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)

Anorexia nervosa (AN) and bulimia nervosa (BN) are potentially fatal eating disorders which primarily affect adolescent females. Differentiating eating disorders from primary gastrointestinal (GI) disease may be difficult. GI disorders are common in eating disorder patients, symptomatic complaints being seen in over half. Moreover, many GI diseases sometimes resemble eating disorders. Inflammatory bowel disease, acid peptic diseases, and intestinal motility disorders such as achalasia may mimic eating disorders. However, it is usually possible to distinguish these by applying the diagnostic criteria for eating disorders and by obtaining common biochemical tests. The primary features of AN are profound weight loss due to self starvation and body image distortion; BN is characterized by binge eating and self purging of ingested food by vomiting or laxative abuse. GI complications in eating disorders are common. Recurrent emesis in BN is associated with dental abnormalities, parotid enlargement, and electrolyte disturbances including metabolic alkalosis. Hyperamylasemia of salivary origin is regularly seen, but may lead do an erroneous diagnosis of pancreatitis. Despite the weight loss often seen in eating disorders, serum albumin, cholesterol, and carotene are usually normal. However, serum levels of trace metals such as zinc and copper often are depressed, and hypophosphatemia can occur during refeeding. Patients with eating disorders frequently have gastric emptying abnormalities, causing bloating, postprandial fullness, and vomiting. This usually improves with refeeding, but sometimes treatment with pro-motility agents such as metoclopromide is necessary. Knowledge of the GI manifestations of eating disorders, and a high index of suspicion for one condition masquerading as the other, are required for the correct diagnosis and management of these patients.
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PMID:Gastrointestinal and nutritional aspects of eating disorders. 840 9

Resinferatoxin (100 micrograms/kg, s.c.), the ultrapotent analogue of capsaicin, when given acutely blocked radiation-(200 rads) and copper sulphate (40 mg% 30 ml, p.o.)-induced emesis in ferrets and substantially decreased loperamide (0.5 mg/kg, s.c.)-induced vomiting, without significantly affecting the von Bezold-Jarisch reflex or gag reflex. It also produced a decrease in core temperature as has been reported for capsaicin. The observation that resinferatoxin reduced or blocked emesis induced by both centrally (loperamide) and peripherally (CuSO4, radiation) acting stimuli suggests a novel anti-emetic action that may provide an insight into clinically useful innovative anti-emetics. The mechanism by which resinferatoxin has its anti-emetic effect is at present unknown, although the combination of results from the present study suggest a central site of action involving modulation of release of neurotransmitter, possibly in the nucleus tractus solitarius.
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PMID:Resinferatoxin, an ultrapotent capsaicin analogue, has anti-emetic properties in the ferret. 841 43

Mitchell et al. (1976, 1977) suggested that pica, eating of nonnutritive substances such as kaolin, is an illness-response behavior in rats. In the present study, we first confirmed their suggestion and then examined the effects of antiemetics on emetic-induced pica in rats. Intraperitoneal injection of apomorphine induced dose-dependent kaolin consumption. Pretreatment with domperidone inhibited apomorphine-induced kaolin intake. Oral administration of copper sulfate and intraperitoneal injection of cisplatin also induced dose-dependent kaolin consumption. Pretreatment with ondansetron inhibited cisplatin-induced kaolin intake. These findings suggest that pica in rats was induced through 1) dopamine D2 receptors in the chemoreceptor trigger zone, and 2) the stomach, partly via 5-HT3 receptors in the visceral afferents in the stomach wall. The present findings support the conclusion that pica in rats is analogous to vomiting in other species and suggest that pica in rats is mediated by the same mechanisms as vomiting in humans. Accordingly, we extended the utility of the animal model to pharmacological research of emesis with pica as an analogue to emesis.
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PMID:Pica in rats is analogous to emesis: an animal model in emesis research. 841 20

Methemoglobinemia among infants is a rare and potentially fatal condition caused by genetic enzyme deficiencies, metabolic acidosis, and exposure to certain drugs and chemicals. The most widely recognized environmental cause of this problem is ingestion of nitrate-containing water. Ingestion of copper causes abdominal discomfort, nausea, diarrhea, and in cases of high-level exposure, vomiting. This report summarizes an investigation by the Division of Health, Wisconsin Department of Health and Social Services of methemoglobinemia associated with ingestion of nitrate- and copper-containing water in an infant during 1992.
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PMID:Methemoglobinemia in an infant--Wisconsin, 1992. 845 Aug 25

Unexplained fractures are characteristic of both osteogenesis imperfecta (OI) and non-accidental injury (NAI) but in most cases the diagnosis is straightforward. However, in a few OI patients an initial diagnosis of NAI is made. Factors contributing to such difficulties include failure to recognise that OI can occur without a family history, without blue sclerae, without osteopenia, without an excess of Wormian bones, or with metaphyseal fractures. In addition we report on 39 patients with an unusual history in that fractures only occurred in the first year of life. Rib fractures, metaphyseal abnormalities and periosteal reactions were common. The initial diagnosis was usually OI if the fractures occurred in hospital, but NAI if they appeared to have been sustained at home. Additional findings such as anaemia, vomiting, hepatomegaly, and apnoeic attacks were often found in these patients. The disorder has some similarities to the syndrome of infantile copper deficiency. Like the latter it is particularly common in preterm infants and in twins. Therefore, we are attempting to examine the incidence of significant hypocupraemia in unselected preterm infants. We suggest that the likely cause of this "temporary brittle bone disease" is a temporary deficiency of an enzyme, perhaps a metalloenzyme, involved in the post-translational processing of collagen.
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PMID:Osteogenesis imperfecta: the distinction from child abuse and the recognition of a variant form. 817 41

A 33 year-old man with undiagnosed neuropathy showing mental retardation and involuntary movements has been nourished for a long period by total parenteral nutrition (TPN) because of frequent vomiting and repeated aspiration pneumonitis. After ten months' TPN, macrocytic anemia and neutropenia developed and iron preparation was administered without hematological improvement. Bone marrow examination revealed normocellular marrow without features of megaloblastosis and dysplasia. In some erythroblasts and immature myeloid cells, vacuoles were observed and mature granulocytes were reduced in the bone marrow. Both serum copper and ceruloplasmin were very low (12 micrograms/dl and 7mg/dl, respectively). Thus, oral administration of copper sulfate resulted in marked increase of reticulocytes and subsequent improvement of anemia and neutropenia within two months. Copper deficiency is a rare condition, but during an unusual nutrition such as TNP, hematological abnormality due to copper deficiency must be noticed to occur.
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PMID:[Anemia and neutropenia due to copper deficiency during long-term total parenteral nutrition]. 849 15

We have shown previously that Suncus murinus, a species of the insectivore, can vomit in response to various emetogenic stimuli. In the present study we investigated whether or not Sorex unguiculatus, which belongs to different subfamily (Soricinae) of insectivore, vomits in response to emetogenic drugs. Subcutaneous injection of veratrine and oral administration of copper sulfate caused emesis in the animal. Histological study showed that bilateral structure of the area postrema was not important for the emetic reflex. Therefore, the capability of emesis may be common to the family of soricidae of the insectivore, and the Sorex unguiculatus is the smallest known mammal which can vomit.
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PMID:Emetic responses of Sorex unguiculatus. 851 99

The potential of dexamethasone (0.5-20 mg/kg i.p.) to antagonize the emesis induced by cisplatin (10 mg/kg i.v.), apomorphine (0.25 mg/kg s.c.), morphine (0.5 mg/kg s.c.) and copper sulphate (100 mg/kg intragastric) was investigated alone and in combination with ondansetron in the ferret. There was a trend for dexamethasone 0.1-5 mg/kg to reduce cisplatin-induced emesis and for 0.05-2.5 mg/kg to delay the onset of apomorphine-induced emesis but doses of dexamethasone up to 20 mg/kg were without effect to modify morphine- or copper sulphate-induced emesis. The combination of dexamethasone 2.5 mg/kg with ondansetron 0.1 mg/kg did not have additive effects to reduce cisplatin-induced emesis but did reduce significantly the total numbers of episodes recorded. Ondansetron 1 mg/kg was without effect to modify apomorphine-, morphine- or copper sulphate-induced emesis but the combination pretreatment of ondansetron 1 mg/kg with dexamethasone 2.5 and 5 mg/kg reduced significantly apomorphine-induced retching. Data are discussed in terms of the antiemetic effectiveness of dexamethasone to antagonize chemotherapy-induced emesis in man.
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PMID:The interaction of dexamethasone with ondansetron on drug-induced emesis in the ferret. 868 1

1. Following our earlier observations that the tachykinin NK1 receptor antagonist CP-99,994 is an effective anti-emetic in ferrets, we have examined the anti-emetic effects of a more potent and novel NK1 receptor antagonist, GR203040, against various emetic stimuli in the ferret, dog and house musk shrew (Suncus murinus). 2. In ferrets, GR203040 (0.1 mg kg-1 s.c. or i.v.) is effective against emesis induced by radiation, cisplatin, cyclophosphamide, copper sulphate, ipecacuanha or morphine. 3. In animals in which emesis had been established with cisplatin, GR203040 (1 mg kg-1 s.c.) was fully effective as an interventional treatment. No further emesis was seen in animals treated with GR203040 whilst saline-treated animals continued to vomit. 4. GR203040 (0.1 mg kg-1 s.c.) retains anti-emetic efficacy in the ferret, even when given as a 6 h pretreatment, indicating that this compound has a long duration of action. The compound is also effective orally at the same dose, when given as a 90 min pretreatment. 5. GR203040 (0.1 mg kg-1 i.v.) is fully effective against ipecacuanha-induced emesis in the dog. 6. GR203040 is effective against motion- and cisplatin-induced emesis in Suncus murinus. These effects were seen at doses an order of magnitude greater than those shown to be effective against cisplatin in the ferret. 7. In conclusion, GR203040 is a novel anti-emetic agent, and the broad spectrum of anti-emetic activity, together with activity observed in three species, suggests that this compound is worthy of clinical investigation.
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PMID:The broad-spectrum anti-emetic activity of the novel non-peptide tachykinin NK1 receptor antagonist GR203040. 871 90

The potent, selective, tachykinin NK1 receptor antagonist, CP-122,721 ([(+)-(2S,3S)-3-(2-methoxy-5-trifluoromethoxybenzyl)amino-2- phenylpiperidine]), at 0.01-1 mg/kg, s.c. reduced retching and vomiting elicited by loperamide, copper sulfate, ipecac syrup and cisplatin in a dose-dependent manner. ID50 values after subcutaneous administration ranged from 0.02 mg/kg (loperamide) to 0.08 mg/kg (ipecac). Oral CP-122,721 reduced cisplatin-induced emesis with an ID50 of approximately 0.08 mg/kg. The less active (2R, 3R)-enantiomer, CP-132.687, did not significantly suppress retching or vomiting induced by any of the emetogens. These data support the hypothesis that CP-122,721 blocks emesis by a specific action at tachykinin NK1 receptors. Its broad spectrum of antiemetic activity suggests a central site of action.
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PMID:Broad spectrum antiemetic effects of CP-122,721, a tachykinin NK1 receptor antagonist, in ferrets. 881 51


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