Gastric acid secretion and enteric infection in Bangladesh

We present three lung transplant recipients who had sigmoid colonic diverticular perforation within 4 weeks of transplantation, giving an overall incidence of 8.6% (3 of 35) in our population. Our cases are unusual because they all occurred in the early posttransplantation period and because the incidence of perforation is substantially higher than that reported in other transplant populations. The reason for the apparent increased incidence of perforation in our lung transplant recipients is unclear, but it is likely related to the short follow-up period, intense posttransplantation immunosuppression, perioperative hypoperfusion, and increased intraluminal pressure from the use of narcotics and bowel stimulants. We discuss these potential causes and comment on preventive measures being undertaken at our program.     

Stimulated gastrinemia, parietal cell mass and stimulated acid secretion in autonomous chronic gastritis: Helicobacter pylori influence

BACKGROUND/AIMS: In the present experience, an evaluation has been carried out of stimulated gastrinemia, parietal cell mass, and acid secretion in the course of a paradigmatic condition, such as autonomous chronic gastritis, in order to reveal possible changes induced by the presence of Helicobacter Pylori (HP). MATERIALS AND METHODS: We evaluated 153 patients with chronic gastritis of the antrum and/or body fundus, in different combinations not associated with peptic pathology. RESULTS: In the group of subjects with antral superficial chronic gastritis associated with normal body-fundic mucosa or with body-fundic superficial chronic gastritis, about 40% of the subjects in the HP positive group show gastrinemia values which are higher than the norm. The evaluation of parietal cell and stimulated acid secretion yielded no differences between the HP positive and HP negative groups: it emerges that these parameters vary exclusively according to the histologic state of the body-fundic mucosa. In the patients group with hypergastrinemia, the study has revealed no variations in parietal cell mass and acid secretion. CONCLUSION: Evidently the increase in gastrinemia in these subjects was not important enough to induce an increase in parietal cell mass and acid secretion. It emerges how the presence of HP does not imply substantial changes on the gastric cyto-functional parameters: these variations depend mainly on the histologic state of the gastric mucosa.     

The relationship between atrophic gastritis and gastric ulcer

The physiological and biochemical effects of a carefully graduated course of vigorous gymnasium training with two or three weekly exercise sessions lasting only 15 minutes have been studied in middle-aged London business men. Activity diaries and psychological questionnaires indicated that these men had a positive attitude to exercise which was probably greater than average. The gymnasium exercises caused a large oxygen debt and considerable rises in plasma catecholamines and lactate levels. A close correlation was found between the pulse rate during exercise and the Borg scale of perceived exertion, so that both could be used to ensure that short periods of exercise were sufficiently vigorous to produce a training effect, and protect against over-exertion. The acceptability of this particular exercise regime was shown by the low fall-out and injury rate. It is suggested that this exercise training programme possesses many features which are advantageous if increased physical activity is to be more widely used as a method of reducing some of the risk factors in coronary heart disease.     

Serum gastrin and atrophic gastritis in achlorhydric patients with and without pernicious anemia

Forty-two patients with pernicious anemia (PA) and 35 patients with achlorhydria but without PA were investigated by means of serum gastrin determination and estimation of circulating parietal cell and thyroidal autoantibodies. In 38 of the 77 patients, gastroscopic and histopathological examinations of the antral and corpus mucosa were performed. The patient groups were similar with regard to distribution of high and normal serum gastrin levels, the frequencey of autoantibodies and antrum-sparing atrophic gastritis. In the present selection of patients, therefore, the achlorhydria group was supposed to represent a precursor state of the group with PA. A minor proportion of patients with severe atrophic gastritis of the antrum as well as of the corpus mucosa was found in the two groups.     

Significant improvement of atrophy after eradication therapy in atrophic body gastritis

Chronic atrophic body gastritis may be induced by H. pylori. Results on the effect of H. pylori eradication therapy have been conflicting. Here, we report on the effect of eradication therapy on both body atrophy and inflammation in 7 patients. They presented with severe or moderate atrophy of the oxyntic mucosa and positive H. pylori histology (Warthin-Starry) and/or serology. Eradication was performed with a standard double or triple therapy regimen. At least 6 weeks after successful eradication therapy, patients underwent rebiopsy and histopathological evaluation of the gastric body. In all 7 patients, the grade of body gastritis improved significantly. Among the patients with severe atrophy before H. pylori eradication, 2 had normal mucosa, 3 low-grade atrophy, and one moderate atrophy after treatment. The one case with moderate atrophy before treatment had normal mucosa after H. pylori eradication. In addition, inflammatory infiltration of the mucosa cleared up in 6 cases and improved from severe to mild in one case after treatment. From these results, we conclude that in patients with histologically demonstrated H. pylori and/or positive H. pylori serology atrophic body mucosa can recover after successful eradication therapy.     

Gastric secretion as a function of acute and chronic stress in the gastric fistula rat.

Conducted 2 experiments using a total of 54 male Long-Evans rats chronically implanted with gastric cannulas. In Exp I Ss exposed to signaled and unsignaled grid shock secreted more gastric acid after shock stress (chronic stress) for 8 days compared to the 1st 12 hrs of shock stress (acute stress). However, Exp II indicated that the higher gastric acid values under chronic stress were not significantly greater than prestress baseline values. Results are interpreted to reflect an inhibition of gastric acid secretion as a function of acute stress. During chronic stress this inhibition was followed by an habituation of gastric secretory processes which was observed as a return of secretion volume to baseline levels. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of pentagastrin and heptagastrin on acid secretion in man (author's transl)

Gastrin analogues are known to stimulate acid secretion with higher potency the more amino acids prolong the peptid chain towards the N-terminal end. In order to compare the response of pentagastrin (Gastrodiagnost, Merck, Darmstadt) and Heptagastrin (HOE 293, Hoechst AG, Frankfurt/M.) in 12 healthy subjects the two peptides were given subcutaneously in doses of 1 microgram/kg, 3 microgram/kg and 6 microgram/kg body weight. Additionally in 8 subjects 1 microgram/kg/h and 2 microgram/kg/h of the gastrins were given intravenously. Gastric content was aspirated under basal and stimulated conditions in portions of 15 minutes, volume (ml) and acid concentration (meq/l) of each fraction was measured and acid secretion (meq/90'), BAO and PAO were calculated. As compared with pentagastrin the dose response curve was shifted to the left, when heptagastrin was given subcutaneously. The amount of acid secretion over a time period of 90 min. was about 17% higher after heptagastrin than after pentagastrin. There was no difference between the peak acid outputs (PAO). Stimulation of acid secretion was prolonged after heptagastrin as compared to pentagastrin. Both gastrins acted similarly on all parameters measured when administered intravenously. Side effects as nausea and dizziness were observed in two subjects of each group.     

Positive result by serology indicates active Helicobacter pylori infection in patients with atrophic gastritis

Patients with atrophic corpus gastritis and elevated Helicobacter pylori antibody titers but 13C-urea breath test (13C-UBT) and histology results negative for H. pylori were randomized into eradication therapy or follow-up only. Antibody levels decreased significantly in six out of seven patients in the eradication group, while in the follow-up group, the titers declined in only one out of eight patients. In patients with atrophic corpus gastritis, positive serology results may indicate an ongoing infection in spite of negative 13C-UBT and histology results.     

Gastric ulcer: effect of healing on gastric acid secretion and fasting serum gastrin levels

In 15 patients with uncomplicated gastric ulcers, basal and peak gastric acid outputs and fasting serum gastrin levels were studied before and after healing. The mean basal acid output [4.0 +/- 1.3 (SEM) mEq H+/hr], the mean peak acid output (29.5 +/- 5.1 mEq H+/hr), and the mean fasting serum gastrin level (80.3 +/- 16.7 pg/ml) in these patients did not change significantly with healing. Failure of gastric secretory function to change with healing suggests that mucosal resistance factors are more important than gastric acid secretion in the pathogenesis of a gastric ulcer.     

Effects of anaesthetics and trauma on stimulated gastric acid secretion in chronic fistula dogs

1. The present study was undertaken to determine whether various anaesthetic agents affect canine gastric acid secretion independently of other experimental variables. 2. Acid secretory output was determined in dogs with chronic fistulae, by administering sedating doses of anaesthetics commonly used for studying gastric secretory mechanisms in laboratory animals. 3. The anaesthetic agents inhibited gastric acid secretion. As the inhibitory effect of the mixture of anaesthetics was pronounced, an attempt was made to study the effect of each individual anaesthetic agent separately. 4. Acetopromazine was given to sedate dogs. Although it has a long duration of action, it only had a transient inhibitory action on gastric acid secretion of 15-30 min duration. Moreover the drug reduced pentagastrin-stimulated secretion, but had no effect on histamine-stimulated secretion. 5. Thiopentone sodium given with acetopromazine produced a mild inhibitory effect on histamine-stimulated secretion for 45 min, but produced a more pronounced and sustained inhibitory effect on pentagastrin-stimulated secretion. 6. Trilene significantly inhibited both histamine- and pentagastrin-stimulated secretion. The effect on the latter was more pronounced and sustained. 7. Trauma had no significant effect on histamine-stimulated secretion, but showed a slight inhibitory effect on pentagastrin-stimulated secretion. 8. Experiments to study gastric secretory mechanisms and antisecretory drugs should take account of the potential inhibitory effects of anaesthetics. Where possible, studies in conscious dogs with gastric fistulae are preferable to experiments on anaesthetized animals.     

Gastric secretion and activity-stress lesions in the rat.

In Exp I with 40 male Sprague-Dawley rats, gastric samples were obtained by means of a pylorus ligation procedure on either the first or last day of an activity-stress procedure. Experimental Ss had more stomach lesions and showed a drop in gastric acid on the last day collection. In Exp II, 32 similar rats were surgically prepared with gastric cannulas and pyloric cuffs, and first and last day collections were obtained from the same animal. Experimental activity Ss revealed more stomach lesions and a corresponding drop in gastric acid of the last collection than did controls, which suggests that acid was not a significant etiological variable. The destruction of acid-bearing parietal cells or the back diffusion of hydrogen ions could also explain the low acid values in Ss with stomach lesions. (18 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Treatment of gastritis in cheetahs (Acinonyx jubatus)

Three cheetahs (Acinonyx jubatus) had a clinical history of chronic spiral bacteria-associated gastritis and three cheetahs had no clinical history of gastritis. Gastric biopsies were obtained from all six cheetahs prior to treatment for gastritis and 3 wk and 1 yr posttreatment. The cheetahs were treated with tetracycline hydrochloride 500 mg p.o. q.i.d., metronidazole 250 mg p.o. q.i.d., and bismuth subsalicylate 300 mg p.o. q.i.d. Each drug was administered concurrently for 7 days. Following this treatment, each cheetah was maintained on 300 mg bismuth subsalicylate p.o. s.i.d. for 1 yr. The three cheetahs with a history of gastritis were culture positive for Helicobacter acinonyx and remained positive during the entire study. The three cheetahs with no clinical history of gastritis were culture negative for H. acinonyx, but gastric biopsies revealed Gastrospirillum-like bacteria (tentatively named Helicobacter heilmannii) pretreatment. Gastric biopsies were negative for H. heilmannii on subsequent examinations. Although the treatment did not eradicate H. acinonyx, it did provide symptomatic relief from the vomiting, anorexia, and weight loss associated with clinical gastritis. The use of endoscopically guided gastric mucosal biopsies for urease testing and histopathologic examination of Warthin-Starry-stained sections is a sensitive and specific method of diagnosing spiral bacteria-associated gastritis. Treatment of spiral bacteria-associated gastritis in cheetahs should include the rational use of antibiotics (tetracycline or amoxicillin and metronidazole), bismuth compounds, and omeprazole and evaluation of husbandry methods to reduce stress.     

Gastric mucosal hepatocyte growth factor in Helicobacter pylori gastritis and peptic ulcer disease

OBJECTIVES: Hepatocyte growth factor (HGF) is increasingly recognized for its role in a variety of hepatic and systemic diseases. Its relationship to gastritis has not been studied. We aimed at measuring gastric mucosal HGF levels in the presence or absence of Helicobacter pylori gastritis, in peptic ulcers, and in response to H. pylori eradication. METHODS: Fifty one patients were studied. Patients were not entered if they had liver disease, malignancy, or any systemic illness. HGF was measured in gastric antral incubates using an enzyme-linked immunosorbent assay. Assessments were repeated 6 wk after a 2-wk course of anti-H. pylori triple therapy in 12 patients. Code numbers were used for blinding. RESULTS: The median gastric mucosal HGF level was 36 ng/gm/tissue in patients with H. pylori gastritis (n = 33) compared with 19 ng/gm in 18 negative controls (p = 0.0024), 18 ng/gm after the eradication of H. pylori (p = 0.021), 23 ng/gm in all patients with ulcers (n = 10), and 26 ng/gm/tissue in H. pylori-positive ulcers (n = 7). CONCLUSIONS: Gastric mucosal HGF levels were elevated in H. pylori gastritis and reduced by its eradication. These results are relevant to our understanding of the increased gastric cell proliferation in patients with H. pylori-related gastritis.     

Influence of Helicobacter pylori on gastric secretion. Study on variously associated gastric body, fundus and antrum chronic gastritis

Among the various themes related to Helicobacter pylori (HP) which is still a subject of discussion, there is the possible influence of this bacterium on gastric secretory physiology. In the present study, an evaluation has been carried out of stimulated gastrinemia, stimulated acid secretion and total peptic activity in gastric juice in the course of a paradigmatic condition, as autonomous chronic gastritis, in order to reveal possible modifications induced by the HP infection. In cases of HP positive chronic superficial antral gastritis associated either with normal body-fundic mucosa or with superficial gastritis, there is a significant increase of stimulated gastrinemia in comparison to HP negative groups and controls. In the course of body-fundic atrophic and preatrophic chronic gastritis associated either with antral superficial chronic gastritis or with antral atrophic gastritis, there are no statistically significant differences between HP positive and HP negative subjects. As regards acid and pepsin secretion no significant differences emerge in any group between HP positive and HP negative subjects. In the HP positive subjects with antral superficial gastritis and higher gastrin values the study of acid and pepsin secretion has yielded no significant variations. From the results of this study it emerges how gastric secretory parameters vary exclusively according to the histologic state of gastric mucosa. Therefore, the lesion action of HP may mainly be attributed to a direct action, rather than to substantial gastric secretory changes.     

Confabulation in atrophic and vascular disease of old age (clinico-psychopathologic findings)

The paper is concerned with a study of confabulation seen in 95 patients. A gradual development of the confabulatory syndrome (from mnemonic confabulations to ecmnestic) was seen in senile dementia (5 cases) and in its combination with vascular atherosclerosis (61 cases). An acute development of confabulations (with a prevalence of mnemonic false reminiscence over ecmnestic) was seen in cerebral atherosclerosis (9 cases). Rudimentary ecmnestic confabulations, without mnemonic were seen in Alzheimer's disease (20 cases). The author established a certain correlation between ecmnestic confabulations and disturbances of fixation, between mnemonic confabulations and disorders of selective reproductivity, between their expressiveness and emotional liveliness and the degree of actualization of the past events. In a complacent-euphoric and anxiety affect the confabulations were spontaneous and were accompanied by psuedoactivity. In depressive states they were fragmentary and were detected only in response to questions. Aphatic disorders and the severity of dementia influence the mnestic confabulations making them poorer and incomplete.