The natural history of portal hypertensive gastropathy in patients with liver cirrhosis and mild portal hypertension

BACKGROUND: Portal hypertensive gastropathy is a potential cause of bleeding in patients with liver cirrhosis. Studies on its natural history have often included patients submitted to endoscopic or pharmacological treatment for portal hypertension. PATIENTS AND METHODS: A total of 222 cirrhotic patients with mild degree of portal hypertension (i.e., with no or small varices at entry, without previous gastrointestinal bleeding and medical, endoscopic, or angiographic treatment) were followed up with upper endoscopy every 12 months for 47 +/- 28 months. RESULTS: Upon enrollment 48 patients presented portal hypertensive gastropathy (43 mild and 5 severe) and the presence of esophageal varices was the only independent predictor of the presence of this gastric lesion at multivariate analysis. The incidence of portal hypertensive gastropathy was 3.0% (1.1-4.9%) at 1 yr and 24% (18.1-29.9%) at 3 yr, while the progression was 3% (1-6.9%) at 1 yr and 14% (4.2-23.8%) at 3 yr. The presence of esophageal varices and the Child-Pugh class B or C at enrollment were predictive of the incidence of portal hypertensive gastropathy, while only Child-Pugh class B or C was correlated with the progression from mild to severe, at multivariate analysis. During follow-up 16 patients bled from portal hypertensive gastropathy (9 acutely and 7 chronically) and one patient died of exsanguination from this lesion. CONCLUSIONS: The natural history of portal hypertensive gastropathy is significantly influenced by the severity of liver disease and severity of portal hypertension. Acute bleeding from portal hypertensive gastropathy is infrequent but may be severe.     

Is there ileopathy in portal hypertension?

BACKGROUND AND AIMS: Portal hypertensive gastropathy and colopathy are well described endoscopic abnormalities in patients with portal hypertension. Endoscopic abnormalities in the ileum in patients with portal hypertension have not been well described. The aim of the present study was to evaluate endoscopic abnormalities in the ileum of patients with portal hypertension. METHODS: Patients with portal hypertension of various etiologies were included in the study. Upper gastrointestinal endoscopy was performed to record esophageal varices, gastric varices and portal hypertensive gastropathy. Colonoscopy with retrograde intubation of the ileum was performed and the presence of colorectal varices, colopathy and mucosal findings in the ileum were noted. RESULTS: Forty-one patients (age 16-80 years, 33 men) were studied. Esophageal varices were present in all. Portal hypertensive gastropathy was present in 27/41 (66%) patients. Rectal varices were noted in 22/41 (54%) patients and 17/41 (42%) patients had features suggestive of colopathy. Ileum could be intubated in 38 patients (93%). Endoscopic abnormalities in the ileum were noted in 13/38 (34%) patients. Ileopathy as evident by endoscopic mucosal abnormalities was observed in 10/38 (26%) patients. Ileal varices were present in 8/38 (21%) patients. Three of these had ileal varices alone while the remaining five patients also had associated ileopathy The presence of ileopathy was significantly associated with the presence of portal hypertensive gastropathy and colopathy but not with esophageal, gastric or rectal varices. CONCLUSIONS: Ileopathy occurs in one-third of patients with portal hypertension and is significantly associated with the presence of portal hypertensive gastropathy and colopathy.     

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%).     

The influence of endoscopic variceal ligation on the portal pressure gradient in cirrhotics

BACKGROUND/AIMS: After variceal eradication by endoscopic ligation, fundal varices and worsening of portal hypertensive gastropathy can occur. The aim of this study is to verify the impact of the eradication of esophageal varices by endoscopic ligation on the portal pressure gradient, worsening of portal hypertensive gastropathy and development of fundal varices. METHODOLOGY: Twenty-two (15M/7F, mean age: 54.5 years) cirrhotics with previous variceal bleeding were submitted to measurement of hepatic venous pressure gradient before and after variceal eradication by endoscopic ligation. RESULTS: The mean hepatic venous pressure gradient in the first measurement was 14.1 mmHg and after eradication, 13.5 mmHg (p = 0.403). After eradication, 12 patients experienced a reduction in portal pressure and 10, an elevation. Three patients developed fundal varices. Their mean gradient before treatment was 22 mmHg and 18.8 mmHg after therapy (p = 0.368). The gastropathy worsened in 9 patients (mean gradient before therapy of 15.2 mmHg; and 16.1 mmHg after treatment) (p = 0.303). The initial pressure gradient of these patients was not different from the other 13 cases (p = 0.463). CONCLUSIONS: The esophageal variceal eradication by endoscopic band ligation does not alter the hepatic venous pressure gradient. There is no significant variation in the portal pressure of patients in whom there was a worsening of portal hypertensive gastropathy or fundal varices development.     

Portal colopathy: prospective study of colonoscopy in patients with portal hypertension

Twenty patients with portal hypertension related to a variety of causes prospectively underwent colonoscopy for hematochezia (n = 10), hemoccult positive stool and anemia (n = 9), or polyp found with screening flexible sigmoidoscopy (n = 2) (includes 1 patient with anemia/heme-positive stool). Twelve patients (60%) had previously undergone a course of sclerotherapy, and 10 (50%) had endoscopic evidence of congestive gastropathy. Colonoscopic findings included mucosal abnormalities resembling multiple vascular ectasias in 14 (70%), 4 of whom also had endoscopic features suggesting a mild, chronic colitis. Neither signs of chronic liver disease nor stigmata suggestive of more severe portal hypertension correlated with the colonoscopic findings. Two patients required heater probe therapy for actively oozing lesions resembling vascular ectasias and an additional two patients sclerotherapy for bleeding midrectal varices. Although likely an overestimate of the frequency, this study suggests that portal colopathy can occur in portal hypertension. Vascular ectasialike lesions in such settings may be associated with acute as well as chronic gastrointestinal bleeding and may require pharmacological, directed endoscopic, or portal decompressive therapy. Additional studies are required to determine not only the pathophysiology but also the true frequency of this entity.     

The etiology of upper gastrointestinal bleeding in patients with liver cirrhosis

108 patients suffering from the cirrhosis of the liver and acute bleeding into the upper digestive tract underwent a prospective endoscopic examination with diagnostic and therapeutic objectives. The most frequent causes of acute bleeding included oesophagus varices (57.4%) followed by peptic gastric ulcer (13.9%) and peptic ulcer of duodenum (11.1%), then portal hypertension gastropathy (5.6%), gastric varices (4.6%), reflux oesophagitis (2.8%), Mallory-Weiss syndrom (2.8%) and erosive gastropathy (0.9%). The endoscopy of the upper digestive tract in one patient resulted in negative diagnosis. 69% of examinations showed multiple findings in the upper digestive tract, each of which could have been a potential cause of bleeding. To determine the source of bleeding the specialist's attitude presented at the end of the endoscopic examination was taken into consideration. In 67.6% of patients the bleeding was a direct consequence of portal hypertension, in 62% it was caused by varices. The emphasis is put on early and thorough endoscopic examinations aimed at proper diagnosis and therapy.     

Mucosal abnormalities of the small bowel in patients with cirrhosis and portal hypertension: a capsule endoscopy study

BACKGROUND: The frequency of small-bowel mucosal changes in patients with portal hypertension is not known. The objective of the study is to better define the mucosal abnormalities of portal hypertensive enteropathy (PHE) and to determine whether these findings are associated with the severity of liver disease, esophageal varices, portal gastropathy, portal colonopathy, or other clinical characteristics. METHODS: We compared the medical records of 37 patients with cirrhosis and portal hypertension with 34 control patients who underwent capsule endoscopy over a 3-year period. RESULTS: Mucosal changes were found to be significantly more common in the cirrhotic patients than in the control patients (67.5% vs. 0, p < 0.001). The lesions included telangiectasias or angiodysplastic-like lesions in 9 (24.3%) patients, red spots in 23 (62.2%), and varices in 3 (8.1%). Active bleeding was seen during endoscopic examinations in 4 (10.8%) patients. A comparison of patients with and those without PHE showed that grade 2+ or larger esophageal varices, portal gastropathy, portal colonopathy, and Child-Pugh class C cirrhosis were all significantly associated with PHE. There were no differences between these two groups of patients with regard to the etiology of cirrhosis, gender, or history of esophageal variceal bleeding. CONCLUSIONS: Mucosal abnormalities in portal jejunopathy include edema, erythema, and vascular lesions findings. A standardized grading system to classify the endoscopic appearance and the severity of portal enteropathy is proposed. The clinical import of these changes remains to be explained.     

The effects of endoscopic variceal ligation and propranolol on portal hypertensive gastropathy: a prospective, controlled trial

BACKGROUND: Endoscopic treatment of esophageal varices may accentuate portal hypertensive gastropathy. The impact of the combination of band ligation and propranolol on this condition remains unknown. METHODS: Patients with history of variceal bleeding were randomized to receive band ligation alone (control group, 40 patients) or a combination of band ligation and propranolol (propranolol group, 37 patients). Serial endoscopic evaluation of gastropathy was performed. Gastropathy was classified into 3 grades and scored as 0, 1, or 2. RESULTS: Before endoscopic treatment, 17% of the control group and 22% of the propranolol group had gastropathy (p = 0.78). The occurrence of gastropathy after endoscopic treatment was significantly higher in the control group than in the propranolol group (p = 0.002). Serial endoscopic follow-up revealed that the mean gastropathy score was significantly higher in the control group than in the propranolol group (p < 0.05). In patients with gastropathy the gastropathy score reached a peak at 6 months after endoscopic treatment in both the control and propranolol groups (85% vs. 48%, respectively). After variceal obliteration, accentuation of gastropathy was significant in the control group (p < 0.01) but not in the propranolol group. Gastropathy was less likely to develop in patients who developed gastric varices. Esophageal variceal recurrence was not related to the development of gastropathy after variceal obliteration with banding. Only one patient in the control group bled from gastropathy. CONCLUSION: Band ligation of esophageal varices may accentuate gastropathy, which in this study was partly relieved by propranolol.     

The role of endoscopy in portal hypertension

Endoscopy plays a major role in the management of gastrointestinal varices in portal hypertension. It is used for the prophylaxis of the first bleeding episode, therapy of active bleeding and prophylaxis of recurrent bleeding. Today not only nonselective betablockers, but also endoscopic band ligation is an option in the primary prophylaxis of the first bleeding episode in patients with large esophageal varices. Acutely bleeding varices should be treated by ligation, pharmacological and antibiotic therapy. Prophylaxis of recurrent bleeding despite endoscopic and pharmacologic treatment is patient dependent: shunt surgery is an option in young patients in a good medical condition (Child-Pugh class A). In patients with refractory ascites and a bilirubin level below 3 mg/dl, TIPS is a good option. Nevertheless, the first-line treatment in most patients in Germany is endoscopic band ligation. Bleeding from ectopic varices and due to hypertensive gastropathy should be treated individually either by endoscopy, TIPS or drug therapy.     

Portal hypertension and gastrointestinal bleeding:Diagnosis,prevention and management

Bleeding from esophageal varices is a life threatening complication of portal hypertension.Primary prevention of bleeding in patients at risk for a first bleeding episode is therefore a major goal.Medical prophylaxis consists of non-selective beta-blockers like propranolol or carvedilol.Variceal endoscopic band ligation is equally effective but procedure related morbidity is a drawback of the method.Therapy of acute bleeding is based on three strategies:vasopressor drugs like terlipressin,antibiotics and endoscopic therapy.In refractory bleeding,self-expandable stents offer an option for bridging to definite treatments like transjugular intrahepatic portosystemic shunt(TIPS).Treatment of bleeding from gastric varices depends on vasopressor drugs and on injection of varices with cyanoacrylate.Strategies for primary or secondary prevention are based on non-selective beta-blockers but data from large clinical trials is lacking.Therapy of refractory bleeding relies on shuntprocedures like TIPS.Bleeding from ectopic varices,portal hypertensive gastropathy and gastric antral vascular ectasia-syndrome is less common.Possible medical and endoscopic treatment options are discussed.     

Capsule endoscopy in the investigation of patients with portal hypertension and anemia.

INTRODUCTION: Data on small bowel abnormalities in patients with portal hypertension (PHT) are limited. Bleeding from the gastrointestinal tract and anemia are common complications in these patients. Capsule endoscopy (CE) was used to evaluate small bowel (SB) pathology in patients with PHT and anemia, and possible associations with various parameters were examined. METHODS: Thirty-five patients with PHT referred for CE investigation of the SB for anemia were prospectively enrolled in the study, as well as 70 age- and sex-matched control patients with anemia, normal liver function and no evidence of PHT who underwent CE. RESULTS: Findings compatible with portal hypertensive enteropathy (PHE) were detected in 65.7% of the patients and in 15.7% of the controls chi2=26.641, P=0.000). Abnormalities in PHT patients included varices in 25.7%, diffuse changes of mucosa with inflammatory-like appearance in 42.9%, and angiodysplasias and/or spider angiomas in 22.9% of cases. The presence of PHE was significantly associated only with the presence of severe portal hypertensive gastropathy, while the presence of SB varices alone was significantly associated with the presence of severe portal hypertensive gastropathy, larger esophageal varices and the presence of colonic varices. CONCLUSIONS: Varices, diffuse changes of mucosa with inflammatory-like appearance, and angiodysplasias and/or spider angiomas are detected more often in patients with PHT than in controls, and probably constitute the endoscopic characteristics of PHE. CE of the SB added a significant number of likely important findings to those detected by conventional endoscopic techniques for the clinical management of patients with PHT and anemia.     

内镜下套扎、硬化剂及组织胶注射治疗食管静脉曲张破裂出血的近期疗效观察

目的观察肝硬化食管静脉曲张破裂出血患者行内镜下套扎、硬化剂及组织胶注射治疗后食管静脉曲张程度、红色征及门静脉高压性胃病的变化。方法回顾性分析本院2011年9月-2013年9月收治的75例食管静脉曲张破裂出血患者,行首次内镜下套扎、硬化剂或组织胶注射治疗。2~4周后复查胃镜,对比治疗前后曲张食管静脉的数目与直径、红色征及门静脉高压性胃病在内镜下的改变。组内治疗前后的比较采用配对t检验,率的比较采用卡方检验。结果治疗后曲张食管静脉的数目及直径均小于治疗前[(3.08±0.96)vs(3.75±0.60),t=5.26,P0.05;(1.05±0.46)cm vs(1.49±0.26)cm,t=9.84,P0.05)],差异均有统计学意义。红色征的发生率较治疗前降低,差异有统计学意义(26.67%vs 57.33%,χ2=14.48,P0.05)。治疗后门静脉高压性胃病虽有所好转,但差异无统计学意义(70.67%vs 72.00%,χ2=0.03,P0.05)。结论内镜下套扎、硬化剂及组织胶注射治疗食管静脉曲张破裂出血的方法安全、有效。     

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.     

Nodules in antrum after variceal eradication a new finding in patients with portal hypertension

Portal hypertension is known to cause esophageal varices, gastric varices and portal hypertensive gastropathy (PHG). The prevalence of gastric varices and PHG is known to increase after eradication of esophageal varices. PHG includes the presence of a mucosal mosaic pattern, cherry red spots, and/or black-brown spots and gastric vascular ectasia (GAVE). Patients with portal hypertension in whom esophageal varices were eradicated were on follow up endoscopy for detection of recurrence of esophageal varices. Their status of PHG was assessed and patients antral nodules were enrolled. Twenty patients with antral nodules were identified over one year. Fifteen out of 20 patients had cirrhosis as etiology of portal hypertension, three had non-cirrhotic portal hypertension and two had extra-hepatic portal vein thrombosis. GAVE was seen more commonly (n=8, 40%) in patients with PHG with nodules. PHG with antral nodules is a novel endoscopic finding present both in cirrhotic and non-cirrhotic portal hypertension with unknown pathogenesis, and is seen more commonly in patients with eradicated varices who are on long-term follow up.     

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.     

肝硬化患者门静脉高压性胃病发病因素的研究

背景：门静脉高压性胃病是肝硬化患者上消化道出血的原因之一．但其发病机制目前尚不完全清楚。目的：探讨肝硬化患者门静脉高压性胃病的发生与肝硬化分级、食管胃底静脉曲张程度、腹水量和胃肠激素血管活性肠肽（VIP）水平的关系。方法：45例肝硬化患者行胃镜检查观察食管胃底静脉曲张程度和胃黏膜改变．行腹部B超检查观察腹水量，同时检测血清白蛋白、总胆红素、胆碱酯酶、凝血酶原时间等肝功能指标和血浆VIP水平。结果：Child—Pugh A、B、C级肝硬化患者、不同程度食管胃底静脉曲张患者以及不同程度腹水患者之间的门静脉高压性胃病发生率均无显著差异（P〉0．05）。但肝硬化伴门静脉高压性胃病患者的血浆VIP水平较无门静脉高压性胃病者显著升高（P〈0．001）。结论：门静脉高压是门静脉高压性胃病的必要条件，而其他因素．如血浆VIP水平与门静脉高压性胃病的发生也有一定关系。     

Gastrointestinal bleeding in portal hypertension in liver cirrhosis

There are three major goals in the prophylaxis and treatment of upper gastrointestinal bleeding in portal hypertensive patients: prophylaxis of the first bleeding episode, therapy of active bleeding and prophylaxis of recurrent bleeding. Several therapeutic options are available: non-selective beta-blockers are the treatment of choice in the primary prophylaxis of the first bleeding episode in patients with large esophageal varices. Alternatively, endoscopic band ligation therapy is an option. Acute bleeding varices should be treated by ligation pharmacological and antibiotic therapy. Prophylaxis of recurrent bleeding is patient-dependent: shunt surgery is an option in young patients in a good medical condition (Child-Pugh class A). In patients with refractory ascites and a bilirubin below 3 mg/dl, TIPS is a good option together with recurrent bleeding. At the moment, there are no trials showing that endoscopic ligation therapy is superior to prevent pharmacological therapy. Nevertheless, the first-line treatment in most patients in Germany is endoscopic band ligation. Bleeding from ectopic varices and bleeding from hypertensive gastropathy should be treated individually either by endoscopy, TIPS or drug therapy.     

Natural history of portal hypertension in patients with cirrhosis

All patients with cirrhosis will eventually develop portal hypertension and esophagogastric varices. Bleeding from ruptured esophagogastric varices is the most severe complication of cirrhosis and is the cause of death in about one third of patients. The rate of development and growth of esophageal varices is poorly defined but in general seem to be related to the degree of liver dysfunction. Once varices have formed, they tend to increase in size and eventually to bleed. In unselected patients, the incidence of variceal bleeding is about 20% to 30% at 2 years. Variceal size is the single most important predictor of a first variceal bleeding episode. Several prognostic indexes based on endoscopic and clinical parameters have been developed to predict the risk of bleeding; however, their degree of accuracy is unsatisfactory. Death caused by uncontrolled bleeding occurs in about 6% to 8% of patients; the 6-week mortality rate after a variceal hemorrhage is 25% to 30%. There are no good prognostic indicators of death caused by uncontrolled bleeding or death within 6 weeks. Untreated patients surviving a variceal hemorrhage have a 1- to 2-year risk of rebleeding of about 60% and a risk of death of about 40% to 50%. The risk of bleeding is greatest in the first days after a bleeding episode and slowly declines thereafter. All patients surviving a variceal hemorrhage must be treated to prevent rebleeding. Varices can also be found in the stomach of cirrhotic patients, alone or in association with esophageal varices. Gastric varices bleed less frequently but more severely than esophageal varices. Portal hypertensive gastropathy is a common feature of cirrhosis, and its prevalence parallels the severity of portal hypertension and liver dysfunction. Portal hypertensive gastropathy can progress from mild to severe and vice-versa or even disappear completely. Acute bleeding from portal hypertensive gastropathy seems to be relatively uncommon, and less severe than bleeding from varices.     

Natural history of portal hypertensive gastropathy in patients with liver cirrhosis. The New Italian Endoscopic Club for the study and treatment of esophageal varices (NIEC)

BACKGROUND & AIMS: The clinical importance of portal hypertensive gastropathy (PHG) as a source of gastrointestinal bleeding in patients with cirrhosis is poorly defined. We investigated the natural history of this condition in a large series of patients. METHODS: All patients with cirrhosis seen at 7 hospitals during June and July 1992 were followed up with clinical and endoscopic examinations every 6 months for up to 3 years. Gastropathy was classified according to the classification of the New Italian Endoscopic Club. RESULTS: The prevalence of gastropathy was 80% and was correlated with the duration of disease, presence and size of esophagogastric varices, and a previous history of endoscopic variceal sclerotherapy. During 18+/-8 months of follow-up, gastropathy was stable in 29% of patients, deteriorated in 23%, improved in 23%, and fluctuated with time in 25%. The evolution of gastropathy with time was identical in patients with and without previous or current sclerotherapy. Acute bleeding from gastropathy occurred in 8 of 315 patients (2.5%). The bleeding-related mortality rate was 12.5%. Chronic bleeding occurred in 34 patients (10.8%). CONCLUSIONS: PHG is common in patients with cirrhosis, and its prevalence parallels the severity of portal hypertension. Gastropathy can progress from mild to severe and vice versa or even disappear completely. Bleeding from this lesion is relatively uncommon and rarely severe. Sclerotherapy of esophageal varices does not seem to influence the natural history of this condition.     

GENERAL RULES FOR RECORDING ENDOSCOPIC FINDINGS OF ESOPHAGOGASTRIC VARICES (2ND EDITION)

General rules for recording endoscopic findings of esophageal varices were initially proposed in 1980 and revised in 1991. These rules have widely been used in Japan and other countries. Recently, portal hypertensive gastropathy has been recognized as a distinct histological and functional entity. Endoscopic ultrasonography can clearly depict vascular structures around the esophageal wall in patients with portal hypertension. Owing to progress in medicine, we have updated and slightly modified the former rules. The revised rules are simpler and more straightforward than the former rules and include newly recognized findings of portal hypertensive gastropathy and a new classification for endoscopic ultrasonographic findings.