Background. Portal hypertension resulted from the increased pressure in the portal system is one of the leading syndromes of liver cirrhosis. A frequent and often fatal manifestation of portal hypertension is upper gastrointestinal bleeding mainly due to varicose veins of the esophagus and the stomach. Objective. To study the prevalence of esophageal and gastric varices and their association with other phenotypic stigmas of cirrhosis. Material and methods. A total of 108 patients with cirrhosis, including 46 (42.59%) men and 62 (57.41%) women, were included in the study. Results. Varicose veins were detected in 77 (71,3%) of 108 examined patients. All varices were localized in the esophagus. Of all patients examined, 36 patients (33.33%) were Child-Pugh class A, 58 patients (53.70%) were class B, and 14 patients (12.96%) were class C. Among Class A patients, 9 patients (11.7%) had grade I varicose veins, 9 patients (11.7%) had grade II, 8 patients (10.4%) had grade III, while 13 patients (16.9%), 24 patients (31.2%) and 3 patients (3.9%) had grade B varicose veins, respectively. All patients classified as class C had large varicose veins. The size of varices was associated with the severity of liver cirrhosis (τ=0.2, 95% CI: p˂0.05). Grade II-III varices were seen in 55 patients (50.9%), 9 of whom (16.4%) had a history of gastrointestinal bleeding. Such complication was not observed in any patient with class A cirrhosis, but occurred in all patients with Child-Pugh class C cirrhosis. Conclusions. Patients with liver cirrhosis should undergo follow-up upper GI endoscopy for early detection of varices and, if necessary, for prescription of prophylactic therapy to reduce the risk of bleeding and associated high mortality.

Гомельский государственный медицинский университет, Гомель, Беларусь В обзоре приведены современные данные по проблеме профилактики кровотечения из варикозно-расширенных вен пищевода (ВРВП) с помощью различных адренергических средств. Освещены доказательства связи полиморфизмов гена b2-адренорецептора (ADRB2) с более значимым снижением градиента печеночно-венозного давления (ГПВД) в ответ на лечение неселективными бета-адреноблокаторами.

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