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At least 19 recordsLinked to original sources
PubMed1985

Calcium absorption and achlorhydria.

Defective absorption of calcium has been thought to exist in patients with achlorhydria. I compared absorption of calcium in its carbonate form with that in a pH-adjusted citrate form in a group of 11 fasting patients with achlorhydria and in 9 fasting normal subjects. Fractional calcium absorption was measured by a modified double-isotope procedure with 0.25 g of calcium used as the carrier. Mean calcium absorption (+/- S.D.) in the patients with achlorhydria was 0.452 +/- 0.125 for citrate and 0.042 +/- 0.021 for carbonate (P less than 0.0001). Fractional calcium absorption in the normal subjects was 0.243 +/- 0.049 for citrate and 0.225 +/- 0.108 for carbonate (not significant). Absorption of calcium from carbonate in patients with achlorhydria was significantly lower than in the normal subjects and was lower than absorption from citrate in either group; absorption from citrate in those with achlorhydria was significantly higher than in the normal subjects, as well as higher than absorption from carbonate in either group. Administration of calcium carbonate as part of a normal breakfast resulted in completely normal absorption in the achlorhydric subjects. These results indicate that calcium absorption from carbonate is impaired in achlorhydria under fasting conditions. Since achlorhydria is common in older persons, calcium carbonate may not be the ideal dietary supplement.

Achlorhydria↗
PubMed1983

Is discrimination between type A and B atrophic gastritis clinically useful in achlorhydria?

We tested the validity of the concept that chronic atrophic gastritis can be subdivided into type A and B in hospital patients and normal subjects with proven pentagastrin-refractory achlorhydria. Classification was based on the determination of the basal serum gastrin and parietal cell antibodies. Of 59 hospital patients with achlorhydria, 71% could be classified as belonging to either type A or B; for 29% the criteria for neither type were fulfilled. Of 14 asymptomatic persons with achlorhydria found in 564 normal persons, five could be classified as having type A gastritis, and one as type B gastritis. In eight (53%) persons, an elevated serum gastrin was found in the absence of parietal cell antibodies, representing an intermediate type of atrophic gastritis. Because one-third of the hospital patients and more than half the persons with achlorhydria in a normal population had to be classified as belonging to an intermediate type, the discrimination between type A and B atrophic gastritis in achlorhydria seems to be of limited practical value.

Achlorhydria↗
PubMed1999

Molecular forms of gastrin in the circulation of patients with achlorhydria.

BACKGROUND/AIM: To study circulating gastrin profile, both fasting and postprandially, in patients with achlorhydria due to auto-immune atrophic gastritis, comparing these with normal healthy controls. METHODS: Circulating gastrins were measured using three region-specific radio-immunoassays: amidated gastrins (R98), N-terminal G34 (R526) and N-terminal G17 (GP168). Samples were analysed further using gel chromatography. RESULTS: Fasting gastrin concentrations were elevated in achlorhydria as measured using all three antisera: median 714 pmol/l (range 107-5176) in achlorhydria versus 12 pmol/l (2-33) in controls (R98), 343 pmol/l (45-4316) versus 10 pmol/l (5-41) (R526), and 720 pmol/l (14-6000) versus 2 pmol/l (1-10) (GP168). In patients, 47% of gastrin was amidated (95% in controls) and 30% was processed N-terminally only to G71 (4% in controls). Gastrin rose significantly postprandially: 1643 pmol/l (269-7142) in patients versus 24 pmol/l (5-142) in controls (R98), 432 pmol/l (113-4756) versus 15 pmol/l (7-45) (R526) and 2189 pmol/l (304-7150) versus 15 pmol/l (7-45) (GP168). Only 25% was amidated in the patient group (93.5% in controls) and 21% remained as component I (4% in controls). CONCLUSIONS: This abnormal gastrin profile associated with hypergastrinaemia secondary to achlorhydria is consistent with saturation of the enzymes involved in the processing of the pro-hormone, in particular amidation of the C-terminus.

Achlorhydria↗
PubMed1994

Magnesium hydrogen breath test using end expiratory sampling to assess achlorhydria in pernicious anaemia patients.

A modified magnesium hydrogen breath test, using end expiratory breath sampling, is described to investigate achlorhydria. The efficacy of this test in the diagnostic investigation of pernicious anaemia was compared with that of serum pepsinogen I. Twenty one patients with pernicious anaemia--that is, patients with achlorhydria--and 22 with healed duodenal ulcer and normal chlorhydria were studied. Magnesium hydrogen breath test, serum pepsinogen I, serum gastrin, and standard gastric acid secretory tests were performed in all subjects. The mean (SEM) hydrogen peak value was lower in patients with pernicious anaemia than in the duodenal ulcer group (21.7 (1.9) v 71.3 (5.2) ppm; p = 0.00005). The hydrogen peak value had a 95.2% sensitivity and a 100% specificity to detect pentagastrin resistant achlorhydria. Mean serum pepsinogen I concentrations were also significantly lower in patients with pernicious anaemia than in the duodenal ulcer group (10.7 (2.7) v 123.6 (11.8) micrograms/l p = 0.00005). Sensitivity and specificity to detect pernicious anaemia were both 100% for pepsinogen I. It is concluded that this modified magnesium hydrogen breath test is a simple, noninvasive, cost effective, and accurate method to assess achlorhydria and may be useful in the diagnostic investigation of patients with suspected pernicious anaemia.

Achlorhydria↗
PubMed2000

Heterogeneity of gastric histology and function in food cobalamin malabsorption: absence of atrophic gastritis and achlorhydria in some patients with severe malabsorption.

BACKGROUND: The common but incompletely understood entity of malabsorption of food bound cobalamin is generally presumed to arise from gastritis and/or achlorhydria. AIM: To conduct a systematic comparative examination of gastric histology and function. SUBJECTS: Nineteen volunteers, either healthy or with low cobalamin levels, were prospectively studied without prior knowledge of their absorption or gastric status. METHODS: All subjects underwent prospective assessment of food cobalamin absorption by the egg yolk cobalamin absorption test, endoscopy, histological grading of biopsies from six gastric sites, measurement of gastric secretory function, assay for serum gastrin and antiparietal cell antibodies, and direct tests for Helicobacter pylori infection. RESULTS: The six subjects with severe malabsorption (group I) had worse histological scores overall and lower acid and pepsin secretion than the eight subjects with normal absorption (group III) or the five subjects with mild malabsorption (group II). However, histological findings, and acid and pepsin secretion overlapped considerably between individual subjects in group I and group III. Two distinct subgroups of three subjects each emerged within group I. One subgroup (IA) had severe gastric atrophy and achlorhydria. The other subgroup (IB) had little atrophy and only mild hypochlorhydria; the gastric findings were indistinguishable from those in many subjects with normal absorption. Absorption improved in the two subjects in subgroup IB and in one subject in group II who received antibiotics, along with evidence of clearing of H pylori. None of the subjects in group IA responded to antibiotics. CONCLUSIONS: Food cobalamin malabsorption arises in at least two different gastric settings, one of which involves neither gastric atrophy nor achlorhydria. Malabsorption can respond to antibiotics, but only in some patients. Food cobalamin malabsorption is not always synonymous with atrophic gastritis and achlorhydria, and hypochlorhydria does not always guarantee food cobalamin malabsorption.

Achlorhydria↗
PubMed1988

Reciprocal regulation of antral gastrin and somatostatin gene expression by omeprazole-induced achlorhydria.

Gastric acid exerts a feedback inhibition on the secretion of gastrin from antral G cells. This study examines whether gastrin gene expression is also regulated by changes in gastric pH. Achlorhydria was induced in rats by the gastric H+/K+ ATPase inhibitor, omeprazole (100 mumol/kg). This resulted in fourfold increases in both serum gastrin (within 2 h) and gastrin mRNA levels (after 24 h). Antral somatostatin D cells probably act as chemoreceptors for gastric acid to mediate a paracrine inhibition on gastrin secretion from adjacent G cells. Omeprazole-induced achlorhydria reduced D-cell activity as shown by a threefold decrease in antral somatostatin mRNA levels that began after 24 h. Exogenous administration of the somatostatin analogue SMS 201-995 (10 micrograms/kg) prevented both the hypergastrinemia and the increase in gastrin mRNA levels caused by omeprazole-induced achlorhydria. Exogenous somatostatin, however, did not influence the decrease in antral somatostatin mRNA levels seen with achlorhydria. These data, therefore, support the hypothesis that antral D cells act as chemoreceptors for changes in gastric pH, and modulates somatostatin secretion and synthesis to mediate a paracrine inhibition on gastrin gene expression in adjacent G cells.

Achlorhydria↗
PubMed1986

Diagnosis of achlorhydria by plasma secretin determination--a tubeless approach.

To investigate the value of plasma secretin determination in the diagnosis of impaired gastric secretion, blood samples were drawn for secretin assay (radioimmunoassay) at specified intervals before and after pentagastrin stimulation in 10 healthy volunteers and 11 subjects with suspected hypo- or achlorhydria (less than 10 mEq HCl/2 h). The tests were performed twice, once with and once without aspiration of gastric juice for estimation of acid output. In six other patients with proven achlorhydria, the test was performed once without gastric aspiration. The best discrimination of a single plasma secretion level between controls and patients with hypo- and achlorhydria was obtained 60 min after pentagastrin stimulation. All controls and four subjects with an acid output more than 10 mEq/2 h had secretin levels within normal limits. In contrast, 12 of the 13 subjects with hypochlorhydria had abnormally low basal corrected secretin levels at 60 min, including nine achlorhydria patients. It is concluded that secretin determinations after pentagastrin stimulation may be a valuable diagnostic and epidemiological tool to identify patients with impaired gastric secretion.

Achlorhydria↗
PubMed1984

Prevalence of achlorhydria in a normal population and its relation to serum gastrin.

In a middle-aged group of normal subjects achlorhydria after maximal stimulation with pentagastrin was found in 12 out of 366 males (3%) and 2 out of 198 females (1%); 13 of these 14 (93%) had an elevated serum gastrin, of which nine were more than two times normal. In another 11 persons a moderately elevated serum gastrin - less than two times normal - was found in absence of achlorhydria. At least seven of them had hypochlorhydria. Of 540 persons with a normal serum gastrin one had achlorhydria. Determination of the serum gastrin appeared to be fairly reliable as a method of detecting achlorhydria.

Achlorhydria↗
PubMed1985

Sustained fasting achlorhydria: a comparison of medical regimens.

The effects on fasting gastric pH of eight medical regimens were evaluated during a 10-h period in 8 duodenal ulcer patients. Our goal was to find a regimen that would produce sustained, fasting achlorhydria (pH greater than 7.0) in every patient. The effects of commonly prescribed bolus doses of cimetidine, antacid, or their combination were studied first. Mean gastric pH with cimetidine (300 mg/6 h intravenously), antacid (30 ml/h intragastrically), and their combination was 3.5, 4.6, and 6.8, respectively. Although mean pH with the combination was significantly higher than with either drug alone (p less than 0.05), sustained achlorhydria was not achieved. Next we tested constant-infusion regimens of cimetidine (50 mg/h intravenously), antacid (0.5 ml/min intragastrically), and their combination. Whereas infusions of cimetidine or antacid alone produced mean pH levels of 4.3 and 5.2, respectively, not significantly different from their bolus counterparts, the combination regimen resulted in a mean pH of 7.4. However, sustained achlorhydria was still not produced in each patient. Only when the dose of cimetidine infusion was doubled to 100 mg/h and administered with a constant infusion of antacid was sustained achlorhydria achieved in each patient.

Adult↗
PubMed1987

Influence of chronic drug-induced achlorhydria by substituted benzimidazoles on the endocrine stomach in rats.

The release of gastric somatostatinlike immunoreactivity and gastrin was studied in rats with chronic achlorhydria induced by the substituted benzimidazole BY 308. In vitro, stimulation of gastrin release by acetylcholine was slightly enhanced after 1 day of treatment but no further effects were observed compared to placebo controls. Four weeks of treatment evoked marked gastrin hypersecretion, which was atropine-resistant. Stimulation of gastrin release was inversely correlated to enhancement of basal gastrin levels. Chronic achlorhydria distinctly reduced somatostatin responses to isoproterenol, whereas potent stimulation was observed in controls. Treatment with BY 308 for 1 wk was associated with fully developed gastrin hypersecretion but isoproterenol-stimulated somatostatin release was still unaffected. Hypergastrinemia accompanied by increased antral gastrin and reduced antral and fundic somatostatin concentrations was also found in vivo after 4 wk of treatment with BY 308. It is concluded that chronic achlorhydria not only enhances storage and secretion of gastrin but also diminishes the secretion and tissue stores of somatostatin; adaptive changes of the somatostatin cell occur, however, with a much longer delay.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1991

Development of sustained achlorhydria in a patient with the Zollinger-Ellison syndrome treated with omeprazole.

Spontaneous remission of gastric acid hypersecretion in the Zollinger-Ellison syndrome occurs rarely. This study shows the development of gastric secretory mucosal atrophy resulting in achlorhydria and loss of pepsin secretion in a 63-year-old woman with the Zollinger-Ellison syndrome. Reduced secretion began soon after starting treatment with omeprazole, and achlorhydria became complete 6 months later. The patient remains well with normal endoscopy results and is achlorhydric 4 years after the start of treatment and 34 months after stopping omeprazole. She was not colonized with Helicobacter pylori until 36 months after developing achlorhydria. Serum gastrin has increased from 1000 to between 5000 and 12,500 ng/L (pg/mL), was not suppressible by gastric acidification, and was not associated with G-cell hyperplasia. She also has a normal Schilling test and normal immunoglobulins, and lacks antibodies to parietal cells or H+, K(+)-ATPase. Moderate enterochromaffinlike cell hyperplasia is apparent for the first time on the latest biopsy sample.

Achlorhydria↗
PubMed1981

Reassessment of the management of benign gastric ulcer with achlorhydria.

Previous reports of benign gastric ulcer with achlorhydria have recommended surgical removal of the ulcer, even though a malignant process had not been demonstrated. We report a patient with achlorhydria and a gastric ulcer who, at exploration 4 weeks after discovery, had only a healed ulcer. Its benign nature was demonstrated by endoscopic biopsies and cytology and confirmed at surgery. The patient has remained achlorhydric on follow-up and has not had further ulcers. We recommend that, after multiple endoscopic biopsies and cytology have adequately excluded a malignant process, a gastric ulcer be followed to complete healing, even in the presence of achlorhydria. If healing is incomplete by 6-12 weeks, surgical intervention should be contemplated, just as for more routine gastric ulcers.

Achlorhydria↗