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)

Eight indices of the immunological function were studied in 246 adult epileptic patients with 100 normal adults as control, it was found that mean contents of blood IgA, and IgM decreased, that of complement C3 increased, and the rates of lymphocyte transformation as well as rosette formation decreased in this group of epileptic patients. The decrease of IgA was related to the types of seizures and the taking of antiepileptic drugs. Suggesting that immunological abnormality did exist in the epileptic patients. The mean content of circulating immune complexes. (CIC) had a negative correlation with the period of time after seizures. It was much higher than that of the controls within the first 3 days after the seizures with its highest levels reached on the first day. Suggesting that immune reactions took part in the process of seizure episodes.
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PMID:[An immunologic study of patients with epilepsy]. 239 Aug 92

This is a report of a 9-year-old epileptic boy, who was studied over a period of 7 years. The seizures started when he was 2 months old. He was treated with phenytoin from the age of 2 years and 7 months. Serum and salivary IgA were absent with high IgE serum total. The routine immunologic studies were normal. The IgA was normalized after phenytoin withdrawal, but IgE determination increased progressively without any atopic symptoms. The T4 (helper)/T8 (suppressor) ratio decreased (1.0 and 1.2) on two different days, although above the normal limit. The phenytoin only modified the IgA levels. These data suggest that a primary immunoregulatory abnormality may be present in drug induced IgA deficiency.
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PMID:Transient phenytoin induced IgA deficiency and permanent IgE increase. 303 84

In a survey of 1011 pediatric patients with seizure disorders, 93 children (9.2%) were found to have depressed serum IgA concentrations when compared with age-matched controls; 27 of these values were less than 0.1 g/L (less than 10 mg/dL). Two thirds (64/93) of these patients were being treated with phenytoin, and ten had been previously treated with phenytoin. No relationship between IgA deficiency and serum phenytoin concentration nor use of other anticonvulsant medications was found. The prevalence of phenytoin-induced IgA depression was similar in patients with "primary" or "secondary" seizure disorders. Approximately 40% of the patients with low serum IgA concentrations had mild to moderate depression of serum IgG and/or IgM concentrations when compared with age-matched controls.
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PMID:Phenytoin-induced IgA depression. 363 Oct 17

Bacterial infections are frequent events in premature and newborn infants. The reason is a defective specific and nonspecific defence of bacterial organisms. Some immunoglobulins like IgM and IgA including secretory IgA are absent. Premature infants also show a decreased level of IgG. Cellular immunity is anatomically intact but functionally defective. A number of complement factors are lacking, the activation of the alternative pathway is impaired. Newborn infants with perinatal problems like asphyxia or difficult delivery, show defects of leucocyte function like decreased deformability, defective chemotaxis and defective killing of ingested bacteria. Certain diseases, like hypoxia and malformations of immature organ functions in this age group (decreased acid production in the stomach), facilitate bacterial colonization of surface epithelia and the invasion of tissues. Consequences of these pathogenetic mechanisms are an unimpaired propagation of bacterial organisms into the blood and meninges without localization of the infecting organisms at the entry site. Bacterial meningitis is not considered a separate disease entity but a complication of bacteremia and sepsis. Clinical symptoms are nonspecific at the onset of the infection. Fever is frequently absent; decreased appetite, vomiting, a bloated abdomen, diarrhea, tachycardia, tachypnea are early signs of a bacterial infection, a grey mottled appearance, cyanosis, jaundice, petechiae, apneic spells, seizure activity and a metabolic acidosis are symptoms of advanced infection. Successful treatment at this stage is often not possible. Every sign of a decreased well being of a newborn of premature infant warrants laboratory and bacteriologic work up for septicemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chemotherapy of severe bacterial infections in pediatrics]. 631 69

A 34-year-old man had polar extremes of B cell dysfunction: systemic lupus erythematosus evolving into common variable hypogammaglobulinemia. He presented in 1974 with seizures and six other criteria for systemic lupus erythematosus; his antinuclear antibody titer was 1:1024 and IgG level, 2870 mg/dL. After 5 months of immunosuppressive treatment, a 79% decrease in serum IgG and 95% decrease in IgA levels occurred and manifestations of systemic lupus erythematosus disappeared. Six years later, he developed panhypogammaglobulinemia, had recurrent sinopulmonary infections, and showed nodular lymphoid hyperplasia on rectal biopsy. For comparison, serum immunoglobulin concentrations were measured serially in 13 other patients with systemic lupus erythematosus. Three developed severe depressions of these levels, two with IgG levels less than 300 mg/dL and one with an IgA level of 8 mg/dL. These decreases were transient, related to treatment, and not associated with infections. Daily high-dose prednisone therapy (60 mg/d) rather than treatment with cytotoxic drugs correlated with decreased immunoglobulin concentrations.
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PMID:Transition from systemic lupus erythematosus to common variable hypogammaglobulinemia. 685 20

Humoral and cell-mediated immunity was determined in 28 epileptics, in 22 patients observed and investigated because of an only one seizure, and 26 healthy controls. Anticonvulsants had not been used in the treatment of these cases up to that time. The total lymphocyte count and the count of lymphocytes forming spontaneously rosettes with sheep erythrocytes were found to be significantly lower in the group of patients with epilepsy of unknown aetiology in relation to controls. The quantitative changes in the composition of the lymphocyte population were not significant and caused, probably, no immunological deficit, but were only a reaction to organic damage to the nervous system. Slight disturbances in the functions of the immune system cannot be, however, ruled out since this group showed also a significantly higher IgG level which suggests long-standing antigenic stimulation. No defect in IgA synthesis and disorders of the cell-mediated immunity (blastic transformation test, leucocyte migration inhibition test, skin test) were demonstrated in this study, although they had been reported by some authors in cases of epilepsy, mainly, however, in patients treated with anticonvulsants. In the patients having started anticonvulsive treatment these investigations will be repeated for establishing the effect of drugs on the immune reactions.
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PMID:[Non-specific immunologic reactivity in epilepsy]. 696 44

In a prospective study performed in 1977-1978 (one year), all 90 children (age 6 months to 5 1/2 years, median 21 months) admitted due to febrile seizures were examined for blood brain barrier function and intrathecal immunoglobulin synthesis. The CSF/serum albumin ratio and CSF total protein reflected the blood brain barrier function, while intrathecal immunoglobulin synthesis was presented by determination of the CSF IgG index [CSF/serum IgG ratio]:[CSF/serum albumin ratio] and the corresponding CSF IgA index. CSF IgM concentrations were also determined. CSF and serum taken at admission were available from 64 children, and CSF and serum taken three to four weeks from 28. Intrathecal synthesis of one or more of the immunoglobulins was concluded to occur in 42% of the children at admission and in 25% at the follow-up examination. Normal blood brain barrier function and normal serum immunoglobulin concentrations were found. There were no relations to clinical variables.
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PMID:Immunoglobulin abnormalities in cerebrospinal fluid and blood in children with febrile seizures. 707 7

The results of this prospective study fail to confirm previously reported phenytoin suppression of lymphocyte responsiveness to mitogens. Our data show a significantly greater than expected percentage (p less than 0.0001) of patients requiring phenytoin treatment have low lymphocyte responsiveness to mitogens prior to phenytoin therapy. Analysis of changes in each individual's response during phenytoin treatment as compared with their pre-phenytoin responses shows a consistent trend to increased responsiveness to concanavalin A, pokeweed mitogen, and to a suboptimal concentration of phytohemagglutinin. This trend was most pronounced for patients whose serum IgA concentration was decreased while taking phenytoin, whereas there was no such trend for individuals whose serum IgA levels were not decreased. This phenomenon was not related to neurological disease classification. Phenytoin added directly to lymphocyte cultures depressed lymphocyte responses to all mitogens in a small (less than 20%) but significant degree, confirming similar in vitro studies by other investigators. Because of limited serum proteins for phenytoin binding in culture medium, these in vitro studies have little application to possible phenytoin effects on lymphocytes of patients taking it to prevent seizures. Thus, the suggestion that phenytoin causes depressed lymphocyte responses to mitogens in epileptic patients appears unwarranted.
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PMID:Phenytoin influence on human lymphocyte mitogen response: a prospective study of epileptic and nonepileptic patients. 709 4

A 49-year-old man suffered from progressive dementia and seizures leading to death after 2 years. CT scans showed severe cortical-subcortical atrophy and hypodensity of the white matter. His father had died at about the same age with similar clinical signs. Two sisters and one brother were also affected. Neuropathological study revealed predominant involvement of the cerebral white matter with myelin loss, gliosis and type I lacunes. The small arteries and arterioles of the white matter and basal ganglia, and, to a lesser extent those of the subarachnoidal space, displayed fibrosis and replacement of the media by an eosinophilic, PAS positive, Congo Red negative, granular substance. Electron microscopy showed swollen myocytes surrounded by collagen, elastin and a compact electron-dense material. Immunofluorescence using antibodies against IgA, IgG, IgM, C1q and C3 stained the abnormal media weakly. In the cortex, there were diffuse senile plaques and neurofibrillary tangles. Immunohistochemistry demonstrated beta/A4 positive material in cortical senile plaques but not in arterial walls. Adventitial macrophages were, however, immunoreactive for gamma-trace. Systemic arterioles were normal. The vascular changes and leukoencephalopathy are comparable to those described in 'Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy' (CADASIL). Similar vascular changes were also observed in nonfamilial cases. An association with Alzheimer changes in the cortex has not been described previously. The relationship between both diseases and the role of each in the causation of the dementia is unclear.
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PMID:Autosomal dominant arteriopathic leuko-encephalopathy and Alzheimer's disease. 820 37

Approximately 10% of patients with systemic lupus erythematosus (SLE) develop epileptic seizures. When occurring before the onset of generalized SLE, the seizures are mainly primary generalized. Accordingly, long-term treatment with anti-epileptic drugs may precipitate SLE, or epilepsy and SLE may both occur as manifestations of a genetically determined predisposition. Some patients develop IgA deficiency during phenytoin treatment. This condition is reversible and IgA becomes normalized when phenytoin is withdrawn (drug-induced IgA deficiency). Some epileptic patients have a drug-independent IgA deficiency. Patients with drug-induced IgA deficiency are usually HLA-A2, while those with drug-independent IgA deficiency are HLA-A1,B8. The gene coding for IgA deficiency seems to be located in the HLA complex on chromosome 6. The gene locus for juvenile myoclonus epilepsy and related disorders is also on chromosome 6 and in close relation to the gene locus for the HLA system. Juvenile myoclonic epilepsy may be accompanied by drug-induced IgA deficiency, but there are also cases with other sometimes less-defined epilepsies, associated with this anomaly. It is possible that the relationship between epilepsy and immune disturbances is related to a common genetically determined susceptibility.
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PMID:Immunological aspects of epilepsy. 833 10


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