The American journal of gastroenterology · 1994
Congestive gastropathy: factors influencing development, endoscopic features, Helicobacter pylori infection, and microvessel changes.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Parikh S S, Desai S B, Prabhu S R, Trivedi M H, Shankaran K, Bhukhanwala F A, Kalro R H, Desai H G
Аннотация
OBJECTIVES: To study 1) the factors influencing the development of congestive gastropathy (CG) in patients with portal hypertension (PHT), 2) the changes in gastric microvessels in patients with PHT with and without CG, and 3) to determine whether Helicobacter pylori plays any role in the pathogenesis of CG.
METHODS: One hundred eighteen patients with PHT (102 cirrhosis, 16 noncirrhotic portal fibrosis) were evaluated by videogastroscopic examination. Antral biopsy tissue was examined for microvessel changes, histological gastritis, and H. pylori infection in 85 of 118 patients and 45 controls. Portal venous pressure (PVP) was determined by hepatic venous pressure gradient in 17 patients with CG.
RESULTS: CG was present in 71 (60%) patients with PHT, of whom 41 (58%) had mild and 30 (42%) had severe CG. CG was observed with equal frequency in cirrhosis (63%) and noncirrhotic portal fibrosis (44%). The incidence of CG was higher in patients with severe liver disease, a past history of hemetemesis, in those with esophageal varices, and in those with gastric varices. Severe CG was commonly observed in patients with large size esophageal varices and in those with gastric varices. There was significant dilation of gastric mucosal vessels in patients with PHT, but in this regard there was no significant difference between patients with and without CG. The presence of H. pylori, histological gastritis, degree of PVP, or degree of capillary dilation did not influence the severity of CG.
CONCLUSIONS: CG occurs commonly in patients with PHT, especially those with severe liver disease, past history of hemetemesis, and esophagogastric varices. Patients with PHT have significant gastric microvessel changes. The severity of CG appears to be independent of PVP, capillary dilation, H. pylori infection, or histological gastritis.
METHODS: One hundred eighteen patients with PHT (102 cirrhosis, 16 noncirrhotic portal fibrosis) were evaluated by videogastroscopic examination. Antral biopsy tissue was examined for microvessel changes, histological gastritis, and H. pylori infection in 85 of 118 patients and 45 controls. Portal venous pressure (PVP) was determined by hepatic venous pressure gradient in 17 patients with CG.
RESULTS: CG was present in 71 (60%) patients with PHT, of whom 41 (58%) had mild and 30 (42%) had severe CG. CG was observed with equal frequency in cirrhosis (63%) and noncirrhotic portal fibrosis (44%). The incidence of CG was higher in patients with severe liver disease, a past history of hemetemesis, in those with esophageal varices, and in those with gastric varices. Severe CG was commonly observed in patients with large size esophageal varices and in those with gastric varices. There was significant dilation of gastric mucosal vessels in patients with PHT, but in this regard there was no significant difference between patients with and without CG. The presence of H. pylori, histological gastritis, degree of PVP, or degree of capillary dilation did not influence the severity of CG.
CONCLUSIONS: CG occurs commonly in patients with PHT, especially those with severe liver disease, past history of hemetemesis, and esophagogastric varices. Patients with PHT have significant gastric microvessel changes. The severity of CG appears to be independent of PVP, capillary dilation, H. pylori infection, or histological gastritis.