1/52. Autoimmune atrophic gastritis with hypergastrinemia. Elevation in fasting serum gastrin levels was found in three patients being evaluated for persistent upper abdominal pain without radiographic evidence of peptic ulcer disease. Fiberoptic endoscopy of the upper gastrointestinal tract in each patient revealed characteristic changes of chronic atrophic gastritis. Gastric biopsies showed diffuse chronic inflammation in the lamina propria, a decrease in the number of parietal cells, and "intestinalization" of gastric mucosa. Total achlorhydria was demonstrated after a maximal histalog stimulus; however, serum levels of vitamin B12 and schilling test values were normal in all three patients. Parietal cell antibodies were found in the serum in all patients in a dilution of 1:20 to 1:80. These cases represent autoimmune (type A) chronic atrophic gastritis and should be distinguished from chronic simple (type B) gastritis, in which serum gastrin levels are normal and no parietal cell antibodies are found in the serum. patients with autoimmune gastritis should be observed at frequent intervals for the occurrence of pernicious anemia or gastric carcinoma. ( info) |
2/52. Symptomatic hypergastrinaemia with achlorhydria: reflief by antrectomy. A women had hypergastrinaemia associated with the variety of gastritis (Type A) that is associated usually with pernicious anaemia, together with recurring bouts of severe abdominal pain. fasting serum gastrin levels ranged between 600 and 2750 pg/ml. There was a rise in serum gastrin levels after a standard protein meal, indicative of a large G cell mass, and a fall after intragastric HCI, which led to a trial of treatment with HCI; this gave some symptomatic relief. After surgical antrectomy there was a profound fall of serum gastrin from a pre-operative level of 2500 pg/ml to constant values of 16--25 pg/ml, and complete and lasting relief from the bouts of abdominal pain. ( info) |
3/52. giardiasis following gastric surgery. A patient is presented who developed acute life-threatening diarrhoea due to infestation with giardia lamblia. We propose that the severity of the illness may have been related to hypochlorhydria following gastric surgery. ( info) |
4/52. 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. ( info) |
5/52. 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. ( info) |
6/52. 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. ( info) |
7/52. 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. ( info) |
8/52. Pernicious anaemia in Africans. Ten cases of pernicious anaemia seen over a 15-year period (1973-1988) in a Lagos hospital are presented. Their ages ranged from 34 to 67 with a mean of 53.6 years. Females outnumbered males 6 to 4. Complications seen include gastric carcinoma, myelopathy, peripheral neuropathy, skin hyperpigmentation, hair depigmentation and diarrhoea. Reluctance to consider the diagnosis owing to firmly held notions of its rarity and a penchant for empirically treating chronic anaemias with all available haematinics and blood transfusion are probably contributory to its underdiagnosis. The fact that seven of the patients presented were seen in the last three years and three of them in the last one year raises the possibility of an increasing incidence of pernicious anaemia in Africans. The disease may be much less rare in Africans than once believed, and medical education should emphasize its existence and advocate greater care in the management of chronic anaemias. ( info) |
| A 49-year-old man presented with a 3-week history of vomiting and diarrhea. He reported foamy stools but no blood or melena and had crampy epigastric pain. He denied usage of antibiotics. He had been taking ranitidine for intermittent epigastric pain for the last few months and noted an 11-pound weight loss during the 3 weeks before admission. Stool was positive for clostridium difficile toxin and giardia lamblia antigen. Cultures and occult blood tests were negative. Oral metronidazole, 500 mg 3 times a day, was administered, and the patient was hydrated. The diarrhea resolved, and patient was discharged on the fourth hospital day. Prior antibiotic therapy is the most common risk factor for C difficile colitis. This patient developed concomitant infection with C difficile and G lamblia while he used ranitidine. He had no other risk factors for these infections. Hence, we propose that ranitidine-induced hypochlorhydria predisposed this patient to the enteric infections. ( info) |
| Hypochlorhydric states such as atrophic gastritis and partial gastrectomy have long been known to cause iron deficiency anemia. However, studies to date have failed to show a similar association with omeprazole, a proton pump inhibitor that also produces achlorhydria. These studies, however, have primarily involved nonanemic, iron-replete individuals. The effect of the drug has not been studied in patients with established iron deficiency, and to our knowledge the patients presented here are the first of their kind to be reported. Our observations support the probability that the profound hypochlorhydria induced by omeprazole may indeed impair the optimal absorption of orally administered iron in iron-deficient individuals, precluding them from obtaining therapeutically adequate amounts to establish the positive balance necessary for the resolution of anemia and the replenishment of stores. The possible explanations for this phenomenon are also discussed. ( info) |