Influence of achlorhydria on aspirin-induced occult gastrointestinal blood loss: studies in Addisonian pernicious anaemia.
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The effect of aspirin (acetylsalicylic acid) ingestion on occult gastrointestinal blood loss has been studied in patients with treated Addisonian pernicious anaemia and proved achlorhydria and in control patients able to secrete hydrochloric acid. A highly significant increase in gastrointestinal blood loss (1.9 ml./day of treatment) occurred with aspirin ingestion in the achlorhydric patients. The control group had a significantly greater increase in blood loss (4.29 ml./day of treatment). Thus aspirin can produce occult gastrointestinal blood loss by a mechanism unrelated to hydrochloric acid. Half of the control patients had losses of similar magnitude to those in the pernicious anaemia group, and the degree of blood loss in individual control patients appeared unrelated to gastric acidity. Differences in gastric mucosal characteristics, in the rate of gastric emptying, or in systemic effects of aspirin may explain the variation between individuals in the degree of occult gastrointestinal blood loss after aspirin. (+info)
Radio-immunoassay of gastrin in human plasma.
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1. A radio-immunoassay for gastrin has been developed using partially purified porcine gastrin to raise antibodies and highly purified natural porcine gastrin I for radio-iodination with (125)I. The separation of antibody-bound from free hormone was performed by a double-antibody method.2. In this assay highly purified natural porcine gastrin I, synthetic human gastrin I, radio-iodinated porcine gastrin I, gastrin in the plasma of a healthy volunteer, a patient with pernicious anaemia and another patient with the Zollinger-Ellison syndrome were immunologically identical.3. The fasting plasma gastrin concentration of fourteen gastric ulcer patients was significantly higher than that of the 113 hospital controls with no history of gastro-intestinal disease, while twenty-seven duodenal ulcer patients had gastrin levels within the normal range.4. Plasma gastrin concentration was significantly elevated in pernicious anaemia (fifty-one patients), achlorhydria (thirty-three patients), hypochlorhydria (eleven patients) and in nine patients with histologically proven Zollinger-Ellison syndrome.5. In human volunteers a protein meal stimulated endogenous gastrin release while a carbohydrate meal did not. Atropine sulphate I.M., and hydrochloric acid orally, produced a significant fall in the level of circulating gastrin. (+info)
The functional 'G' cell mass in atrophic gastritis.
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The serum gastrin response to a standard protein meal has been determined in achlorhydric patients with atrophic gastritis and contrasted with the response in normal subjects whose gastric contents were kept continuously neutral by intragastric bicarbonate instillation. Five normal subjects showed a significant increase in serum gastrin from a mean (+/- SEM) of 17 +/- 3 pg/ml to 119 +/- 10 pg/ml but their response did not approach that of four patients with atrophic gastritis and antral sparing (605 +/- 133 pg/ml to 1418 +/- 186 pg/ml). By contrast, in four patients with antral gastritis, there was no significant change in gastrin levels (24 +/- 13 pg/ml to 55 +/- 19 pg/ml). These studies indicate that the gastrin-secreting cell mass is increased in atrophic gastritis with antral sparing and decreased in atrophic gastritis with antral involvement, as compared to the normal state. They provide further evidence for the existence in man of two distinct forms of atrophic gastritis. (+info)
Serum gastrin and the antral mucosa in atrophic gastritis.
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The gastric antral mucosa was studied histologically in 22 patients with atrophic gastritis, of whom 11 had high levels and 11 had normal levels of serum gastrin. The antrum was graded histologically from normal to grade 3 gastritis. All patients with hypergastrinaemia (nine seropositive and two seronegative for parietal cell antibody) had either a normal antrum or minimal (grade 1) antral gastritis. In contrast all but one patient without raised serum gastrin (nine seronegative and two seropositive for parietal cell antibody) had severe (grades 2-3) antral gastritis. Thus circulating gastrin levels observed in patients with gastritis and achlorhydria can be directly related to the presence or absence of antral mucosal damage.Comparison of the histological appearances of the antral mucosa with serum gastrin and parietal cell antibody status has provided a basis for the separation of two distinctive forms of atrophic gastritis. (+info)
Spontaneous achlorhydria with atrophic gastritis in the Zollinger-Ellison syndrome.
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This case report describes the occurrence of spontaneous, persistent achlorhydria in a patient with markedly raised basal acid secretion and diarrhoea for over two years (Zollinger-Ellison syndrome). Achlorhydria was due to the rapid development of severe atrophic gastritis in a gastric mucosa that had previously shown markedly increased numbers of parietal cells. (+info)
Serum gastrin in chronic gastritis.
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Fasting gastrin levels in serum were measured in 49 patients with different types of chronic gastritis and in matched controls. In 15 patients with established pernicious anaemia the mean (+/- S.E. of mean) level of gastrin was greatly raised (699 +/- 99 pg/ml). In 17 patients with chronic atrophic gastritis, seropositive for parietal cell antibody but with adequate vitamin-B(12) absorption, the level was also raised (476 +/- 74 pg/ml). By contrast, in "simple" atrophic gastritis seronegative for parietal cell antibody the gastrin levels were significantly lower for both diffuse atrophic gastritis (129 +/- 31 pg/ml) and multifocal gastritis (14 +/- 4 pg/ml). These levels were similar to those in the controls (46 +/- 7 pg/ml).The mechanism of the raised gastrin levels remains uncertain, but neither achlorhydria nor in vivo action of the parietal cell antibody wholly accounted for the hypergastrinaemia.We conclude that hypergastrinaemia is characteristic of gastritis associated with autoimmune reactions to gastric antigens and pernicious anaemia and that a raised serum gastrin is a useful marker of the type of gastritis that tends to progress to the gastric lesion of pernicious anaemia. The findings suggest that this type of gastritis is an essentially different disease from "simple" atrophic gastritis, and the differences in gastrin levels may be due to sparing of the antral mucosa in the autoimmune type but not in "simple" gastritis. (+info)
Determination of vitamin B 12 absorption by a simple whole body counter.
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This paper reports the results of estimating vitamin B(12) absorption by whole body counting in patients without known gastrointestinal disorder, and in patients with pernicious anaemia, idiopathic achlorhydria, achlorhydria following gastric operations, and various forms of small intestinal disease. Patients with pernicious anaemia absorbed less than 30% of the test dose; they could be distinguished from patients without gastrointestinal abnormality and from most achlorhydric patients who secreted more than 300 mg units of intrinsic factor in the post-histamine hour. Nevertheless, the wide range of normal absorption and the variable absorption from the normal gastrointestinal tract is emphasized and discussed. There is no relation between histamine-stimulated intrinsic factor production and vitamin B(12) absorption in patients with small intestinal disease. (+info)
Gastric carcinoma following operation for peptic ulcer disease.
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Gastric carcinoma following operation for benign peptic ulcer disease has been considered rare but nine patients have been seen during the past five years. All were male patients, the average time interval from prior ulcer operation to development of cancer was 17 years, but was a short as ten years. The symptoms of cancer are vague and the diagnosis is often delayed. Fiberoptic endoscopy with biopsy of suspicious areas is the most accurate diagnostic approach. Resection of the tumor is indicated if feasible. The poor prognosis of this malignancy is documented. The evidence is reviewed that the creation of achlorhydria with bile reflux increases the risk of development of gastric carcinoma. All patients who undergo peptic ulcer operation require careful long-term follow-up. Vague gastrointestinal symptoms occurring ten years or more after peptic ulcer operation require full evaluation to exclude the presence of gastric cancer. (+info)