Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The carcinoid syndrome can arise when effluent blood from carcinoid tumor tissue gains access to the systemic, as opposed to the portal, venous system. Features include facial flushing, diarrhea, wheezing, right-sided cardiac lesions, and retroperitoneal fibrosis. Attacks of flushing, diarrhea, and wheezing can be provoked by bolus injections of adrenaline, noradrenaline, or pentagastrin. While serotonin usually predominates, carcinoid tumors can also secrete, in varying proportions, 5-hydroxytryptophan, kallikrein, kinins, substance P and other neuropeptides, prostaglandins, catecholamines, and histamine. Of these, serotonin, kinins, histamine, and substance P are possible mediators of flushes; serotonin and substance P of hyperperistalsis; and serotonin, kinins, or histamine of bronchial constriction. Despite the gross excess of circulating serotonin, nearly all is platelet bound and therefore inactive. Very little is free in plasma. Demonstration of a contribution of serotonin to carcinoid attacks requires assay of free plasma serotonin; measurements of whole blood or serum serotonin are of little value. Some, but not all, provoked flushes have been shown to be accompanied by a rise in free plasma serotonin or substance P; an increase in circulating kinins has been more consistently shown. The 5HT2 antagonist ketanserin has been found to inhibit both provoked and spontaneous attacks of flushing, diarrhea, and dyspnea in a proportion of patients with carcinoid syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carcinoid syndrome and serotonin: therapeutic effects of ketanserin. 228 51

Granisetron, a potent and selective 5-hydroxytryptamine receptor (5-HT3) antagonist was reported to be an effective antiemetic agent both in animal studies and in patients given highly emetogenic chemotherapy. A sample of 43 patients with breast cancer was accrued from September to November 1992 in a phase II study to assess the efficacy of granisetron in patients receiving FEC (5-FU, epirubicin, cyclophosphamide). Each patient received 3 mg intravenous granisetron as a single dose just prior to chemotherapy. Oral metoclopromide was prescribed to each patient as a rescue anti-emetic. The emetic episodes and degree of nausea were evaluated on a daily basis. Good control of emesis (0-2 episodes of vomiting) and nausea (mild or no nausea) was in the range 77%-98% and 77%-93% respectively. There was a complete response (no emetic episodes throughout the 6-day period) in 16 patients (37.2%). Onset of emesis tends to occur on day 1 and tend to subside after day 3; 85% of patients had onset of emesis in the first 2 days after chemotherapy. Control of emesis and nausea tends to improve after day 3, which could be the result of the reduced emetogenicity of the combination FEC with time. Altogether, 77% had good control of acute emesis; control of delayed emesis was better with 84% achieving a major response on day 2 after chemotherapy, which improved to more than 90% after day 4. Granisetron was generally tolerated with headache being the most common side-effect followed by constipation and flushing. This study suggests that granisetron is an effective and well-tolerated anti-emetic agent, which deserves randomised trials to elucidate its efficacy further.
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PMID:Control of emesis by intravenous granisetron in breast cancer patients treated with 5-FU, epirubicin and cyclophosphamide. 803 7