Relationship of serum gastrin and Helicobacter pylori in the gastric antral and body mucosa.

OBJECTIVE: To evaluate the relationship between serum gastrin and Helicobacter pylori status in the antrum and body of gastric mucosa. METHODS: Fasting and post-meal serum gastrin level were studied by radioimmunoassay in 41 patients with dyspepsia. These patients were divided into three groups depending on H pylori status ie H pylori present in both antrum and body; (A+B+; n = 13), present in antrum but not in the body; (A+B-; n = 7) and absent in both antrum and body A-B-; n = 21. RESULTS: There was no difference in fasting or post meal serum gastrin levels between the groups A+B+ and A+B-. Serum gastrin values 20 and 40 minutes post meal were significantly higher (p < 0.05) in the group A+B+ as compared to A+B-. CONCLUSION: Post meal serum gastrin levels are higher in patients with dyspepsia in whom Helicobacter pylori is present in the antral and body mucosa as compared to those in whom it is present in the antrum only.

Relationship of serum gastrin and Helicobacter pylori in the gastric antral and body mucosa.

OBJECTIVE: To evaluate the relationship between serum gastrin and Helicobacter pylori status in the antrum and body of gastric mucosa. METHODS: Fasting and post-meal serum gastrin levels were studied by radioimmunoassay in 41 patients with dyspepsia. These patients were divided into three groups depending on H pylori status ie H pylori present in both antrum and body; (A + B+; n = 13), present in antrum but not in the body; (A + B-; n = 7) and absent in both antrum and body; (A - B-; n = 21). RESULTS: There was no difference in fasting or post meal serum gastrin levels between the groups A + B+ and A - B-. Serum gastrin values 20 and 40 minutes post meal were significantly higher (p < 0.05) in the group A + B+ as compared to A + B-. CONCLUSION: Post meal serum gastrin levels are higher in patients with dyspepsia in whom Helicobacter pylori is present in the antral and body mucosa as compared to those in whom it is present in the antrum only.

Helicobacter pylori in dental plaque of children and their family members.

A prospective study was undertaken to determine the presence of Helicobacter pylori in the dental plaque of children and their family members. 22 children (age range: 2-12 years; males: 16) admitted to the paediatric ward for various disorders and 17 healthy family members (age range: 7-40 years; males: 9) of 13 of these children were screened for presence of Helicobacter pylori in the dental plaque by the rapid urease test. H. pylori was detected in dental plaque of 82% (18/22) children and 88% (15/17) of family members. In 85% (28/33) of the positive cases the rapid urease test was positive within 1 hour. Our observations indicate that Helicobacter pylori is present in the dental plaque of majority of children and their family members.

Age-related prevalence of Helicobacter pylori antibodies in Indian subjects.

OBJECTIVE: To determine the age-related prevalence of Helicobacter pylori antibodies in Indian subjects without upper gastrointestinal symptoms. MATERIAL AND METHODS: Sera of 340 subjects without any upper gastrointestinal complaints were screened for IgG and IgA Helicobacter pylori antibodies by the ELISA technique. RESULTS: The prevalence of IgG and IgA antibodies was 22%, 56% and 87% and 48%, 58% and 83% in 0-4, 5-9 and 10-19 year age groups respectively; thereafter it remained almost constant upto fifth decade. A significant fall in IgG and IgA prevalence was observed from fifth to seventh decades. CONCLUSION: Our data indicate that in India exposure to Helicobacter pylori occurs early in life and is widespread; about 83% of the population is exposed to Helicobacter pylori during the first two decades of life. The comparable prevalence rates of IgG antibodies to Helicobacter pylori and hepatitis A virus, in different age groups, in India and in the West, suggest a feco-oral mode of transmission for Helicobacter pylori.

Wilson's disease: varied hepatic presentations.

BACKGROUND: Wilson's disease is an inherited disorder of copper metabolism. Previous Indian studies have high-lighted the neurological manifestations of this disorder. Eleven patients with Wilson's disease with different hepatic manifestations are reported. METHODS: Patients referred to the gastroenterology department of a tertiary referral center were investigated for Wilson's disease, based on clinical suspicion, with slit-lamp examination for Kayser-Fleischer rings, serum ceruloplasmin and 24-hour urinary copper estimation. Liver biopsy was done whenever possible. RESULTS: Patients with Wilson's disease presented as acute viral hepatitis (n = 5), fulminant hepatic failure (n = 2), subacute hepatic failure (n = 2) and cryptogenic cirrhosis (n = 2). Therapy with penicillamine/trientene and zinc sulphate was started in 9 patients; 5 showed good response to therapy, one had to be switched to trientene due to penicillamine toxicity, two died, and one was lost to follow-up. CONCLUSION: Wilson's disease has varied hepatic presentations and should be suspected in all patients with unexplained liver disease. Any young adult presenting with acute hepatitis or fulminant hepatic failure who has evidence of underlying chronic liver disease or associated hemolytic anemia should be investigated for Wilson's disease. Therapy with penicillamine or trientene combined with zinc sulphate shows improvement in a majority of patients.

Electron microscopic observations in gastric mucosa of habitual tobacco chewers.

Clinical evaluation, upper gastrointestinal endoscopy and electron microscopy of mucosal biopsies from antrum, body and fundus of stomach were performed in three control subjects and 17 habitual tobacco chewers. Electron microscopic abnormalities such as discontinuous, fragmented basement membrane with reduction in hemidesmosomes, and widened intercellular spaces filled with clusters of desmosomes were found in the gastric mucosa of habitual tobacco chewers; these were similar to those reported in experimental carcinogenesis and leukoplakia. It is concluded that habitual chewing of tobacco produces electron microscopic alterations in the human gastric mucosa which may be important precursors for gastric malignancy.

Genetic hemochromatosis presenting as asymptomatic hepatomegaly.

A case of genetic hemochromatosis presented with asymptomatic hepatomegaly. The diagnosis was based on elevated serum iron, serum ferritin and transferrin saturation, a characteristic picture on magnetic resonance imaging, and liver biopsy showing cirrhosis with excessive iron deposits in the liver parenchyma. The extreme rarity of this disease in our country is perhaps determined by hereditary factors.

Helicobacter pylori and acid secretion.

BACKGROUND. Helicobacter pylori has been implicated in the aetiopathogenesis of peptic ulcer but data on the effect of infection by this organism on gastric acid secretion are equivocal. We, therefore, examined the effect of the presence of Helicobacter pylori in the antrum and body of the stomach on acid secretion. METHODS. We used the augmented histamine test and intragastric titration in three groups of patients. In one group Helicobacter pylori was present in both the antrum and body of the stomach, in the second it was present in the antrum but not the body, and in the third the organism was absent. RESULTS. There were no significant differences in acid secretion between these three groups. CONCLUSION. The presence of Helicobacter pylori in the mucosa of the gastric antrum and body has no effect on acid secretion.

Stomach in portal hypertension.

365 consecutive patient of portal hypertension [Cirrhosis 285, Non-cirrhotic portal fibrosis (NCPF) 50, Extrahepatic portal vein obstruction (EHPVO)-30] were evaluated prospectively over a period of 2 years. Of these, 33 patients underwent successful sclerotherapy with evaluation before and after the same. Portal hypertensive gastropathy (PHG) was found in 56.4% (mild 28.2%, Severe 28.2%) of total patients; while its incidence was 60.6% in cirrhosis, 54% in NCPF and 20% in EHPVO. Incidence of PHG was significantly higher in cirrhotics when compared with non-cirrhotics (60.7% vs 41.25%: p < 0.05). PHG is more common in patients with large esophageal varices as compared to those with small varices (64.1% vs 50.8%: p < 0.05). Overall incidence of gastric varices was 29.3% while its incidence in cirrhosis, NCPF and EHPVO was 22.1%, 44% and 73.3% respectively. Incidence of gastric varices was significantly higher in non-cirrhotics (NCPF + EHPVO) when compared with cirrhotic (p < 0.05) and in patients with large esophageal varices when compared with patients having small esophageal varices (p < 0.05). Peptic ulcer was found in 10.9% patients with portal hypertension. (More than 90% were cirrhotics, mainly alcoholics). 33 patients underwent successful sclerotherapy of which 11 had PHG (mild--6, severe--5) at the beginning of sclerotherapy. After successful sclerotherapy 26 patients had PHG (mild--14, severe--12) p < 0.001). There was no significant difference in incidence of gastric varices before and after sclerotherapy. Incidence of PHG was significantly higher in cirrhotics while gastric varices were seen more commonly in patients with non-cirrhotic portal hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Ultrastructural changes in esophageal mucosa of chronic tobacco chewers.

Seventeen chronic tobacco chewers and three control subjects underwent clinical evaluation, upper gastrointestinal endoscopy and esophageal mucosal biopsies. The esophageal biopsies were processed and examined under the electron microscope. A large number of ultrastructural abnormalities such as discontinuous, fragmented basement membrane, with reduction in hemidesmosomes, widened intercellular spaces were found in the esophageal mucosa of chronic tobacco chewers which resembled the ultrastructural features of experimental carcinogenesis and leukoplakia. It is concluded that chronic chewing of tobacco produces ultrastructural abnormalities in the esophageal mucosa which could be important precursors for esophageal malignancy.