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)

Acute hepatic failure is characterized by a sudden catastrophic compromise of hepatic failure that causes clinical signs such as anorexia, depression, vomiting, diarrhea, icterus, and encephalopathy. Injurious hepatotoxins, drugs, infectious agents, or metabolic disturbances can cause acute hepatic failure; however, in many cases, the inciting cause is not determined. Treatment is aimed at controlling complications such as fluid-electrolyte imbalances, hepatic encephalopathy, hypoglycemia, bleeding diathesis, gastric ulcer, sepsis, and endotoxemia, in order to provide time for liver regeneration and recovery.
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PMID:Acute hepatic failure. 387 99

A 68-year-old woman with a history of mild hypertension developed a toxic encephalopathy following myelography with metrizamide. Concomitant with the symptoms of vomiting, headache, muscle twitching, and hallucinations was a sudden and marked increase in arterial pressure. Treatment with parenteral vasodilators caused a partial, but transient lowering of the blood pressure. The mental status abnormalities were resolved by treatment with parenteral lorazempam and, subsequently, the blood pressure returned to the premyelography levels. This report demonstrates that metrizamide can induce a severe, accelerated form of hypertension.
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PMID:Accelerated hypertension associated with the central nervous system toxicity of metrizamide. 394 59

Vomiting, drowsiness, metabolic acidosis, polymorphonuclear leucocytosis, and encephalopathy developed in thirteen infants within hours of ingestion of margosa oil. Liver biopsy of one infant and necropsy examination of ICR strain mice after experimentally induced margosa-oil poisoning demonstrated pronounced fatty infiltration of the liver and proximal renal tubules as well as cerebral oedema. Electron microscopy demonstrated mitochondrial damage. These findings indicate that margosa oil may be involved in the aetiology of Reye's syndrome among Indians in Malaysia.
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PMID:Margosa oil poisoning as a cause of Reye's syndrome. 611 Jan

In a comparative randomized double-blind study, 73 patients underwent myelography using iopamidol (36 patients) or metrizamide (37 patients) as contrast medium. The overall diagnostic adequacy of iopamidol myelography was found to be comparable to that of metrizamide myelography. The incidence of examinations graded as superior (64%) or adequate (36%) with iopamidol was equivalent to that with metrizamide (57% superior, 43% adequate). Adverse reactions after iopamidol myelography were fewer, less severe, and generally of shorter duration than those associated with metrizamide. In the iopamidol group, adverse reactions occurred in nine (25%) patients, all of whom experienced mild or moderate headache, one with nausea, vomiting, and fatigue. In the metrizamide group, adverse reactions occurred in 17 (46%) patients, all of whom experienced mild or moderate headache, six with nausea and vomiting and four with back and leg pain. Of nine individuals who underwent myelography using 300 mg 1/ml metrizamide injected via lateral C1-C2 puncture, three experienced a toxic encephalopathy with confusion, dysphasia, headache, nausea, and vomiting, and a fourth individual suffered severe nausea, vomiting, fever, and irregular pulse. Encephalopathy was not observed in any of the 11 patients in whom myelography was performed via lateral C1-C2 puncture with a similar concentration of iopamidol. No seizures were encountered, and no clinically significant changes in laboratory studies were observed with either contrast medium.
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PMID:Iopamidol and metrizamide for myelography: prospective double-blind clinical trial. 638 81

A 4-year-old girl with juvenile rheumatoid arthritis developed fever, protracted vomiting, disturbance of consciousness and decorticate posture following the administration of salicylate. There were elevated levels of transaminases in serum, hyperammonemia and a fatty liver. However, the fatty droplets were different electronmicroscopically from that of Reye's syndrome. This observation emphasizes the importance of electronmicroscopic observation of the liver in the differential diagnosis between Reye's syndrome and aspirin-induced encephalopathy, because the clinico-pathological findings of intoxication are so similar.
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PMID:Simulated Reye's syndrome and salicylate therapy. 646 45

A 55-year-old man with a subacute onset of slurred speech, ataxia, nystagmus, extrapyramidal rigidity, decreased tendon reflexes, vomiting, bilateral optic atrophy, and clonic jerks died of bronchopneumonia and respiratory failure. Neuropathological examination showed lesions characteristic of subacute necrotizing encephalopathy. Clinicopathological observations of reported cases of Leigh's syndrome in the adult are reviewed.
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PMID:Leigh's syndrome in an adult. 652 Jun 17

Two cases of triglyceride storage in liver, kidney, heart, and skeletal muscle are described in infants who died at the age of 1 1/2 years and 4 d, respectively. In the first patient, a previously normal girl, the clinical symptoms began two months before death with encephalopathy (vomiting, unconsciousness), liver enlargement, hypoglycemia, increase in serum transaminases. These signs disappeared within the following days. Some weeks later she died during the second attack. The 4-d-old boy, the second child of healthy consanguineous parents, showed at the third day of life an impaired sucking, muscular hypotonia, respiratory arrest and bradycardia. An intensive therapy was inefficient. At autopsy gross examination showed only a moderately enlarged yellow liver and an edematous brain in the first case and pale organs in the second one but no cause of death. The microscopial examination of all tissues of both cases showed fat storage within the four organs mentioned above. The common histochemical methods for neutral lipids were positive, the Schultz-reaction for cholesterol and cholesterol esters was negative. The lipid loaden cells did not show birefringence in polarized light. A predominance and strong fat storage of the type I fibres was found in the skeletal muscle. The storage of triglyceride could be confirmed by histochromatography, a thin-layer chromatography of tissue sections. The triglyceride accumulation in liver, heart, kidney, and skeletal muscle is a characteristic feature of systemic carnitine deficiency. The clinical symptoms of the first patient are in agreement with reports of this disease also. A carnitine deficiency in a newborn was not yet described. Family studies revealed a low carnitine concentration in the mother's serum in both cases, while the serum of father and brother resp. sister showed normal carnitine levels.
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PMID:[Metabolic triglyceride storage disorders. A report of 2 cases of systemic carnitine deficiency]. 652 56

An acute episode of encephalopathy after the infusion of 16 g methotrexate is reported in a 12-year-old girl with osteogenic sarcoma. The complication occurred during the 11th treatment course, when severe vomiting and diarrhea were followed by a low urine output with consecutive toxic concentrations of methotrexate in serum and cerebrospinal fluid leading to severe systemic and central nervous system toxicity. The onset of the central nervous system toxicity was acute with slurred speech, paresis of the external rectus eye muscles, ataxia, and hemiparesis, and symptoms resolved completely after 30 hours by treatment with calcium leucovorin and forced diuresis. After management of the cerebral and systemic toxicity, high-dose methotrexate treatment could be reinstituted, and was followed by no further complications. In contrast to the transient cerebral dysfunctions, probably caused by embolization of tumor tissue in the early course of high-dose methotrexate treatment, the acute neurologic syndrome observed in the current case after the prolonged use of methotrexate seemed to be related to direct central nervous system toxicity of the drug.
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PMID:Transient encephalopathy during the late course of treatment with high-dose methotrexate. 658 97

Reye's syndrome is a virus-associated biphasic disease that causes acute encephalopathy in infants and children. Epidemiologic and experimental data support the hypothesis that it is a multifactorial disease of modern civilization. Just as young patients seem to be recovering uneventfully from the first phase of the illness, usually a nonspecific viral-like illness such as a respiratory tract infection or gastroenteritis, the second phase, encephalopathy, starts unexpectedly, with vomiting and sensorial changes. Identifying the syndrome early ;in the second phase and referring the child to a specialized centre with the experience, staff and facilities to manage this phase has improved the numbers and neurologic condition of survivors, though the overall mortality is still about 20%. Therapy is primarily directed at facilitating adequate cerebral perfusion pressure.
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PMID:Reye's syndrome: a clinical review. 678 91

The clinical features and the computed tomographic appearances of the brain in seven children with ornithine carbamoyl transferase deficiency are described. Episodic vomiting and drowsiness, acute encephalopathy, failure to thrive and developmental retardation were common, but focal neurological symptoms and signs were also observed. The CT appearances were non-specific with generalised or focal changes. They were related to the severity, the duration and the age of onset of the hyperammonaemia. Since the CT changes may suggest conditions other than metabolic disease, the emergency investigation of a child with an encephalopathy should include the estimation of plasma ammonium and, if elevated, the appropriate investigations to establish the cause.
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PMID:Neurological features and computed tomography of the brain in children with ornithine carbamoyl transferase deficiency. 684 97


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