[Gastric lesions caused by anti-inflammatory drugs].
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Biomedical subjects
Publications and source records attributed to F Molinari.
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The actions of cimetidine are well known: an inhibitor of gastrin hydrochloric secretion, cimetidine modifies neither the motility nor any of the other functional factors. Numerous authors also attribute a cytoprotective role to cimetidine, one that is apparently carried out independently of the inhibitory effect on hydrochloric secretion. The cytoprotective mechanism itself is not yet fully understood. Numerous hypotheses have been made, including increased production of bicarbonates, inhibition of cyclic AMP, increased mucosal blood flow, and increased mucous production. However, all these hypotheses have not been fully explained, hence the problem remains open to further contributions. Well accepted, instead, is the possibility that the drug may not only intervene in acid-hydrochloric inhibition but may also, by broadening its mechanisms, enhance the powers of the mucosal barrier.
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The parietal cell mass (PCM) was evaluated on endoscopically obtained biopsy specimens of fundus mucosa from 20 duodenal ulcer patients before and after cimetidine treatment. Patients were given cimetidine, 1 g/day, for 28 days. Six out of the 18 cases which healed after short-term therapy went on taking 400 mg/day of cimetidine for 9 months. The PCM was expressed by means of an index (PI) obtained by multiplying the mean cell number per mm of section surface by the mean parenchymal thickness. The analysis of the obtained data failed to demonstrate any significant difference between the PI observed before and after 28 days treatment with cimetidine, while after long term treatment for 9 months, a significant increase of the PI was achieved.
A double-blind 4-week trial of cimetidine (1 g daily) versus placebo was conducted in 68 adult outpatients with active duodenal ulceration endoscopically confirmed. 3 of the patient admitted to the study (1 on cimetidine and 2 on placebo) did not complete the trial. After 4 weeks of treatment, 25 of 33 patients (76%) receiving cimetidine had healed their ulcers compared with 15 (47%) of 32 patients receiving placebo (p less than 0.02). Antacid consumption was also significantly decreased by cimetidine when compared with placebo. Tolerability of the drug was good.
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A case of ulcerous rectocolitis presenting a remarkable haematic and tissue eosinophilia, both rectal and gastric, is described. After therapy, the eosinphil complement decreased in the blood but not in the colic mucosa. It is suggested that eosinphilia is not a particular characteristic of ulcerous colitis, but the expression of an inidvidual reaction to an inflammatory stimulus.
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Duodeno-gastric reflux measured in 18 patients without gastrointestinal complaints showed a wide variation of regurgitation rates. Duodeno-gastric reflux was significantly diminished during duodenal acidification. The effect was more intense and lasted longer after olive oil infused intraduodenally, leading practically to a closed pylorus.
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33 cases of cancer of the gastric stump after gastrectomy for peptic ulcer observed between 1963 and 1972 are reviewed. In 26 patients the average interval between operation and carcinoma detection was over 20 years. No cases of carcinoma occurred in less than 10 years. All patients came too late for surgery, since they had attributed their symptoms to the previous operation. The gradual increase in the gastric-cancer risk of operated patients with time suggests a continuous carcinogenic influence. Regurgitation of duodenal contents through the Billroth II anastomosis seems to be the most important cause of postoperative atrophic gastritis, which is now considered by many authors to be a condition predisposing to gastric cancer. Gastric resection patients should be regarded as a high gastric-cancer risk group. The periodic use of modern procedures for early gastric cancer detection in this group of patients is therefore justified.
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