Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000729 (abdominal cramps)
 531 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inclusion of vagotomy and pyloroplasty in the surgical treatment of gastroesophageal reflux associated with hiatal hernia has long been controversial. To evaluate the morbidity of vagotomy in the treatment of reflux esophagitis, a retrospective study of 311 patients treated by the Hill posterior gastropexy technique of hiatal hernia repair was tabulated. Vagotomy with the anti-reflux operation was performed upon 159 patients (51%). Vagotomy was not included for 152 patients (49%). The incidence of postoperative symptoms with or without vagotomy was almost equally divided--41% without vagotomy and 47% with vagotomy. However, the major postoperative symptoms that occurred in both groups were abdominal cramps and bloating which usually disappeared in the early postoperative period and were attributed to the anti-reflux procedure and not to vagotomy. When vagotomy was included with the anti-reflux operation, the incidence and duration of long term, disabling postoperative symptoms were significantly increased. Diarrhea occurred two times more frequently. Nausea and vomiting occurred ten times more frequently and dumping was present only in vagotomized patients. Long term postoperative symptoms, judged on a basis of symptoms lasting longer than three months duration, occurred in 1% of patients without vagotomy and 26% when vagotomy was included. This study revealed that no additional protection against recurrent symptoms of gastroesophageal reflux or radiographic evidence of recurrent hiatal hernia was provided by inclusion of vagotomy. In conclusion, vagotomy is contraindicated in the treatment of gastroesophageal reflux except in the presence of peptic ulcer disease.
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PMID:Complications of vagotomy in the treatment of hiatal hernia. 97 50

The effect of intragastric and intraduodenal 16,16-dimethyl prostaglandin E2 (dm PGE2) on meal-stimulated gastric acid secretion and gastrin release was studied in patients with inactive duodenal ulcer. Compared to placebo, doses of 0.75, 1.00, 1.33, and 1.77 mug per kg of dm PGE2 instilled into the stomach inhibited meal-stimulated gastric acid secretion by 61 to 94% (P less than 0.01). The 1.00, 1.33, and 1.77 mug per kg doses inhibited acid secretion significantly (P less than 0.05) more than an optimal dose of propantheline bromide. Intragastric dm PGE2 (1 mug per kg) was significantly (P less than 0.05) more effective than intraduodenal dm PGE2 (1 mug per kg) in inhibiting both gastric acid secretion and gastrin release. After 1.33 and 1.77 mug per kg, some patients experienced abdominal cramps, or diarrhea, or both, but at doses of 1.00 mug per kg or less no apparent untoward side effects were observed. It is concluded that 16,16-dm PGE2 significantly inhibits meal-stimulated gastric acid secretion and gastrin release, and may be of therapeutic value in patients with peptic ulcer provided it is free of untoward side-effects with chronic administration.
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PMID:The effect of 16,16-dimethyl prostaglandin E2 on meal-stimulated gastric acid secretion and serum gastrin in duodenal ulcer patients. 125 35

Hypochlorhydria induced by potent antisecretory drugs is followed by a marked elevation of serum gastrin levels which leads to changes in ECL cell density in rats. "Soft" antiulcer drugs like prostaglandins do not increase gastrin levels. Their use in peptic ulcer disease seems to be mainly limited by a relatively high incidence of diarrhea and abdominal cramps. Rioprostil is a new prostaglandin E1 analogue. We compared the potency and duration of action of rioprosil 600 micrograms nocte with 300 micrograms bid on human gastric secretion in a placebo-controlled double-blind study. We further evaluated the clinical effectiveness of rioprostil 600 micrograms nocte in the acute treatment of duodenal ulcer. Nocturnal gastric acidity (24:00 to 08:00) was inhibited from 54.5 +/- 1.7 mmol H+/L (placebo experiments; n =9) to 26.7 +/- 3.5 mmol H+/L (52%) by rioprostil 300 micrograms bid (p less than 0.05) and to 14.4 +/- 3.8 mmol H+/L (74%) by rioprostil 600 micrograms nocte (p less than 0.05). During the daytime (09:00 to 18:00), H+ activity was reduced by 33% and 15% respectively (n.s.). Two hundred and three patients with endoscopically proven duodenal ulcers were randomly allocated to treatment with either rioprostil 600 micrograms nocte or ranitidine 300 mg nocte for 4 weeks in a prospective double-blind study. The two groups were similar. After 2 and 4 weeks treatment respectively, about 55% and 85% of patients healed on rioprostil 600 micrograms nocte and 55% and 90% on ranitidine 300 mg nocte. There were no differences between the treatment groups in ulcer pain relief.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostaglandins and peptic ulcer disease: nocturnal administration of rioprostil vs ranitidine in duodenal ulcer healing. 310 57

Misoprostol has been evaluated in healthy subjects for both antisecretory and pharmacological activity. Doses used were determined initially from acute and chronic tolerance testing in healthy subjects. In the single dosage range of 50-200 micrograms, misoprostol inhibits gastric acid secretion in a dose-related manner both in the basal state and after stimuli such as histamine and standard test meals. The 200 micrograms dose differs significantly from placebo as an antisecretory agent. A preliminary study in six subjects suggested that the 400 micrograms dose does not produce a substantial increase in activity over the 200 micrograms dose. Furthermore, side-effects such as diarrhea and abdominal cramps appear to be dose related. The antisecretory action of misoprostol is maximal one hour after drug administration and is negligible after 4-5 hours. These factors have until now dictated a 50-200 micrograms q.i.d. dosing regimen for misoprostol in clinical trials against peptic ulcer. Misoprostol does not significantly affect platelet function in terms of ADP-, collagen- and thrombin-induced platelet aggregation. Measurements of FEV1, vital capacity, and peak expiratory flow rate have revealed that misoprostol has no significant bronchodilating or bronchoconstricting effect. Studies of endocrine function revealed only a slight rise within the normal range in serum cortisol in women.
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PMID:Misoprostol clinical pharmacology. Establishment of activity in man. 393 46