Cases reported "Achlorhydria"

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1/17. Benign gastric ulcer in a patient with pernicious anemia.

    This is the report of the presence of a benign gastric ulcer in a patient with achlorhydria and documented pernicious anemia. The pernicious anemia was established by a Histalog-fast achlorhydria, a schilling test of 2.1% excretion of tagges vitamin B12 in a 24-hr urine, and reticulocytosis after administration of cyanocobalamine. Following Histalog (1.5 mg per kg of body weight), the gastric volume was 40 ml, there was no acid, and the pH was 8.1. The ulcer demonstrated by gastroscopy was confirmed at gastrectomy. Histological examination of the ulcer and the remainder of the stomach showed no malignancy. The principal conclusion of this paper is that the patient did not have an acid-produced ulcer, but that bile regurgitation coupled with alcohol ingestion produced the lesion. Surgical investigation of the ulcer seemed mandatory because of the known increased incidence of gastric carcinoma in patients with pernicious anemia.
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2/17. Gastrointestinal dysfunction in immunoglobulin deficiency. Effect of corticosteroids and tetracycline.

    Idiopathic late-onset immunoglobulin deficiency in a young man was associated with achlorhydria and a severe intestinal malabsorption syndrome that did not respond to conventional therapy. Combined therapy with high doses of prednisone and tetracycline hydrochloride resulted in weight gain, cessation of diarrhea, improved absorption of water, fat, and vitamin B12, and production of gastric acid after stimulation with histamine. serum immunoglobulin levels, however, did not increase.
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3/17. polyps caused by gastric erosions.

    Gastric erosions, a disease with a tendency to recur through decades, may in advanced age and anacidity give rise to polyps. These histologically benign polyps may be recognized by clinical methods of examination.
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4/17. Interrelationships between the B-vitamins in B12-deficiency neuromyelopathy. A possible malabsorption-malnutrition syndrome.

    Five patients presenting clinically with a form B12-deficiency neuromyelopathy, with cord involvement in all and proximal muscle weakness in two of them, were investigated for their neurologic, hematologic and vitamin status. Megaloblastosis and achlorhydria were present in all, and impaired absorption of 57Co vitamin B12 and of D-xylose was detected in four. Total cyanide extracted vitamin B12 (A) was lowered in all cases and noncyanide extractable (B) in four of the five, being zero in three. All five responded to injections of hydroxocobalamin. In two patients sequential estimations showed that both A and B, especially the latter, rose steeply initially, normalizing at 50% of A after some weeks. Moiety B is suggested to be physiologically the more active and dissociable form of vitamin B12. Markedly elevated initial serum folate levels, and their subsequent fall under treatment with B12, indicated the operation of the "methyltetrahydrofolate trap". blood levels of thiamin, nicotinic acid and pantothenic acid were within normal limits. However, serum riboflavin (B2) total vitamin B6 and pyridoxal were reduced in all where tested. Vitamin B6 deficiency could have resulted from its own malabsorption and have contributed to be B12 deficiency. Vitamin B2 and B6 levels also corrected themselves on B12 therapy. The B-vitamin deficiencies in our patients probably resulted from intestinal malabsorption, with a possible factor of malnutrition consequent to their strictly vegetarian diet.
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5/17. achlorhydria, parietal cell hyperplasia, and multiple gastric carcinoids: a new disorder.

    We describe a 54-year-old woman who had multiple gastric carcinoid tumors arising in the setting of marked hypergastrinemia associated with a lack of acid production by hypertrophic parietal cells. The serum gastrin level was 1,400 pg/mL, and investigation revealed no evidence for either of the recognized causes for hypergastrinemia-associated carcinoids, autoimmune gastritis, and Zollinger-Ellision syndrome. Partial gastrectomy was performed. Pathologic examination showed multiple intramucosal and invasive carcinoid tumors of the body and fundus in a background of marked ECL cell hyperplasia. There were no gastric or duodenal ulcerations. One perigastric lymph node was metastatically involved. The oxyntic mucosa showed marked hyperplasia and hypertrophy of the parietal cells. Some of these cells were vacuolated, and many displayed protrusions of apical cytoplasm into dilated oxyntic glands filled with inspissated eosinophilic material. Similar findings have occurred in 1 other patient, strongly indicating that the clinicopathologic alterations in the 2 cases are not random but, on the contrary, represent a very rare disorder of gastric carcinoids associated with an intrinsic acid secretion abnormality of the parietal cells.
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6/17. 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.
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7/17. Recurrent obstipation as a complication of partial pancreatectomy for non-beta cell adenoma of the pancreas.

    Verner and Morrison, in 1958, reported non-insulin-secreting tumours of the pancreas that were associated with a syndrome of refractory diarrhea, achlorhydria and hypokalemia. Surgical resection of such tumours results in rebound acid hypersecretion and cessation of the watery diarrhea. The authors report the case of an 84-year-old man who had three of the four major criteria for diagnosis of the Verner Morrison syndrome. hypokalemia was absent, but this was possibly due to the large doses of potassium chloride that he was taking in conjunction with diuretics. After resection of the tumour severe obstipation with resultant bowel obstruction developed in addition to rebound hypersecretion and relief of watery diarrhea. Treatment, consisting of bulk laxatives in appropriate amounts, alleviated the obstipation.
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8/17. Multifocal gastric carcinoid tumours, achlorhydria, and hypergastrinaemia.

    Multiple polypoidal carcinoid tumours of the stomach were found in 5 patients with achlorhydria (4 of whom had pernicious anaemia) as a result of autoimmune atrophic gastritis. The tumours were small (nearly all less than 1 cm diameter) and appeared to grow very slowly, if at all; no significant enlargement or complications were seen during periods of observation of up to 6 years. No extragastric hormonal syndromes were identified. They differed from the carcinoid tumours usually found in the intestinal tract by being composed of argyrophil (not argentaffin) cells of the enterochromaffin-like (ECL) type. fasting plasma levels of gastrin, which is believed to be trophic to ECL cells, were very high in all patients. Thus, chronic hyperplasia of gastric ECL cells (as a result of hypergastrinaemia) may have been responsible for development of the tumours. Long-term, uninterrupted achlorhydria produced by potent inhibitors of gastric acid secretion might therefore predispose to carcinoid tumours of the stomach.
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keywords = gastric acid, acid
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9/17. Iatrogenic campylobacter pylori infection is a cause of epidemic achlorhydria.

    On a number of occasions, there have been descriptions of epidemic achlorhydria in subjects undergoing repeated gastric secretory studies, typically as part of research protocols. We observed a case in a 37-yr-old healthy man undergoing weekly gastric analyses, along with endoscopy and gastric biopsy, as part of a research protocol studying gastric adaptation to aspirin. In the middle of the 2nd wk of aspirin administration, he developed severe nausea and epigastric discomfort. aspirin administration was discontinued, but, as per protocol, gastric analyses, endoscopies, and biopsies were continued. Compared to the week preceding the acute illness, biochemical analyses showed a transient 7.4-fold increase in basal gastric acid, 3.6-fold increase in pepsin secretion, 8.8-fold increase in dna loss, 5.6-fold increase in mucus secretion, and 12-fold increase in gastric bleeding. Basal acid secretion was zero, and pepsin secretion was one-third of control during the 2nd wk of the infection. endoscopy at the time of symptoms showed erosions in the gastric body and antrum, as well as numerous mucosal hemorrhages and an acute ulcer in the antrum. endoscopy 7 days later revealed that the gastric mucosa had almost completely recovered, with only a shallow erosion seen at the site of the previous ulcer. Gastric biopsies were normal before and during the first 2 wk of aspirin ingestion. Gastric biopsies taken at the time of the acute illness (associated with increased basal acid secretion) showed marked acute inflammation of the antrum with many campylobacter pylori bacilli. At that time, neither acute inflammation nor C. pylori were found in biopsies from the body of the stomach. Biopsies obtained 1 wk later (zero basal acid) showed acute inflammation of both the gastric body and antrum. One week later, biopsies from the gastric body showed mild focal acute inflammation, moderate chronic inflammation, and an occasional lymphoid follicle; the gastric antrum showed chronic inflammation. Antral biopsies obtained 2 yr later showed persistent chronic gastritis with prominent lymphoid follicles and scattered foci of acute inflammatory cells; C. pylori bacilli were still present, but were less apparent. We believe that the syndrome of acute (epidemic) gastritis is often iatrogenic C. pylori infection. Our case shows that increased basal acid and pepsin secretion occur before onset of basal acid hypochlorhydria in the acute phase of C. pylori infection.
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ranking = 1131.80133868
keywords = gastric acid, acid
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10/17. Positive intravenous secretin test in patients with achlorhydria-related hypergastrinemia.

    The intravenous secretin test is widely used to distinguish gastrinoma (zollinger-ellison syndrome) from other causes of fasting hypergastrinemia. We report 2 patients with fasting hypergastrinemia and a rise of greater than 200 pg/ml in serum gastrin concentration after intravenous injection of 2 CU/kg body wt of pure natural secretin. Both patients had pentagastrin-fast achlorhydria. Thus, the intravenous secretin test may be positive in patients with achlorhydria-related hypergastrinemia. gastric acid secretion should be measured in hypergastrinemic patients before embarking on a secretin test.
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