Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dyspepsia, defined as chronic or recurrent upper abdominal pain or nausea, is a common occurrence. Dyspepsia without an ulcer (non-ulcer dyspepsia) is diagnosed in patients at least twice as often as peptic ulceration. Diseases that may present with similar symptoms include gastroesophageal reflux, biliary tract disease, chronic pancreatitis, and irritable bowel syndrome. A careful history and physical examination, supplemented by selected tests, usually lead to a correct diagnosis. The pathogenesis of non-ulcer dyspepsia remains unknown. Gastric acid secretion, duodenogastric reflux, psychological factors, environmental exposures, and heredity probably do not play a major role. Some patients may have motility disturbances, but whether these disturbances cause dyspepsia is unknown. Campylobacter pylori infection and associated gastritis are common in non-ulcer dyspepsia, but their etiologic role is controversial, as is the importance of chronic duodenitis. By recognizing the heterogeneity of patients who present with non-ulcer dyspepsia, more rational management may be possible. Although an empiric trial of antacids or H2 blockers has been recommended to treat dyspepsia, most controlled trials show that although these substances reduce severity of symptoms, they are no more effective than placebos in non-ulcer dyspepsia.
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PMID:Non-ulcer dyspepsia: potential causes and pathophysiology. 328 48

Dyspepsia or indigestion is one of the most common disorders that is managed by general practitioners and gastroenterologists. Non-ulcer dyspepsia can be defined as upper abdominal pain or nausea in patients in whom endoscopy reveals no evidence of peptic ulceration or gastric cancer. Non-ulcer dyspepsia is a heterogeneous disorder and can be the result of such diverse entities as the irritable bowel syndrome, duodenitis or gastro-oesophageal reflux, or may be idiopathic ("essential" dyspepsia). This review traces the development of modern thought on dyspepsia and non-ulcer dyspepsia, from the 16th century to the present.
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PMID:Dyspepsia and non-ulcer dyspepsia: an historical perspective. 354 May 42

Methyl tert-butyl ether (MTBE) has been recently proposed as a new therapeutic modality for the dissolution of cholesterol gallstones. To further evaluate efficacy and tolerability of this new litholytic agent, we have administered MTBE to 3 patients with nonobstructive radiolucent common bile duct stones after recent surgery. Methyl tert-butyl ether (8-11 ml/day) was infused after aspiration of bile via a Teflon catheter inserted through the postoperative T tube. Gentle aspiration and reinfusion were performed continuously to generate stirring. The total amount of MTBE retrieved during the entire procedure was equivalent to approximately 30% of the volume infused. In all cases, MTBE failed to dissolve the radiolucent stones, which were then dissolved with continuous infusion of monooctanoin via the biliary catheter. The characteristic odor of MTBE was detected on the breath of the patients, and nausea and somnolence developed during the treatment. Serum hepatic and pancreatic enzymes did not change after MTBE. In the third subject, who received 11 ml/day of MTBE for 2 consecutive days (total of 22 ml), histologic evidence of duodenitis was found around the papilla. In our opinion, the lack of efficacy of MTBE in dissolving retained radiolucent common bile duct stones was mainly related to its leakage from the common bile duct into the duodenum and the ensuing local chemical toxicity and systemic absorption. As MTBE needs a persistent stone-solvent contact to exert its litholytic action and, at the same time, its toxicity prevents the infusion of larger doses, MTBE use should be restricted to stones placed in closed chambers, such as the gallbladder.
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PMID:Methyl tert-butyl ether fails to dissolve retained radiolucent common bile duct stones. 375 21

We report the case of a 59-year-old man who was treated with intraarterial chemotherapy for metastatic colonic adenocarcinoma. After the second course he developed persistent symptoms of nausea, vomiting, and pain. Endoscopic examination demonstrated severe erosive gastritis and duodenitis, and histological examination of the antral tissue showed severe atypia and histological appearances suggestive of in situ carcinoma. A 2-month course of sucralfate and cimetidine was used and successfully produced symptomatic relief as well as complete normalization of the dysplastic changes.
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PMID:Erosive gastroduodenitis with marked epithelial atypia after hepatic arterial infusion chemotherapy. 392 27

Controversy exists as to whether or not duodenitis alone can cause peptic ulcer symptoms. A modified provocation perfusion test has been performed in 10 symptomatic patients with duodenitis confirmed by endoscopy and histology. The test was conducted without the patient being aware of whether 0.1 N hydrocholoric acid, normal saline, or 8.5% sodium bicarbonate was being perfused directly on the area of duodenitis through the endoscopic irrigation cannula at a fixed rate of 10 ml/min for 10 min. The test was also performed in eight patients with dyspepsia alone and in five patients with chronic duodenal ulceration. Intraduodenal infusion of acid reproduced the epigastric pain in all patients with peptic duodenitis and duodenal ulcer patients, including the feeling of nausea in several which was partially relieved by bicarbonate infusion. In patients with dyspepsia but no peptic duodenitis, the symptoms were not reproduced. It would appear that "peptic duodenitis" can cause symptoms and that this "pain provocation test" may prove useful in its diagnosis.
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PMID:Pain provocation test in peptic duodenitis. 631 25

Nodular duodenum, frequently described as nodular duodenitis, is endoscopically characterized by multiple erythematous nodules in the proximal duodenum and may represent a variant of duodenal inflammation. This study examines the incidence, clinical presentation, histologic correlates, natural history, and response to therapy of nodular duodenum in 83 patients who presented with epigastric pain, heartburn, early satiety, bloating, nausea, vomiting, or gastrointestinal bleeding. There was a previous history of peptic ulcer disease in 58% of patients and gastroesophageal reflux in 33%. None of the patients had associated end-stage renal disease. Endoscopically, in addition to nodular duodenum, esophagitis was found in 17% of patients and gastritis in 32%. Histology of duodenal nodules revealed chronic inflammation in 58% of patients, Brunner's gland hyperplasia in 9%, gastric heterotopia in 7%, and normal mucosa in 26% of patients. In a group of 34 patients studied prospectively, high dosage (300 mg orally bid) therapy with the H2-antagonist ranitidine for 8 wk significantly improved symptoms and endoscopic appearance (p < 0.05). In 26 patients who completely or partially failed H2-antagonist therapy, continuation of therapy with omeprazole (40 mg orally qd) for 8 wk significantly improved symptoms and endoscopic findings (p < 0.05) in 10 patients. These therapeutic approaches led to improvement in the endoscopic findings, but to no statistically significant changes in the underlying histologic appearance of the duodenum. We conclude that nodular duodenum is an endoscopically distinct entity that may respond clinically to antisecretory therapy, but remains difficult to eradicate completely.
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PMID:Clinical and pathologic features of the nodular duodenum. 831 6

Cryptosporidial oocyst infection is a common cause of diarrhea in patients with AIDS. Concomitant symptoms can include crampy abdominal pain, nausea, vomiting, and anorexia. Esophagogastroduodenoscopy is then useful for delineating potentially treatable pathogens. We report a case of cryptosporidial duodenitis with characteristic endoscopic findings, biopsy correlate, and a review of the current literature. The endoscopic appearance illustrated strongly suggests proximal small bowel mucosal involvement with cryptosporidial oocysts.
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PMID:Endoscopic appearance of cryptosporidial duodenitis. 885 57

The important long-term outcomes after Helicobacter pylori eradication are the proportion of patients with continuing symptoms, and the rate of recrudescence of the infection. Patients with proven H. pylori infection prior to treatment and a negative urea breath test at least 4 weeks after completing treatment were invited to return for a further urea breath test and a questionnaire. There were 167 patients and the mean interval since the post-treatment urea breath test was 16 months. The endoscopic diagnoses were duodenal ulcer 72, duodenitis 17, gastric ulcer 26, normal or oesophagitis 52. The ethnic groups were European 86, Maori 25, Pacific Island 28 and other ethnic groups 28. Ten patients (6%) had a positive urea breath test at follow up. The proportion of patients showing recrudescence of H. pylori was related to the delta value (delta) of the post-treatment urea breath test: delta 0-2, five of 146 (3.4%); delta 2-3, two of 18 (11%); and delta 3-4, three of five (60%). A symptom questionnaire was given to 147/157 patients with a persistently negative breath test; 60 had no symptoms, 31 had heartburn, 30 had epigastric pain, 15 had both heartburn and epigastric pain, and 11 had nausea or other symptoms. There were fewer symptoms in patients with gastric ulcer (GU) compared with patients with duodenal ulcer (DU) and non-ulcer patients. Twenty-four patients (16%) were taking H2-antagonists (including seven DU and five GU), 15 were taking antacids and four were taking omeprazole. There was no difference in medication use between diagnostic groups. Eighteen of the 46 patients (39%) with heartburn stated that this was a new symptom. Heartburn was a common symptom for duodenal ulcer patients after eradication (24/74, 32%). A second urea breath test 6-12 months after eradication is required to definitely prove eradication. Patients with a breath test delta value of 2-4 should have a repeat urea breath test.
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PMID:Follow up after successful eradication of Helicobacter pylori: symptoms and reinfection. 971 95

Alendronate sodium is an aminobiphosphonate, an analog of inorganic pyrophosphate, indicated for the treatment of osteoporosis in post-menopausal women. We analyzed events reported in patients prescribed alendronate by general practitioners (GPs) in England. A non-interventional observational cohort study was conducted using the technique of prescription event monitoring (PEM). Exposure data were obtained from dispensed prescriptions issued between October 1995 and January 1997. Outcome data were obtained by sending questionnaires to prescribing GPs. The cohort comprised 11,916 patients. Events most frequently reported as suspected adverse drug reactions and reason for stopping alendronate were recognized gastrointestinal events listed in the Summary of Product Characteristics. These included nausea/vomiting, abdominal pain, dyspepsia, esophagitis and esophageal reflux. Events with the highest incidence density (ID(1) per 1000 patient months treatment) were dyspeptic conditions (32.2), nausea/vomiting (20.8) and abdominal pain (13.8). The term dyspeptic conditions included dyspepsia, esophagitis, esophageal reflux, duodenitis, gastritis and heartburn. Serious suspected adverse reactions possibly related to alendronate were single reports of angioedema, erythema multiforme, hypercalcemia and hypocalcemia. There were 540 deaths in this elderly cohort. This study suggests that alendronate appears to be well tolerated, though there may be risk of developing gastrointestinal side effects including esophagitis and esophageal ulcers.
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PMID:Pharmacovigilance study of alendronate in England. 1273 Jul 57

We sought to determine the cause of gastrointestinal (GI) intolerance of a ketogenic diet (KD) using an endoscopic investigation, and to examine the relationship between endoscopic lesions and dietary tolerance. Thirty-five patients were enrolled in this study and underwent gastrofiberscopy prior to initiation of the KD. We observed the relationship between abnormal endoscopic findings and prior use of antiepileptic drugs (AEDs) and symptoms of GI disturbance. We treated patients with GI symptoms, and observed whether the KD was subsequently better tolerated. Of the 35 patients enrolled, 20 patients (57%) had abnormal endoscopic findings: ten cases of erosive gastritis, four of duodenitis, three of hemorrhagic gastritis, two of esophagitis, and one case of duodenal ulcer. The incidence of abnormal endoscopic lesions was 78% in the polypharmacy group (14/35) and 81% in steroid consumers (16/35). Symptoms of GI disturbance, such as nausea, vomiting, unusual irritability, cramping abdominal pain, and diet refusal for over a day, were observed in 17 (85%) of those patients with abnormal endoscopic lesions and in five (33%) patients without such lesions. Steroids and polypharmacy with more than three AEDs were factors associated with abnormal endoscopic lesions (p < 0.05). After active management with GI medications, GI symptoms subsided, and in all cases except one, patients were able to continue the KD treatment. In conclusion, symptoms of GI disturbance were frequently associated with abnormal endoscopic findings prior to initiation of the KD. Active management with GI medications increased the tolerability of the KD in patients treated with multiple AEDs and steroids.
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PMID:Improving tolerability of the ketogenic diet in patients with abnormal endoscopic findings. 1822 66


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