Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High gastric residual volumes (RVs) are a frequent cause for cessation of total enteral nutrition (TEN). This study was designed to determine the RV that indicates intolerance or inadequate gastric emptying and to compare the RV findings in a blinded fashion with those findings obtained on physical examination and radiography. Twenty healthy normal volunteers (HNV), 8 stable patients with gastrostomy tubes (GTP), and 10 critically ill patients (CIP) were evaluated prospectively for 8 hours while receiving TEN. No subjects were clearly intolerant (ie, vomiting, aspiration). Of the total RVs recorded, 13.1% were greater than or equal to 150 mL in the CIP group, whereas only 2.4% of the RVs were greater than or equal to 150 mL in the HNV group. None of the RVs in the GTP group were greater than or equal to 150 mL. Objective scores on physical examination failed to correlate with RV (p = .397), as did objective scores on radiography (p = .742). However, objective scores on physical examination were significantly related to scores on radiography (p = .016). Abnormal physical examination findings were found in 4 out of 11 patients (GTP + CIP) with RVs less than 100 mL and in 6 out of 7 with RVs greater than or equal to 100 mL. Abnormal radiographic results were found in 6 out of 11 patients with RVs less than 100 mL, in 7 out of 7 patients with RVs greater than or equal to 100 mL, and in 4 out of 20 HNVs. There was no difference in RVs obtained from the supine or right lateral decubitus positions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of residual volume as a marker for enteral feeding intolerance: prospective blinded comparison with physical examination and radiographic findings. 155 25

Tiazofurin (2-B-D-Ribofuranosylthiazole-4-Carboxamide: NSC 286193) is a nucleoside antimetabolite that acts as a potent inhibitor of IMP dehydrogenase resulting in a guanine nucleotide deprivation. Recent in vivo biochemical observations in rats bearing hepatoma suggested a correlation between depletion of guanine nucleotides and antitumor effect. The present phase I trial utilized a weekly x 3 bolus infusion schedule, repeated every 5 weeks. Biochemical measurements of GTP and dGTP were performed in patients at each dose level. Twelve patients received 16 courses of the drug in doses ranging from 1100 to 2050 mg/m2 weekly x 3. The dose limiting toxicities were pericarditis and clinical symptoms suggestive of a more generalized serositis (chest and abdominal pain). Other toxicities included reversible elevations in CPK (MM band only) and SGOT, nausea, vomiting, and arthralgias. Neurotoxic effects were generally mild, including headaches, anxiety, and malaise. Only 1 of 6 patients evaluated for tiazofurin's biochemical activity showed a sustained depletion of guanine nucleotide pools. No antitumor activity was observed. The maximally tolerated dose of tiazofurin on this intermittent weekly x 3 schedule was 1650 mg/m2. Toxicity and the overall lack of biochemical and biologic effect at clinically achievable doses may preclude further clinical evaluation of this drug on a weekly schedule. The toxicities observed in our study were similar to those reported for phase I investigations using a considerably higher dose intensity with daily x 5 schedules.
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PMID:Phase I trial and biochemical evaluation of tiazofurin administered on a weekly schedule. 234 2

Most anticancer drugs are cytotoxic and produce various side-effects, among which nausea and vomiting are almost ubiquitous and usually extremely distressing to the patient. Cancer chemotherapy elicits two main phases of vomiting: an intense, acute phase of vomiting that occurs almost immediately following anti-cancer therapy and a milder, delayed phase of nausea and vomiting of longer duration. The mechanisms underlying the induction of nausea and vomiting after cancer chemotherapy are poorly understood but may be mediated by serotonin (5-hydroxytryptamine or 5-HT), particularly in the acute phase. Serotonin activates 5-HT3 receptors, which function as ligand-gated ion channels located either in the periphery and/or in the central nervous system to produce emesis, among other effects. The peripheral 5-HT3 receptors may be pharmacologically distinct from the central 5-HT3 receptors and may exhibit some association with GTP-binding proteins. In addition, different populations may exist as distinct subtypes of the same receptor. The 5-HT3 receptor antagonist ondansetron (GR 38032F) is effective in preventing the emesis induced by cytotoxic agents currently used in the treatment of many forms of cancer. Ondansetron has, comparatively, a much higher efficacy in the treatment of acute emesis following cancer chemotherapy than it does in the delayed phase, suggesting that the late phase of emesis may be mediated by other distinct mechanisms.
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PMID:Role of 5-hydroxytryptamine3 (5-HT3) antagonists in the prevention of emesis caused by anticancer therapy. 876 66