Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Institutionalized epileptic patients on long-term anticonvulsant diphenylhydantoin (DPH) therapy were examined clinically. DPH plasma levels were unexpectedly high in 54% despite rather poor seizure control. No patient was free from side effects, which included gingival hypertrophy (90% of patients), increased alkaline phosphatase activity (55%), suggestion of a sensory peripheral neuropathy (34%), central nervous system (CNS) intoxication (22%), coarsened facial features (19%), tendency to bleed excessively (15%), hirsutism (12%), and mild megalocytic anemia (5%). CNS intoxication correlated with high plasma DPH levels, reports of deteriorating behavioral and motor performance, and the findings of nystagmus on vertical gaze or truncal ataxia, though not all patients with high plasma levels were clinically intoxicated. Alarming were the often disfiguring changes of gums and facial structures and the tendency to develop signs of vitamin D deficiency secondary to therapy. Hirsutism was rare in black patients. Plasma DPH level determinations are recommended as part of the management of mentally retarded epileptic patients but do not replace clinical acumen and skill.
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PMID:Effects of diphenylhydantoin in 41 epileptics institutionalized since childhood. 19 Jul 7

Biochemical evidence for hypoparathyroidism and roentgenographic evidence for hyperparathyroidism were present in a 7-year-old girl with seizures and tetany. She was hypocalcemic (4.7 mg/dl), hyperphosphatemic (11 mg/dl), and normomagnesemic, with elevated parathyroid hormone level (2,603 pg/dl and 3,693 pg/dl in immunoassays utilizing two different antisera). Somatic features of pseudohypoparathyroidism were absent. Increased serum alkaline phosphatase activity (335 IU/liter) with evidence of subperiosteal bone resorption suggested parathyroid hormone activity on bone. Intramuscular administration of parathyroid extract caused a rise in serum calcium level (9.6 mg/dl) and a fall in serum phosphorus level (7.9 mg/dl). The serum calcium, phosphorus, and alkaline phosphatase activity became normal during vitamin D therapy. Parathyroid hormone values and bone roentgenograms became normal. With serum calcium and phosphorus levels normal, ethylenediaminetetraacetic acid infusion was followed by an increase in plasma parathyroid hormone level but not in urinary cyclic adenosine monophosphate (AMP) or phosphaturia; in contrast, parathyroid extract induced cyclic AMP excretion and phosphaturia. These results suggest that endogenous parathyroid hormone in this patient affects bone resorption but not renal handling of phosphate. We infer that this represents a defective endogenous parathyroid hormone.
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PMID:Hypo-hyperparathyroidism: evidence for a defective parathyroid hormone. 19 77

Long-term treatment with antiepileptic drugs is based on a differentiated diagnosis. Medication appropriate for a special type of seizures has to be chosen. Treatment must be controlled carefully to avoid side effects. Total blood count, urinalysis and determination of enzymes (alkaline phosphatase etc.) are necessary in regular intervals. Essential in treatment is the psychological guidance of the patient and his parents to handle various problems which arise during development. The treatment is terminated carefully after years when the seizures are controlled and the EEG has been normalized.
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PMID:[Long-term treatment with anticonvulsants in childhood. Guidelines for the practice]. 40 40

Liver function tests were carried out in 206 adults and children taking anticonvulsants to ascertain the prevalence of biochemical abnormalities in asymptomatic patients. It was observed that serum gamma-glutamyl transpeptidase was elevated in 74.6% of patients, alkaline phosphatase in 29.7% and alanine aminotransferase in 25.2% of cases. These figures are similar to those previously reported in the literature and probably reflect hepatic enzyme induction by the anticonvulsants. It is suggested that there is no value in the routine performance of liver function tests in patients with epilepsy. However, such patients should be informed of the symptoms of hepatic dysfunction and asked to report for liver function tests should they have such symptoms.
Seizure 1992 Sep
PMID:Liver function tests in persons receiving anticonvulsant medications. 134 66

Although valproic acid as well as its derivatives are effective in the treatment of some epileptic seizures, they are not free of adverse side effects. The purpose of this work was to describe the collateral clinical effects of valproic acid, the associated changes that take place in some serum laboratory parameters, and correlations among these adverse clinical effects, drug serum level and therapeutic response. One hundred patients aged 7 months to 19 years (average 5 year and 6 month old) were followed for at least 13 months. Clinical collateral effects were observed in 14% patients, anorexia and hair loss being the most frequent. One third of patients showed raised serum alkaline phosphatase and transaminases values, while lower than normal prothrombin time and platelet counts were detected in 4% and 1% of patients, respectively. In one patient treatment was interrupted because of low platelet counts which persisted in spite of drug withdrawal, but basal counts were not done, so it is not possible to establish causal relationships between both events. No correlation between adverse clinical symptoms and valproic acid plasma levels was observed. In spite of the fact that basal laboratory values were not known and that abnormal tests were not repeated for confirmation, collateral clinical effects and laboratory findings associated to treatment with valproic acid seemed not severe in this series. Anyway, taking into account drug characteristics, it should always be used with caution.
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PMID:[Adverse effects of valproic acid in epileptic infants and adolescents]. 184 42

The subacute toxicity of compound 1 was investigated in rats and dogs. Compound 1 was administered orally to rats of both sexes at daily doses of 0.5, 1.0 or 2.5 g/kg for 3 months. No change attributable to the administration of compound 1 was found either in blood count or in histopathological examination. Decreases in SGPT, alkaline phosphatase and lactic acid dehydrogenase and an increase in serum cholesterol were detected. Compound 1 was mixed with food and given to dogs of both sexes daily at doses of 0.2 or 0.5 g/kg for 3 months. Severe toxic symptoms including anorexia, emesis, ataxia and convulsive seizures were observed. A decrease in SGPT and increase in alkaline phosphatase were also detected. Hyperemia of the duodenal mucosa and severe kidney lesions were found in histopathological examination. Neither abnormality of appearance nor histopathological change was found in a pig receiving compound 1 at the daily dose of 0.1 g/kg for 3 months. The results suggest that there are differences of compound 1 metabolism among the species used in this study.
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PMID:[Species differences in subacute toxicity of pyrrole aldehyde N4-(4-methoxyphenyl) semicarbazone]. 215 Dec 66

Following acute accidental death of 26 cows exposed to boron fertilizer, effects of inorganic boron treatment in goats were studied. Goats were orally dosed with toxic but sublethal amounts of the fertilizer. Multiple hematologic and serum chemistry parameters were assessed, as were cerebrospinal fluid (CSF) neurotransmitters and some of their metabolites. Significant increases in packed cell volume, hemoglobin, inorganic phosphate, creatine phosphokinase, conjugated bilirubin, sodium, glucose, cholesterol, and aspartate transaminase were recorded. The following serum components were significantly decreased after boron dosing: alkaline phosphatase, magnesium, glutamyltransferase and potassium. There was evidence of a stimulatory effect on both serotonergic and dopaminergic neurons as reflected in elevated CSF monoamine metabolites. Aberrations in clinical behavior, including seizure-like activity, also suggested a central nervous system effect of inorganic boron.
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PMID:Experimental acute inorganic boron toxicosis in the goat: effects on serum chemistry and CSF biogenic amines. 216 93

Nutritional rickets was diagnosed in 18 infants aged eight to 24 months. Clinical features included progressive leg bowing, poor linear growth, a diet deficient in vitamin D, seizures, and abnormal serum calcium, phosphate and alkaline phosphatase levels. Wrist radiographs and serum alkaline phosphatase levels were the most useful confirmatory tests. Breast milk may not contain enough vitamin D to protect infants, particularly dark-skinned children and those living in cloudy, northern U.S. cities, from rickets after six months of age. As breast feeding becomes more widely practiced, care is required to ensure that infants at high risk for rickets receive appropriate vitamin D supplementation.
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PMID:Nutritional rickets. 223 38

Acute zinc toxicosis from the ingestion of pennies was diagnosed in a dog with Heinz body hemolytic anemia (PCV = 14%), leukocytosis (51,000 cells/ml) with a left shift (3,060 band neutrophils; 37,740 segmented neutrophils) and monocytosis (4,080 cells/ml), azotemia (BUN = 60 mg/dl), bilirubinemia (total bilirubin = 5.3 mg/dl), hypokalemia (3.0 mEq/L), high serum alkaline phosphatase activity (691 U/L), high total plasma solids (8.1 g/dl), hemoglobinuria, and proteinuria. Despite aggressive medical treatment, renal failure ensued, and the dog died of cardiac arrest. The clinical signs, clinical course, and laboratory findings in this dog were similar to what has been reported in other cases of acute zinc toxicosis in dogs, with the exception of a history of generalized seizures and the findings of Heinz bodies. Although a causative relationship between plasma zinc values and Heinz body formation cannot be proven, their association suggests that oxidative damage to erythrocyte hemoglobin and cell membrane proteins may be involved in the pathogenesis of zinc-induced hemolysis.
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PMID:Heinz body hemolytic anemia associated with high plasma zinc concentration in a dog. 226 50

Plasma phenytoin and phenobarbitone levels were estimated in 123 adult Ethiopian epileptics by gas-liquid chromatography. Thirty four (38.2%) of the patients on phenytoin, and 52 (52%) of those on phenobarbitone, had plasma levels in the conventional therapeutic ranges of 10-20 micrograms/ml and 10-30 micrograms/ml respectively. Of the 89 patients who were taking phenytoin either singly or combined with phenobarbitone, motor disturbances (ataxia and nystagmus) were seen in 31 (34.8%) and dysmorphic and idiosyncratic side effects including gum hypertrophy, hirsutism, acne and skin rash in 37 (41.6%). Subnormal serum calcium levels were noted in 15 (30.6%) and high alkaline phosphatase was found in 13 (26.5%). Phenobarbitone was found to be an effective anticonvulsant (78.1% seizure control rate), with adverse effects of sedation and intellectual depression. Seizure control was achieved in 77.1% of patients on a single drug as opposed to 55.6% on combination of phenytoin and phenobarbitone (p less than 0.05). The overall seizure control rate was 66%.
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PMID:Plasma level distribution, effect and toxicity of antiepileptic drugs among Ethiopian epileptics. 230 55


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