Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ninety-three consecutive patients referred to a gastroenterology unit with unexplained dyspeptic symptoms were sent a postal questionnaire 6-12 months after endoscopy. It inquired into their current physical symptoms and subjective improvement since investigation, satisfaction with treatment, past history and current psychological well-being. A comparison group of 47 patients with peptic disease were similarly surveyed. Those with unexplained dyspepsia reported more current physical symptoms, more dissatisfaction with their treatment and less subjective improvement than those with peptic disease. The two groups were similar in terms of psychological distress but previous consultation for abdominal and other somatic complaints were more common in those with unexplained dyspepsia. The implications for management of dyspeptic patients are discussed.
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PMID:The outcome of unexplained dyspepsia. A questionnaire follow-up study of patients after endoscopy. 143 65

Forty-five healthy men aged 21-34 years took part in a double-blind, parallel-group, placebo-controlled study of the effects of 28 days' treatment with lornoxicam 4 mg twice daily or indomethacin 50 mg twice daily on faecal blood loss and the endoscopic appearances of gastric and duodenal mucosa. After an initial endoscopic examination, subjects received, intravenously, on day 0, autologous erythrocytes labelled with 51Cr. Complete daily faecal collections were then made from days 6-12, 20-26 and 34-40. The drug treatments or placebo were given from days 13-41. Faecal blood loss was calculated from 51Cr-specific activity of blood and faeces. Endoscopy was repeated 4-8 hours after the last dose of medication; mucosal appearance was graded on a 5-point scale. Lornoxicam caused no more adverse events than placebo; indomethacin caused more indigestion and central nervous system effects, and one subject in this group was withdrawn from the study. Median total blood losses during the pre-treatment and the second and fourth weeks of treatment were respectively 3.33, 3.95 and 5.71 ml for lornoxicam, 2.87, 7.04 and 7.75 ml for indomethacin, and 4.55, 3.64 and 4.13 ml for placebo. Differences between treatments were not statistically significant (P = 0.081 for second week of treatment, P = 0.383 for fourth week of treatment; Kruskal-Wallis test). The effect of chlortenoxicam on faecal blood loss in this study was thus intermediate between placebo and indomethacin, but within- and between-subject variability was such that the differences were not statistically significant. Endoscopic findings were normal in most subjects before and after all treatments, but indomethacin was associated with a slightly greater deterioration in endoscopic score and was the only treatment associated with Grade 3 appearance (in a single patient) in post-treatment endoscopy.
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PMID:Lornoxicam, indomethacin and placebo: comparison of effects on faecal blood loss and upper gastrointestinal endoscopic appearances in healthy men. 221 30

The discussion reports on the history, etiology, and the relationship of prostaglandins to primary dysmenorrhea, reviews old and new drugs used in the treatment; and considers future research. The history of dysmenorrhea dates back to the Greeks who defined the word as "painful menstrual flow." In 1865 the 1st surgical approach was used, consisting of a bilateral oophorectomy followed by other procedures. The relationship of dysmenorrhea and ovulation was discovered in 1938 and was treated by ovulatory suppression with estrogen. The psychogenic theory was advanced in the 1940s and many feel it still remains part of the etiology of dysmenorrhea. Until the discovery of prostaglandins and the subsequent relationship of them to dysmenorrhea, the known therapies were oral contraceptives (OCs), childbirth, sedation, narcotic analgesics, other hormones to suppress ovulation, and bed rest. The relationship of prostaglandins to primary dysmenorrhea is most likely the best explanation medical science can offer. Prostaglandins are thought by many as the etiologic agent of disease. The newest link of research deals with the implication of arginine vasopressin (AVP) as another possible integrated factor in the etiology of primary dysmenorrhea. AVP has been shown to be elevated in women with dysmenorrhea, but how AVP integrates into the sequence of events surrounding painful uterine contractions is unknown. The 2 main modes of therapy are OCs and nonsteroidal anti-inflammatory drugs (NSAIDS). Each has separate indications for use. It is recommended that when relief is not found in 6-12 months that causes of secondary dysmenorrhea be ruled out. OCs have been shown to be quite effective in all groups of women with dysmenorrhea, significantly reducing symptoms in 80-98% of the population. The use of OC in dysmenorrhea is recommended in women who are young, sexually active and who seek contraception, and relief of symptoms related to dysmenorrhea where secondary dysmenorrhea and premenstrual tension syndrome has been ruled out. NSAIDs have come to surface as the mainstay of therapy for dysmenorrhea. The major effect is that they inhibit cyclo-oxygenase. The NSAIDs are recommended for use in any woman with primary dysmenorrhea who may not want therapy with OCs and who does not have a history of peptic ulcer, dyspepsia, hepatic or renal disease, aspirin allergy, asthma, or a bleeding diathesis. At times, short term use can be permissible with some of the contraindications. Guidelines for the use of anti-PGs prophylactically are somewhat nuclear at this time.
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PMID:Primary dysmenorrhea: current concepts. 646 99

Non-steroidal anti-inflammatory drug use is associated with gastrointestinal side-effects including complications such as bleeding and perforation, which occur in 1-2% of patients after 6-12 months of therapy. A high level of non-prescription non-steroidal anti-inflammatory drug use is observed among those presenting complications. More common side-effects are symptomatic gastro-duodenal ulcers (annual incidence of 4-8%) and dyspepsia (25-50%). Low-dose aspirin use is also associated with an increased risk of upper gastrointestinal bleeding, but the increase is about 3 times lower than that found with common non-steroidal anti-inflammatory drugs. Recent studies suggest that the risk of bleeding in patients taking preferential cyclooxygenase-II inhibitors (e.g. nimesulide) is similar to that in patients taking non-selective non-steroidal anti-inflammatory drugs. Epidemiological studies have also shown that nitric oxide donors and antisecretory drugs reduce the risk of upper gastrointestinal bleeding both in non-steroidal anti-inflammatory drug and low-dose aspirin users.
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PMID:Cyclo-oxygenase-1/cyclo-oxygenase-2 non selective non-steroidal anti-inflammatory drugs: epidemiology of gastrointestinal events. 1182 60

NICE recommends immediate referral for patients with dyspepsia and significant acute GI bleeding and urgent specialist referral for investigation if any of the following alarm symptoms are present: progressive difficulty swallowing; chronic GI bleeding; unintentional weight loss; persistent vomiting; abdominal mass; iron deficiency anaemia; suspicious findings on barium meal. Patients aged > 55 with unexplained and persistent dyspepsia, despite H. pylori testing and acid suppression therapy, should also be considered for endoscopy, as should those with previous gastric ulcer or surgery, continuing need for NSAIDs or raised risk of gastric cancer. Patients with uninvestigated dyspepsia should be managed by empirical treatment with a PPI or testing for and treating H. pylori if present. Testing by urea breath test, stool antigen test, or locally validated lab-based serology is suggested. H. pylori eradication is usually given as triple therapy, for seven days, involving a PPI, clarithromycin and either amoxicillin or metronidazole. It is important to take a thorough history and to enquire about any medication the patient is taking. Drugs that are common culprits for dyspepsia include: NSAIDs; calcium antagonists; bisphosphonates; steroids; theophyllines; nitrates. NSAIDs can also cause GI bleeding. Absence of dyspepsia in patients taking NSAIDs does not indicate a reduced risk of bleeding. Peptic ulcers fall into three categories: H. pylori associated ulcers; drug-induced ulcers (particularly NSAIDs); and ulcers in H. pylori-negative patients not taking causative medication. H. pylori is associated with both gastric and duodenal ulcer disease but it is in the duodenum where the closest relationship exists. In any 6-12 month period, 20-40% of healthy people, more commonly men, will experience symptoms of heartburn. Oesophageal reflux can progress to more serious disease such as erosive oesophagitis, stricture or Barrett's oesophagus.
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PMID:Managing dyspepsia in primary care. 1993 59

Urginea indica Kunth. (Family; Liliaceae) was studied for its gastrointestinal stimulant effect to rationalize the traditional medicinal uses as a digestive aid, stomachic and laxative. The crude aqueous-methanol extract of Urginea indica bulb (Ui.Cr) was tested on mice and isolated gut preparations. Ui.Cr, which was tested positive for alkaloids, tannins and coumarins, increased faecal output and accelerated charcoal meal transit in mice (6-12 mg/kg, p.o.), similar to that caused by carbachol (10 mg/kg). Ui.Cr (0.01-1 mg/mL) caused a spasmogenic effect in guinea-pig ileum that was reproduced in rabbit jejunum (0.01-0.3 mg/mL) followed by relaxation at a higher concentration. Like carbachol, the stimulant effect of Ui.Cr was blocked by atropine, suggesting the activation of muscarinic receptors mediating the prokinetic effect. Ui.Cr (0.01-5.0 mg/mL) also inhibited K(+) (80 mm)-induced contraction in rabbit jejunum and shifted the Ca(2+) concentration-response curves to the right, similar to verapamil, a standard calcium channel blocker. These data, indicating the presence of a gastrointestinal stimulant effect in Urginea indica possibly mediated through a cholinergic mechanism, provide a rationale for the use of Urginea indica in indigestion and constipation. The presence of a calcium antagonist effect in the plant may help to alleviate untoward effects of the plant that may result from an excessive increase in gut motility.
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PMID:Gastrointestinal stimulant effect of Urginea indica Kunth. and involvement of muscarinic receptors. 2200 63