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 fatty liver of pregnancy is a rare clinical entity unique to pregnancy that can lead to hepatic failure and encephalopathy and, if the diagnosis is delayed, to death for the baby and the mother. The characteristic histological picture demonstrates microvesicular fatty infiltration of hepatocytes. Acute fatty liver of pregnancy is a disease of the third trimester of pregnancy. The most significant clinical findings are nausea or vomiting, abdominal pain, jaundice, hepatic encephalopathy, increased transaminase levels, decreased platelet count, increased prothrombin time, and renal failure. Hypertension and proteinuria are common. Liver biopsy is not always necessary for diagnosis but may be useful in atypical cases. The primary therapy is early delivery and supportive care. Both the obstetric team and the medical consultants must have a high index of suspicion for this disease because early delivery is lifesaving and has transformed the prognosis for the mother and the baby. Collaboration between obstetricians and gastroenterologists is necessary to make the diagnosis and also to improve our understanding of this disease of unknown etiology.
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PMID:Acute fatty liver of pregnancy: the hepatologist's view. 805 22

Ondansetron, a selective 5-HT3 antagonist, has been shown to be effective in preventing chemotherapy-induced nausea and vomiting. From July and August 1991, 25 patients were accrued in a phase II study to assess the efficacy of ondansetron in patients receiving cisplatin-containing chemotherapy. Patients received intravenous cisplatin 100 mg/m2, given either as a 24-hour infusion on day 1 or in divided doses as eight-hour infusions daily on days 1 to 3. Each patient received 24 mg of ondansetron per day for six days. Intravenous dexamethasone 24 mg was given daily on the days of cisplatin infusion. The emetic episodes and degree of nausea were evaluated daily. "Good" control of emesis (0-2 episodes of vomiting) and nausea (mild or no nausea) ranged from 64-100% and 88-100% respectively. Failure in emesis control occurred most frequently on days 3 and 4. Ondansetron was generally well tolerated with only minimal side-effects. One patient developed unexplained encephalopathy which resolved completely. Our results suggest that ondansetron is an effective anti-emetic agent with minimal toxicities. Randomised studies comparing ondansetron against "standard" anti-emetics should be conducted.
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PMID:Use of oral and intravenous ondansetron in patients treated with cisplatin. 812 53

BW12C79 stabilizes the oxyhemoglobin molecule resulting in a reversible left-shift of the oxygen saturation curve. The activity of a number of bioreductive anticancer drugs, such as mitomycin C, may be enhanced under hypoxic conditions. Twenty-four patients with various malignancies received BW12C79 and mitomycin C. BW12C79 was administered i.v. with a loading dose (20-50 mg/kg) over 1 h followed by a maintenance infusion of 4 mg/kg/h for 5 h. Percentage modification of the oxyhemoglobin (degree of left-shift) was dose related with maximum modification of 56% and was maintained for the duration of maintenance infusion of BW12C79. Hemoglobin electrophoresis showed a fast moving band consistent with the BW12C79-oxyhemoglobin complex. Side effects at the top dose level comprised headache, nausea/vomiting, vein irritation, and myocardial ischemia. One other patient suffered from an acute encephalopathy of unknown etiology a few days following BW12C79. 31P magnetic resonance spectroscopy of exercising calf muscles showed increased breakdown of high energy phosphate stores and a greater reduction in pH. Recovery of the high energy phosphate stores after exercise was slow. These results were consistent with reduced oxygen supply due to either a left shift of the oxygen saturation curve and/or reduced muscle blood flow. BW12C79 did not interfere with the pharmacokinetics of mitomycin C. In conclusion, this phase I study demonstrates the feasibility of achieving a significant left shift in the oxygen saturation curve in cancer patients which is maintained for at least 5 h with acceptable toxicity. The maximum tolerated dose of BW12C79 was 50 mg/kg loading infusion followed by a maintenance infusion of 4 mg/kg/h. Magnetic resonance spectroscopy results were consistent with reduced supply of oxygen to exercising skeletal muscle. BW12C79 may be of potential benefit as an adjunct to bioreductive drugs in the treatment of solid tumors.
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PMID:A phase I study of the left-shifting agent BW12C79 plus mitomycin C and the effect on the skeletal muscle metabolism using 31P magnetic resonance spectroscopy. 824 19

The purpose of this study was to review our experience with the use of OKT3 (a murine monoclonal CD3 antibody) used as immune prophylaxis for pediatric heart transplant recipients. Orthotopic heart transplantation was performed in 18 pediatric patients, 8 girls and 10 boys, ranging in age from 17 days to 17 years. OKT3 therapy was initiated intraoperatively at a dose of approximately 0.2 mg/kg and was administered at a dose of approximately 0.1 to 0.2 mg/kg/day for a period of 11.5 +/- 2.5 days. Daily average OKT3 levels were 1132 +/- 469 ng/ml. Side effects that occurred during OKT3 therapy were fever (59%), diarrhea (24%), headaches (24%), vomiting (18%), encephalopathy (12%), pulmonary edema (6%), and rash (6%). Infections occurred in 24% of patients, all within 6 months of transplantation. In the first year after transplantation, patients experienced 3.4 +/- 2.4 episodes of mild rejection and 1.0 +/- 0.8 episodes of moderate rejection. No patient experienced severe rejection. Five of the surviving 14 patients (36%) have been weaned from chronic steroid therapy, and 42% are being maintained on alternate-day prednisone at a dose of 0.06 +/- 0.02 mg/kg/day. Coronary artery disease developed in three patients; two of whom died. Actuarial survival was 83% at 1 year and 73% at 2 years. This report shows that OKT3 prophylaxis in pediatric heart transplantation can be used with acceptable short-term adverse side effects and overall survival.
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PMID:Murine monoclonal CD3 antibody (OKT3)-based early rejection prophylaxis in pediatric heart transplantation. 832 14

Outcome in terms of progression of Korsakoff's psychosis is known to be unlikely when the preceding thiamin deficiency syndrome, Wernicke's encephalopathy, does not follow heavy alcohol use. There is evidence that alcohol potentiates thiamin-related brain damage. It is argued here that in heavy drinkers, if vomiting precedes the onset of the encephalopathy, then the latter might develop at a time when tissue alcohol levels are close to zero. Any progression to Korsakoff's psychosis could then be associated with less or even no impairment. This outcome would not be expected if ingestion of alcohol continued during the vomiting stage. In a follow-up study of 61 cases of alcoholic Wernicke's encephalopathy, these concepts are given some support by the results obtained.
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PMID:A feature of alcoholic Wernicke's encephalopathy favourable to the maintenance of memory function: vomiting. 835 45

A 9-year-old girl was referred to our hospital after recurrent episodes of hypoglycemia, altered consciousness and persistent vomiting without acetonemia or myopathic symptoms. Other pertinent laboratory data included elevated BUN, hyperammonemia and very low levels of triglycerides with elevated free fatty acids. The patient was born from unaffected but related parents (second cousins) and the illness was previously diagnosed as Reye encephalopathy. Recurrence of similar attacks suggested an underlying metabolic disorder. Several syndromes of impaired FFA beta oxidation were taken into account and discarded successively after laboratory investigations: systemic carnitine deficiency, Medium and Long Chain Acyl-CoA Dehydrogenase deficiency and Multiple Acyl CoA Dehydrogenation deficiency (Glutaric aciduria, Ethylmalonic-adipic aciduria and riboflavin-responsive multiple acyl CoA dehydrogenation deficiency). Urinary and hematic gas-chromatography and Mass-Spectrometry show no abnormality in Medium Chain fatty acids and in C6-C10 dicarboxylic acids. Carnitine plasma concentrations (both total and free) were above normal levels while in urine acetyl carnitine was low in respect to longer acyclic radicals. Among metabolic defects located at the level of hepatic fatty acid oxidation, only Carnitine Transferase deficiency can explain this peculiar mosaic of data (precursors of the blocked reaction are elevated in blood whereas lack of the metabolites derived uniquely from this reaction explains all the clinical manifestations).
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PMID:[Non-ketotic hypoglycemia caused by carnitine palmitoyl transferase 1 deficiency]. 848 29

Two previously healthy women are described who in their late thirties suffered transient strokelike episodes, consisting of initial headache and vomiting, with various subsequent neurological signs that were only partially reversible. Investigations revealed elevated serum creatine kinase, lactic acidosis, hypertriglyceridaemia, and ragged red fibres in the muscle biopsy specimens. In both patients in vitro studies were performed on intact muscle mitochondria and muscle homogenate. Only in one was a mitochondrial defect found, located at the level of coenzyme Q. We conclude that these patients suffered from adult-onset mitochondrial encephalopathy, lactic acidosis and strokelike episodes (MELAS syndrome). Although the syndrome is often associated with long-standing neurological multisystem disease from childhood onwards, it should also be suspected in adults with strokelike signs of otherwise unexplained origin.
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PMID:Mitochondrial encephalomyopathy, lactic acidosis and stroke in adults: two cases. 849 10

We studied the seizure and polygraphic patterns of 18 patients with Angelman's syndrome. All patients showed movement problems. Eleven patients were also reported to have long-lasting periods of jerky movements. The polygraphic recording showed a myoclonic status epilepticus in nine of them. Seven patients had partial seizures with eye deviation and vomiting, similar to those of childhood occipital epilepsies. These seizures and electroencephalographic patterns suggest that Angelman's syndrome occurs in most of the patients as a nonprogressive, age-dependent myoclonic encephalopathy with a prominent occipital involvement. These findings indicate that, whereas ataxia is a constant symptom in Angelman's syndrome, the occurrence of a transient myoclonic status epilepticus may account for the recurrence of different abnormal movements, namely the jerky ones.
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PMID:Seizure and EEG patterns in Angelman's syndrome. 857 58

Migraine and the MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) syndrome have some clinical features in common. First, cerebral infarctions, most often in the posterior cerebral regions, which are a main symptom of MELAS, may complicate migraine. Second, migrainous headache with vomiting is also a characteristic feature of the MELAS syndrome. Less frequently, hemicranial headache is present in another mitochondrial disease, myoclonic epilepsy with ragged-red fibers (MERRF). Moreover, there is a mild bias toward maternal transmission in migraine. Apart from clinical resemblance, there is some experimental evidence for mitochondrial dysfunction in migraine. There may be depression of respiratory chain enzyme activity in muscle and platelets, and magnetic resonance spectroscopy has revealed a defective energy metabolism in brain and muscle of migraine patients. There has not been a systematic study of mitochondrial DNA in migraine, however. We therefore analyzed the mitochondrial DNA in lymphocytes of 23 migraine patients with aura. Southern blot and polymerase chain reaction analysis of mitochondrial DNA failed to detect any large-scale deletions or point mutations at base pair 3243 (MELAS) and base pair 8344 (MERRF). Our data show that deletions of mitochondrial DNA and the most frequent point mutations of MELAS and MERRF syndromes are not common in migraine with aura. In particular, these data do not support the hypothesis that some cases of migraine may be monosymptomatic forms of a MELAS syndrome. We cannot exclude, however, that migraine may be associated with different point mutations of mitochondrial DNA or with mutations of autosomally coded respiratory chain subunit genes.
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PMID:Mitochondrial DNA in migraine with aura. 864 80

To describe the clinical manifestations of dengue haemorrhagic fever (DHF) all children with a clinical diagnosis of DHF admitted to the paediatric ward of the Dr. Hassan Sadikin General Hospital (Bandung, Indonesia) between April 1st 1991 and September 30th 1993 were enrolled in a prospective study. Of the 306 children with a clinical diagnosis of DHF on admission in only 128 (41.8%) the diagnosis of DHF was confirmed by HI test. Of the confirmed cases, 24 (19%) developed shock and 1 (0.7%) died. Of the 174 cases with a negative HI test, 33 (19%) developed shock and 4 (2%) died. Four of the children died of shock before an hemagglutination inhibitor (HI) test was performed. The overall case mortality rate was 2.9%. The symptoms and signs of the 128 children with serologically confirmed DHF included fever or a history of fever (100%), petechiae (29.7%), epistaxis (39.1%), other forms of bleeding (5.5%), a positive Tourniquet test (78.1%), hepatomegaly (46.9%), epigastric pain (61.7%), vomiting (55.5%), thrombocytopenia < 100,000/mm3 (3.2% on admission and 15.3% during hospitalisation). Four (3%) children developed encephalopathy and 1 child an acute liver failure. In order to decrease the mortality associated with DHF early diagnosis and adequate case management are essential.
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PMID:Clinical manifestations of dengue haemorrhagic fever in children in Bandung, Indonesia. 866 76


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