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)

Using a 12-hour infusion of salmon synthetic calcitonin (S-CT), distinct and sustained inhibition of gastric acid and pepsin secretion has been demonstrated in 4 normal subjects, 3 patients with peptic ulcer disease and 3 high risk patients. In 3 patients with Zollinger-Ellison syndrome, treated in the same way, elevated serum gastrin was reduced by about 50% and acid secretion by more than 90%. In healthy volunteers oral administration of human synthetic CT (H-CT) led to reduction in basal and pentagastrin-stimulated acid and pepsin secretion by about 50%, lasting for more than 2 hours after the instillation of CT. In 4 subjects receiving CT intravenously, slight nausea and headache were registered, while there were no side effects after the oral route. Serum calcium did not change after i.v. or oral administration of CT. Wheras therapeutical applications of CT, given by i.v. route, seem to be restricted to selected cases, i.e. acute gastric ulcerations with imminent or existent bleeding, the eventual benefit or orally administered CT in peptic ulcer disease should be evaluated in controlled long-term trials.
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PMID:Long-term effects of calcitonin on gastric secretion in normals, peptic ulcer and high risk patients. 6 56

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of omeprazole are reviewed. Omeprazole, a substituted benzimidazole, has a unique site and mechanism of action because it inhibits the proton pump--i.e., hydrogen, potassium adenosine triphosphatase (H+,K+-ATPase)--and consequently blocks the final common step in the gastric acid secretory pathway. Omeprazole inhibits basal and histamine-, gastrin- and pentagastrin-stimulated gastric hydrochloric acid secretion. It produces a dose-dependent reduction in gastric acidity, gastric acid output, and gastric juice volume and has variable effects on pepsin secretion. Omeprazole has no documented effect on esophageal motility or lower esophageal sphincter pressure. Omeprazole is variably absorbed from the gastrointestinal tract, and food appears to decrease the rate, but not the extent, of drug absorption. The drug is approximately 95% bound to plasma proteins and is metabolized to inactive components that are enterohepatically or renally eliminated. Omeprazole is more effective (in most studies) than H2-receptor antagonists in treating duodenal ulcer, at least as effective in treating benign gastric ulcer, and more effective in treating reflux esophagitis. Omeprazole has been used successfully in patients with Zollinger-Ellison syndrome refractory to treatment with H2-receptor antagonists. Gastrointestinal complaints (nausea and diarrhea) are the most commonly reported adverse effects associated with omeprazole therapy. The most frequently reported laboratory abnormality occurring with omeprazole use is elevation of serum aspartate aminotransferase and alanine aminotransferase concentrations. Omeprazole will serve a valuable role in the management of gastrointestinal tract ulcers and hypersecretory conditions.
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PMID:Therapeutic evaluation of omeprazole. 306 85

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

On a number of occasions, there have been descriptions of epidemic achlorhydria in subjects undergoing repeated gastric secretory studies, typically as part of research protocols. We observed a case in a 37-yr-old healthy man undergoing weekly gastric analyses, along with endoscopy and gastric biopsy, as part of a research protocol studying gastric adaptation to aspirin. In the middle of the 2nd wk of aspirin administration, he developed severe nausea and epigastric discomfort. Aspirin administration was discontinued, but, as per protocol, gastric analyses, endoscopies, and biopsies were continued. Compared to the week preceding the acute illness, biochemical analyses showed a transient 7.4-fold increase in basal gastric acid, 3.6-fold increase in pepsin secretion, 8.8-fold increase in DNA loss, 5.6-fold increase in mucus secretion, and 12-fold increase in gastric bleeding. Basal acid secretion was zero, and pepsin secretion was one-third of control during the 2nd wk of the infection. Endoscopy at the time of symptoms showed erosions in the gastric body and antrum, as well as numerous mucosal hemorrhages and an acute ulcer in the antrum. Endoscopy 7 days later revealed that the gastric mucosa had almost completely recovered, with only a shallow erosion seen at the site of the previous ulcer. Gastric biopsies were normal before and during the first 2 wk of aspirin ingestion. Gastric biopsies taken at the time of the acute illness (associated with increased basal acid secretion) showed marked acute inflammation of the antrum with many Campylobacter pylori bacilli. At that time, neither acute inflammation nor C. pylori were found in biopsies from the body of the stomach. Biopsies obtained 1 wk later (zero basal acid) showed acute inflammation of both the gastric body and antrum. One week later, biopsies from the gastric body showed mild focal acute inflammation, moderate chronic inflammation, and an occasional lymphoid follicle; the gastric antrum showed chronic inflammation. Antral biopsies obtained 2 yr later showed persistent chronic gastritis with prominent lymphoid follicles and scattered foci of acute inflammatory cells; C. pylori bacilli were still present, but were less apparent. We believe that the syndrome of acute (epidemic) gastritis is often iatrogenic C. pylori infection. Our case shows that increased basal acid and pepsin secretion occur before onset of basal acid hypochlorhydria in the acute phase of C. pylori infection.
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PMID:Iatrogenic Campylobacter pylori infection is a cause of epidemic achlorhydria. 341 50

Trichinella spiralis is an important zoonotic nematode causing trichinellosis which is associated with human diseases such as malaise, anorexia, nausea, vomiting, abdominal pain, fever, diarrhea, and constipation. microRNAs (miRNAs) are endogenous small non-coding RNAs that play important roles in the regulation of gene expression. The objective of the present study was to examine the miRNA expression profile of the larvae of T. spiralis by Solexa deep sequencing combined with stem-loop real-time polymerase chain reaction (PCR) analysis. T. spiralis larvae were collected from the skeletal muscle of naturally infected pigs in Henan province, China, by artificial digestion using pepsin. The specific identity of the T. spiralis larvae was confirmed by PCR amplification and subsequent sequence analysis of the internal transcribed spacer of ribosomal DNA. A total of 17,851,693 reads with 2,773,254 unique reads were obtained. Eleven conserved miRNAs from 115 unique xsmall RNAs (sRNAs) and 12 conserved miRNAs from 130 unique sRNAs were found by BLAST analysis against the known miRNAs of Caenorhabditis elegans ( ftp://ftp.ncbi.nih.gov/genomes/Caenorhabditis_elegans ) and Brugia malayi dataset ( http://www.ncbi.nlm.nih.gov/genomeprj?Db=genomeprj&cmd=ShowDetailView&TermToSearch=9549 ) in miRBase, respectively. One novel miRNA with 12 precursors were identified and certified using the reference genome of B. malayi, while no novel miRNA was found when using the reference genome of C. elegans. Nucleotide bias analysis showed that the uracil was the prominent nucleotide, particularly at the 1st, 6th, 18th, and 23th positions, which were almost at the beginning, middle, and the end of the conserved miRNAs. The identification and characterization of T. spiralis miRNAs provides a new resource to study regulation of genes and their networks in T. spiralis.
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PMID:Identification and characterization of microRNAs in Trichinella spiralis by comparison with Brugia malayi and Caenorhabditis elegans. 2132 87