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)

The clinical spectrum of toxic effects and serum concentrations after ingestion of carbamazepine were studied in 82 pediatric patients. Serum carbamazepine level was related to the depth of coma (p less than 0.001), convulsions (p = 0.002), hypotension (p less than 0.001), and the requirement for mechanical ventilation (p less than 0.001). In 10 patients in deep coma with a Glasgow Coma Scale (GCS) of 3-4, the mean serum level was 213 mumol/L (range 143 to 343); seizures, ventilatory failure, or hypotension caused by myocardial failure and conduction defects were observed. In four of these, large doses of inotropic agents were required, one patient was treated with plasmapheresis, and two died--one of cardiac failure and one of aspiration pneumonitis. In 27 patients with moderate coma (GCS 5-8), the mean serum level of carbamazepine was 112 mumol/L (range 63 to 176); convulsions were observed in two patients in this group. In 45 patients whose conscious state was mildly depressed or normal (GCS 9-15), the mean serum level was 73 mumol/L (range 37 to 128); additional effects were drowsiness (80%), ataxia (53%), nystagmus (38%), vomiting (17%), and dystonia (7%). I conclude that patients with serum carbamazepine levels of approximately 100 mumol/L require close observation, whereas those with levels greater than 150 mumol/L may require intensive life support.
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PMID:Acute toxic reaction to carbamazepine: clinical effects and serum concentrations. 164 Mar 2

Fourteen new cases of cytochrome oxidase (COX)-associated Leigh syndrome (LS) are combined with 20 reported cases to describe the clinical, laboratory, and radiological features of this devastating metabolic condition. Three clinical stages are identified. Most patients have normal neurological development during the first 8-12 months (stage I). Somatic complaints are common, including chronic diarrhea, recurrent vomiting, anorexia, and decelerating body and head growth. The second stage evolves during late infancy and early childhood when motor regression becomes evident. Eye signs, altered breathing patterns, pyramidal, extrapyramidal, and cerebellar signs emerge and sudden clinical deterioration occurs during intercurrent infectious or metabolic stress. The last stage may extend from 2 to 10 years and is manifested by extreme hypotonia, swallowing difficulties and undernutrition. Feeding assistance is necessary and seizures may occur. The CSF lactate concentration is consistently elevated and MRI abnormalities are seen in the subcortical structures. COX deficiency affects most tissues, but is not always generalized. For example, 3 patients with a cardiomyopathy had normal COX activity in cultured skin fibroblasts. Nearly normal amounts of cross-reacting material are present by ELISA and immunoblot analyses. Parental consanguinity has been found in several families, the hereditary pattern is recessive and males are affected more commonly (2:1). The biomolecular abnormality causing COX deficiency in LS is unknown, but the available evidence implicates a nuclear-encoded protein that affects the structure or the stability of the holoenzyme complex.
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PMID:Cytochrome c oxidase-associated Leigh syndrome: phenotypic features and pathogenetic speculations. 165 84

Acute i.m. injections of benzodiazepine receptor ligands were administered to baboons before 1-h observational sessions. The agonist midazolam produced sedative effects, the antagonist flumazenil produced no behavioral effects, the inverse agonist FG7142 produced tremor and the inverse agonist 3-carboethoxy-beta-carboline hydrochloride (beta CCE) produced tremor, vomiting, jerks and seizures. Co-administration of these drugs (midazolam + beta CCE, midazolam + flumazenil or flumazenil + beta CCE) produced a mutual antagonism of these effects. Compared to the non-dependent condition, in the diazepam-dependent condition (baboons maintained on 20 mg/kg per day diazepam) and withdrawn condition (dependent baboons tested during withdrawal), midazolam produced decreased sedative effects, flumazenil produced increased effects (i.e., tremor, vomiting and jerks), and beta CCE produced increased frequency of seizures. Taken together, these data suggest that (1) benzodiazepine receptor ligands lie on a continuum of behavioral activity, and (2) chronic diazepam administration alters the behavioral effects of these benzodiazepine ligands, producing a shift in the direction of the inverse agonist.
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PMID:Behavioral effects of benzodiazepine ligands in non-dependent, diazepam-dependent and diazepam-withdrawn baboons. 166 65

This is a report of an infant with 3-hydroxy-3-methylglutaryl-CoA-lyase deficiency. During infancy vomiting and feeding difficulties had been found repeatedly. Nutrition consisted in a mixture of one third of milk diluted with two thirds of water. Shortly before admission a change to whole milk had taken place. The one year old girl was admitted to the hospital because of vomiting and diarrhoea. Liver was enlarged and consciousness reduced. There was acidosis, hypoglycemia and an elevation of the transaminases. The typical pattern of organic acids in urine and dicarboxylic aciduria was pathognomonic. The diagnosis was proved by a deficiency of 3-hydroxy-3-methylglutaryl-CoA-lyase in fibroblasts. A protein and fat restricted diet, but also carnitine supplement was introduced. With the exception of severe hypoglycemia seizures on one morning the more than 2 1/2 year old girl is developed normally. It is of importance for future to avoid hypoglycemia after fasting, infections diseases or stress. The possible impairment of pancreatic function even in a normal clinical condition with normal values of transaminases is especially pointed out.
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PMID:[3-hydroxy-3-methylglutaraturia. Clinical aspects, follow-up and therapy in a young child]. 169 26

Citalopram is an antidepressant belonging to a new class of drugs which enhance serotoninergic neurotransmission through potent and selective inhibition of serotonin reuptake. Preliminary trials suggest that its short term therapeutic efficacy is significantly greater than that of placebo and mianserin, and comparable to that of amitriptyline, maprotiline and imipramine. It appears to be a weaker antidepressant agent than clomipramine, but better tolerated. Its elimination half-life of 33 hours permits once daily oral administration. Symptomatic improvement obtained with short term treatment has been maintained when therapy has been extended for up to 1 year; in the few patients studied for this extended period, the relapse rate was lower than with fluvoxamine, fluoxetine or imipramine. Compared to standard antidepressant agents, citalopram is well tolerated. It does not appear to be cardiotoxic, has not been associated with seizures in humans, and is relatively nonsedating. Unlike the tricyclic antidepressants, citalopram has minimal anticholinergic effects. Mild and transient nausea, with or without vomiting, is the most frequent adverse effect--occurring in 20% of patients--and increased perspiration, headache, dry mouth, tremor and insomnia are experienced by 15 to 18% of patients. Citalopram thus offers similar therapeutic efficacy and a more favourable tolerability profile than the tricyclic antidepressants. Preliminary data suggest that it may be particularly useful in patients who cannot tolerate the anticholinergic or cardiovascular side effects of tricyclic antidepressants and in those for whom sedation is not indicated.
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PMID:Citalopram. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in depressive illness. 171 47

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

A 39-year-old man developed paroxysmal cough, occasional vomiting after cough, and subconjunctival hemorrhage. His illness was complicated by episodes of seizure, with clonic movements of the arms and legs, brief loss of consciousness, and confusion. The episodes were triggered by mild, unremarkable coughing paroxysms. A diagnosis of pertussis was confirmed serologically by measurement of IgG, IgA, and IgM antibodies to pertussis toxin and filamentous hemagglutinin. Serologic studies confirmed the presence of Bordetella pertussis infection in the patient's 10-year-old daughter and suggested that his wife was infected as well. This case report illustrates the occurrence of typical pertussis with serious complications in an adult. Further research is required to determine the scope of this problem and the need for a program of adult immunization against pertussis.
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PMID:Pertussis encephalopathy in an adult: case report and review. 177 35

Cases of penicillin-resistant pneumococcal meningitis have been reported in other countries since 1977, but never before reported in Taiwan. In 1990, two cases of the disease were diagnosed here. Case one was a two-year-old boy who had had fever and vomiting for several days prior to admission. Under the impression of meningitis, a spinal tap was done. The CSF yielded pneumococcus, which was misinterpreted as sensitive to penicillin. Penicillin (400,000 units/kg/day) was given parenterally without effect. On the 12th day after admission, another spinal tap still yielded pneumococcus. This time the sensitivity test was reread with great care, and then reported to be penicillin-resistant pneumococcus. Minimal inhibitory concentration (MIC) of penicillin was performed simultaneously and it revealed 0.1 microgram/ml. Vancomycin (60 mg/kg/day) was substituted for penicillin. The patient became afebrile two days later, and was discharged ten days later without sequelae. Case two, a five-month-old girl, was diagnosed to have meningitis because of fever, vomiting, tense fontanel and seizure on admission. After a spinal tap was done, she was put on ampicillin and cefotaxime. The fever subsided two days later. At that time, the CSF was reported to grow pneumococcus, again misread as sensitive to penicillin. The antibiotics was switched to penicillin, but fever recurred. The second spinal tap still yielded pneumococcus which was sensitive to penicillin but resitstant to oxacillin. Based on experience with the first case, penicillin was changed to vancomycin, and performed MIC immediately. The MIC was 1.0 microgram/ml. The patient became afebrile two days later, and was discharged in good condition after ten days of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Penicillin-resistant pneumococcal meningitis: report of two cases]. 177 62

A case of propionic acidemia is reported. The main features of this patient were recurrent vomiting, ketosis and occasional episodes of seizure. Serum concentrations of propionic acid and glycine were within the normal range. Blood ammonia was slightly elevated. Characteristic organic acids were present in the patient's urine. they were: 3-hydroxypropionic acid, propionylglycine, methyl-citric acid, tiglyglycine, 3-hydroxyvaleric acid, etc. The etiology, pathogenesis, clinical features, diagnosis, and treatment of propionic acidemia are briefly discussed.
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PMID:[Propionic acidemia: one case report]. 183 12

Alpers disease consists of diffuse cerebral degeneration manifested as developmental delay, seizures, vomiting, and progressive neuromuscular deterioration, with liver disease and death. We report the clinical course of the liver disease, histologic progression of the hepatic lesions, and etiologic investigations in five patients (four girls, three kinships). All had grown and developed normally until seen at 6 to 36 months of age (mean 20 months), with vomiting (n = 5), progressive hypotonia (n = 3), or seizures (n = 2). All had been given anticonvulsants, including valproic acid in three. Liver disease was noted at a mean age of 35 months (range 9 to 67 months), with hepatomegaly (two patients), abnormal hepatic synthetic function (three) or transaminase values (three), and cirrhosis in one. Patients survived for a mean of 4.6 weeks (range 1 to 8 weeks) after the identification of liver disease; all died of hepatic failure. Results of evaluation for infectious and metabolic causes of liver disease and causes of degenerative neuromuscular disease were negative in all patients. Premortem liver biopsy specimens (n = 3) demonstrated an early lesion consisting of lobular disarray, microvesicular steatosis, periportal acute and chronic inflammation, and individual hepatocyte necrosis. Autopsy findings (n = 5) consisted of macrovesicular steatosis, massive hepatocyte dropout, and proliferation of bile ductular elements, with almost complete replacement of hepatocytes by proliferating bile ductular elements in two patients. Brain showed characteristic neuronal degeneration. We conclude that Alpers disease can be a cause of rapidly progressive liver failure in early childhood. Although the cause of this autosomal recessive disease is not known, it does not appear to be related to peroxisomal dysfunction.
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PMID:Liver involvement in Alpers disease. 186 Dec 11


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