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)

12 patients with adverse reactions to foods are discussed, including 1 with biopsy-proven ulcerative proctitis. 10 had predominantly gastrointestinal symptoms (diarrhoea, abdominal pain, vomiting) and two had rhinitis and headache. Skin tests (in all but two) and radioallergosorbent tests (RAST) in some patients were negative. All of the patients were challenged in hospital with the offending food, either alone or preceded by a prostaglandin synthetase-inhibiting drug (aspirin, indomethacin or Ibuprofen). In 11 of the 12 patients this premedication prevented both the gastrointestinal and the more remote symptoms. Blood and stool prostaglandin measurements (PGE2 and PGF2 alpha) showed changes which correlated with clinical symptoms and did not occur if one of the inhibiting drugs had been given prior to challenge.
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PMID:Prostaglandin synthetase inhibitors and food intolerance. 11 24

Three patients suffering from Bartter's syndrome were studied before and after 5 days of treatment with the prostaglandin synthetase inhibitors, aspirin and indomethacin. Saralasin was given by intravenous infusion in increasing doses from 0.6 to 42 micrograms/min.kg/BW. During saralasin infusion a blood pressure reduction was observed in all patients. Aspirin treatment did not affect this response and nor did it affect other manifestations of the syndrome. Indomethacin treatment changed the blood pressure response to saralasin in such a way that the blood pressure was increased in one patient and was unchanged in the other. Indomethacin also tended to normalize other features of Bartter's syndrome, such as the hyperreninaemia and angiotensin unresponsiveness, but did not affect the hypokalaemia. The saralsin effect on blood pressure is thus evidently inversely related to the prevailing activity of the renin-angiotensin system in this condition also, and the patients obviously depended on the renin-angiotensin system to maintain their blood pressure. Our findings, together with data in the literature, indicate that angiotensin unresponsiveness of the vascular bed is not a primary feature in Bartter's syndrome. Chloride loss is currently thought to be the basic abnormality and this may link the Bartter's syndrome with other diseased states characterized by chloride loss, such as the syndrome of habitual vomiting and chronic treatment with loop diuretics.
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PMID:Effect of Sar1-ala8-angiotensin II on blood pressure and renin in Bartter's syndrome, before and after treatment with prostaglandin synthetase inhibitors. 11

Thirty-two patients were treated with placebo tablets or indomethacin (25 mg three times daily) in a six-month, double-blind, cross-over trial. During indomethacin therapy, 75 per cent of patients experienced significant pain relief while associated vomiting and diarrhoea were relieved in 44 per cent and 64 per cent of patients respectively. The efficacy of indomethacin was comparable to that of other prostaglandin synthetase inhibitors.
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PMID:Indomethacin in the treatment of primary dysmenorrhoea. 38 65

Serum progesterone, human chorionic gonadotropin, prostaglandin E2, F2 alpha and 13,14-dihydro-15-keto-PGF2 alpha and urinary immunoractive prostaglandins E2 and F2 alpha were measured throughout gestation in a woman who previously had experienced three abortions, an immature birth of a twin and a term single pregnancy. Prostaglandin-mediated symptoms such as uterine sensitivity and contractions, backache, spotting, vomiting and diarrhea were carefully registered and have been correlated with the variations in prostaglandin levels. The effect of therapy with a prostaglandin synthetase inhibitor and a beta-adrenergic drug on prostaglandin levels was also studied. The rise of prostaglandin E2 level observed during implantation is discussed.
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PMID:Successful pregnancy in an abortion-prone woman: prostaglandin and hormone levels during implantation, gestation and lactation. 739 61

A food poisoning case due to the ingestion of 'ogonori', an edible red alga, occurred at Yokohama, Kanagawa Prefecture, Japan, in late October 1993, resulting in two victims, including one death (female). No causative agent present in the ogonori was found from a routine bioassay for marine toxins. From the production of increased amounts of prostaglandins (PGs), mainly PGE2, by the alga on stimulation by cutting or soaking in fresh water, and further increase of PGE2 by addition of arachidonic acid, it appeared that an enzyme, probably fatty acid cyclooxygenase, in the ogonori and the body of the victim, was acting on the highly unsaturated fatty acids in the oil of the ingested seafood and in the blood hemorrhaged from the stomach of the victim. This resulted in the production of over 30 mg of PGE2 and small amounts of other PGs in a comparatively short time. With this dosage the victim suffered from nausea, vomiting, and hypotension, and died of hypotensive shock. PGE2 seems to work more selectively on females. This type of poisoning is very unusual, and differs from the more familiar forms of poisoning occurring after ingestion of marine organisms.
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PMID:Poisoning by the red alga 'ogonori' (Gracilaria verrucosa) on the Nojima Coast, Yokohama, Kanagawa Prefecture, Japan. 772 21