Ripoll Cristina, Garcia-Tsao Guadalupe
Guadalupe Garcia-Tsao, MD Digestive Diseases Section, Yale University School of Medicine, 333 Cedar Street--1080 LMP, New Haven, CT 06510, USA.
Curr Treat Options Gastroenterol. 2007 Dec;10(6):483-94. doi: 10.1007/s11938-007-0048-5.
Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) are two distinct gastric mucosal lesions that may cause acute and/or chronic upper gastrointestinal hemorrhage in patients with cirrhosis. Whereas PHG is associated with portal hypertension, GAVE may present in patients without portal hypertension or liver disease. Diagnosis is made upon visualization of the characteristic lesions with upper gastrointestinal endoscopy, although the differential may be difficult at times. PHG is characterized endoscopically by a mosaic pattern with or without red signs and a proximal distribution. PHG mainly causes chronic blood loss and anemia in patients with cirrhosis but also can cause acute hemorrhage. First-line therapy for chronic hemorrhage from PHG is a nonselective beta-blocker (propranolol or nadolol) and iron supplementation. If bleeding/anemia are not controlled with these measures and the patient is transfusion-dependent, shunt therapy (transjugular intrahepatic portosystemic shunt or shunt surgery) should be considered. Management of acute bleeding from PHG, an infrequent event, should be accomplished with a vasoactive drug, somatostatin (or its analogues) or terlipressin. If bleeding responds, the patient must be switched to a nonselective beta-blocker. Shunt therapy should be considered in patients who rebleed or continue to bleed despite adequate beta-blocker therapy. GAVE is less common than PHG. It is characterized by red spots without a background mosaic pattern, typically in the gastric antrum. When lesions have a linear distribution, the lesion is called "watermelon stomach." GAVE is a cause of chronic gastrointestinal bleeding and anemia in patients with cirrhosis. If lesions are localized, first-line therapy is argon plasma coagulation. In more diffuse lesions, therapy with argon plasma coagulation is more complicated. Preliminary data suggest that cryotherapy may be a reasonable option for diffuse GAVE lesions. Neither beta-blockers nor TIPS reduces the bleeding risk in patients with GAVE and thus should not be used in this setting.
门静脉高压性胃病（PHG）和胃窦血管扩张症（GAVE）是两种不同的胃黏膜病变，可导致肝硬化患者发生急性和/或慢性上消化道出血。PHG与门静脉高压有关，而GAVE可出现在无门静脉高压或肝病的患者中。通过上消化道内镜检查发现特征性病变即可确诊，尽管有时鉴别可能困难。PHG在内镜下的特征是有或无红色征的马赛克样改变及近端分布。PHG主要导致肝硬化患者慢性失血和贫血，但也可引起急性出血。PHG慢性出血的一线治疗是使用非选择性β受体阻滞剂（普萘洛尔或纳多洛尔）及补充铁剂。如果这些措施不能控制出血/贫血且患者依赖输血，则应考虑分流治疗（经颈静脉肝内门体分流术或分流手术）。PHG急性出血不常见，处理时应使用血管活性药物，如生长抑素（或其类似物）或特利加压素。如果出血得到控制，患者必须改用非选择性β受体阻滞剂。对于尽管接受了充分的β受体阻滞剂治疗仍再出血或持续出血的患者，应考虑分流治疗。GAVE比PHG少见。其特征是无背景马赛克样改变的红点，通常位于胃窦。当病变呈线性分布时，该病变称为“西瓜胃”。GAVE是肝硬化患者慢性胃肠道出血和贫血的一个原因。如果病变局限，一线治疗是氩离子凝固术。对于更弥漫的病变，氩离子凝固术治疗更复杂。初步数据表明，冷冻疗法可能是弥漫性GAVE病变的一个合理选择。β受体阻滞剂和经颈静脉肝内门体分流术均不能降低GAVE患者的出血风险，因此在这种情况下不应使用。
