During a study of gastric secretion four out of six previously healthy subjects developed hypochlorhydria after a transient illness with nausea, vomiting, and abdominal pain. Mean basal and peak acid outputs were 0 and 2.3 mmol (84 mg)/h one month after the onset of illness and 1.5 and 27.0 mmol/h (55 and 984 mg/h) at eight months' follow up. Two of the subjects were followed up at 18 months, when mean basal and peak acid outputs were 3.9 and 33.5 mmol/h (142 and 1221 mg/h). No endoscopic abnormality was seen at one and eight months, but biopsies showed active superficial gastritis, which resolved in one subject and became chronic in two. Schilling tests performed in three subjects at eight months showed diminished retention of vitamin B12. During hypochlorhydria a 24 hour intragastric analysis was performed for total and nitrate reducing bacteria, pH, and concentrations of nitrite and total and stable N-nitroso compounds. Of the 48 samples of gastric juice examined, 47 had bacterial growth of more than 10(6) organisms/ml and 46 had growth of nitrate reducing bacteria of more than 10(5) organisms/ml. Mean intragastric nitrite concentrations were 10 times higher than in a group of eight healthy controls. Both mean total and mean stable N-nitroso compound concentrations, however, were not appreciably different from those in controls. Although community transmission was a possibility, serological screening and electron microscopy of gastric biopsy specimens failed to show an infective cause. Transmission of an unidentified enteric pathogen via a contaminated pH electrode was therefore suspected. Thus gastric juice should not be returned to the stomach after contact with a contaminated glass electrode as this is a possible cause of atrophic gastritis. (+info)
On the natural history of hypergastrinemia.
(50/79)
We determined total gastrin and pepsinogen I in frozen serum samples from 175 overnight-fasted women 54 years old, and from 81 overnight-fasted women 60 years old, who took part in a population study in 1968-69. We also assayed samples from some of these women, who participated in clinical follow-up studies in 1974-75 and 1980-81: all of the women in the initial group whose serum gastrin concentration exceeded the 85th centile value and, as a reference group, a randomized subsample of women whose initial serum gastrin concentration was less than the 80th centile. Samples with total gastrin concentration greater than 400 ng/L were also assayed for gastrin-17 and gastrin-34. We found that: a pronounced increase of serum gastrin persisted throughout the study period for most of these postmenopausal women, indicating that conversion of type A gastritis (antrum-sparing) to pan-gastritis is uncommon; unexplained high concentrations of pepsinogen I in relation to the reference interval for young and middle-aged adults, as well as in relation to serum gastrin, were common; and the gastrin-17/gastrin-34 ratio is not correlated with the outcome of pronounced hypergastrinemia. (+info)
Microbial and metabolic profile of achlorhydric stomach: comparison of pernicious anaemia and hypogammaglobulinaemia.
(51/79)
The microbial flora and some of its metabolites and enzymes in the stomach were compared in patients with achlorhydria, pernicious anaemia, and primary hypogammaglobulinaemia and in patients with dyspepsia with normal gastric acidity. Detailed analysis of the flora of the gastric juice and of the mucosa from the antrum, body, and fundus in six patients with hypogammaglobulinaemia (mean pH 8.2), seven patients with pernicious anaemia (mean pH 7.3), and five patients with dyspepsia (mean pH 1.9) yielded 22 different genera of bacteria, mainly from the patients with achlorhydria, the most common being streptococci, micrococci, staphylococci, veillonella, and lactobacilli. A similar flora was found associated with the mucosa at all three sites. Various metabolites were also looked for. beta Glucoronidase and C14 lipase were found in patients with hypogammaglobulinaemia but not in those with pernicious anaemia or dyspepsia. Volatile fatty acids were not found. Relatively high concentrations of ethanol were found in the patients with hypogammaglobulinaemia compared with those with pernicious anaemia (p = 0.02). Similar concentrations of dimethylamine were found in all three groups, but the concentrations of trimethylamine were much higher in patients with pernicious anaemia and hypogammaglobulinaemia. The high concentrations of some microbial enzymes and ethanol differentiated the group with hypogammaglobulinaemia from the rest, and these may bear some relation to the high incidence of gastric cancer in patients with hypogammaglobulinaemia. (+info)
Gastric hypochlorhydria in ferret distemper.
(52/79)
In the present investigation 42 female ferrets were studied in regard to the influence of canine distemper in this species on gastric acid secretion. A total of fifteen naturally-infected and 27 non-infected ferrets were fasted and pylorus-ligated, and were either injected with corticosterone (10 or 50 mg/kg, s.c. one injection/day for 4 days) suspended in corn oil, injected with corn oil, on non-injected. Prior to autopsy blood samples were acquired for corticosterone analysis, and at autopsy the volume, pH, free and combined acidity of the gastric contents were evaluated. It was apparent that distemper induced hypochlorhydria in ferrets under the conditions of these experiments, an effect which was probably mediated through the central nervous system, but may also relate to a direct effect of distemper virus upon the gastric mucosa. Administration of corticosterone did not prevent hypochlorhydria in distemperous ferrets. Blood levels of corticosterone were elevated due to the stress effect of distemper infection, and also as a reflection of exogenous corticosterone administration. Prior immunization against canine distemper failed to immunize the ferrets in this study against the natural precipitation of this disease. (+info)
Surgical management of reflux gastritis.
(53/79)
Reflux gastritis is now recognized with increasing frequency as a complication following operations on the stomach which either remove, alter, or bypass the pyloric phincter mechanism. The entity may occasionally occur as a result of sphincter dysfunction in the patient who has not undergone prior gastric surgery. The diagnosis is made on the basis of symptoms (postprandial pain, bilious vomiting and weight loss), gastroscopic examination with biopsy and persistent hypochlorhydria. Remedial operation for correction of reflux is indicated in the presence of persistent symptoms when conservative measures fail. Only operative procedures which divert duodenal contents from the stomach or gastric remnant are effective. Both the isoperistaltic jejunal segment (Henley loop) and the Roux-en-Y diversion have been effective as remedial operations for reflux gastritis and merit greater awareness by gastroenterologists and surgeons. Our choice is the Roux-en-Y because of its technical simplicity and lower morbidity rate. (+info)
Gastric acid barrier to ingested microorganisms in man: studies in vivo and in vitro.
(54/79)
Reassessment of the ;gastric bactericidal barrier' to enteric bacteria in man included studies of the bactericidal activity of (1) the normal and achlorhydric stomach in vivo and (2) normal and achlorhydric gastric juice and other media in vitro. Within 30 minutes virtually all bacteria (Serratia marcescens) were eliminated in the normal stomach whereas no reduction occurred in the achlorhydric stomach in one hour. In vitro, identical bactericidal activity was observed at the same pH (from 2.0 to 7.0) in normal gastric juice, achlorhydric gastric juice, aqueous HCl, and nutrient broth. At pH less than 4.0, 99.9% of the bacteria were killed within 30 minutes. The presence of profuse bacterial flora, including coliforms, found in markedly acid-deficient but not in normal stomachs, correlates well with the absence of bactericidal activity. Thus, the ;gastric bactericidal barrier' is primarily pH-hydrochloric acid dependent, with other constituents of gastric juice contributing little, if any, detectable effect on the destruction of microorganisms. (+info)
Progressive increase in the functional G cell mass with age in atrophic gastritis.
(55/79)
Patients with atrophic gastritis but normal antral mucosa and achlorhydria were divided into three groups according to age-under 40, 40 to 70, and over 70 years. Serum gastrin, both basal and following a standard protein meal, was estimated in all patients by radioimmunoassay. There was a significant correlation between the magnitude of the gastrin response and age, the older the patient the greater the response. These results suggest that with increasing duration of gastritis and continued stimulation of a normal antrum in the absence of inhibition by acid, the functional G (gastrin) cell mass increases. However the possibility exists that each cell may secrete more gastrin in response to the same stimulus with age. This may be resolved by counting the number of G cells in the stomachs of subjects with atrophic gastritis and different ages. (+info)
Survey of haemorrhagic erosive gastritis.
(56/79)
Fluorescent-antibody studies in 22 patients out of a total of 40 cases of acute erosive gastritis showed no antibodies to gastric parietal cells. Hence erosive gastritis seems unlikely to be an autoimmune phenomenon.In this series 57.5% of cases belonged to blood group A. This suggests that there is a correlation between the instability of the gastric mucosa and blood group A.The operative mortality in erosive gastritis is high. Operation should be delayed as long as possible in the hope that the bleeding will stop spontaneously. Erosive gastritis may be idiopathic or precipitated by drugs, particularly aspirin. The highest risk was found to occur in those cases where bleeding was drug-induced. (+info)