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)

Ifosfamide is an oxazaphosphorine alkylating agent with a broad spectrum of antineoplastic activity. It is a prodrug metabolised in the liver by cytochrome P450 mixed-function oxidase enzymes to isofosforamide mustard, the active alkylating compound. Mesna, a uroprotective thiol agent, is routinely administered concomitantly with ifosfamide, and has almost eliminated ifosfamide-induced haemorrhagic cystitis and has reduced nephron toxicity. Therapeutic studies, mostly noncomparative in nature, have demonstrated the efficacy of ifosfamide/mesna alone, or more commonly as a component of combination regimens, in a variety of cancers. In patients with relapsed or refractory disseminated nonseminomatous testicular cancer, a salvage regimen of ifosfamide/mesna, cisplatin and either etoposide or vinblastine produced complete response in approximately one-quarter of patients. As a component of both induction and salvage chemotherapeutic regimens, ifosfamide/mesna has produced favourable response rates in small cell lung cancer, paediatric solid tumours, non-Hodgkin's and Hodgkin's lymphoma, and ovarian cancer. Induction therapy with ifosfamide/mesna-containing chemotherapeutic regimens has been encouraging in non-small cell lung cancer, adult soft-tissue sarcomas, and as neoadjuvant therapy in advanced cervical cancer. As salvage therapy, ifosfamide/mesna-containing combinations have a palliative role in advanced breast cancer and advanced cervical cancer. Ifosfamide/mesna can elicit responses in patients refractory to numerous other antineoplastic drugs, including cyclophosphamide. With administration of concomitant mesna to protect against ifosfamide-induced urotoxicity, the principal dose-limiting toxicity of ifosfamide is myelosuppression; leucopenia is generally more severe than thrombocytopenia. Reversible CNS adverse effects ranging from mild somnolence and confusion to severe encephalopathy and coma can occur in approximately 10 to 20% of patients after intravenous infusion, and the incidence of neurotoxicity may be increased to 50% after oral administration because of differences in the preferential route of metabolism between the 2 routes of administration. Other adverse effects of ifosfamide include nephrotoxicity, alopecia, and nausea/vomiting. In general, intravenously administered mesna is associated with a low incidence of adverse effects; however, gastrointestinal disturbances are common following oral administration. Thus, ifosfamide/mesna is an important and worthwhile addition to the currently available range of chemotherapeutic agents. It has a broad spectrum of antineoplastic activity and causes less marked myelosuppression than many other cytotoxic agents. At present, the role of ifosfamide/mesna in refractory germ cell testicular cancer is clearly defined; however, its overall place in the treatment of other forms of cancer awaits delineation in future well-controlled comparative studies.
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PMID:Ifosfamide/mesna. A review of its antineoplastic activity, pharmacokinetic properties and therapeutic efficacy in cancer. 172 Mar 82

From 65 reported cases of medium chain acyl-CoA dehydrogenase deficiency, we found an average presenting age of 13.5 months and a mean age at death of 18.5 months. One quarter of patients died of a Reye-like syndrome and/or sudden infant death. In half the cases there had been at least one sibling death. Asymptomatic cases were not uncommon (12% of cases). The crises were generally induced by a prolonged fast and after a viral prodromal phase in three quarters of cases. The crises consisted of somnolence progressing to lethargy which could lead to coma. Vomiting was frequent (60% of cases). Seizures, which were found in 29% of cases, represented a bad prognosis. The physical examinations revealed frequently a variable and regressive anicteric hepatomegaly. Blood and urine analysis revealed in most instances hypoglycaemia (96% of cases) with hypoketonuria and sometimes metabolic acidosis. Hepatic and muscular cytolytic enzymes were frequently raised, as were plasma ammonia, urea, and uric acid. Plasma total or free carnitine concentrations, especially non-fasting, were diminished in most cases. Plasma saturated medium chain fatty acids and particularly unsaturated cis-4-decenoate were on the other hand raised during the crises or during fasting. Urinary organic acid analysis revealed a characteristic profile of medium chain aciduria: C6-C10 dicarboxylic acids, hydroxy acids, glycine conjugates, and carnitine conjugates. Oral loading tests with carnitine or phenylpropionate allow a precise diagnosis. The diagnosis is confirmed by specific assays in various tissues. Avoidance of prolonged fasting seems to be the mainstay of treatment.
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PMID:Medium chain acyl-CoA dehydrogenase deficiency. 173 32

Over 10% of emergency room patients are diagnosed as having alcohol (6.0%) or drug intoxication. In the present study 196 alcohol intoxications treated in a hospital were studied retrospectively; 49.2% of the patients had abnormal acid-base values, alcoholics more often than non-alcoholics (p = 0.04). Mean blood ethanol concentration (BAC) was 310 mg/dl (SD 120); alcoholics had higher concentrations of alcohol. BAC was the higher the lower the serum pH was (p less than 0.002, r = -0.45). The deeper the coma the lower the serum pH (p less than 0.05) and the higher the BAC (p less than 0.0001). Respiratory acidosis (31.7%) was an important finding in those intoxicated. Metabolic acidosis (7.9%) could be explained by the presence metabolites of ethanol in the serum and by decreased extra-cellular fluid volume. Metabolic alkalosis related to vomiting and an extra-cellular fluid volume decrease was found in 7.9% of the patients. Respiratory alkalosis was a rare finding (1.6%). Hypokalemia (22.5%) and hypernatremia (15.3%) were the most important electrolyte changes. Chronic alcoholics had lower serum potassium than had non-alcoholics; 3.6% (n = 7) of the patients had to be intubated. Acid-base disturbances were frequent in adults with alcohol intoxication. Serum pH correlated well with the state of consciousness and the BAC.
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PMID:Acid-base balance in alcohol users seen in an emergency room. 174 42

Serum NEFA profiles in Reye's syndrome are reportedly unique with a disproportionate percent made up of polyunsaturated fatty acids some of which are not ordinarily found in the serum. This pattern is also reflected in the serum triglyceride composition as well. As the liver is probably the sole source of the serum triglyceride in Rye's syndrome because patients are vomiting or in coma, the fatty acid acid composition of the liver triglyceride was examined for insight regarding the lipid abnormalities in this disease. Palmitic acid (16:0) and the sum of all the saturated fatty acids in the liver triglycerides were significantly decreased whereas the sum of the monoenoic fatty acids and the products of delta 9 desaturase activity were increased in Reye's samples. When these data were compared to the fatty acid composition of the serum triglyceride from a separate cohort of Reye's and control subjects, certain inferences regarding hepatic delta 9, delta 6, delta 5, and delta 4 desaturase activities and the elongases can be drawn from the liver and serum triglyceride fatty acid profiles which are unique. Collectively, these data reflect considerable intrahepatic fatty acid desaturation and elongation activity and/or acyl transfer from lipid to lipid of various polyunsaturated fatty acids in Reye's syndrome.
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PMID:Fatty acid composition of hepatic triglycerides in Reye's syndrome: implications for hepatic desaturase abnormalities. 181 59

Headaches, vomiting and altered sensorium can be seen in patients with migraines as well as in patients with shunt malfunctions. This is a report of 10 patients with hydrocephalus and CSF shunts who presented with headache, vomiting, varying degrees of impairment of consciousness, and coma. Various diagnostic considerations were made: shunt malfunction, slit ventricle syndrome and low pressure (overshunting). Repeated operative procedures were performed in all. 7 of 10 patients had a family history of migraines when the diagnosis of migraine was entertained, 8 patients improved on propranolol therapy, 1 failed with this therapy but responded to verapamil. In the remaining 2 patients, after a transient response to propranolol, compartmentalized hydrocephalus became obvious and improvement followed with shunt procedures. It is concluded that in those patients with hydrocephalus and small ventricles on neuroimaging and a family history of migraines, and in the face of documented adequate shunt function, the diagnosis of migraines be entertained before further operative interventions.
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PMID:Clinical course and diagnosis of migraine headaches in hydrocephalic children. 184 Aug 19

A 47 year-old woman with juvenile myoclonic epilepsy received anticonvulsant therapy with valproate, 200 mg 4 times a day. Severe abdominal pain and vomiting developed 3 days after initiation of therapy, and she became comatose requiring artificial ventilation. Increased urinary output of delta-amino-levulinic acid (48 uM/24 hr, 8 times normal) and porphobilinogen (9 uM/24 hr, twice normal) were demonstrated. Complete recovery took place 5 days after discontinuation of valproate.
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PMID:[Porphyria induced by valproic acid: clinical case]. 184 75

A case is reported of ruptured dissecting aneurysm of the intracranial vertebral artery (VA) operated on with VA trapping and bilateral posterior inferior cerebellar artery (PICA) side-to-side anastomosis. A 42-year-old male suddenly developed severe headache and vomiting. On admission, 3 hours later, he was in a state of moderate confusion (Japan Coma Scale 3) and had neck stiffness. Computed tomography (CT) revealed diffuse subarachnoid hemorrhage, especially thick in the posterior fossa with right side dominance. Right vertebral angiography disclosed a fusiform dilatation with proximal narrowing of the right VA which originated just proximal to the VA-PICA junction. Lateral suboccipital craniectomy was undertaken with the patient in a left park bench position. Right VA was dilated and discolored black, and right PICA arose from the proximal portion of this aneurysmal dilatation. Since it was impossible to clip the VA distal to the PICA for the proximal clip-occlusion, the VA including the VA-PICA junction was trapped. Considering the risk of developing infarction at the PICA territory, bilateral PICA was anastomosed at their posterior medullary segment in a side-to-side fashion because the occipital artery (OA) had been cut at the skin incision and could not be used for the OA-PICA anastomosis. The postoperative course was benign, but a mild lateral medullary syndrome developed. CT revealed no abnormal low density area and left vertebral angiography demonstrated the patency of the bypass. Thereafter, the deficit subsided gradually and the patient was discharged. He is presently working without neurological deficit.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Vertebral dissecting aneurysm treated with trapping and bilateral posterior inferior cerebellar artery side-to side anastomosis; case report]. 188 26

In Japan, acute encephalopathy with hepatic steatosis resembling Reye's syndrome has been reported to occur after treatment with the pantothenic acid antagonist, calcium hopantenate. We studied the causal relationship and the pathogenesis in dogs. The agent was administered to seven dogs at increasing doses over a period of 8 weeks. Anorexia, vomiting, and diarrhea were common clinical findings. In four dogs, coma suddenly developed after the appearance of gastrointestinal signs. Three animals died during periods when they were not under direct observation. The effects of the agent appear to be related to dose. Laboratory findings representing significant changes at the time of coma included hypoglycemia, leukocytosis, hyperammonemia, hyperlactatemia, and elevated levels of serum transaminases. Microvesicular hepatic steatosis and mitochondrial abnormalities were consistent pathological findings. The hepatic mitochondria were enlarged and characterized by an increased number of cristae and the presence of crystalloid inclusions. In a second group of four dogs, pantothenic acid was given in addition to and in the same amount as calcium hopantenate at increasing doses over a period of 8 weeks. All four dogs survived the 8 weeks and only one developed mild anorexia. No significant biochemical changes were found and neither hepatic steatosis nor mitochondrial abnormalities were observed. The addition of pantothenic acid prevented the development of the disorder in the four animals. These results show that calcium hopantenate produces acute encephalopathy with hepatic steatosis in dogs, by inducing a deficiency of pantothenic acid. The hepatic mitochondrial changes of this reaction differ from those of Reye's syndrome.
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PMID:Acute encephalopathy with hepatic steatosis induced by pantothenic acid antagonist, calcium hopantenate, in dogs. 188 58

An outbreak of food poisoning resulting in 13 deaths in children occurred in Malaysia during the Chinese Festival of the Nine-Emperor Gods in 1988. The offending food was a Chinese noodle called 'Loh See Fun' (LSF). The source was traced to a factory where a banned food preservative was added to make the LSF. The food poisoning was attributable to aflatoxins and boric acid. The clinical features included vomiting, pyrexia, diarrhoea, abdominal pain, anorexia, giddiness, seizures, and eventual coma. Initially, many presented with a Reye-like syndrome. Eleven post-mortem examinations were performed. The pathological findings included extensive coagulative necrosis of the liver with proliferative 'ductal/ductular metaplasia of the hepatocytes'. Giant cell formation, central vein sclerosis, bile stasis, and steatosis were also noted. There was presence of acute tubular necrosis, superficial upper gastrointestinal erosions, and ensuing encephalopathy. The eventual cause of death is acute hepatic and renal failure.
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PMID:An outbreak of aflatoxicosis and boric acid poisoning in Malaysia: a clinicopathological study. 189 May 47

Dehydration, in childhood as in adulthood, may origin from an inadequate water ingestion or an excessive water elimination. Causes may be found in fever, vomiting, scalds, pulmonary hyperventilation, diabetes. Water loss during acute diarrhea in children can be even 6-7 times higher in comparison with an healthy child. Together with water, electrolytes are lost. We differentiate dehydration in isonatremic d. (70% of cases), hyponatremic d. (10%) and hypernatremic d. (20%) basing on Sodium loss. Important dehydration causes severe clinical symptoms as shock, renal and cardiocirculatory failure, convulsion, coma. Symptoms at the central nervous system level derivate both from hyperosmolarity in brain cells and from thrombosis or hemorrhages in subdural sites. Dehydration, following acute diarrhea, is slight when weight loss is lower than 5%. The child health conditions still remain good. Dehydration become moderate if weight loss reaches 5% and the child starts suffering. When the weight loss reaches 10%, dehydration is now severe and circulatory deficiency becomes evident. When it is higher than 10%, prognosis is very severe and shock and coma may be observed. In the present work, we illustrate the different ways of rehydration after acute diarrhea. Initially, oral rehydration must be established with one of the oral solutions, differing each other for amount of electrolytes and glucose. Recently, a new solution, "supersolution", has been presented differing from the other ones for electrolytes concentration and for the presence of rice starch instead of glucose. In most cases of diarrhea, oral rehydration appears adequate but sometimes an intravenous rehydration becomes necessary, e.g. in case of vomiting, CNS depression and in any case of severe gastroenteric symptomatology.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Dehydrated child]. 189 82


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