Abstract
We report three Japanese patients with psoriasis vulgaris associated with nonalcoholic fatty liver disease in which the skin lesions dramatically resolved after treatment of the fatty liver disease with ursodeoxycholic acid (UDCA). According to the literature, arachidonic acid is released from phospholipid by phospholipase A(2) (PLA(2)) and is a precursor of eicosanoids, including prostaglandins, leucotrienes, and thromboxanes, which are potent inflammatory mediators. PLA(2) activity has been reported to be significantly raised in the serum and skin tissue of patients with psoriasis. UDCA has been reported to suppress the increased activity of group IIA PLA(2), a secretory low-molecular-weight PLA(2) (PLA(2)IIA), in HepG2 cells (a human hepatoblastoma-derived cell line) and in gallbladder and gallbladder bile samples from patients with cholesterol stones. Thus, UCDA may improve the skin lesions of patients with psoriasis by suppressing PLA(2)IIA activity.
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