboratory signs showed a marked trend to normalisation. The presented medical history seems to suggest that there may be some kind of interplay between psoriasis and digestive system disorders.

Prevalence and Possible Role of Candida Species in Patients with Psoriasis: A Systematic Review and Meta-Analysis

“…However, in some genetically predisposed individuals, bacteria or fungi on the mucous membranes may lead to the activation of the local innate immune system and, in turn, induce an adaptive immune response [ 34 ]. These recent findings partially explain the presence of gastrointestinal symptoms in patients with psoriasis as well as coexistence with inflammatory bowel diseases [ 35 , 36 ].…”

The Risk of Chronic Pancreatitis in Patients with Psoriasis: A Population-Based Cohort Study

“…[ 28 – 29 ] The pivotal mediators of inflammation in psoriasis, including tumor necrosis factor (TNF) -α, interleukin (IL)-1, IL-17, and IL-18, are also overexpressed in patients with pancreatitis and their expressions are related to the severity of pancreatic destruction and eventual mortality. [ 28 , 30 – 33 ] Mews et al showed that persistent activation of the stellate pancreatic cells by TNF-α and IL-1 could be a factor in the progression of CP. [ 34 – 35 ] In murine models, TNF-α has been shown to induce severe pancreatitis and be involved in subsequent pancreatic fibrosis by inducing TGF-β.…”