Efficacy of argon plasma coagulation for gastric antral vascular ectasia associated with chronic liver disease.

Gastric antral vascular ectasia (GAVE) is a rare cause of chronic gastrointestinal bleeding. The aim of this study was to evaluate the relationship between GAVE with cirrhotic patients and liver dysfunction, portal hypertension and the safety and efficacy of argon plasma coagulation (APC) in treating GAVE with cirrhotic patients. Eight cirrhotic patients with the characteristic endoscopic findings of GAVE were registered. In this study, APC was performed for GAVE in all eight patients. The patients-liver function was classified by Child-Pugh classification and classifications were: two class A, five class B and one class C (mean score: 7.8). Five patients had previously received prophylactic endoscopic injection sclerotherapy for esophageal varices and one had esophageal varices. Balloon-occluded retrograde transvenous obliteration (B-RTO) for gastric varices had been performed in other one patient. Portal hypertensive gastropathy (PHG) was recognized in only one case. APC was performed in all eight patients and one to three treatment sessions were needed (mean: 1.8 sessions). No complications were observed in the initial treatment. During follow-up, endoscopies revealed the recurrence of GAVE in two patients requiring further treatment by APC (recurrence rate: 25%). After APC treatment, the recurrence of GAVE was not observed with endoscopy in the other six patients. The results suggest that GAVE is related to severe liver damage and portal hypertension in cirrhotic patients. APC is a safe and effective treatment against GAVE.     

Disappearance of gastric antral vascular ectasia after percutaneous transhepatic obliteration

We report on a patient with severe iron deficiency anemia due to gastric antral vascular ectasia (GAVE), complicating hepatocellular carcinoma (HCC) and esophageal varices. Esophago-gastro-duodenoscopy (EGDS) 6 months after transarterial embolization (TAE) for the HCC and percutaneous transhepatic obliteration (PTO) for esophageal varices, showed the absence of GAVE. As GAVE did not recur in spite of the recurrence of the tumor thrombus later, lowered antral congestion by PTO might be the main cause of disappearance of GAVE. This case suggests that PTO may be an effective treatment against GAVE with portal hypertension with uncontrollable bleeding.     

Portal hypertensive gastropathy: A systematic review of the pathophysiology,clinical presentation,natural history and therapy

AIM: To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy(PHG) based on a systematic literature review.METHODS: Computerized search of the literature was performed via Pub Med using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy". The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS: PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG.PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt or liver transplantation is highly successful ultimate therapies because they reduce the underlying portal hypertension.CONCLUSION: PHG is important to recognize in patients with cirrhotic or non-cirrhotic portal hypertension because it can cause acute or chronic GI bleeding that often requires pharmacologic therapy.     

Treatment of gastropathy and gastric antral vascular ectasia in patients with portal hypertension

Opinion statement 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 β-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 [TIPS] 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 β-blocker. Shunt therapy should be considered in patients who rebleed or continue to bleed despite adequate β-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 β-blockers nor TIPS reduces the bleeding risk in patients with GAVE and thus should not be used in this setting.     

Portal hypertensive gastropathy in chronic hepatitis C patients with bridging fibrosis and compensated cirrhosis: results from the HALT-C trial

OBJECTIVES: The clinical significance of portal hypertensive gastropathy (PHG) in patients with compensated liver disease is not well established. The aim of this study was to determine the prevalence and correlates of PHG in a large cohort of patients with chronic hepatitis C virus (HCV) infection and bridging fibrosis/compensated cirrhosis entering the randomized phase of the Hepatitis C Antiviral Long-term Treatment against Cirrhosis trial (HALT-C). METHODS: The presence and severity of PHG in 1,016 HCV patients with no prior history of gastrointestinal bleeding was determined at surveillance endoscopy using the New Italian Endoscopy Club criteria. RESULTS: Overall, 37% of HALT-C patients had PHG with 34% having mild and 3% with severe changes. The mucosal mosaic pattern was identified in 33%, red marks in 15%, and gastric antral vascular ectasia (GAVE) features in only 3%. Independent correlates of PHG included biochemical markers of liver disease severity (lower serum albumin, higher bilirubin), portal hypertension (lower platelet count), insulin resistance (higher glucose), and non-African American race. Independent correlates of GAVE included a history of smoking, nonsteroidal anti-inflammatory drugs (NSAIDs) use within the past year, and higher serum bilirubin and glucose levels. There was a strong positive association between the presence of PHG and esophageal varices (p < 0.0001). CONCLUSIONS: PHG is associated with the histological and biochemical severity of liver disease in patients with HCV and advanced fibrosis but is mild in most patients. The clinical relevance of these findings will be further explored during the randomized phase of the HALT-C study.     

Portal Hypertensive gastropathy

Portal hypertensive gastropathy (PHG), a term used to describe the endoscopic appearance of gastric mucosa with a characteristic mosaic-like pattern with or without red spots, is a common finding in patients with portal hypertension. Current classification systems that describe the severity of PHG have many limitations, but it appears that simple grading systems have better inter- and intraobserver agreement. The wide variation in the reported prevalence of PHG is probably related to selection bias, absence of uniform criteria and classification, and more importantly, the differences in inter- and intraobserver variation. Pathogenesis of PHG is not clearly defined, but there is a very close relationship between portal hypertension and development of PHG. GAVE is a separate entity from PHG, but patients with severe PHG may have a GAVE-like appearance in the gastric antrum. Acute bleeding from PHG, seen usually in the presence of severe PHG, is often mild and self-limiting. Currently, the only treatment that could be recommended for prophylaxis of bleeding from PHG is nonselective B-blockers.     

The effects of transjugular intrahepatic portosystemic shunt on portal hypertensive gastropathy

In addition to variceal bleeding, haematemesis may occur due to haemorrhagic gastritis in patients with portal hypertension. This has been known as portal hypertensive gastropathy (PHG). We have evaluated the effects of the transjugular intrahepatic portosystemic shunt (TIPS) on portal venous pressure (PVP) and endoscopic gastric mucosal changes observed in patients with portal hypertension. We performed TIPS in 12 patients with complications due to portal hypertension as follows: variceal bleeding in nine patients (bleeding from oesophageal varices in seven and gastric varices in two), refractory ascites in three and haemorrhage from severe PHG in one. Endoscopic examinations were performed before and after TIPS for all patients. Changes of PVP and gastric mucosal findings on endoscopy were analysed. Before TIPS, PHG was seen in 10 patients. Portal venous pressure decreased from an average of 25.1 ± 8.8 to 17.1 ± 6.2 mmHg after TIPS ( P < 0.005). On endoscopy, PHG improved in nine of 10 patients. Oesophagogastric varices improved in eight of 11 patients. In one patient with massive haematemesis, haemorrhage from severe PHG completely stopped after TIPS. Because TIPS effectively reduced PVP, this procedure appeared to be effective for the treatment of uncontrollable PHG.     

The natural history of portal hypertensive gastropathy: influence of variceal eradication

OBJECTIVE: The natural history and likelihood of bleeding from portal hypertensive gastropathy (PHG) present in patients with portal hypertension before endoscopic variceal obliteration may differ from that in patients who develop PHG during or after variceal eradication. METHODS: A total of 967 variceal bleeders who had achieved variceal eradication by endoscopic sclerotherapy in the recent past were prospectively studied. In all, 88 (9.1%) patients (cirrhosis in 54, noncirrhotic portal fibrosis in 18, and extrahepatic portal vein obstruction in 16) had distinct mucosal lesions. PHG alone was present in 78, PHG with gastric antral vascular ectasia (GAVE) in eight, and GAVE alone in two patients. PHG was graded as mild or severe and according to whether present before (group A) or after endoscopic intervention (group B). Patients underwent regular endoscopy at follow-up to see if the PHG was transitory (disappearing within 3 months), persistent (no change), or progressive. Bleeding from PHG lesions was defined as acute or chronic. RESULTS: Twenty-two (26%) patients had PHG before (group A) and 64 (74%) developed PHG after variceal eradication (group B). During a mean follow-up of 25.1 +/- 14.2 months, PHG lesions disappeared in group A in only two patients (9%), but in group B in 28 (44%) patients (p < 0.05). PHG lesions more often progressed in the former as compared to the latter (18% vs 9.4%, p = NS). The incidence of bleeding was higher in group A than group B (32% vs 4.7%, p < 0.02). Bleeding from PHG occurred in 10 patients (11.6%); seven of them were from group A, and all had either progressive (n = 3) or persistent (n = 4) lesions. CONCLUSIONS: PHG developing after variceal eradication is often transitory and less severe. If PHG is pre-existing, endoscopic therapy for varices could worsen the PHG, with a likelihood of bleeding. Such patients may be benefited by concomitant beta-blocker therapy.     

内镜治疗食管静脉曲张对门脉高压性胃病的影响

探讨内镜下硬化剂(EST)和套扎(EVL)治疗食管静脉曲张术后对门脉高压性胃病(PHG)和胃底静脉曲张(GV)的影响,对21例注射硬化剂治疗和27例套扎治疗的共48例患者进行了1年的内镜随访,观察PHG和GV的程度。结果在接受治疗3个月和1年后,PHG发生率较治疗前(35％,17/48)明显增加,分别为75％(36/48)和87％(42/48);GV较治疗前(17％,8/48)增多,分别为33％(16/48)和43％(21/48)。结论:食管静脉曲张的内镜下硬化剂和套扎治疗将加重PHG和GV且有可能增加PHG和GV的出血机会。     

内镜下聚桂醇治疗食管静脉曲张对门脉高压性胃病的影响

[目的]探讨内镜下聚桂醇治疗食管静脉曲张对门脉高压性胃病(PHG)的影响.[方法]对连续100例门脉高压食管静脉曲张出血后接受内镜下硬化剂聚桂醇治疗的患者开展临床随访研究,评估聚桂醇治疗后对PHG的影响.[结果]注射聚桂醇前33例患者存有PHG(33％);初次注射聚桂醇治疗后PHG患者为74例,其中新增轻度PHG患者41例;2次及以上注射聚桂醇治疗后PHG患者达88例,经注射聚桂醇后PHG发生率明显增高(P＜0.01).注射聚桂醇的次数与PHG的发生相关(P＜0.01).[结论]内镜下硬化剂聚桂醇治疗术(EIS)治疗食管静脉曲张,在控制出血和消退曲张静脉的同时,具有产生和加重PHG的可能,但大多为轻度PHG.患者经硬化剂治疗后控制出血,全身状况好转后应择期手术治疗或长期应用降门脉压药物,控制和改善PHG,预防食管静脉曲张和PHG出血.     

Reliability in endoscopic diagnosis of portal hypertensive gastropathy

AIM: To analyze reliability among endoscopists in diagnosing portal hypertensive gastropathy (PHG) and to determine which criteria from the most utilized classifications are the most suitable.METHODS: From January to July 2009, in an academic quaternary referral center at Santa Casa of São Paulo Endoscopy Service, Brazil, we performed this single-center prospective study. In this period, we included 100 patients, including 50 sequential patients who had portal hypertension of various etiologies; who were previously diagnosed based on clinical, laboratory and imaging exams; and who presented with esophageal varices. In addition, our study included 50 sequential patients who had dyspeptic symptoms and were referred for upper digestive endoscopy without portal hypertension. All subjects underwent upper digestive endoscopy, and the images of the exam were digitally recorded. Five endoscopists with more than 15 years of experience answered an electronic questionnaire, which included endoscopic criteria from the 3 most commonly used Portal Hypertensive Gastropathy classifications (McCormack, NIEC and Baveno) and the presence of elevated or flat antral erosive gastritis. All five endoscopists were blinded to the patients’ clinical information, and all images of varices were deliberately excluded for the analysis.RESULTS: The three most common etiologies of portal hypertension were schistosomiasis (36%), alcoholic cirrhosis (20%) and viral cirrhosis (14%). Of the 50 patients with portal hypertension, 84% were Child A, 12% were Child B, 4% were Child C, 64% exhibited previous variceal bleeding and 66% were previously endoscopic treated. The endoscopic parameters, presence or absence of mosaic-like pattern, red point lesions and cherry-red spots were associated with high inter-observer reliability and high specificity for diagnosing Portal Hypertensive Gastropathy. Sensitivity, specificity and reliability for the diagnosis of PHG (%) were as follows: mosaic-like pattern (100; 92.21; High); fine pink speckling (56; 76.62; Unsatisfactory); superficial reddening (69.57; 66.23; Unsatisfactory); red-point lesions (47.83; 90.91; High); cherry-red spots (39.13; 96.10; High); isolated red marks (43.48; 88.31; High); and confluent red marks (21.74; 100; Unsatisfactory). Antral elevated erosive gastritis exhibited high reliability and high specificity with respect to the presence of portal hypertension (92%) and the diagnosis of portal hypertensive gastropathy (88.31%).CONCLUSION: The most suitable endoscopic criteria for the diagnosis of PHG were mosaic-like pattern, red-point lesions and cherry-red spots with no subdivisions, which were associated with a high rate of inter-observer reliability.     

Case report: portal hypertension secondary to isolated liver tuberculosis

In this report, we present a case of isolated liver tuberculosis (TB) as a cause of non-cirrhotic portal hypertension leading to bleeding esophageal varices. Although TB has been known to cause portal hypertension in a variety of ways, this case was notable for the presence of periportal inflammation and granulomas, also seen in hepatic schistosomiasis. Herein, we discuss isolated liver TB and the differential diagnosis of non-cirrhotic portal hypertension. In endemic areas, TB should be considered in the differential diagnosis of non-cirrhotic portal hypertension.     

Portal hypertensive bleeding

Portal hypertension bleeding is a common and serious complication of cirrhosis. All patients with cirrhosis should undergo endoscopy and be evaluated for possible causes of current or future portal hypertensive bleeding. Possible causes of bleeding include esophageal varices, gastric varices, and PHG. Patients with esophageal varices at high risk of bleeding should be treated with nonselective beta-blockers for primary prevention of variceal hemorrhage. HVPG measurements represent the optimal way to monitor the success of pharmacologic therapy. EVL may be used in those with high-risk varices who do not tolerate beta-blockers. When active bleeding develops, simultaneous and coordinated attention must be given to hemodynamic resuscitation, prevention and treatment of complications, and active control of bleeding. In cases of acute esophageal variceal (Fig. 5) and PHG bleeding, terlipressin, somatostatin, or octreotide should be started. Endoscopic treatment is provided for those with bleeding esophageal varices. If first-line therapy fails, TIPS or surgery may need to be performed. Unlike esophageal variceal or PHG bleeding, there is no established optimal treatment for gastric variceal bleeding. Individual and specific treatment modalities for acute gastric variceal bleeding must be calculated carefully after considering side effects.     

Antral Varices

Varices of the gastric fundus, often associated with esophageal varices, are a common complication of portal hypertension or splenic vein occlusion. However, varices of the gastric antrum have been reported rarely. We describe a 61-yr-old man with antral and esophageal varices caused by portal hypertension due to hepatic cirrhosis.     

Prevalence of upper and lower gastrointestinal tract findings in liver transplant candidates undergoing screening endoscopic evaluation

OBJECTIVE: The incidence of esophageal and gastric varices and portal hypertensive gastropathy (PHG) has been well studied in cirrhotic patients. Because little is known of the prevalence of other upper and lower gastrointestinal tract pathology in pre-liver transplant candidates, we retrospectively studied the prevalence of and factors associated with these findings. METHODS: One hundred and twenty pre-liver transplant candidates underwent esophagogastroduodenoscopy to evaluate for varices, and 71 of them also underwent flexible sigmoidoscopy to screen for colorectal carcinoma. The association of upper and lower GI tract pathology with Child-Pugh Class, etiology of cirrhosis, and signs of portal hypertension, including presence and size of esophageal varices, presence of gastric varices, PHG, ascites, and splenomegaly, was analyzed using univariate and multivariate analysis. RESULTS: Etiology of cirrhosis among 87 men and 33 women (mean age, 52 yr) included 25% hepatitis C, 27% hepatitis C/alcohol, 15% alcohol, 10% primary sclerosing cholangitis/primary biliary cirrhosis, 9% cryptogenic, 8% metabolic, and 6% hepatitis B. Prevalence of Child-Pugh Classes A, B, and C were 34%, 49%, and 17%, respectively; 73% of patients had esophageal varices (23% were large), 62% PHG (23% were severe), and 16% gastric varices. Excluding varices and PHG, endoscopic findings in the upper GI tract (n = 120) included: 13% esophagitis/ulcers, 7.5% gastritis, 8% duodenitis, 2% Barrett's esophagus, 3% duodenal ulcers, and 2% gastric ulcers. Findings in the lower gastrointestinal tract (n = 71) included 21% adenomatous polyps, 21% internal hemorrhoids, 15% diverticulosis, 7% rectal varices, 3% colopathy, and 3% vascular ectasias. Univariate analysis revealed that there was a significant association between rectal varices and severe PHG (p < 0.05). This association was not maintained when multivariate analysis was performed. CONCLUSIONS: Among all the findings, only rectal varices and colopathy were of higher prevalence in the pre-liver transplant population than that reported for the general population. No significant associations were found between these gastrointestinal tract lesions and patient characteristics.     

Association of nodular regenerative hyperplasia of the liver with porto-pulmonary hypertension in a patient with systemic lupus erythematosus

A 37-year old woman with systemic lupus erythematosus (SLE) complicated by pulmonary hypertension (PHT) was admitted to evaluate abnormal liver function. Radiological imaging study, including ultrasonography, computed tomography and magnetic resonance imaging and upper gastrointestinal endoscopy, revealed multiple hepatic nodules, hepatosplenomegaly and esophageal varices. Percutaneous needle liver biopsy showed non-cirrhotic hepatic nodules with hyperplastic hepatocytes surrounded by atrophic hepatocytes, confirming the diagnosis of nodular regenerative hyperplasia (NRH) associated with non-cirrhotic portal hypertension (PT). NRH of the liver is known to be a very rare hepatic manifestation in rheumatic diseases. This case shows the association of NRH with porto-pulmonary hypertension in SLE.     

Portal hemodynamics in patients with gastric varices. A study in 230 patients with esophageal and/or gastric varices using portal vein catheterization

The hemodynamic features of gastric varices are not well documented. The purpose of this study was to investigate the nature of hepatofugal collateral veins, their origins, the direction of blood flow in the major veins and collateral veins, and portal venous pressure. To this end, 230 patients, mostly cirrhotic, who had esophageal or gastric varices, or both, demonstrated by endoscopy were investigated by portal vein catheterization. The findings were correlated with endoscopically assessed degrees of varices. Gastric varices were seen in 57% of the patients with varices due to portal hypertension. In most of the patients with advanced gastric varices, esophageal varices were minimal or absent. When patients with gastric varices were compared with those having predominantly esophageal varices, it was found that advanced gastric varices were more frequently supplied by the short and posterior gastric veins, they were almost always associated with large gastrorenal shunts, and portal venous pressure in patients with large gastric varices was lower. Chronic portal systemic encephalopathy was more common in patients with large gastric varices due to hepatofugal flow of superior mesenteric venous blood in the splenic vein than in patients with predominantly esophageal varices. Thus, the hemodynamics in patients with large gastric varices are distinctly different from those in patients with mainly esophageal varices, and such differences seem to account for the differing incidence of chronic encephalopathy and variceal bleeding.     

Effect of Portal Hypertension in the Small Bowel: An Endoscopic Approach

BACKGROUND AND AIM: The effects of portal hypertension in the small bowel are largely unknown. The aim of the study was to prospectively assess portal hypertension manifestations in the small bowel. METHODS: We compared, by performing enteroscopy with capsule endoscopy, the endoscopic findings of 36 patients with portal hypertension, 25 cirrhotic and 11 non-cirrhotic, with 30 controls. RESULTS: Varices, defined as distended, tortuous, or saccular veins, and areas of mucosa with a reticulate pattern were significantly more frequent in patients with PTH. These two findings were detected in 26 of the 66 patients (39%), 25 from the group with PTH (69%) and one from the control group (3%) (P < 0.0001). Among the 25 patients with PTH exhibiting these patterns, 17 were cirrhotic and 8 were non-cirrhotic (P = 0.551). The presence of these endoscopic changes was not related to age, gender, presence of cirrhosis, esophageal or gastric varices, portal hypertensive gastropathy, portal hypertensive colopathy, prior esophageal endoscopic treatment, current administration of beta-blockers, or Child-Pugh Class C. More patients with these endoscopic patterns had a previous history of acute digestive bleeding (72% vs. 36%) (P = 0.05). Active bleeding was found in two patients (5.5%). CONCLUSIONS: The presence of varices or areas of mucosa with a reticulate pattern are manifestations of portal hypertension in the small bowel, found in both cirrhotic and non-cirrhotic patients. The clinical implications of these findings, as regards digestive bleeding, are uncertain, although we documented acute bleeding from the small bowel in two patients (5.5%).     

肝硬化门静脉高压性胃病的胃镜表现及相关因素分析

目的探讨门静脉高压性胃病(PHG)胃镜下胃黏膜特征及其与食管胃静脉曲张、溃疡病及肝硬化并发症之间的关系。方法回顾性分析2012年8月-2018年6月陆军军医大学大坪医院867例肝硬化患者临床资料,统计其胃镜下食管胃静脉曲张、PHG、溃疡病发生的情况,收集肝硬化并发自发性细菌性腹膜炎、肝性脑病、原发性肝癌的数据资料。计数资料组间比较采用χ2检验,相关性分析采用Spearman相关性检验。结果肝硬化患者PHG发生率高达66.2%(574/867),轻度PHG胃黏膜改变以红点灶(68.6%)和蛇皮征(56.8%)为主,而重度PHG以弥漫红斑为主(76.5%)。PHG在不同程度的食管静脉曲张中发生率差异显著(χ2=304.712,P<0.05),并且随着食管静脉曲张加重,PHG程度亦越来越重(r=0.515,P<0.05)。不同程度胃静脉曲张的患者PHG发生率差异有统计学意义(χ2=81.004,P<0.05),且PHG程度与胃静脉曲张程度相关(r=0.292,P<0.05)。不同部位静脉曲张患者PHG的发生率差异显著(χ2=41.361,P<0.05),当患者仅出现胃静脉曲张时,PHG发生率(34.8%)最低,且均为轻度;而食管和胃均出现静脉曲张时,PHG发生率(85.6%)最高。未合并PHG患者中有71例(24.2%)因呕血和(或)黑便就诊住院,而574例PHG患者中有316例(55.1%)因此而住院,二者差异显著(χ2=74.562,P<0.05)。结论不同PHG严重程度的患者胃黏膜特征差异显著,PHG的发生和严重程度与食管胃静脉曲张程度密切相关,且是肝硬化消化道出血重要原因,应积极治疗和预防PHG以降低消化道出血风险和相关并发症。