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)

Mitomycin was approved for marketing by the Food and Drug Administration in 1974 for use in gastric and pancreatic carcinomas when combined with other chemotherapeutic agents. Since then, mitomycin has been used extensively in combination chemotherapy for a variety of tumors, particularly in the past seven years. However, the contribution of this agent to the various drug regimens has not been adequately defined. Clear evidence of the drug's activity as a single agent has been seen in the intravesical treatment of superficial bladder carcinoma. Common toxicities include anorexia, vomiting, and myelosuppression. Less common, but potentially lethal, toxicities in the form of fibrosing alveolitis and microangiopathic hemolytic anemia with renal failure are being reported with increasing frequency. These potentially severe adverse effects, coupled with the still undefined role of mitomycin in systemic cancer chemotherapy, suggest that selection of this drug for other than investigational use should be made with care.
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PMID:Mitomycin: ten years after approval for marketing. 388 63

Strychnine toxicosis is characterized by inducible tetanic seizures and metaldehyde poisoning by fine fasciculations progressing to generalized tremors and seizures. Intoxication with 1080 causes seizures, random running movements, vomiting, defecation, urination, acidosis and hyperglycemia. Intoxication with rodenticides causing coagulopathy is characterized by hemorrhage into body cavities but not necessarily external hemorrhage. Anticholinesterase insecticides cause salivation, urination and defecation, while chlorinated hydrocarbon insecticides cause CNS disturbances. Ethylene glycol intoxication results in ataxia, depression, coma, vomiting and tachypnea, followed by acute renal failure. Urea poisoning causes bloat and CNS signs in cattle. Monensin intoxication in horses lasts several days and causes stiffness, colic, uneasiness and recumbency. Salt poisoning results in depression, seizures and hypernatremia. Lead poisoning is associated with central and peripheral nervous system signs, as well as increased numbers of nucleated RBC and basophilic stippling of RBC. Arsenic poisoning results in GI pain, diarrhea, weakness and death. Copper toxicosis in sheep is manifested by hemolytic anemia, hemoglobinemia and hemoglobinuria. Plants that may intoxicate domestic animals include sorghum, greasewood, halogeton, water hemlock, Japanese yew, larkspur, lupine, milk-weed, philodendron, oleander, castor bean and precatory bean.
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PMID:Practical toxicologic diagnosis. 649 3

The case of a 32-year-old primigravida, 32 weeks gestation, with nausea, vomiting, thrombocytopenia, and abnormal liver function tests is presented. A diagnosis of severe preeclampsia was made and the patient underwent emergency cesarean section. Improvement of clinical symptoms and laboratory studies followed over the succeeding days. These less common manifestations of preeclampsia indicate severe disease necessitating aggressive management, even in the setting of a normal blood pressure. Thrombocytopenia, microangiopathic hemolytic anemia, or abnormal liver functions in a patient presenting in the latter half of pregnancy may be manifestations of severe preeclampsia.
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PMID:Preeclampsia. 671 36

IMPY was given to 25 patients with advanced cancer on a twice weekly schedule in escalating doses from 165 to 3000 mg/m2. Nausea, vomiting, fatigue, generalized weakness, and decreases in performance status were dose-limiting. In one patient treated at a dose of 3000 mg/m2 for three doses, hemolytic anemia resulted, with a 6-g/dl decrease in hemoglobin. No tumor regression occurred. A reasonable starting dose for phase II studies is 1200 mg/m2 twice weekly for 3 weeks, with planned rapid escalation to 1800 mg/m2 in patients tolerating the lower dose level.
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PMID:Phase I evaluation of IMPY in a twice weekly schedule. 723 64

To evaluate the toxic effect of ethanol on erythropoiesis in alcoholic ketoacidosis (AK), 6 male patients were studied in the acute and remittent phase of AK. Episodes of metabolic acidosis in nondiabetic chronic alcoholics were associated with protracted vomiting and prolonged intestinal symptoms. AK was associated with elevated beta-hydroxybutyrate, acetoacetate and lactate/pyruvate plasma levels. Analysis of plasma lipids showed raised HDL cholesterol, fatty acids and phospholipids resulting in a concomitant disorder of lipid metabolism in red cell ghosts. A red cell metabolic disorder with reduced ATP and glutathione levels was also observed in patients suffering from mild hemolytic anemia. On admission, miscellaneous toxic effects on erythropoiesis were detected when bone marrow was aspirated. This study lends further support to the hypothesis that there is a linkage of different factors producing serious but transient hematologic and oncologic implications of ethanol in patients with AK.
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PMID:[Disorders of erythropoiesis in alcoholic ketoacidosis in patients with chronic liver diseases]. 745 61

A 78-year-old woman was admitted to our hospital because of disorientation and fever on January 21, 1992. Two days before admission she experienced vomiting, anorexia and general malaise. Laboratory examinations on admission disclosed a hemoglobin level of 11.1 g/dl and a platelet count of 8,000/microliters. The peripheral blood smear revealed anisocytosis with numerous schistocytes and poikilocytes. Polychromatophilic and nucleated red blood cells were also seen, and the reticulocyte count was 38/1000. Her serum lactate dehydrogenase (LDH) value was 2,977 WU and the total serum bilirubin level was 3.5 mg/dl with 2.7 mg/dl indirect reacting fraction. Serum creatinine was 4.7 mg/dl. Her consciousness became semicomatose after a systemic seizure which lasted approximately 15 seconds and her hemoglobin level decreased to 8.5 g/dl on hospital day 2. Therefore, we diagnosed her as having thrombotic thrombocytopenic purpura (TTP) because of the presence of all 5 features, that is, thrombocytopenia, microangiopathic hemolytic anemia, fluctuating neurologic abnormalities, renal dysfunction and fever. A plasmapheresis with fresh frozen plasma (FFP) replacement was begun on that day. She was also treated with anti-platelet agents, 80 mg/day aspirin, and 300 mg/day dipyridamole. Moreover, packed red blood cells (PRC) were infused. While also receiving diphenylhydantoin and phenobarbital to prevent convulsions, status epilepticus developed on day 3. Because of inhibited spontaneous respiration which was an adverse effect derived from diazepam and sodium thiamylal administered intravenously to treat the status epilepticus, an artificial respiration was initiated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An elderly case of thrombotic thrombocytopenic purpura]. 848 87

A dysentery outbreak in the Central African Republic village of Zemio was diagnosed as "Shigella flexneri" by the Pasteur Institute in Bangui (IPB) in February 1996; 2 months later there was an outbreak of hemorrhagic colitis. 108 patients presented with bloody diarrhea; cramping abdominal pain, fever, nausea, and vomiting were uncommon. The illness lasted between 5 days and 3 weeks (average, 8 days). Antibiotics were ineffective. Four patients died and several developed hemolytic-uremic syndrome. Stool cultures done at IPB tested negative. PCR was used to detect enterohemorrhagic Shiga-like toxin (SLT) 1 and 2, the invasivity gene ipaH, and the attaching and effacing gene eaeA. DNA fragments of 130 and 494 nucleotides corresponding to amplified SLT1 and eaeA were found in 80% of the specimens tested. No amplification was obtained for SLT2 or for ipaH in specimens collected during the second epidemic. These results suggest the presence of enterohemorrhagic Escherichia coli and the absence of Shigella. The number of reported cases of acute bloody diarrhea in infants and adults in Bangui has increased since 1996. E. coli O157:H7 was isolated from two fatal adult cases. Smoked zebu meat was suspected in several hospital cases (bloody diarrhea, hemolytic anemia, and renal insufficiency) in which non-fermenting sorbitol E. coli O157:H7 was not isolated. In two cases of acute diarrhea, other serotypes of E. coli were indicated by retrospective PCR on stools which were positive for SLT1 and for eaeA and negative for invasivity. A study was conducted in Bangui on 290 cases (33 with bloody diarrhea) and 140 controls. Patients were not paired because of civil unrest in the city. The questionnaire included demographic and socioeconomic characteristics, environmental factors, and habitual food consumption. The major contributing factor was consumption of locally made meat pies (kanda), which were made with smoked zebu meat. Kanda is stored at ambient temperature, often for days, before it is sold in markets or along roads. Before 1996, E. coli was not reported as a cause of bloody diarrhea in the Central African Republic.
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PMID:Enterohaemorrhagic Escherichia coli in Central African Republic. 918 91

A 29-year-old woman with a triplet pregnancy received emergency caesarean section in the 33rd week of pregnancy. She lost 2 babies, one of whom was a fetal death and the other a neonatal death. Three weeks before delivery, she was admitted to hospital suffering from vomiting, diarrhea and polyuria. There were no laboratory abnormalities such as a slightly elevated levels of liver enzymes, nor any clinical symptoms of preeclampsia. At the end of the operation, disseminated intravascular coagulation (DIC) occurred and HELLP syndrome was diagnosed. However, the hemoglobin level was in the normal range at this point. On the 2nd postoperative day, hemolytic anemia developed in spite of the resolution of other problems. We suggested that the hemolysis, which may have been caused by a latent hemoconcentration and a membrane disorder of the red cells, was an osmotic hemolysis. This case was unique for the following reasons; 1) a lack of symptoms of hypertension, proteinuria and edema, 2) complications due to diabetes insipidus, 3) postpartum severe hemolysis following latent hemoconcentration, and 4) slow progress of the condition after onset. Early detection of HELLP syndrome is difficult. It should be considered in the management of patients with unrecognizable hemoconcentration and nonspecific complications.
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PMID:[HELLP syndrome in triplet pregnancy complicated by DIC and transient diabetes insipidus]. 951 34

Thirteen-week oral repeated dose toxicity of ecabapide, a gastroprokinetic drug, was investigated in dogs at dosage levels of 50, 175 or 600 mg/kg, and in rats at dosage levels of 25, 100, 400 or 1600 mg/kg. In dogs, vomiting, aqueous salivation, body weight gain inhibition, and hemolytic anemia, together with an increase in Heinz body formation, were observed at 175 and/or 600 mg/kg. Histological examination revealed enhanced hemosiderin deposition in the liver and spleen, retention of erythrocytes in the splenic sinus and enhanced erythropoiesis in bone marrow at 175 and/or 600 mg/kg. In the rat study, although increases in serum total protein, albumin and calcium, as well as increased liver and kidney weights, were observed at 400 and/or 1600 mg/kg, no obvious morphological changes were seen. The hemolytic anemia and an increased Heinz body formation were not observed in rats, indicating a species difference. On the basis of these results, the non-toxic dose of ecabapide was considered to be 50 mg/kg in dogs and 100 mg/kg in rats.
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PMID:Thirteen-week repeated oral dose toxicity study of ecabapide, a gastroprokinetic drug, in dogs and rats. 976 Apr 13

Many of the adverse events induced by rifampin have been considered allergic in origin. The flu-like syndrome and other hypersensitivity reactions seem to be caused by immune complexes, although their pathogenetic mechanisms are not fully elucidated. Many cases have been reported of the flu-like syndrome, thrombocytopenia, hemolytic anemia, and renal failure caused by rifampin. In almost all of the patients in whom they were sought, nonreaginic antirifampin antibodies were detected. On the other hand, anaphylactic reactions seem to be IgE-mediated. We have analyzed the 18 reported cases of anaphylactic reactions severe enough to cause marked hypotension. The interval between the onset of treatment and the anaphylactic reaction was highly variable. Most patients presented with prodromes, mainly rash, before the development of anaphylactic symptoms, and, in most cases, the reaction occurred after reexposure to rifampin. Clinical findings include a variety of symptoms, such as fever, exanthem, dyspnea, abdominal pain, and vomiting. Seven of the 9 patients in whom HIV status was known were seropositive, including the only 2 patients who died. We believe that, in case of a non-life-threatening adverse reaction caused by immune complexes, rifampin could be readministered, if necessary, at a more frequent and reduced dose, perhaps with the addition of corticosteroids. In case of anaphylactic reactions the drug should be avoided, although desensitization procedures may be useful. Certain laboratory findings may serve as a clue to predict anaphylactic reactions in patients who have experienced minor adverse events to rifampin. However, the diagnostic value of such findings is not well established and, therefore, patients with previous adverse reactions should be carefully monitored if reexposure to rifampin is essential.
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PMID:Hypersensitivity reactions to rifampin. Pathogenetic mechanisms, clinical manifestations, management strategies, and review of the anaphylactic-like reactions. 1057 18


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