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Five‐year history of pruritic plaques

hyperthyroidism, alcoholism, carcinoid syndrome with liver metastases, and even in healthy individuals. The most accepted theory is that it may result from a localized increase in estrogen receptors caused by a somatic mosaicism, which explains the distribution in a segmental pattern. These lesions become unmasked in situations of estrogen excess. Estrogens promote endothelium-dependent relaxation by increasing nitric oxide and prostacyclin and inhibiting the mechanisms of vascular smooth muscle contraction, contributing to the formation of telangiectasias. Clinically it manifests as an asymptomatic, segmental distribution of telangiectasias, frequently found in C3–C4 or the trigeminal dermatomal areas. The histopathology is characterized by a normal-appearing epidermis with underlying superficial dermal telangiectatic vessels. As this is a benign condition, there is no need for treatment. Nevertheless, the treatment of choice is the pulsed-dye laser therapy. In most cases, the cosmetic result is excellent. In both our patients, the history of chronic hepatic disorders along with the characteristic distribution of the lesions and the histopathological confirmation of superficial telangiectasias confirmed the diagnosis of UNT. In both cases, estrogen levels were not performed, which would be helpful to support the diagnosis, if increased. Hyperestrogenism in liver diseases is attributed to reduced hepatic catabolism of estrogens and weak androgens. The weak androgens are converted to estrogenic compounds in peripheral tissues, thereby adding to the burden of circulating estrogens. Hyperestrogenism is much more evident when extrahepatic portal hypertension due to cirrhosis is present, as the portal-systemic shunts permit these hormones to bypass the liver.