Severe Gastropathy Research Articles

HELICOBACTER PYLORI OIPA VIRULENCE GENE AS A MOLECULAR MARKER OF SEVERE GASTROPATHIES.

Helicobacter pylori is an etiologic agent of gastroduodenal diseases. The microorganism, considered a type I carcinogen, affects about 50% of the global population. H. pylori virulence factors are determinant for the clinical outcome of the infection. The outer inflammatory protein A (oipA) gene encodes an outer membrane adhesin and is related to severe gastropathies, such as gastric cancer. The aim of this study was to evaluate the association of the oipA gene with the severity of gastroduodenal diseases in dyspeptic patients in region Central Brazil. The polymerase chain reaction (PCR) was used to determine the presence of H. pylori. Samples positives were used for molecular screening of the oipA gene. Gastropathies were categorized as non-severe and severe diseases. Approximately 68% of patients had H. pylori and 36% were infected with H. pylori oipA+ strains. Infection was significantly associated in patients aged over 44 years (P=0.004). However, there was no association between oipA and patients' age (P=0.89). Approximately 46% of patients infected with oipA+ strains had some severe illness. Gastric adenocarcinoma was the most frequent severe gastropathy. The H. pylori oipA genotype was inversely associated with the severity of gastroduodenal diseases (OR=0.247, 95%CI: 0.0804-0.7149 and P=0.007). The characterization of possible molecular markers will contribute to personalized medicine, impacting the prognosis of patients. • Evidence points to an association between the H. pylori oipA gene and gastropathies. • There is a high prevalence of H. pylori infection with a relevant percentage of oipA+ strains. • More severe gastropathies were observed in those infected with H. pylori oipA+ strains.

Frequency of virulence-associated genotypes of Helicobacter pylori and their correlation with clinical outcome and histological parameters in infected patients

Helicobacter pylori (H. pylori) is a gram-negative which can cause several gastroduodenal diseases, including gastritis and peptic ulcer disease (PUD). H. pylori specific genotypes have been related to increased occurrence of gastritis and PUD. The aim of this study was to investigate the clinical relevance of the major virulence factors of H. pylori with clinical outcomes and histological parameters in Iranian patients. Totally, 200 subjects with PUD and gastritis disease who underwent gastroduodenal endoscopy were enrolled in this study. The presence of the cagA, vacA, oipA, babA2, and iceA genes in antral gastric biopsy specimens were determined by polymerase chain reaction (PCR) and the results were compared with clinical outcomes and histological parameters. The frequency of babA2+, oipA+, vacA s1/m2, and vacA m2 genes was significantly higher in patients with peptic ulcer disease compared with patients with gastritis. In contrast, the frequency of vacA s1/m1 gene was significantly higher in gastritis subjects than PUD subjects. The high-density scores of H. pylori were strongly associated with iceA1¯, babA2+, and oipA+ genes. Additionally, the high polymorphonuclear cell infiltration and high mononuclear cell infiltration scores were strongly associated with the cagA+, iceA1¯, oipA+ genes and cagA+, babA2+, oipA+ genes, respectively. Our study indicated that the vacA, babA2, and oipA virulence factors are related to a higher risk of PUD in subjects with H. pylori-infection. Infection with these strains was associated with a more severe gastropathy.

Presence of cagPAI genes and characterization of vacA s, i and m regions in Helicobacter pylori isolated from Alaskans and their association with clinical pathologies.

Introduction. Gastric cancer is a health disparity in the Alaska Native people. The incidence of Helicobacter pylori infection, a risk factor for non-cardia gastric adenocarcinoma, is also high. Gastric cancer is partially associated with the virulence of the infecting strain.Aim. To genotype the vacA s, m and i and cag pathogenicity island (cagPAI) genes in H. pylori from Alaskans and investigate associations with gastropathy.Methodology. We enrolled patients with gastritis, peptic ulcer disease (PUD) and intestinal metaplasia (IM) in 1998-2005 and patients with gastric cancer in 2011-2013. Gastric biopsies were collected and cultured and PCR was performed to detect the presence of the right and left ends of the cagPAI, the cagA, cagE, cagT and virD4 genes and to genotype the vacA s, m and i regions.Results. We recruited 263 people; 22 (8 %) had no/mild gastritis, 121 (46 %) had moderate gastritis, 40 (15%) had severe gastritis, 38 (14 %) had PUD, 30 (11 %) had IM and 12 (5 %) had gastric cancer. H. pylori isolates from 150 (57%) people had an intact cagPAI; those were associated with a more severe gastropathy (P≤0.02 for all comparisons). H. pylori isolates from 77 % of people had either the vacA s1/i1/m1 (40 %; 94/234) or s2/i2/m2 (37 %; 86/234) genotype. vacA s1/i1/m1 was associated with a more severe gastropathy (P≤0.03 for all comparisons).Conclusions. In this population with high rates of gastric cancer, we found that just over half of the H. pylori contained an intact cagPAI and 40 % had the vacA s1/i1/m1 genotype. Infection with these strains was associated with a more severe gastropathy.

2672 Gastric Amyloidosis: A Rare Cause of Gastropathy and GI Bleeding

INTRODUCTION: Amyloidosis is a disorder of protein deposition that often presents with systemic symptoms. Symptoms of GI amyloidosis include abdominal pain, upper and lower GI bleeding, weight loss, diarrhea, malabsorption, esophageal reflux, and spontaneous bowel perforation. GI amyloidosis involves, from most to least common, the duodenum, stomach, colorectum, and the esophagus. In this case report, we will present a rare case of symptomatic AL amyloidosis localized to the stomach in which diagnosis and management was delayed by 3 months. CASE DESCRIPTION/METHODS: The patient was a 64-year-old African American woman who presented with a one-day history of fatigue and shortness of breath and a one-week history of dark stools. She had a past medical history significant for untreated plasma cell myeloma and chronic anemia. The patient had an EGD for intermittent dark stools 3 months prior to this admission which demonstrated severe gastropathy on endoscopic exam, but unfortunately no biopsies were taken at that point. The etiology of gastropathy remained unclear and nonspecific. During this hospitalization, with the patient’s ongoing history of melena, she underwent a repeat EGD which again showed severe localized gastropathy in the proximal stomach. A gastric biopsy was obtained from the area. On pathology review, the biopsy showed deposition of amorphous, eosinophilic material, suspicious for amyloid. Congo Red stain highlighted apple green birefringent material, consistent with amyloid. Patient remained hemodynamically stable during the hospital admission and was discharged before the pathology results were back. A week later, she was called to notify her of the results and to follow up with hematology oncology, but unfortunately patient had passed away at home, and the reason of death remained unclear. DISCUSSION: In a patient with GI bleed or other GI symptoms such as abdominal pain, nausea/vomiting, or change in bowel habits a probable etiology of amyloidosis should be on the differential, especially with history of plasma cell dyscrasia. Evaluation should include endoscopy with biopsy and specific amyloid staining if any obvious lesion is noted. Localized gastric amyloidosis presenting with GI bleeding is rare. This rarity may lead clinicians to dismiss it as a possibility which can delay diagnosis and proper management. This case report demonstrates such a situation in which a patient with plasma cell myeloma and symptoms of GI bleeding was delayed diagnosis and management by 3 months.

34. A study of prevalence of helicobacter pylori and its relation with severity of gastropathy in patients with portal hypertensive gastropathy owing to liver cirrhosis

Background and Aims: The role of Helicobacter pylori in pathogensis of PHG in cirrhotic patients is poorly defined. The Aim of this study is to evaluate the prevalence of Helicobacter pylori infection in patients with portal hypertension due to liver cirrhosis and its relation with severity of gastropathy. Methods: Forty adult patients with cirrhosis of liver were included in present observational study, carried out in the Department of Gastroenterology, Gandhi Hospital from November 2017 to May 2018. Data collected include detailed history, physical examination and relavent investigations. All patients were subjected to UGIE and rapid urea test for H. Pylori. The diagnosis and severity of PHG was evaluated on UGIE. Results: Out of 40 liver cirrhotic cases studied, 32 (80%) were males, 8 (20%) were females. Rapid urease test was positive in 28 (70%) patients. Presence of H. pylori observed in 22 (55%) cirrhotic patients with PHG compared to 6 (15%) cirrhotic patients with out PHG. The risk estimated showed a significant association between H. Pylori and PHG in cirrhotic patients (P = 0.0133). Out of 22patients with PHG & H. Pylori infection, 15 (37.5%) had severe PHG while 7 (17.5%) had mild PHG. In H. Pyloli negative group (2.5%) had mild, 4 (10%) had severe PHG. The difference was statistically significant (p = 0.018). Conclusions: Our results showed a significant association between H. Pylori Infection and PHG in cirrhotic patients which is also related to severity of PHG. Hence H. Pylori needs to be eradicated in patients with cirrhosis. The authors have none to declare.

Helicobacter pylori Infection in Patients with Portal Hypertensive Gastropathy Owing to Liver Cirrhosis: Prevalence and Relation with Severity of Gastropathy

ABSTRACT Background and Aim: Helicobacter pylori is a major human pathogen. Its role in the pathogenesis of portal hypertensive gastropathy (PHG) is debated. The aim of this study was to evaluate the prevalence of this infection in patients with portal hypertension due to liver cirrhosis and its relation with severity of gastropathy. Patients and Methods: Sixty consecutive patients with liver cirrhosis were enrolled in the study. All patients were subjected to an upper gastrointestinal endoscopy (UGIE), and rapid urease testing for H. pylori was performed. The diagnosis and severity of PHG was evaluated on UGIE. ChildαTurcotteαPugh (CTP) and model for endαstage liver disease (MELD) scores were calculated to assess the severity of liver cirrhosis. Results: H. pylori infection was reported in 33 patients with overall prevalence 55%. The presence of H. pylori was observed in 26 (67%) cirrhotic patients with PHG compared to 7 (33%) cirrhotic patients without PHG. The risk estimate showed a significant association between H. pylori and PHG in cirrhotic patients (P = 0.0133, odds ratio [OR]: 4.00, 95% confidence interval [CI]: 1.298–12.325). Out of the 26 patients with PHG and H. pylori infection, 17 had severe PHG (65.3%) and 9 had mild PHG (34.6%) whereas 4 patients had severe PHG (30.8%) and 9 had mild PHG (69.2%%) in the group of H. pyloriαnegative patients. The difference was statistically significant (P = 0.04, OR: 4.25, 95% CI: 1.0188–17.729). Of the 39 patients with PHG, 21 (53.85%) had severe PHG and 18 (46.15%) had mild PHG. No significant relation was found between H. pylori infection and severity of liver cirrhosis as regards CTP score (P = 0.76) and MELD score (P = 0.56). Conclusion: Our results showed a significant association between H. pylori infection and the occurrence and also the severity of gastropathy in patients with liver cirrhosis. Yet, the severity of liver cirrhosis itself did not correlate with H. pylori or the severity of gastropathy.

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.

Blood ammonia level in chronic liver disease: clinical and pathogenetic importance

Aim. To evaluate blood ammonia concentration in patients with chronic liver diseases. Methods. 87 patients with chronic liver disease were examined. Ammonia concentration was determined using the enzymatic test. Results. Ammonia concentrations ranged from 18.16 to 118.36 μmol/l (median 43.7 μmol/l). Depending on blood ammonia level, 2 groups of patients were identified: with blood ammonia level below (first group) and above the median level (second group). The first group included 35 (79.5%) patients with liver cirrhosis and 9 (20.5%) patients with chronic hepatitis, the numbers were similar in the second group: 36 (83.7%) and 7 (26.3%) patients correspondingly. Signs of portal gastropathy were identified in 25 (58.1%) and 26 (60.5%) patients correspondingly, while Helicobacter pylori infection was found in 5 (21.7%) and 8 (31.8%) patients with blood ammonia level below and above the median level correspondingly. Mean ammonia concentration in patients with liver cirrhosis and chronic hepatitis, with and without portal gastropathy, with mild and severe gastropathy did not differ significantly. Conclusion. Ammonia blood concentration can not reliably indicate liver failure, hepatic encephalopathy development and stage, portal hypertension and collateral development as well as predict gastric lesions.

Reactive Increase in Gastric Mucus Secretion Is an Adaptive Defense Mechanism Against Low-Dose Aspirin-Induced Gastropathy

Gastric mucus is considered to play an essential role in gastric mucosal defense mechanisms, especially when irritants are present in the stomach. To investigate the relationship between low-dose aspirin-induced gastropathy and gastric secretory function, especially gastric mucus secretion, in healthy volunteers. Thirty male, asymptomatic, Helicobacter pylori pylori-negative healthy volunteers were asked to take 100 mg of enteric-coated aspirin (Bayaspirin) once a day for 10 days. Endoscopic examination was performed before and 3 and 10 days after drug administration. The extent of endoscopically assessed gastric mucosal injury was semi-quantitatively evaluated according to the modified Lanza score. The pentagastrin-stimulated gastric juice was collected for 10 min during the endoscopic examination and subjected to analysis for gastric acid (mEq/10 min) or mucus (mg hexose/10 min) output. Overall, the 10-day aspirin treatment significantly increased gastric mucus secretion from 0.8 (interquartile range 1.7) to 1.6 (1.6) mg hexose/10 min (P < 0.05), with a concomitant and significant decrease in the gastric acid/mucus ratio from 4.3 (5.2) to 2.9 (4.7) (P < 0.01). Subsequent analysis of two subgroups of volunteers categorized according to their endoscopic status ("severe gastropathy" vs. "modest gastropathy") revealed that changes in gastric secretory parameters occurred exclusively in those subjects without severe gastric injury; there was no alteration in these parameters in subjects with severe gastric injury. The results of this study suggest that the reactive increase in gastric mucus secretion is an adaptive defense mechanism against low-dose aspirin-induced gastropathy. In some individuals, such a response may be insufficient to prevent the development of severe mucosal injury and even ulcers and their complications.

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.

Association of gastric acid and mucus secretion level with low-dose aspirin-induced gastropathy

Low-dose aspirin is known to cause upper gastrointestinal complications. The mechanism by which the aspirin disrupts gastric mucosal integrity remains to be clarified. In this study we investigated the temporal association of gastric secretory parameters (acid and mucus) with aspirin-induced gastropathy. In 42 long-term low-dose aspirin-takers and the same number of sex- and age-matched controls, pentagastrin-stimulated gastric juice was collected for 10 min during endoscopic examination. The collected gastric juice was divided and half was submitted to analysis for gastric acid (mEq/10 min) and the other half was analyzed for mucin (mg hexose/10 min) output. The grade of gastric mucosal injury was assessed endoscopically according to the modified Lanza score, and a score of more than 4 was defined as the presence of severe gastropathy. While gastric acid secretion did not differ significantly between aspirin-takers and controls, gastric mucus secretion, in terms of mucin output, was significantly increased in aspirin-takers compared to controls (4.1 (SD 4.8) vs. 2.3 (1.4) mg hexose/10 min, P < 0.05). Consequently, the acid/mucin ratio was significantly decreased in aspirin-takers compared to controls (1.2 (1.0) vs. 1.7 (1.4), P < 0.05). In the subanalysis of 25 aspirin-takers without severe gastropathy, gastric mucus secretion was increased and the acid/mucus ratio was decreased compared with controls, but there was no such association in the remaining 17 aspirin-takers with severe gastropathy. Overall, gastric mucus secretion is increased in aspirin-takers, suggesting a functional adaptive response to long-term administration of the drug. However, it is possible that the adaptive response is impaired in some aspirin takers, who might be susceptible to severe upper gastrointestinal complication.

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.

Mucin Expression in Reactive Gastropathy: An Immunohistochemical Analysis

Reactive gastropathy is the second most common diagnosis made on gastric biopsies. Increased epithelial proliferation and modifications of epithelial cytokeratin profile, distinct from those of Helicobacter pylori gastritis, have been previously reported. However, the evaluation of mucins, important components of the protective mucosal mucous layer, has not been reported. To investigate alterations of membrane and secreted mucins in reactive gastropathy of various etiologies using antibodies against mucin glycoproteins. Thirty-eight gastric biopsies diagnosed as reactive gastropathy, related to nonsteroidal anti-inflammatory drugs (n = 18) or bile reflux (n = 6) or of indeterminate etiology (n = 14), were evaluated using antibodies to MUC1, MUC5AC, MUC6, and MUC2. All cases were confirmed to be negative for H. pylori. The biopsies were classified in 3 groups based on the severity of cytoarchitectural changes (mild, moderate, and severe). Mucin expression and its distribution were recorded and the results correlated with the cytoarchitectural alterations and etiologies. Loss of MUC1, either patchy or complete, was noted in 67% of the cases. Aberrant expression of MUC5AC in pyloric glands was observed in 81% of the cases, and aberrant expression of MUC6 in the upper foveolar epithelium was diffusely seen in 14% of the cases. Aberrant expression of MUC2 in non-goblet cells was observed in a single case. Aberrant expression of MUC6 was less extensive in the nonsteroidal anti-inflammatory drugs group than in other 2 groups (P = .03). Concurrently, the diffuse distribution of aberrant MUC6 expression was seen only in the cases of severe gastropathy (P = .09). There was no correlation between modifications in expression of other mucins and either the etiologies or the severity of cytoarchitectural changes. Expressions of membrane (MUC1) and secreted (MUC5AC, MUC6) mucins are frequently modified in reactive gastropathy. The alteration of MUC1, which is involved in cell adhesion and polarity, may play a role in the development of the serrated profile of reactive gastropathy. Milder modifications of the secreted mucins may be explained by the reactive/regenerative nature of the process. Importantly, theses changes are different from the increase in MUC6 and reduction of MUC5AC expression reported in H. pylori gastritis, underlying their mechanistic differences. It is worth noting that similar alterations of mucin expression are shared by various etiologies, that is, nonsteroidal anti-inflammatory drugs and bile reflux, consistent with the nonspecific nature of reactive gastropathy.

Prevalence of portal hypertensive duodenopathy in cirrhosis: clinical and haemodynamic features

To estimate the prevalence of portal hypertensive duodenopathy (PHD) in patients with cirrhosis and portal hypertension, and to evaluate its relationship with clinical and haemodynamic parameters. Endoscopy reports and clinical history of 549 consecutive patients with cirrhosis and portal hypertension were evaluated retrospectively. A diagnosis of PHD was obtained in those patients with a congestive vascular pattern of the duodenum. PHD was found in 46 patients (8.4%). Previous endoscopic band ligation and coexistence of severe gastropathy were significantly more frequent in PHD group. Systemic and hepatic haemodynamic evaluations were performed in 20 patients with PHD and 160 without PHD: the mean hepatic venous pressure gradient was higher in those cases with PHD (22.5 (5.4) vs. 19.8 (5.5) mmHg, P=0.045). Hypertensive colopathy was found in seven out of the 10 patients with PHD and a colonoscopic evaluation. In five of six patients PHD disappeared after liver transplant. PHD is an uncommon finding of portal hypertension in cirrhotic patients. It is associated with previous endoscopic band ligation, to manifestations of portal hypertension in other sites of the gastrointestinal tract and to greater values of hepatic venous pressure gradient. The clinical relevance of this syndrome remains to be determined.

An endoscopic study of upper-GI mucosal changes in patients with congestive heart failure

Congestive heart failure results in an increase in systemic venous pressure that is transmitted to the inferior vena cava and to the hepatic veins. This can cause GI vascular and mucosal congestion. The aim of this study was to define upper-GI mucosal changes in patients with congestive heart failure. A total of 57 patients with congestive heart failure presenting with GI symptoms underwent upper endoscopy. Echocardiography was performed in all patients to determine the ejection fraction and the degree of tricuspid regurgitation. Transabdominal US was performed to measure the diameters of the hepatic veins, the inferior vena cava, and the portal vein. The presence and the severity of gastropathy and duodenopathy were compared with the parameters relating to severity of cardiac failure. Of the 57 patients studied, gastric mucosal changes were observed in 50 (88%), duodenal mucosal changes in 31 (54%), and esophageal mucosal changes in none. Gastric mucosal changes were the following: mosaic-like pattern (n = 50), punctate spots (n = 34), thickened folds (n = 5), watermelon stomach (n = 3), and telangiectasia (n = 10). Duodenal mucosal changes were the following: mosaic-like pattern (n = 29), thickened folds (n = 8), and telangiectasia (n = 2). Upper-GI symptoms were associated with gastropathy ( p = 0.027) and duodenopathy ( p = 0.003). The presence and the severity of duodenopathy showed a high degree of positive correlation with the presence and the severity of gastropathy (gamma value 0.690; p value <0.001). Patients with gastropathy and duodenopathy had higher mean inferior vena cava and hepatic vein diameters than those without gastropathy and duodenopathy. The severity of duodenopathy but not that of gastropathy was significantly associated with increasing severity of tricuspid regurgitation ( p = 0.001), larger portal vein diameter ( p = 0.02), and lower ejection fraction ( p = 0.008). Among patients with congestive cardiac failure with GI symptoms, changes of congestive gastropathy are evident in 88% and duodenopathy in 54%. The presence and the severity of duodenopathy was significantly associated with increasing severity of features of congestive heart failure.

American Diabetes Association annual meeting, June 2003: gastrointestinal and dietary aspects of diabetes.

At the 63rd annual scientific session of the American Diabetes Association (ADA), held in New Orleans, Louisiana, June 2003, a number of fascinating topics were discussed. This is the first of approximately six articles reviewing presentations at this meeting. Mark Burge, Albuquerque, New Mexico, introduced the topic of diabetic gastroparesis. The role of the stomach is to mix, pulverize, and deliver food to the duodenum. Gastric motor activity is controlled by many factors, including extrinsic parasympathetic and sympathetic and intrinsic enteric nerves and hormones such as gastrin, motilin, glucagon-like peptide-1, neuropeptide-Y, and nitric oxide. The glucagon-like peptide-1 agonist NN-211 delays gastric emptying in people with diabetes and may be beneficial for the overly rapid gastric emptying, which appears to worsen postprandial glycemia, of many individuals with type 1 diabetes. Gastric peristalsis is controlled by electrical impulses originating from gastric pacemaker cells, depolarizing three times per minute, with the fundus exhibiting receptive relaxation, while the antrum has regular contractions leading to vigorous mixing and grinding. Gastroparesis is potentiated by a number of factors, including gastric dysrhythmia, discoordination of antral contractions, failure of the fundus to relax, and hypomotility or inappropriate dilation of the antrum. Nausea, particularly following meals, vomiting, abdominal pain, bloating with malodorous eructation, early satiety, and anorexia are usual symptoms, although not typically with weight loss, which may indicate an eating disorder or additional gastrointestinal illness. There is poor relationship between the severity of gastropathy and the symptoms exhibited by a given person. For many patients, erratic glycemia, Burge noted, are “the only clue.” This is complicated, however, as hyperglycemia delays gastric emptying of solids and liquids in individuals without diabetes; therefore, those with poorly controlled diabetes may only appear to have gastroparesis, showing the importance of achieving glycemic control. As symptoms alone are insufficient, it is important to …

Gastroduodenal ulcer and erosions are related to portal hypertensive gastropathy and recent alcohol intake in cirrhotic patients.

Gastroduodenal ulcers and gastroduodenal erosions are particularly frequent in cirrhotic patients, but their precise cause is unclear. The aim of this study was to identify pathogenic factors associated with ulcers and erosions in patients with cirrhosis. We studied 64 consecutive patients with cirrhosis referred for gastroscopy. The severity of portal hypertensive gastropathy was graded with an endoscopic score. H. pylori status was determined by histological examination of gastric biopsy samples or by the [13C] urea breath test. The daily alcohol intake within the preceding week was recorded. The Child-Pugh score was determined. Fifteen patients had gastroduodenal ulcer and 20 had gastroduodenal erosions. Cirrhosis was related to alcohol in 44 patients and hepatitis B or C virus in 14 patients. The portal hypertensive gastropathy was graded as severe in 12 patients and mild in 25 patients. H. pylori infection, found in 37 patients, was not related to the gastroduodenal lesions. Univariate and multivariate analysis showed the links between gastroduodenal erosions and hypertensive gastropathy and recent heavy drinking. Gastroduodenal ulcer was independently associated only with the severity of the gastropathy. In conclusion, in these patients with cirrhosis, the presence of gastroduodenal ulcer was significantly related to hypertensive gastropathy but not to H. pylori infection. Recent alcohol intake favored the occurrence of gastroduodenal erosions.

Gastritis and gastropathy of childhood.

Gastritis and gastropathy of childhood.

TIPS Allowing for an Endoscopic Mucosal Resection of Early Gastric Cancer in a Cirrhotic Patient with Severe Hypertensive Gastropathy: Report of a Case

TIPS Allowing for an Endoscopic Mucosal Resection of Early Gastric Cancer in a Cirrhotic Patient with Severe Hypertensive Gastropathy: Report of a Case

Findings of Portal Hypertensive Gastroenteropathy Using Infrared Electronic Endoscopy

Abstract: The aim of this study was to ascertain how and in what form portal hypertensivive gastroenteropathy affects the submucosal vasculature using an infrared electronic endoscope (IREE), which is capable of visualizing the submucosal vasculature. Subjects were 46 patients with liver cirrhosis (19 in Child‐Pugh class A, 21 in B, and 6 in class C). In 37 of 46 patients, the submucosal vasculature of the stomach was visualized using IREE and morphologic features were studied in relation to the severity of portal hypertensive gastropathy (PHG; none, mild and severe). In the remaining 9 patients, the submucosal vasculature of the rectum and sigmoid colon was observed with IREE. IREE images of blood vessels of the gastric submucosa demonstrated withered branch‐like vessels (35.1%), multiple dotted or spotted stains at terminations of branches (32.4%), vascular ectasia‐like circular stains (11%) and dilated tortuous venules of relatively large caliber around the cardia and in the upper region of the stomach (18.8%). This feature around the cardia was observed more frequently in patients with complications of gastric varices (55.6%). In relation to the severity of PHG, the incidence of withered branch‐like vessels was significantly higher in the severe gastropathy group than in the non‐gastropathy group. Dotted or spotted stains were most frequently observed in the severe gastropathy group. Visual examination of the colorectal mucosa with IREE noted withered branch‐like vessels in 7 of 9 cases. In 3 of 9 patients, dilated venules were seen running in the anorectal submucosa and joining the rectal varices. In conclusion, morphological changes due to congestion were found in portal hypertensive gastroenteropathy using IREE in submucosal venules of relatively large caliber and even in the venous plexus in the vicinity of the muscularis mucosa. (Dig Endosc 1999; 11: 144–149)