Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Enprostil, a synthetic analogue of prostaglandin E2, is effective in the treatment of patients with duodenal or gastric ulcers. As demonstrated in pharmacological studies in healthy volunteers and in patients with inactive ulcer disease, gastric acid secretion is suppressed by up to 80% for almost 12 hours after single doses of enprostil. The drug also reduces the secretion of pepsin, another 'aggressive' factor in peptic ulcer disease. Interestingly, in contrast to the H2-receptor antagonists, which either increase or have no effect on serum gastrin concentrations, enprostil inhibits basal and postprandial gastrin release. Although the possible effects of enprostil on 'defensive' factors in peptic ulcer disease-which are thought to protect the mucosa-require much further clarification, some evidence obtained in man indicates that bicarbonate secretion is enhanced by enprostil. Further, data from animal studies suggest that microvascular integrity may be preserved by a direct action of enprostil on the gastric mucosa. In healthy volunteers, the administration of enprostil in antisecretory doses protects the gastric mucosa against of enprostil in antisecretory doses protects the gastric mucosa against aspirin-induced injury. Cumulative rates of ulcer healing observed in patients with duodenal ulcers after 4 weeks' treatment with enprostil 35 micrograms twice daily were about 50 to 80%, which were similar to those seen in comparative trials with usual therapeutic doses of cimetidine or pirenzepine, but less than occurred with ranitidine. Moreover, enprostil has been shown to relieve daytime pain in a similar percentage of patients as do these H2-receptor antagonists, but night-time pain appears to respond less well to therapy with the prostaglandin. As evidenced by a few controlled trials in patients with gastric ulcers, treatment with enprostil 35 micrograms twice daily for 6 weeks provides ulcer healing in parallel with pain relief as effectively as cimetidine and ranitidine in a high percentage of patients (about 80% after 6 weeks). Prophylactic treatment with enprostil after initial ulcer healing has reduced the rate of duodenal ulcer relapse in patients 'at risk', but to a lesser extent than has ranitidine. Gastrointestinal symptoms-abdominal cramping and pain, flatulence, nausea and notably, diarrhoea-are the most frequently reported side effects during therapy with enprostil. Diarrhoea occurs in about 10% of patients, but is rarely of a severity necessitating treatment discontinuation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Enprostil. A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in the treatment of peptic ulcer disease. 312 Dec 76

The effect of combined use of pentoxifylline and solcoseryl was studied in 35 patients with chronic pancreatitis. General clinical findings were studied in parallel with the time course of pancreatic exocrine (trypsin) and endocrine (insulin, C-peptide) function. The blood level of gastrin and changes in intestinal function using 131I-lipids were also studied. The incorporation of both drugs in multimodality therapy made a positive therapeutic effect, resulting in a decrease in the pain syndrome and dyspeptic symptoms. At the same time some favorable shifts in pancreatic and GI tract function were noted. Possible mechanisms of a positive therapeutic effect were discussed. A conclusion was made that the incorporation of pentoxifylline and solcoseryl in multimodality therapy of chronic pancreatitis was clinically justified and determined pathogenetically.
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PMID:[Trial of the combined use of trental and solcoseryl in treating patients with chronic pancreatitis]. 336 55

In 16 consecutive patients with systemic mastocytosis, we prospectively evaluated a variety of gastrointestinal functions and examined how they relate to the occurrence of gastrointestinal symptoms. Nine patients had either a duodenal ulcer or duodenitis. Hypersecretion of gastric acid was present in 6 patients, and in these patients the mean basal acid output was 20.7 +/- 4.1 mEq/h (range 14-39 mEq/h). Impaired small intestinal absorption occurred in 5 patients, although this was usually mild. The mean fractional emptying rate of liquids for all patients (14.7% +/- 2.3% per minute) did not differ from that for controls (10.7% +/- 0.6% per minute). Mean mouth-to-cecum transit time measured by breath hydrogen testing was the same among patients (87.7 +/- 6.7 min) and controls (86.7 +/- 8.0 min). Plasma histamine concentrations were increased in all patients (mean 1886 pg/ml, range 480-7450) and correlated with the basal acid output (r = 0.64, p less than 0.02) but not maximal acid output or the presence or absence of pain or diarrhea. Mean fasting plasma concentrations of motilin, substance P, and neurotensin from 6 patients did not differ significantly from controls, whereas gastrin and vasoactive intestinal peptide were significantly less than in controls (p less than 0.01). Gastrointestinal symptoms, consisting of abdominal pain or diarrhea, occurred in 80% of patients. Abdominal pain classified as dyspeptic was usually associated with acid-peptic disease of the duodenum and hypersecretion of gastric acid, whereas abdominal pain of a nondyspeptic character was not. Only in those cases of diarrhea consisting of greater than 200 g stool/day was gastric acid hypersecretion frequently found. Neither fecal urgency nor nondyspeptic pain could be accounted for by alterations of gastrointestinal transit. These results demonstrate that gastrointestinal symptoms, peptic disease, and mild malabsorption are much more common than described previously in patients with systemic mastocytosis. Furthermore, the results provide no evidence for the contention that altered gastrointestinal transit is involved in the pathogenesis of these symptoms.
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PMID:Gastrointestinal dysfunction in systemic mastocytosis. A prospective study. 339 14

In an open clinical trial, 16 hospital outpatients with endoscopically proven duodenal ulcer were given 30 mg omeprazole once daily for four weeks. After two weeks' treatment 14 of the 16 patients had healed and after four weeks all patients were healed. Reduction of pain was rapid and occurred during the first part of the trial. No serious adverse events or clinically significant deviations from normal laboratory values were reported. Serum gastrin levels significantly increased during treatment but returned to normal levels after the treatment was discontinued.
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PMID:Effect and tolerability of omeprazole in the treatment of duodenal ulcer disease. 353 Jun 77

Forty patients with endoscopically proven persistent duodenal ulcer who had been treated for six weeks with cimetidine (1 g/day) were randomly allocated to receive a further six weeks' treatment with cimetidine (1 g/day) or ranitidine (300 mg/day). Ulcers healed in 12 of 19 patients given cimetidine (63%) and in 13 of 21 given ranitidine (62%); two patients on cimetidine and two on ranitidine dropped out. In the unhealed ulcer group the ulcer size was reduced in most patients. There was no change in basal acid output, peak acid output, plasma gastrin and pepsinogen I levels after either treatment. Clinical data, gastric function tests, and endoscopic features did not predict ulcer healing. Both treatments were effective in the relief of pain: 72% of patients with unhealed ulcers were asymptomatic at the end of the trial.
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PMID:Treatment of 'cimetidine-resistant' chronic duodenal ulcers with ranitidine or cimetidine: a randomised multicentre study. 609 Feb 80

Review of a 5 year clinical experience with the histamine H2-receptor antagonists metiamide, cimetidine, and ranitidine in 20 patients with Zollinger-Ellison syndrome disclosed a treatment failure rate of 50 percent. The criterion for failure was hemorrhage in four patients, obstruction followed by hemorrhage in one patient, perforation in one, and intractable pain in four. Nine of the 10 patients in whom treatment failed required total gastrectomy for control of complications; the 10th patient refused operation. Retrospective analysis identified hepatic metastases, the multiple endocrine adenomatosis-type I syndrome, refractory diarrhea, and breaks in the medication schedule as being more common in the treatment failure group, but these trends were not statistically significant in our small series of patients. Nonhealing or recurrent ulcers were found in 90 percent of the patients in whom drug therapy failed and in only 10 percent of those patients in whom therapy was successful (p less than 0.01). There were no differences related to age, sex, duration of symptoms, previous gastric operation, ulcer location, presence of diarrhea, or amount of drug prescribed. Basal and peak acid outputs, basal serum gastrin levels, and response to secretin challenge were also nondiscriminatory. The degree of acid inhibition in response to cimetidine was highly variable from one patient to another and on repeat testing in individual patients, and there was no correlation between acid secretory inhibition and clinical course. When severe complications occurred, reinstituting H2-receptor antagonist therapy or increasing the dose did not avert the need for total gastrectomy. Patients refractory to drug treatment who have persistent or recurrent ulcers should be managed with prompt total gastrectomy to prevent life-threatening complications.
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PMID:Failure of histamine H2-receptor antagonist therapy in Zollinger-Ellison syndrome. 612 12

Decapeptide ceruletide (CRL), chemically related to cholecystokinin and gastrin, proved to have remarkable analgesic properties when administered to a group of 22 burned patients, 15 patients with acute myocardial infarction, and 8 patients suffering from pain caused by malignant tumours with metastases. Its effect was such, that many of the patients required no other analgesics (opiates) even after a prolonged administration (up to 10 days) of CRL. In some of the patients a marked euphoria developed. There were no substantial changes in EEG records during CRL administration in 15 controls, among them 4 epileptics. It is probable that CRL helps to activate the internal analgesic system. In the burned patients cortisol, testosterone, renin, prolactin and tri-iodothyronine (T3) levels in serum (plasma) were measured (radio-immunoassays). CRL did not block the stress response (no drop of increased cortisol levels, no increase in low T3 levels), but it modified (influenced) it (drop of the high renin levels, and a tendency to increase the very low testosterone levels). CRL appears to act as an endorphin releaser, as evidenced by the plasma levels of beta-endorphins (quotations). CRL and similar drugs may represent a new, more physiological and probably safer approach to the management of pain.
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PMID:Endorphin releasers: a new possible approach to the treatment of pain after burns--a preliminary report. 631 91

Billroth II resection was carried out in 1000 duodenal ulcer patients in the period 1948-1956. Twenty-two to thirty years later, gastroscopy and biopsy was performed in 196 of 423 survivors. Chronic atrophic gastritis appeared in 93 per cent of the cases, 47 per cent showed slight and 46 per cent severe changes. Seven per cent had normal mucosa. The microscopic grade of gastritis proved to be independent of age, alcohol and tobacco consumption and serum gastrin. No correlation between clinical status, such as dumping, diarrhoea, vomiting and pain, haematological parameters and the microscopic grade of gastritis, could be found. It is suggested that gastritis might be caused by reflux of bile, pancreatic and intestinal juices, and that postgastrectomy symptoms and anaemia do not depend on the microscopic grade of gastritis.
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PMID:Causes and clinical significance of gastritis following Billroth II resection for duodenal ulcer. 686 Sep 6

The study investigated the relationships between specific demographic, psychosocial, and physiological variables and the severity of duodenal ulcer disease in a population of patients with proved duodenal ulcer. Intercorrelations between psychosocial and physiological variables were also studied. The study design was cross sectional and retrospectively assessed life change units and DUD severity during the previous 6 months in 39 male ulcer clinic outpatients. Anxiety, depression, life change units, the family environment, ABO blood type, secretor status, serum pepsinogen, and serum fasting gastrin were evaluated. A DUD severity score was calculated from self-reported ulcer pain symptoms and ulcer complications. Gastrin levels correlated significantly with three Family Environment Scale (FES) subscales, including: (a) independence, (b) achievement orientation, and (c) expressiveness. Duodenal ulcer disease severity scores correlated with Zung SDS scores, but not with state or trait anxiety, life change units, or the FES.
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PMID:Serum gastrin and the family environment in duodenal ulcer disease. 697 85

The effect of pentagastrin on oesophageal motility was studied in six subjects with idiopathic diffuse oesophageal spasm (IDOS). Pentagastrin was administered by continuous intravenous infusion in doses of 1 microgram/kg/h, 5 micrograms/kg/h, and 10 micrograms/kg/h. Saline infusion was used as a control. No subject experienced pain during pentagastrin infusion. Two developed dysphagia and repetitive contractions with 'wet' swallows during the saline infusion and the lowest pentagastrin infusion. Contraction amplitude was increased only with 'dry' swallows during the 10 micrograms/kg/h infusion period. Contraction duration was increased with both 'wet' and 'dry' swallows during the 1 microgram/kg/h infusions, and with 'dry' swallows during the 10 micrograms/kg/h infusion. Propagation velocity was not altered by pentagastrin. We conclude that gastrin released physiologically by eating probably does not contribute to symptom production in IDOS. Moreover, it seems unlikely that pentagastrin, at least in these doses, can be exploited for diagnostic purposes.
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PMID:Pentagastrin in diffuse oesophageal spasm. 722 56


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