Mild Gastropathy Research Articles

3145 Dieulafoy's Lesion: An Underdiagnosed and Underrecognized Cause of Gastrointestinal Bleed

INTRODUCTION: Acute gastrointestinal bleed accounts for nearly 50-150 cases per 100,000 each year. The etiology in the majority of cases is peptic ulcer disease (PUD). Dieulafoy's lesion is a rare (accounts for 1-2%), but potentially life-threatening cause of gastrointestinal (GI) bleed. We present a case of recurrent hemodynamically significant upper GI bleeding requiring multiple hospitalizations and endoscopies to identify a duodenal Dieulafoy's lesion as the primary source for bleed. CASE DESCRIPTION/METHODS: A 52-year-old male with a history of chronic alcohol use was admitted to the intensive care unit for the third time within a one-year duration for recurrent episodes of melena. During the first two episodes, upper GI endoscopy was positive for mild gastropathy, and a small 4-5 mm partially healed duodenal ulcer respectively. The exam was negative for any esophageal varices or other upper GI pathologies. The patient responded well both times to medical therapy and subsequently discharged home. In the third admission for similar presentation with melena and hemodynamically significant GI bleed, endoscopy was positive for an actively bleeding duodenal Dieulafoy's lesion. Bleeding was controlled with hemostatic clips and epinephrine injections. He was discharged home 48 hours after stabilization. Post-discharge, he was followed for a year, and he remained asymptomatic. It was therefore concluded that Dieulafoy's lesion was the likely cause of GI bleed that had evaded diagnosis during the first two endoscopies. DISCUSSION: Dieulafoy's lesion is a dilated submucosal vessel that erodes the epithelium and most commonly found in the stomach. Approximately one-third of the lesions are extragastric and located in the duodenum and colon. They are typically seen in men, around the fifth decade, in the presence of comorbidities such as hypertension, diabetes, chronic kidney disease, or alcohol abuse. Dieulafoy's lesions are under-diagnosed as they are silent until presentation. Approximately 33% of the lesions may require more than one EGD to identify the active source of bleeding, especially in the presence of other causes of GI bleed such as PUD. In our patient, the culprit for his recurrent GI bleeding was identified as Dieulafoy's lesion on the third endoscopy. We want to highlight the importance of the diagnosis and management of Dieulafoy's lesion as it can significantly decrease the mortality from 80% to 8.6%.

1693 Jejunal Lymphangioma: An Unusual Etiology for Iron Deficiency Anemia

INTRODUCTION: Lymphangiomas are benign tumors characterized by cystic dilation of lymphatic vessels, and can arise from any location throughout the lymphatic system. Small bowel lymphangiomas are rare, and are primarily described in children. When found in adults, these lesions are typically an incidental finding. Pathologic small bowel lymphangiomas are particularly unusual, and have been reported as a rare etiology of massive gastrointestinal bleeding and chronic anemia. CASE DESCRIPTION/METHODS: A 65yo African American man with a history of prostate cancer, coronary artery disease, hypertension, hyperlipidemia, and peripheral artery disease was hospitalized for a 6 month history of symptomatic anemia, without signs of overt gastrointestinal blood loss. Vital signs were stable upon presentation, and initial labs were significant for a hemoglobin 8.7, mean corpuscular volume 94, ferritin 28, and iron saturation of 3%. An esophagogastroduodenoscopy was performed which was significant for mild gastropathy, and a colonoscopy that showed mild diverticulosis, a 3 mm polyp and small internal hemorrhoids, without stigmata of recent bleeding. Iron therapy was initiated, and the patient was referred to the outpatient gastroenterology clinic for further workup. The patient next underwent capsule endoscopy which showed a friable small bowel mass, with evidence of active bleeding. A single balloon enteroscopy was then performed, which revealed a 4 cm circumferential, friable, granular mass in the mid-jejunum which was biopsied and tattooed with India Ink. Biopsies of the mass revealed benign small intestinal mucosa with prominent lymphangiectasia. The patient was then referred to surgical oncology and underwent a laparoscopic assisted enteroscopy which again demonstrated the previously seen lesion occupying 75% of the small bowel lumen. The lesion was further evaluated with endomicroscopy which revealed multiple dilated blood vessels and lymphatic channels, in a background of inflammation. The cells appeared organized and without atypical features. A small bowel resection was performed, and the surgical pathology revealed a benign lymphatic malformation involving the mucosa and submucosa consistent with a lymphangioma. No invasive features or malignant cells were identified. DISCUSSION: Small bowel lymphangiomas are a rare finding, and primarily found within the duodenum. We report an unusual case of a large jejunal lymphangioma presenting as iron deficiency anemia, which completely resolved after resection of the mass. Watch the video: http://bit.ly/2LvNhpc.

Metastatic Gastric Melanoma Masquerading as Bleeding Ulcer: A Challenging Case of Rarity

The most common cause of death secondary to melanoma is widespread metastasis. Malignant melanomas appear to have a particular tendency of metastases to the gut. However, these metastases rarely involve the gastric mucosa of the stomach. We present a case of 68-year-old male with a past medical history of cutaneous melanoma 3 years prior treated with wide excision and no evidence of metastasis at the time, presented with complaints of a one-month history of nausea, dizziness, black stool and a 15-lb weight loss. Initial workup revealed a Hemoglobin 9.4 g/dl (reduced from his baseline of 14g/dl) and positive occult blood in the stool. Physical exam was benign otherwise. Given the presentation of anemia, melena and weight loss, the patient underwent esophagogastroduodenoscopy (EGD), which revealed diffuse mild gastropathy, three large ulcerative gastric polyps about 3-4 cm, and several smaller gastric polyps [Image 1]. Biopsy revealed metastatic gastric melanoma with staining positive for S100+, SOX 10+, MART1+, AMB45 +, and BRAF + [Image 2,3]. CT (Computed Tomography) of the chest and abdomen, revealed lesions affecting the lung and liver. The patient was diagnosed with Stage 4 metastatic melanoma. Chemo and radiation therapy were started, however, he was soon changed to hospice care and died within 4 months of diagnosis. Melanoma can metastasize to the gastrointestinal tract. Studies report up to 60% pathological involvement of the gastrointestinal tract in autopsies of patients with metastatic melanoma. However, rarely do these metastases involve the gastric mucosa of the stomach, only reaching clinical relevance in a median of 2% of patients with metastatic melanoma (range: 0.8-8.9%). Gastric manifestations are non-specific and may present as obstruction, gastrointestinal hemorrhage, anemia, weight loss, or abdominal pain. Non-specific pulmonary, hepatic, or GI symptoms in conjunction with the history of melanoma should raise the suspicion of metastases. Management includes surgical and non-surgical interventions, including, chemotherapy and palliative radiation therapy (XRT). Metastatic gastric melanoma should be considered when evaluating a patient with melanoma, especially in those who manifest with nonspecific GI symptoms. Identification of metastases early on can better guide therapeutic treatment recommendations and improve patient outcomes.2644_A Figure 1. Esophagogastroduodenoscopy (EGD) revealed diffuse mild gastropathy, th ree large ulcerative gastric polyps about 3-4 cm, and several smaller gastric polyps.2644_B Figure 2. Diffuse S100 + staining in the tumor cells supporting the diagnosis of melanoma.2644_C Figure 3. H&E stained section shows gastric mucosa being replaced by tumor. The tumor is growing in a diffuse fashion. It is comprised of cells with round, oval and spindled nuclei. There is a moderate amount of amphophilic to eosinophilic cytoplasm. Mitotic figures are easily identified.

CIRRHOTIC PATIENTS;

At present time portal hypertension is perceived as one of the complications ofadvanced liver disease. It results in various vascular changes in gastrointestinal tract (GI),including esophageal varices, gastric varices and portal hypertensive gastropathy (PHG). PHGand gastric varices are a common cause of acute as well as chronic bleeding from GI tractwhich resulted in significant mortality among patients. Objectives: To determine the frequencyof gastric vascular changes in various causes of cirrhosis. Study Design: Cross sectional study.Setting: Department of Gastroenterology, Pakistan Institute of Medical Sciences, Islamabad.Period: 1st August 2007 to 31st July 2008. Materials and Methods: Patients of age ≥30 years,with clinical evidence of cirrhosis and without prior treatment of esophagiogastric varices wereincluded in the study. Results: A total of 100 patients were enrolled in the study out of which47 were male and 53 were females with mean age of 53.6 years. The most common type ofcirrhosis was turned out to be Hepatitis C affecting 50% of patients and most of the patientswere in Child class C. Portal hypertensive gastropathy was present in 74% of patients. Amongthem 24.3% have mild changes while severe changes were present in75.7% of patients. Gastricvarices were found in 40% of the patients and the most common type was IGV type I whichwas present in 29(72.5%) of the patients. Correlation of severity of PHG was seen with gradingof esophageal varices, grading of gastric varices and Child class. Conclusion: Frequency ofsevere gastropathy is higher than the mild gastropathy. It is also concluded that gastric vascularchanges are associated with cause of cirrhosis, child class and degree of portal hypertension.

English

At present time portal hypertension is perceived as one of the complications ofadvanced liver disease. It results in various vascular changes in gastrointestinal tract (GI),including esophageal varices, gastric varices and portal hypertensive gastropathy (PHG). PHGand gastric varices are a common cause of acute as well as chronic bleeding from GI tractwhich resulted in significant mortality among patients. Objectives: To determine the frequencyof gastric vascular changes in various causes of cirrhosis. Study Design: Cross sectional study.Setting: Department of Gastroenterology, Pakistan Institute of Medical Sciences, Islamabad.Period: 1st August 2007 to 31st July 2008. Materials and Methods: Patients of age ≥30 years,with clinical evidence of cirrhosis and without prior treatment of esophagiogastric varices wereincluded in the study. Results: A total of 100 patients were enrolled in the study out of which47 were male and 53 were females with mean age of 53.6 years. The most common type ofcirrhosis was turned out to be Hepatitis C affecting 50% of patients and most of the patientswere in Child class C. Portal hypertensive gastropathy was present in 74% of patients. Amongthem 24.3% have mild changes while severe changes were present in75.7% of patients. Gastricvarices were found in 40% of the patients and the most common type was IGV type I whichwas present in 29(72.5%) of the patients. Correlation of severity of PHG was seen with gradingof esophageal varices, grading of gastric varices and Child class. Conclusion: Frequency ofsevere gastropathy is higher than the mild gastropathy. It is also concluded that gastric vascularchanges are associated with cause of cirrhosis, child class and degree of portal hypertension.

Conservative Management of an Impacted Capsule Within the Appendiceal Orifice

A fifty year old female with a history of anemia presented with acute worsening of chronic abdominal pain. She admitted to some nausea but no other associated complaints. She had a normal physical exam apart from mild right quadrant abdominal tenderness with palpation. Laboratory work was significant for a hemoglobin of 11.7 g/dl. Gallbladder ultrasound and Computed Tomography scan of the abdomen were normal. Upper endoscopy revealed mild gastropathy with duodenitis. Given her prior work up, a capsule endoscopy was done to exclude concerns for a small bowel etiology such as Crohns disease. The capsule report revealed a tortuous small bowel and the cecum was not visualized on the images. As the capsule was not retrieved, an abdominal X-ray confirmed a retained capsule in the right lower abdominal quadrant. Multiple attempts were made at flushing the capsule out with purgative agents and enemas. As serial abdominal X-rays confirmed the retained capsule even after several days, colonoscopy was performed to retrieve the capsule (Fig 1). Upon endoscopic examination of the cecum, the capsule was noted to be lodged within the appendiceal orifice (Fig 2). We were able to dislodge the capsule using aggressive washing maneuvers and applying gentle pressure around the base of the capsule with the Roth net catheter. The Roth net was then used to remove the capsule from the colon. The patient did well subsequently and was discharged for outpatient follow up. Capsule endoscopy has become the accepted modality for evaluating small bowel pathology. Capsule retention is a complication with an overall incidence of 1-2%. Individuals with Crohn's disease are at highest risk for capsule retention (13%) versus obscure GI bleeding patients with lowest risk. A thorough literature review revealed one other case report of an impacted capsule that was caused by appendicitis requiring an appendectomy. We demonstrate here in this case report the conservative management of an impacted capsule within the appendiceal orifice of a patient without any known bowel pathology, which, to the best of our knowledge, has not been previously described in the literature.Figure 1Figure 2

Effect of Helicobacter pylori and its virulence factors on portal hypertensive gastropathy and interleukin (IL)-8, IL-10, and tumor necrosis factor-alpha levels

Background/Aim:We aimed to assess the influence of Helicobacter pylori and its virulent factors, cytotoxin associated gene (cag) A and E, on portal hypertensive gastropathy (PHG) and the levels of interleukin (IL)-8, IL-10, and tumor necrosis factor-alpha (TNF-α).Patients and Methods:The patients with cirrhosis underwent screening endoscopy and the lesions related to PHG were graded. Biopsies were obtained for histology, and polymerase chain reaction (PCR) of H. pylori 16S rRNA, cagA, cagE, and tissue cytokine levels was carried out. Absent or mild PHG was compared with moderate to severe PHG.Results:One hundred and forty patients with cirrhosis were studied; males numbered 92 and the mean age of the patients was 50.3 ± 12.0 years, H. pylori positivity in 87 (62.1%) patients was associated with male gender (P = 0.032), younger age (P = 0.029), hepatitis D etiology (P = 0.005), higher serum albumin (0.000), lower Child Pugh score (P = 0.001), and lower portal vein diameter (P = 0.001). There was no significant difference in the levels of TNF-α and IL-8. However, a decrease in the anti-inflammatory cytokine IL-10 was noted with moderate to severe gastropathy. Four H. pylori strains were positive for both cagA and cagE, while four were positive for cagA only. All the four patients with both virulent factors had mild gastropathy only.Conclusion:The presence of H. pylori infection neither affected the severity of PHG nor augmented the IL-8 and TNF-α levels. There was a decline of virulent H. pylori strains and IL-10 levels in patients with advanced PHG.

Intestinal Spirochetosis: A Rare Etiology with a Common Presentation

Purpose: A 40-year-old male with past medical history of celiac disease, HIV positive on HAART therapy, Hodgkin's lymphoma and candida esophagitis was referred to the gastroenterology clinic by his primary care physician for evaluation of diarrhea. He had 5-10 loose, watery, non-bloody, brown, bowel movements for the past year, associated with nausea, vomiting and bloating. He also noted he had a >10 lb weight loss over the past three months. He denied nausea, vomiting, hematochezia, melena, fever or chills. His symptoms did not improve with a gluten-free diet. CBC, chemistry, liver function and thyroid function were normal. He was compliant with his HAART therapy. CD4 count was >400 and viral RNA by PCR was undetectable. Tissue transglutaminase antibodies and IgA antibodies were within normal limits and stool culture, ova and parasites, clostridium toxin assay and giardia assay were negative. RPR was reactive at a titer of 1:4. EGD only revealed mild gastropathy. On colonoscopy, the mucosa appeared grossly normal. Random biopsies were performed to rule out lymphocytic or microscopic colitis. Histology subsequently revealed spirochetosis in the ascending, transverse and descending colon. The patient was treated with metronidazole 500 mg three times a day for four weeks resulting in marked improvement of symptoms and weight gain. Spirochetosis is a rare colonic disease caused by spirochete brachyspira pilosicoli or brachyspira aalborgi. Intestinal spirochetosis is a rare disease that is usually seen in HIV positive patients and CD4 counts >200/ml. Patients usually present with chronic diarrhea, abdominal pain and weight loss. It responds well to treatment with metronidazole. We report a case of intestinal spirochetosis in a patient with well controlled HIV with an undetectable viral load in the setting of past medical history of celiac disease. As this case demonstrates, opportunistic infections remain a possibility and should be investigated in all patients with HIV despite high CD4 count and low viral titer.Figure: [1150] Colonic mucosal biopsy demonstrating spirochetes. Giemsa Stain 60 ×.

Gastric Motility and Emptying in Cirrhotic Patients with Portal Hypersensitive Gastropathy

Our aim was to clarify gastric motility and emptying in LC patients with PHG. A total of 30 LC patients (18 with mild gastropathy type, 12 with severe gastropathy type) with a mean age with 65.8 yr were enrolled and 17 healthy participants were recruited as the control group. Electrogastrography was performed to examine gastric motility in the fasting, nocturnal and 2 hr postprandial phase. Subsequently, patients with LC and control were performed to measure gastric emptying of solids with the breath test using 13C for labeling the octanoic acid. Breath samples were obtained every 15 to 30 minutes for 5 hours. The mean frequency of the EGG while fasting with severe PHG was significantly increased compared to mild PHG (p<0.05). The mean frequency of the EGG at 1-hr and 2-hr postprandially with severe PHG was significantly increased compared to mild PHG. The half time of GE with both mild and severe PHG was significantly increased compared to controls. Postprandial EGG and GE in LC patients would be affected by PHG.

A Case of Refractory Peristomal Variceal Bleeding Post-TIPSS and Review of the Therapeutic Options

Purpose: Results: A 69 year old man has a history of Ulcerative Colitis with total abdominal colectomy with ileostomy performed Febuary 2002 due to treatment refractory disease. He presented four years later with presumed lower GI bleed with bright red blood noted in his ostomy bag. Ileoscopy performed at that time showed normal ileal mucosa, while careful inspection of the ileostomy site showed continued oozing from an external source. Upper endoscopy was performed to assess other signs of portal hypertension showing mild gastropathy and small esophageal varices. Non-selective beta-blocker therapy was initiated at that time with a diagnosis of Laennec's Cirrhosis. A diagnosis of peristomal varices was made after confirmation on review of abdominal imaging. Recurrent bleeding continued to require hospitalization and transfusion on three separate presentations leading to initial TIPSS procedure as well as revision bringing porto-systemic pressure gradient from 15 mmHg to 4 mmHg. He was placed prophylactically on lactulose at that time, but progressive difficulties required the addition of rifaximin. Despite the TIPSS procedure, he continued to have episodes of bleeding from his peristomal varices requiring transfusion. Conservative measures were initially employed in attempts to control bleeding after repeat porto-systemic pressure gradient measurement confirmed a widely patent TIPSS. Application of silver nitrate, oversewing with suture, and injection sclerotherapy were all attempted in addition to direct pressure without durable result. After initial consultation with Colorectal Surgery, his ostomy was taken down and re-sited for definitive therapy of his recurrent peristomal variceal hemorrhage. In the 13 months since revision of his ileostomy, he has had far fewer difficulties with bleeding only requiring transfusion on two occasions. Conclusion: Peristomal variceal bleeding is difficult to control and can be a life-threatening complication of portal hypertension in patients with colonic resection requiring ileostomy. In patients with advanced liver disease as defined by Childs Classification, ectopic variceal bleeding frequently represents a terminal event. Stoma revision with devascularization has been found in previous reports to be temporarily effective in reducing recurrent peristomal variceal bleeding and has reduced the need for transfusion in our patient. Liver transplantation remains the only potential therapy for our patient at this time, but given his age and comorbid medical status it has been determined that he is not a candidate.

Portal Hypertensive Duodenopathy: Clinical, Endoscopic, and Histopathologic Profiles

Description of the clinical, endoscopic, and histopathologic detailed profiles of duodenal affection in portal hypertensive patients. A total of 105 patients with chronic liver disease and portal hypertension (PH) were included, upper endoscopy was performed, and two duodenal biopsies were obtained from the bulb and distal to the ampulla, for histopathologic examination. Twenty dyspeptic patients with normal upper endoscopy were included as controls. Of the portal hypertensive patients, 54 (51.4%) had endoscopic duodenopathy (ED) lesions including erythema, erosions, ulcers, telangiectasia, exaggerated villous pattern, duodenal varices, and mixed lesions. ED was significantly higher in patients having severe than mild gastropathy (56.8% vs 23.5%, P<0.05) with no relation to size of esophageal varices or variceal bleeding. ED was a source of overt bleeding in 6.7% and occult bleeding in 2.9% of patients. Histopathologically, vascular changes included either capillary congestion (in more than half of biopsies) or capillary angiogenesis (in more than one-quarter of biopsies). Nonvascular changes included increased apoptosis (in about 16% of biopsies), fibrous proliferation (in about 4% of biopsies), and villous changes (in 11.4% of distal biopsies). All changes were not statistically different between patients with and without ED. In dyspeptic patients, only minimal histopathologic changes were noted. ED is significantly higher in patients with severe gastropathy and causes gastrointestinal bleeding in 9.5% of patients. Capillary angiogenesis is an important vascular mechanism for adaptation to PH. The overall existence of histopathologic duodenopathy is much higher than that of ED and occurs with a similar prevalence in patients with and without ED.

Gastritis and gastropathy of childhood.

Gastritis and gastropathy of childhood.

Weakness of mucosal barrier in portal hypertensive gastropathy of alcoholic cirrhosis. Effects of propranolol and enprostil

Background/Aims: It has been suggested that the vulnerability of gastric mucosa is increased in patients with cirrhosis as a result of a PGE2 deficiency. Therefore, we evaluated whether PGE2 mucosal generation, and gastric potential difference - a reflection of the gastric mucosal barrier - were correlated to endoscopic features and whether these alterations could be alleviated. Methods: The potential difference was measured before (basal) and after a stimulation test by aspirin. The serum levels of gastrin and glucagon were also determined. Finally, the effects of a 1-week administration of propranolol or enprostil were tested on potential difference. The endoscopic grade of portal hypertensive gastropathy was assessed according to McCormack et al. The results are presented respectively for controls, patients with mild gastropathy, and patients with severe gastropathy. Comparisons were made using variance or covariance analysis after adjustment with age. Results: Basal potential difference was significantly different betweeen the three groups: −30.6, −28.8, t-24.9 mV, p<0.05, respectively. The effects of aspirin administration on potential difference parameters were significantly different between the three groups (irritability index: 35±25, 92±98, 114±74 mV 2 · min, p<0.05, respectively) when non-responders to aspirin were excluded. PGE2 mucosal generation was significantly increased in both the antrum (9.8, 19.5, 19.7 ng/mg proteins, p<0.05, respectively) and in the corpus (8.1, 14.0, 20.2 ng/mg proteins, p<0.05, respectively). PGE2 generation was not related to potential difference. Glucagon serum levels were related to the grade of gastropathy. A 1-week administration of 160 mg/d long-acting propranolol, 35 μg/d enprostil or placebo did not significantly modify basal potential difference. Conclusions: Portal hypertensive gastropathy is characterized by a decreased potential difference proportional to the endoscopic severity. The gastric mucosa of patients with cirrhosis seems to be more susceptible to aspirin than that of healthy subjects. It appears that the role of PGE2 is controversial in portal hypertensive gastropathy. Propranolol and enprostil do not improve this decreased potential difference.

Portal hypertensive gastropathy in patients with cirrhosis

Portal hypertensive gastropathy is a recently recognized important complication of cirrhosis. In the present study, the clinical features, portohepatic hemodynamics, and hepatic function were investigated in a series of 47 patients with cirrhosis. Mild gastropathy was found in 15 patients (32%) and severe gastropathy in 17 patients (36%). The presence of gastropathy seemed to be independent of age, sex, cause of cirrhosis, or grade of gastroesophageal varices. However, severe gastropathy was associated with an increase in portal venous pressure gradient (vs. control, P < 0.01; vs. mild gastropathy, P < 0.01), an increase in hepatic sinusoidal resistance (vs. control, P < 0.01; vs. mild gastropathy, NS), and a decrease in hepatic blood flow (vs. control, P < 0.01; vs. mild gastropathy, NS). In addition, patients with severe gastropathy had impaired metabolic activity of the liver, which was assessed by intrinsic clearance of indocyanine green (vs. control, P < 0.01; vs. mild gastropathy, NS). These observations may have important therapeutic implications in patients with cirrhosis and portal hypertensive gastropathy.

Congestive gastropathy in cirrhosis-how bad is red?

In a prospective study of the natural history of congestive gastropathy, 212 consecutive cirrhotic patients (75 treated with sclerotherapy) were included. Mean follow-up was 46 months. Mild gastropathy (mosaiclike pattern) was found in 110 patients and severe gastropathy (granular mucosa with cherry spots) was found in 20. Prevalence of Helicobacter pylori, formerly Campylobacter pylori, was 50% in patients without, 43% in those with mild, and 28% in those with severe gastropathy. Congestive gastropathy was significantly more frequent in patients treated with sclerotherapy (83% vs. 50%, P &lt; 10−5). Sixty-month actuarial proportions of patients free of anemia (in the absence of hematemesis or melena), were 17% with severe, 02% with mild, and 93% without gastropathy (P &lt; 10−8). Corresponding figures for overt bleeding were 25%, 73%, and 87% (P &lt; 10−8), whereas those for survival were 46%. 72%. and 85%(P = 0.0005). respectively. A multivariate regression analysis supported the following conclusions: (a) sclerotherapyand the presence of large esophageal varices significantly increase the risk of congestive gastropathy, which (b) is a significant risk indicator of both chronic and overt bleeding but does not independently affect survival.

Natural history of congestive gastropathy in cirrhosis

In a prospective study of the natural history of congestive gastropathy, 212 consecutive cirrhotic patients (75 treated with sclerotherapy) were included. Mean follow-up was 46 months. Mild gastropathy (mosaiclike pattern) was found in 110 patients and severe gastropathy (granular mucosa with cherry spots) was found in 20. Prevalence of Helicobacter pylori, formerly Campylobacter pylori, was 50% in patients without, 43% in those with mild, and 28% in those with severe gastropathy. Congestive gastropathy was significantly more frequent in patients treated with sclerotherapy (83% vs. 50%, P < 10−5). Sixtymonth actuarial proportions of patients free of anemia (in the absence of hematemesis or melena), were 17% with severe, 62% with mild, and 93% without gastropathy (P < 10−8). Corresponding figures for overt bleeding were 25%, 73%, and 87% (P < 10−7), whereas those for survival were 46%, 72%, and 85% (P = 0.0005), respectively. A multivariate regression analysis supported the following conclusions: (a) sclerotherapy and the presence of large esophageal varices significantly increase the risk of congestive gastropathy, which (b) is a significant risk indicator of both chronic and overt bleeding but does not independently affect survival.

Natural history of congestive gastropathy in cirrhosis

In a prospective study of the natural history of congestive gastropathy, 212 consecutive cirrhotic patients (75 treated with sclerotherapy) were included. Mean follow-up was 46 months. Mild gastropathy (mosaic-like pattern) was found in 11O patients and severe gastropathy (granular mucosa with cherry spots) in 20. Prevalence of Campylobacter Pylori was 50% in patients without, 43% in those with mild and 28% in those with severe gastropathy.