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MeSH Review


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Disease relevance of Vomiting

  • Repetitive oral activated charcoal and control of emesis in severe theophylline toxicity [1].
  • Using a metoclopramide regimen of 2 mg/kg body weight intravenously every 2 hours for four doses, we found that serum levels greater than 850 ng/mL immediately before the third dose were associated with complete control of emesis (less than three episodes) in 78% of patients and partial control (three to five episodes) in 18% [2].
  • Although, clinical hearing loss, neuropathy, emesis, and myelosuppression were equivalent in the two treatment arms, DDTC-treated patients had more nephrotoxicity as determined by changes in serum creatinine concentration [3].
  • The etiologies were diverse and included postoperative status, thiazide diuretics, polydipsia, infection, acute renal failure, chronic alcoholism with emesis, and beer potomania [4].
  • The initially detected side effects, mainly nausea and emesis, appear at least partially overcome by the 'second generation' PDE4 inhibitors, some of which like roflumilast and cilomilast are in the later stages of clinical development for treatment of chronic obstructive pulmonary disease [5].

Psychiatry related information on Vomiting


High impact information on Vomiting


Chemical compound and disease context of Vomiting

  • Among the 76 patients who satisfactorily completed both parts of the study, complete or nearly complete control of emesis (i.e., no episodes of emesis occurred, or only one or two) was achieved in 57 of 76 treatments (75 percent) with ondansetron and in 32 of 76 treatments (42 percent) with metoclopramide (P less than 0.001) [13].
  • Patients given metoclopramide had significantly fewer episodes of emesis than patients given placebo (medians, 1.0 vs. 10.5; P = 0.001) or prochlorperazine (medians, 1.5 vs. 12.0; P = 0.005) [14].
  • Patients receiving megestrol acetate reported significantly less nausea (13% vs. 38%; P = .001) and emesis (8% vs. 25%, P = .009) [15].
  • Activation of CB1r by the agonists (delta)(9)-tetrahydrocannabinol, WIN 55,212-2, and methanandamide inhibited emesis and their action was reversed by a selective CB1r antagonist, which alone had no effect, but potentiated vomiting in response to an emetic stimulus [16].
  • However, the PDE4 inhibitors cilomilast and roflumilast have recently shown efficacy in asthma and COPD, with a reduced propensity to cause nausea and emesis [17].
  • SEA-induced emesis is downregulated by the CB system through decreasing 5-HT release in intestine [18].

Biological context of Vomiting


Anatomical context of Vomiting

  • Continuous i.v. infusion rates resulting in serum phenylacetate concentrations exceeding Km often resulted in rapid drug accumulation and dose-limiting toxicity, which consisted of reversible central nervous system depression, preceded by emesis [24].
  • Since no correlation was observed between the behaviour of these mutants with regard to toxin stability, emesis and T cell proliferation we conclude that SEC1-induced emesis and T cell proliferation are dependent on separate regions of the molecule [25].
  • The biological effects of substance P in the CNS, namely regulation of affective behavior and emesis in the brain and nociception in the spinal cord, are mediated by its binding to the NK1 receptor [26].
  • Intracerebroventricular injection of noradrenaline produced dose-dependent and shortlasting emesis, which was abolished after ablation of the area postrema [27].
  • Dopexamine and dopamine produced a similar incidence of panting and repetitive licking at 3 X 10(-8)mol kg-1 min-1 and emesis at 10(-7)mol kg-1 min-1, due to stimulation of dopamine receptors in the chemoreceptor trigger zone [28].

Gene context of Vomiting

  • The threshold dose for PYY-induced emesis in the dog is less than 120 pmol/kg [29].
  • Emesis was sometimes seen following large IV bolus doses of neuropeptide Y (NPY), but none was seen following IV injection of pancreatic polypeptide (PP) [29].
  • The therapeutic ratio for PDE4 inhibitors is thought to be determined by selectivity on receptor subtypes for relative effects on PDE4B (anti-inflammatory) and PDE4D (emesis) [30].
  • In 12 of the 14 subjects plasma AVP levels increased in association with symptoms of epigastric pressure and discomfort before the onset of overt nausea or emesis [31].
  • Two subunits, the 5-HT3A and 5-HT3B are expressed in anatomical structures known to be involved in the mechanism of acute cytostatic drug induced emesis [32].

Analytical, diagnostic and therapeutic context of Vomiting

  • CONCLUSIONS: The neurokinin-1-receptor antagonist L-754,030 prevents delayed emesis after treatment with cisplatin [12].
  • METHODS: In a multicenter, double-blind, placebo-controlled trial involving 159 patients who had not previously received cisplatin, we evaluated the prevention of acute emesis (occurring within 24 hours) and delayed emesis (on days 2 to 5) after a single dose of cisplatin therapy (70 mg or more per square meter of body-surface area) [12].
  • Recent clinical trials have confirmed the efficacy of NK1 receptor antagonists to alleviate depression and emesis but, surprisingly, not pain [33].
  • Using a sensitive and specific high-pressure liquid chromatographic (HPLC) assay, we measured serum levels of metoclopramide in 18 cancer patients receiving high-dose intravenous (IV) therapy to prevent cisplatin-induced emesis [34].
  • In human volunteers, studies to assess the adverse effects of the carbamate anticholinesterase physostigmine showed that the intramuscular dose observed to induce emesis in 50% of subjects tested (ED50) was 28.1 (23.5-120.7) micrograms/kg [35].


  1. Repetitive oral activated charcoal and control of emesis in severe theophylline toxicity. Amitai, Y., Yeung, A.C., Moye, J., Lovejoy, F.H. Ann. Intern. Med. (1986) [Pubmed]
  2. Optimizing metoclopramide control of cisplatin-induced emesis. Meyer, B.R., Lewin, M., Drayer, D.E., Pasmantier, M., Lonski, L., Reidenberg, M.M. Ann. Intern. Med. (1984) [Pubmed]
  3. Randomized placebo-controlled multicenter evaluation of diethyldithiocarbamate for chemoprotection against cisplatin-induced toxicities. Gandara, D.R., Nahhas, W.A., Adelson, M.D., Lichtman, S.M., Podczaski, E.S., Yanovich, S., Homesley, H.D., Braly, P., Ritch, P.S., Weisberg, S.R. J. Clin. Oncol. (1995) [Pubmed]
  4. Hyponatremic encephalopathy: is central pontine myelinolysis a component? Tien, R., Arieff, A.I., Kucharczyk, W., Wasik, A., Kucharczyk, J. Am. J. Med. (1992) [Pubmed]
  5. PDE4 inhibitors as new anti-inflammatory drugs: effects on cell trafficking and cell adhesion molecules expression. Sanz, M.J., Cortijo, J., Morcillo, E.J. Pharmacol. Ther. (2005) [Pubmed]
  6. Responses to apomorphine, amphetamine, and neuroleptics in schizophrenic subjects. Angrist, B., Rotrosen, J., Gershon, S. Psychopharmacology (Berl.) (1980) [Pubmed]
  7. Bromocriptine in Parkinsonism: long-term treatment, dose response, and comparison with levodopa. Parkes, J.D., Debono, A.G., Marsden, C.D. J. Neurol. Neurosurg. Psychiatr. (1976) [Pubmed]
  8. Chlorpromazine with and without lorazepam as antiemetic therapy in children receiving uniform chemotherapy. Relling, M.V., Mulhern, R.K., Fairclough, D., Baker, D., Pui, C.H. J. Pediatr. (1993) [Pubmed]
  9. Differential action of domperidone to modify emesis and behaviour induced by apomorphine in the ferret. Lau, A.H., Ngan, M.P., Rudd, J.A., Yew, D.T. Eur. J. Pharmacol. (2005) [Pubmed]
  10. Symptomatic low intracranial pressure in shunted hydrocephalus. Foltz, E.L., Blanks, J.P. J. Neurosurg. (1988) [Pubmed]
  11. Prevention of cisplatin-induced emesis by a neurokinin-1-receptor antagonist. Roila, F., Ballatori, E., Del Favero, A. N. Engl. J. Med. (1999) [Pubmed]
  12. Reduction of cisplatin-induced emesis by a selective neurokinin-1-receptor antagonist. L-754,030 Antiemetic Trials Group. Navari, R.M., Reinhardt, R.R., Gralla, R.J., Kris, M.G., Hesketh, P.J., Khojasteh, A., Kindler, H., Grote, T.H., Pendergrass, K., Grunberg, S.M., Carides, A.D., Gertz, B.J. N. Engl. J. Med. (1999) [Pubmed]
  13. Comparison of the 5-hydroxytryptamine3 (serotonin) antagonist ondansetron (GR 38032F) with high-dose metoclopramide in the control of cisplatin-induced emesis. Marty, M., Pouillart, P., Scholl, S., Droz, J.P., Azab, M., Brion, N., Pujade-Lauraine, E., Paule, B., Paes, D., Bons, J. N. Engl. J. Med. (1990) [Pubmed]
  14. Antiemetic efficacy of high-dose metoclopramide: randomized trials with placebo and prochlorperazine in patients with chemotherapy-induced nausea and vomiting. Gralla, R.J., Itri, L.M., Pisko, S.E., Squillante, A.E., Kelsen, D.P., Braun, D.W., Bordin, L.A., Braun, T.J., Young, C.W. N. Engl. J. Med. (1981) [Pubmed]
  15. Controlled trial of megestrol acetate for the treatment of cancer anorexia and cachexia. Loprinzi, C.L., Ellison, N.M., Schaid, D.J., Krook, J.E., Athmann, L.M., Dose, A.M., Mailliard, J.A., Johnson, P.S., Ebbert, L.P., Geeraerts, L.H. J. Natl. Cancer Inst. (1990) [Pubmed]
  16. Cannabinoids inhibit emesis through CB1 receptors in the brainstem of the ferret. Van Sickle, M.D., Oland, L.D., Ho, W., Hillard, C.J., Mackie, K., Davison, J.S., Sharkey, K.A. Gastroenterology (2001) [Pubmed]
  17. PDE4 inhibition: a novel approach for the treatment of inflammatory bowel disease. Banner, K.H., Trevethick, M.A. Trends Pharmacol. Sci. (2004) [Pubmed]
  18. Staphylococcal enterotoxin induces emesis through increasing serotonin release in intestine and it is downregulated by cannabinoid receptor 1. Hu, D.L., Zhu, G., Mori, F., Omoe, K., Okada, M., Wakabayashi, K., Kaneko, S., Shinagawa, K., Nakane, A. Cell. Microbiol. (2007) [Pubmed]
  19. Amifostine pretreatment for protection against cyclophosphamide-induced and cisplatin-induced toxicities: results of a randomized control trial in patients with advanced ovarian cancer. Kemp, G., Rose, P., Lurain, J., Berman, M., Manetta, A., Roullet, B., Homesley, H., Belpomme, D., Glick, J. J. Clin. Oncol. (1996) [Pubmed]
  20. Patient-tailored antiemetic treatment with 5-hydroxytryptamine type 3 receptor antagonists according to cytochrome P-450 2D6 genotypes. Kaiser, R., Sezer, O., Papies, A., Bauer, S., Schelenz, C., Tremblay, P.B., Possinger, K., Roots, I., Brockmöller, J. J. Clin. Oncol. (2002) [Pubmed]
  21. Effects of cholinoceptor and 5-hydroxytryptamine3 receptor antagonism on erythromycin-induced canine intestinal motility disruption and emesis. Qin, X.Y., Pilot, M.A., Thompson, H., Scott, M. Br. J. Pharmacol. (1993) [Pubmed]
  22. The action of dazopride to enhance gastric emptying and block emesis. Costall, B., Domeney, A.M., Gunning, S.J., Kelly, M.E., Naylor, R.J., Nohria, V., Owera-Atepo, J.B., Simpson, K.M., Tan, C.C., Tattersall, D. Neuropharmacology (1987) [Pubmed]
  23. 5-hydroxytryptamine3 receptors in the human brain: autoradiographic visualization using [3H]ICS 205-930. Waeber, C., Hoyer, D., Palacios, J.M. Neuroscience (1989) [Pubmed]
  24. A phase I and pharmacokinetic study of intravenous phenylacetate in patients with cancer. Thibault, A., Cooper, M.R., Figg, W.D., Venzon, D.J., Sartor, A.O., Tompkins, A.C., Weinberger, M.S., Headlee, D.J., McCall, N.A., Samid, D. Cancer Res. (1994) [Pubmed]
  25. Investigation of the role of the disulphide bond in the activity and structure of staphylococcal enterotoxin C1. Hovde, C.J., Marr, J.C., Hoffmann, M.L., Hackett, S.P., Chi, Y.I., Crum, K.K., Stevens, D.L., Stauffacher, C.V., Bohach, G.A. Mol. Microbiol. (1994) [Pubmed]
  26. Neurobiology of substance P and the NK1 receptor. Mantyh, P.W. The Journal of clinical psychiatry. (2002) [Pubmed]
  27. Noradrenaline-induced emesis. Alpha-2 adrenoceptor mediation in the area postrema. Beleslin, D.B., Strbac, M. Neuropharmacology (1987) [Pubmed]
  28. The effects of dopexamine on the cardiovascular system of the dog. Brown, R.A., Farmer, J.B., Hall, J.C., Humphries, R.G., O'Connor, S.E., Smith, G.W. Br. J. Pharmacol. (1985) [Pubmed]
  29. Identification and characterization of the emetic effects of peptide YY. Harding, R.K., McDonald, T.J. Peptides (1989) [Pubmed]
  30. Phosphodiesterase-4 inhibitors for asthma and chronic obstructive pulmonary disease. Lipworth, B.J. Lancet (2005) [Pubmed]
  31. Neurohypophyseal secretion in response to cholecystokinin but not meal-induced gastric distention in humans. Miaskiewicz, S.L., Stricker, E.M., Verbalis, J.G. J. Clin. Endocrinol. Metab. (1989) [Pubmed]
  32. Investigation of the association between 5-HT3A receptor gene polymorphisms and efficiency of antiemetic treatment with 5-HT3 receptor antagonists. Kaiser, R., Tremblay, P.B., Sezer, O., Possinger, K., Roots, I., Brockmöller, J. Pharmacogenetics (2004) [Pubmed]
  33. Discovery of the antidepressant and anti-emetic efficacy of substance P receptor (NK1) antagonists. Rupniak, N.M., Kramer, M.S. Trends Pharmacol. Sci. (1999) [Pubmed]
  34. Clinical pharmacokinetics of high-dose metoclopramide in cancer patients receiving cisplatin therapy. McDermed, J.E., Cohen, J.L., Joseph, C., Strum, S.B. J. Clin. Oncol. (1985) [Pubmed]
  35. A model for carbamate and organophosphate-induced emesis in humans. D'Mello, G.D., Sidell, F.R. Neuroscience and biobehavioral reviews. (1991) [Pubmed]
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