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)

Serum-immunoglobulin concentrations were measured in 364 patients with epilepsy. On dividing the patients into those treated with or without hydantoins, and according to possible aetiological factors, a characteristic pattern emerged. Irrespective of the treatment given, the mean values of IgA were significantly reduced in patients in whom constitutional factors were apparent, including those with familial prevalence of seizures. While IgA was rarely found below 0-6 mg/ml, a limit chosen to define IgA deficiency in patients not treated with hydantoins, the IgA level was subnormal in 20-25% of the patients treated with such drugs. In contrast, the mean concentration of IgA was normal and no individual subnormal values were observed in epileptic patients treated with or without hydantoins whose disease was thought to be secondary to traumatic or infectious events or to metabolic disturbances. The data suggest that epilepsy with constitutional characteristics might predispose to low IgA, but that IgA deficiency only occurs when hydantoins are given. Whether this postulated predisposition is relevant to the aetiology or pathogenesis of epilepsy remained unresolved.
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PMID:IgA deficiency, epilepsy, and hydantoin medication. 5 43

Serum levels of IgA were found to be reduced in some patients with epilepsy. Further studies revealed that only epileptics with constitutional factors for seizures showed, if ever, IgA deficiency, particularly those treated with hydantoins (up to 25%). In order further to substantiate the association of immunoglobulin alterations with epilepsy nine families in whom the disease was clustered were investigated. An IgA deficiency was detected in 16 of the 19 epileptics (three without hydantoin medication), but in none of their 45 non-epileptic relatives. However, four of the relatives had a low IgM. Seven other families were tested in each of which only one IgA deficient epileptic was known. No other family members were found with a low IgA, but 24 of 58 such relatives had increased IgM serum concentrations. The association of IgA deficiency and epilepsy with IgM imbalances in relatives of IgA deficient epileptics gives additional support for the hypothesis that immune imbalances and certain forms of epilepsy might be linked.
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PMID:Immunoglobulin abnormalities in relatives of IgA deficient epileptics. 7 56

Up to 12% of epileptic patients have subnormal IgA serum concentrations. Previous observations suggest that IgA deficiency is correlated with hydantoin treatment and also with the type of seizure. In a followup study it is shown that IgA deficiency in epileptics is a rather constant feature of a given patient. The most pronounced changes in IgA levels were seen in patients in whom the hydantoin medication also changed. However, low IgA levels have also been reported in untreated epileptics. A new classification for the immunodeficiency state in epileptics is introduced.
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PMID:Immunodeficiency in epilepsy: a new view. 9 Jan 39

Anti-muscle nicotinic acetylcholine receptor (nAR) antibodies were sought in epileptic patients without clinical signs of myasthenia gravis. Low titers of such antibodies were found in 3 cases characterized by primary generalized seizures, IgA deficiency and HLA A1 and B8 antigens. These three patients also had anti-brain nAR antibodies. In the serum of one patient with myasthenia gravis, anti-brain nAR antibodies were also detected. The titer was low despite a high titer of anti-muscle nAR antibodies. This may reflect the fact that the immune reaction in the three epileptic patients is primarily directed against the brain nAR.
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PMID:[Antibodies against nicotine-like acetylcholine receptors of central nervous system and muscles in epileptics with IgA deficiency]. 69 79

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

Three children with hair-shaft abnormalities and neurological disorders are reported. The first case is a young girl with monilethrix and Friedreich's ataxia that presented IgG and IgA deficiency, without telangiectasis. The second patient is a young girl with monilethrix and HMSN I. The third patient is a boy with a peculiar face, hypotrichosis and pili torti; he was mentally retarded and had epileptic seizures. His diagnosis was compatible with Noonan's syndrome or with a cardio-facio-cutaneous syndrome, because of the existence of hyperkeratosis and the neurological features. It is our aim to emphasize the heterogeneity of neurotrichosis, whose limits are not well established and whose manifestations are shared by some of them.
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PMID:[Hair disorders and neurological impairments (neurotricosis): three new cases]. 749 1

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

A 9-year-old boy diagnosed as having Rasmussen syndrome had congenital IgA deficiency and juvenile alopecia. He developed auditory hallucination and consciousness disturbance with intractable complex partial epileptic status. Anti-glutamate receptor epsilon2 antibodies were detected in his serum and cerebrospinal fluid. He was administered immunomodulatory agents and his seizures were treated with an intravenous anticonvulsant for 2 months. Subsequently, he developed a nephrotic syndrome, which proved to be membranous nephropathy and was treated with cyclophosphamide. Anti-basement membrane antibodies were detected in his serum. The boy died at the age of 14 years, and autopsy revealed diffuse brain atrophy with neuronal loss, infiltration of glial cells in the cerebrum, and loss of Purkinje cells in the cerebellum. A kidney specimen contained many sclerotic glomeruli, indicative of progressive membranous nephropathy. The patient was considered to have multimodal autoimmune disorder producing juvenile alopecia, autoimmune encephalitis, and a membranous nephropathy, based on the congenital IgA deficiency.
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PMID:Rasmussen syndrome combined with IgA deficiency and membranous nephropathy. 1943 84