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)

The effects of human urogastrone (0-25 mug. per kg. per hour intravenously) in four male patients with proven Zollinger-Ellison syndrome (z.e.s.) and in four healthy control subjects have been studied. After urogastrone in z.e.s. patients gastric acid volume and concentration decreased and basal acid output was reduced by 50-82%; the concentrations of intrinsic factor and pepsin in gastric juice increased by 60-300%; and peak plasma-gastrin concentration increased by 127-164% of basal concentration. A significant negative correlation between increase in plasma-gastrin concentration and decrease in acid output was observed (r=-0-72, P less than 0-01). Ulcer pain was relieved 30-60 minutes after the beginning of urogastrone infusion. These results suggest that urogastrone can inhibit the endogenously stimulated acid hypersecretion in z.e.s.
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PMID:Effect of urogastrone in the Zollinger-Ellison syndrome. 5 Dec 36

The effect of 300 mg cimetidine q.i.d. on ulcer healing was studied in a controlled double-blind clinical trial of 71 in-patients with duodenal ulcer. Healing occurred in 48.5% of patients in the cimetidine group after two weeks, and in 20.6% in the placebo group (P less than 0.05). The healing rate was 88% in the cimetidine group at four weeks, 79.4% in the placebo group. Only during the first day was ulcer pain significantly reduced in the cimetidine-treated patients. Neither basal nor pentagastrin-stimulated acid and pepsin secretions were affected by 17-day administration of cimetidine. The drug had to be withdrawn in two patients because of elevated serum-creatinine levels. There was no other untoward effect.
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PMID:[In-patient treatment of peptic ulcer with cimetidine. I. Effect on duodenal ulcer healing (author's transl)]. 34 17

In a controlled double-blind clinical trial of 39 in-patients with gastric ulcer the effect of cimetidine on ulcer healing, ulcer pain and pentagastrin-stimulated acid and pepsin secretion was measured. A faster healing rate in the cimetidine group was statistically not significant. Cimetidine had no effect on ulcer pain and pentagastrin-stimulated acid and pepsin secretion. There were no serious untoward reactions.
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PMID:[In-patient treatment of peptic ulcer with cimetidine. II. Controlled double-blind trial on gastric ulcer patients (author's transl)]. 34 18

Studies in which the numbers of healed or unhealed ulcers and their correlation with symptoms are availabel are summarized in Table 1. A review of the data and inspection of the Table show that the correlation of GU or DU healing with symptomatic remission is generally poor. The reasons for this are unknown and reflect the very incomplete understanding of the mechanism of ulcer pain and of the pathways through which the pain is mediated. The pathogenesis of pain in GU or DU may be due to the action of acid and pepsin, or of bile, on the tissues exposed in the ulcer crater, to abnormal motility, to normal motility acting on inflamed tissue, to areas of inflammation surrounding the ulcer crater, or to a combination of these factors. The relative importance of each of these variables in DU or GU, or in individual patients (because the mechanism of pain may not be the same in each patient) is not known. Nor is it known how much the pathogenesis of ulcer pain is the result of local release of histamine, kinins, and prostaglandins. These biogenic factors are known to be associated with inflammation and produce, or enhance, somatic pain. Their importance in peptic ulcer in man needs to be studied. Relief of pain after neutralization or buffering of gastric contents with alkali or food suggests strongly that acid must play an important part in the pathogenesis of the ulcer symptoms. The rapidity with which relief of symptoms occurs points towards the direct involvement of hydrogen ions in at least one type of ulcer symptom. Lowering of intragastric acidity by histamine H2- receptor antagonists or high-dose alkali may contribute to the observed discrepancies between ulcer healing and the remission of pain, by creating an environment in the gastroduodenal lumen which favours symptomatic improvement, even in the presence of an unhealed crater. This idea, however, does not explain why there is a discordance between healing and symptoms in patients receiving placebo, or in those treated with other drugs, such as carbenoxolone sodium. In the absence of endoscopic evidence, the presence or absence of symptoms cannot be assumed to indicate with certainty the presence or the absence of a peptic ulcer.
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PMID:Peptic ulceration and its correlation with symptoms. 36 2

An immunofluorescent microscopic method (IF) was compared with conventional culture methods for detection of Actinomyces israelii in smears from the endocervix and IUD of 124 women over a 4-month period at the Royal Women's Hospital, Melbourne. Genital actinomycosis is a non-contagious, chronic, suppurative infection caused by a slowly growing, filamentous, gram-positive anaerobe, and it can lead to fibrosis, abscess or death. The women, attending the Family Planning, Gynecology or Emergency Departments for termination of contraception, replacement of an IUD or for signs or symptoms of pelvic infection, work plastic or copper IUDs. All were screened for Chlamydia and cervical cytology. Actinomyces cultures were screened for 4 weeks and A. israelii identified by morphology, Gram stain and gas-liquid chromatography. The immunofluorescence method involved pepsin treatment of heat-fixed slides, staining with fluorescein-conjugated antibody to A. israelii types I and II, counter-staining, and examination under fluorescence microscopy. Slides were graded subjectively in comparison with positive and negative controls. 9 (11%) of 82 cervical smears, and 2 (4%) of 49 IUD smears were positive by IF, while only 1 was positive by culture: all from 10 patients. One patient has a positive chlamydia culture, and also symptoms of pelvic infection requiring hospitalization. There were 6 others who had symptoms such as pain and discharge, who were treated with IUD removal and antibiotics. 3 women asymptomatic women merely had their IUDs removed. There were no incidents of severe actinomycosis requiring surgery or prolonged hospital treatment although this infection can in rare case be life-threatening. Management of pelvic actinomycosis was discussed.
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PMID:Comparison of immunofluorescence and culture for the detection of Actinomyces israelii in wearers of intra-uterine contraceptive devices. 194 93

The epithelial cells of the stomach and duodenum are normally protected from the damaging effects of acid and pepsin by a balancing mechanism of mucosal resistance. If an imbalance occurs, peptic ulcer may result. Traditional teaching has emphasized the importance of acid (and pepsin) as the cause of this imbalance; however, it is clear that acid and pepsin are not the only important factors in the pathogenesis of peptic ulcer. More recent investigative efforts have been directed at what constitutes mucosal resistance and how it can be disrupted to produce, in the presence of gastric acid, a peptic ulcer. Depletion of endogenous prostaglandins and Helicobacter pylori gastritis have emerged as prominent theories. As evidence exists both to support and refute these theories in humans, any definitive conclusions cannot be made at this time. The acute management of peptic ulcer disease is directed at relieving pain, accelerating ulcer healing, and preventing complications. Peptic ulcers can be healed with antisecretory agents (i.e., H2-receptor antagonists, omeprazole), antacids, prostaglandins, and sucralfate. Because they are effective, safe, and convenient, the H2-receptor antagonists are the most widely used agents for the management of peptic ulcer disease. Because the H2-receptor antagonist agents are equally effective in their indicated uses and are equally safe based on scientifically valid data, selection should be based primarily on cost. Omeprazole is the newest antisecretory agent: a single morning dose of 20 mg suppresses acid secretion for 24 h. The agent offers little advantage over H2-receptor antagonists for the majority of patients with peptic ulcer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathogenesis and therapy of peptic ulcer disease. 197 40

Transient esophageal ulceration is a common finding after sclerotherapy of varices. A small proportion of these ulcers become chronic and resistant to conventional therapy. Such chronic ulcers have been associated with pain, stricture formation, and recurrent hemorrhage. The use of omeprazole, a proton pump inhibitor, was examined in the current study in the treatment of 10 patients (6 women, 4 men; age range, 27-86 years) with cirrhosis (PBC, 4; sclerosing cholangitis, 2; chronic active liver disease, 2; alcohol, 1; and cryptogenic, 1) who developed an esophageal ulcer after a mean of 13 (range, 8-21) sessions of sclerotherapy. The ulcers had been present for 3-54 months despite prolonged treatment with high-dose H2-receptor antagonists and sucralfate. In each case one or more complications had occurred: severe pain in 3, stricture formation in 4, and recurrent hemorrhage in 7 cases. After an 8-week course of omeprazole, 40 mg daily, endoscopy confirmed complete healing of the ulceration in all 10 cases with symptom resolution. In 2 cases the ulcer recurred, with associated bleeding within 6 weeks of discontinuing the treatment in 1 patient. Both cases responded to repeat therapy. These results confirm the efficacy of omeprazole for postsclerotherapy ulceration and imply that acid-pepsin has a role in perpetuating such ulcers.
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PMID:Omeprazole in the management of intractable esophageal ulceration following injection sclerotherapy. 222 99

In peptic ulcer disease, antacids present a therapeutic effect by neutralizing gastric acid and reducing acid delivery to the duodenum. Furthermore, they reduce the activity of pepsin and have the capacity to bind bile acids. Despite the opinion of most clinicians, the effect of antacids relieving pain in patients with peptic ulcer has not been definitely demonstrated. Furthermore, antacids do not seem to improve the healing rate of gastric ulcer. Earlier studies showed that antacids could hasten the healing of duodenal ulcer when administered at a very high dose. However, recent papers demonstrate that this therapeutic effect is also achieved with a dose with very low neutralizing capacity. Severe side effects are rare, although they can occur in high-risk patients. However, minor problems, such as changes in bowel habits, are more frequent.
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PMID:Antacids in the treatment of peptic ulcer disease. 265 91

The author examined 124 patients with duodenal ulcer prior to and after various types of vagotomy. There were 96 males and 28 females whose age ranged from 18 to 76 years. The regional blood flow in the gastric and duodenal mucosa was measured by the hydrogen clearance method. The results provide evidence that along with increase acid- and pepsin-production, the intensity of the local blood flow in the duodenal mucosa is reduced in patients with duodenal ulcer. After vagotomy the debit of hydrochloric acid and pepsin reduces and the intensity of the blood flow in the duodenal mucosa increases. The combination of these two effects of vagotomy facilitates the cessation of pain during the first postoperative days.
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PMID:[Role of blood flow in the etiology of pain caused by ulcer and its cessation after vagotomy]. 273 6

The epidemiology, pathophysiology, diagnosis, clinical presentation, and treatment of peptic ulcer disease (PUD) are reviewed. PUD occurs commonly, with about 4 million Americans affected in a year. Cigarette smoking, aspirin use, and prolonged corticosteroid use are associated with PUD. The disease's etiology is multifactorial; the long-held assumption that ulcers develop solely because of increased gastric acid secretion is no longer valid. Although duodenal ulcer patients are frequently hypersecretors of acid, gastric ulcer patients more commonly have defective mechanisms for protecting the mucosal lining from acid, pepsin, and other agents. PUD is best diagnosed using an upper gastrointestinal roentgenographic series or using endoscopy. The clinical presentations, which involve epigastric abdominal pain that is relieved by food, milk, or antacids, may aid in diagnosis but are not usually definitive. Treatment is designed to relieve symptoms, heal the ulcer, prevent recurrences, and prevent complications. Of the four currently available drug treatments (cimetidine, ranitidine, antacids, and sucralfate), the treatment of first choice is cimetidine or ranitidine for four or six weeks, respectively, for duodenal and gastric ulcer patients. Antacids should be used as needed for pain, and the patient should be reassessed at the end of this period. For most patients, neither cimetidine nor ranitidine is demonstrably superior to one another. Several agents are under investigation in the U.S., including other H2-receptor antagonists (famotidine and nizatidine), proton-pump inhibitors (omeprazole), prostaglandins (misoprostol, arbasprostil, enprostil, and trimoprostil), antimuscarinic agents (pirenzepine), and tricyclic antidepressants (doxepin and trimipramine). peptic ulcer disease is an important disease. It is best treated with H2-receptor antagonists supplemented with antacids as needed for pain.
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PMID:Current concepts in clinical therapeutics: peptic ulcer disease. 286 52


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