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)

The safety of ondansetron has been carefully evaluated through laboratory studies and clinical trials. Preclinical studies demonstrated that there is no end-organ toxicity in rats and dogs administered ondansetron doses 30 to 100 times those used in humans. At near-lethal doses of ondansetron, animals developed subdued activity, ataxia, and convulsions. Modest transient increases in serum transaminase values were observed. Concurrent administration of ondansetron with chemotherapy had no effect on tumor response in animals. The clinical safety of ondansetron has been evaluated in more than 2,500 cancer patients who received intravenous doses as large as 1.5 mg/kg. In adult patients receiving single-day chemotherapy, the incidence of adverse events was 36% with ondansetron (n = 647) and 50% with metoclopramide (n = 498). Diarrhea occurred in 9% of ondansetron patients and 19% of metoclopramide patients. Headache occurred in 14% of ondansetron patients and 8% of metoclopramide patients. Extra-pyramidal symptoms were reported in none of the ondansetron patients and 5% of the metoclopramide patients. The incidence of vascular occlusive events and seizure disorders was nearly identical with ondansetron and metoclopramide and similar to the cancer population in general. In a group of 209 pediatric patients receiving chemotherapy, the incidence of adverse events was 19% with ondansetron. Serum transaminase values increased significantly in 6% to 8% of ondansetron patients and 2% of metoclopramide patients. There was no apparent relationship between the cumulative dose of ondansetron administered and the incidence of increased transaminase values. However, there was an apparent relationship between the cumulative dose of cisplatin administered and the incidence of transaminase abnormalities. These data demonstrate that ondansetron is better tolerated than metoclopramide and is safe for intravenous administration to pediatric and adult patients receiving chemotherapy.
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PMID:Toxicity and side effects of ondansetron. 138 51

A previously healthy breast-fed baby was admitted at 10 days of age to a hospital in the north of Pakistan with diarrhoea and fever. He was treated for suspected sepsis with intravenous cefotaxime and tobramycin. Cultures of blood and faeces at that time proved negative. At 12 days of age, seizures began and examination of CSF revealed evidence of pyogenic meningitis but bacteria were neither seen microscopically nor isolated in culture. Ceftazidime was substituted for cefotaxime and carbenicillin was given also. Since the baby's condition continued to deteriorate with persistent fever, vomiting and recurrent seizures, he was transferred to the Aga Khan University Hospital, Karachi. Examination of CSF there confirmed the diagnosis of pyogenic meningitis and revealed Gram-negative bacteria. Cultures of CSF and faeces yielded Salmonella paratyphi A but the blood culture was negative. The isolate was found to be multiple antimicrobially resistant but sensitive to ciprofloxacin. Treatment with this drug was therefore started 3 days after the baby's admission to the Aga Khan Hospital. Within 36 h, improvement was observed. From then onwards, the baby made a progressive recovery and was healthy when seen at 7 months of age.
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PMID:Eradication of a multiple drug resistant Salmonella paratyphi A causing meningitis with ciprofloxacin. 143 Nov 77

The safety of intravenous (IV) and oral ondansetron has been evaluated in over 7,000 cancer patients in world-wide clinical trials. In adult patients receiving single-day chemotherapy, the incidence of adverse events was 45% with IV ondansetron (n = 317) and 59% with metoclopramide (n = 279). Headache occurred in 17% of ondansetron patients and 10% of metoclopramide patients, whereas diarrhea symptoms were reported in 15% of the former and 29% of the latter. The incidence and types of adverse events were similar following three 0.15 mg/kg IV ondansetron doses and 8- or 32-mg single IV doses. There was a slight increase in the incidence of headache following a single 32-mg dose (25%) compared with a single 8-mg dose (18%) or three 0.15 mg/kg doses (18%). The safety profile of oral ondansetron was similar to that of the IV formulation. Following an 8-mg oral dose administered three times a day for 3 days, the most frequently reported adverse events were headache (21%), constipation (7%), and abdominal pain (5%). In a group of 209 pediatric patients receiving chemotherapy, the incidence of adverse events following IV and oral ondansetron was 19%. The most commonly reported adverse event was headache (4%). In comparative clinical trials, extrapyramidal symptoms were reported in 5% of the metoclopramide patients but none of the ondansetron patients. In open-label trials, two patients who received ondansetron reported symptoms consistent with, but not diagnostic of, extrapyramidal reactions. The incidence of vascular occlusive events and seizure disorders was identical for ondansetron and comparative agents. Serum transaminase values increased significantly in 6% to 8% of ondansetron patients and 2% of metoclopramide patients who received cisplatin. There was no apparent relationship between the dose of ondansetron administered and the incidence of increased transaminase abnormalities. However, there was an apparent relationship between the dose of cisplatin administered and the incidence of transaminase abnormalities. In patients who received non-cisplatin chemotherapy, there was no difference in serum transaminase values between oral ondansetron and placebo. These data demonstrate that ondansetron is better tolerated than metoclopramide and is safe for IV and oral administration to patients receiving chemotherapy. In addition, ondansetron is well tolerated when administered as a single 32-mg infusion over 15 minutes.
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PMID:Clinical safety of ondansetron. 148 79

Aldicarb toxicosis was diagnosed in 200 sheep that died suddenly. Carbamate insecticide toxicosis was suspected based on observed clinical signs (hypersalivation, diarrhea, urination, paddling, seizures, miosis, and deaths occurring within 1 hour). Tissue samples were submitted from 4 Columbian ewes for pathologic and analytical evaluation. Severe diffuse pulmonary edema was observed on gross and histologic examination. Inhibition of cholinesterase activity in retina (21.2-68.1% of normal activity, n = 3), brain (40.6-45.6% of normal activity, n = 3), and whole blood (27% of normal activity, n = 1) supported a diagnosis of carbamate toxicosis. Reversal of brain and whole blood cholinesterase activities (reactivation factor greater than 1.4) following an in vitro 1 hour incubation at 37 C was also consistent with carbamate poisoning. Aldicarb toxicosis was confirmed following its detection in rumen contents at 1.5, 5.5, and 334 ppm using both high-pressure liquid chromatography with UV detection and gas chromatography with nitrogen/phosphorus detection.
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PMID:Aldicarb toxicosis in a flock of sheep. 155 68

Hypovolemic hyponatremia attributable to severe fluid and electrolyte alterations was diagnosed in a foal with diarrhea. Subsequent consumption of water resulted in rapid reduction of serum sodium concentration and serum osmolar depression. Clinical signs of neurologic disease developed including blindness, loss of menace response, and seizures. Treatment of this condition with IV administered fluids included hypertonic saline solution (7.2%; 2 ml/kg of body weight), and frequent monitoring of serum electrolyte concentrations and osmolality resulted in gradual correction of the fluid and electrolyte imbalance and resolution of the neurologic signs. Hyponatremia has been recognized in foals with renal failure, ruptured urinary bladder, and iatrogenic water overload. The key to diagnosis and management of profound hyponatremia is accurate diagnosis of the status of plasma volume and association of the electrolyte imbalance with clinical signs of neurologic disease. This report describes an unusual complication of a commonly encountered problem in equine practice and documents that the severe metabolic and electrolyte abnormalities associated with diarrhea can result in clinical neurologic disease. The differential diagnosis also should include bacterial sepsis, parasitism, thoracic mass, acute renal failure, congenital neurologic deficit, or seizure syndrome. Serum electrolyte disorders should be considered as a potential cause of signs of neurologic disease in foals with diarrhea.
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PMID:Hypovolemic hyponatremia and signs of neurologic disease associated with diarrhea in a foal. 160 18

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

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

Severe watery diarrhea and eosinophilic colitis induced by carbamazepine (CBZ) has not been described previously. We report the first known case of CBZ-induced watery diarrhea and eosinophilic colitis in a 57-year-old man receiving CBZ for secondarily generalized tonic-clonic seizures that developed after a cerebral infarction.
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PMID:Carbamazepine-induced eosinophilic colitis. 173 44

To determine whether severity of the prodromal gastrointestinal illness is associated with the course and complications of the extraintestinal manifestations of hemolytic-uremic syndrome, we conducted a retrospective review of children (n = 509) hospitalized with hemolytic-uremic syndrome. Those who came to the hospital with colitis and rectal prolapse associated with hemolytic-uremic syndrome (group I, n = 40) were compared with an equal number of time-matched children with hemolytic-uremic syndrome but without prolapse (group II). Children in group I had evidence of more severe colitis than children in group II had, as indicated by increased frequency of bloody diarrhea (p less than 0.001) and longer duration of diarrhea (p less than 0.001). However, they also had more severe extraintestinal manifestations during hemolytic-uremic syndrome, including edema (p less than 0.0001), severe thrombocytopenia (p less than 0.0001), prolonged anuria (p less than 0.001), and seizures (p = 0.036). Long-term prognosis for recovery of renal function was worse for group I than group II. Within group II, patients with bloody diarrhea had milder extraintestinal illness than those with prolapse but more severe extraintestinal illness than those with watery diarrhea. Analysis of Kaplan-Meier survival curves demonstrated a better prognosis for return of normal renal function in the children with watery diarrhea but without prolapse (p = 0.009) than in children with bloody diarrhea or prolapse. These data demonstrate that the severity of the gastrointestinal prodrome reflects the severity of the extraintestinal acute microangiopathic process and the resulting long-term outcome. Widespread vascular damage, often followed by permanent sequelae, is characteristic of patients with the most severe colitis.
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PMID:Association between severity of gastrointestinal prodrome and long-term prognosis in classic hemolytic-uremic syndrome. 173 16

Two cases of lithium toxicity are reported on in dogs having had lithium hypochlorite chlorinated water as their sole source of drinking water. Clinical signs in one dog included polyuria, polydipsia, loss of body mass; dehydration, diarrhoea and general weakness and in the other case, polyuria, polydipsia, loss of body mass and seizures. Withdrawal of the water resulted in complete recovery.
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PMID:Lithium toxicity in two dogs. 177 Apr 85


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