Vomiting prostaglandins

Dronabinol (tetrahydrocannabinol), the active principle from cannabis and synthetic cannabinoids, nabilone and levonantradol are effective in treating nausea and vomiting in cancer chemotherapy. The mode of action is unclear but appears to involve cannabinoid CBi receptors. Cannabinoids have been shown to reduce acetylcholine release in the cortex and hippocampus, and have been suggested to inhibit medullary activity by a cortical action. Inhibition of prostaglandin synthesis and release of endorphins may also be involved in the antiemetic effect. A review of trials of dronabinol, nabilone or levonantradol concluded that while the cannabinoids were superior to placebo or dopamine receptor antagonists in controlling emesis... 

It is an antisecretory drug. It is 5-ami-nosalicylic acid with linked sulfapyridine through azo bond. The drug is poorly absorbed from the intestine and the azo linkage is broken down by the bacterial flora in the distal ileum and colon to release 5-ami-nosalicylic acid (5-ASA) and sulfapyridine. 5-ASA inhibits locally prostaglandin synthesis, decreases mucosal secretion. It is used in rheumatoid arthritis and ulcerative colitis. Side effects include fever, rashes, blood dyscrasias, nausea, vomiting and headache. 

Nausea, vomiting, diarrhea, and abdominal pain (107) occur in about 90% of all patients given prostaglandins... 

Nausea, vomiting, diarrhea, and abdominal pain (107) occur in about 90% of all patients given prostaglandins systemically. The frequency and duration of these adverse effects depend on the mode of application, the dosage, and the molecule used, and are very variable (108). 

Two cases of severe vomiting, dyspepsia, and headache, with falls in body weight and plasma albumin, have been reported in patients on chronic peritoneal dialysis (2). Both occurred a few days after they started to take ramipril (dose not reported) and totally resolved after withdrawal. Both patients subsequently took losartan, which was well tolerated. This led the authors to suggest that the mechanism was mediated by bradykinin and/or prostaglandins, through an interaction with gastrointestinal motility, which may also be affected by peritoneal dialysis. 

Fatalities from normal doses and overdoses of intravenous NAC have not been reported. This is most probably due to the fact that the body produces this compound naturally and can rapidly metabolize it in the liver. Toxicity is usually limited to anaphylactoid reactions and nausea/vomiting. The average time for the onset of adverse effects following commencement of the infusion of NAC was 30 min (range, 5-70 min). In vivo and in vitro tests indicate that NAC is an inhibitor of allergen tachyphylaxis by inhibition of prostaglandin E synthesis. Adverse reactions are anaphylactoid in type and have been attributed to cause histamine release. 

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