Immunological abnormalities and HLA antigen frequencies in IgA deficient patients with epilepsy.

Fontana, Adriano; Joller, Helen; Skvaril, F; Grob, Peter J.

doi:10.1136/jnnp.41.7.593

Cited by 46 publications

(16 citation statements)

References 21 publications

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“…IgA synthesis by stimulated peripheral blood lymphocytes from the same patients was, however, defective [11]. Further, it has been speculated that drug-induced deficiency of IgA in epileptic patients is connected with HLA antigen A2 [9]. We found no such association of significant immunoglobulin reduction and the HLA structure of the patients.…”

Section: Discussioncontrasting

confidence: 45%

Transient IgA and IgM deficiencies are frequent in children with ulcerative colitis

1988

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Serum immunoglobulin levels in 22 children with ulcerative colitis were followed for 2 years after diagnosis of the disease. A statistically significant depression of IgA, IgM, and IgG was noticed; depression of IgA and IgM was most frequent. The depression of immunoglobulin levels was transient and was most prominent during the first year of treatment. All patients in the study received sulphasalazine. Disease activity or steroid medication had no influence on immunoglobulin levels. The development of immunoglobulin deficiencies was not connected with any HLA antigen; we found decreased frequency of antigen B7 in the whole group.

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Section: Discussioncontrasting

confidence: 45%

Transient IgA and IgM deficiencies are frequent in children with ulcerative colitis

1988

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“…Antibodies against AChRs have been found in the cerebrospinal fluid of MG patients [15,18], but their relevance remains speculative. AChR antibodies have also been reported in the serum of patients with seizures and IgA deficiency but with no evidence of MG [12,13,25]. The frequency of epilepsy in patients with juvenile-onset MG in this series was six times higher than in the normal population [4].…”

Section: Discussionmentioning

confidence: 87%

Outcome in juvenile-onset myasthenia gravis: a retrospective study with long-term follow-up of 79 patients

Lindner

Schalke

Toyka

1997

Journal of Neurology

107

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Randomised and controlled treatment studies of juvenile-onset myasthenia gravis have not been published. We therefore report our retrospective analysis of 79 patients with juvenile-onset myasthenia gravis observed for as long as 30 years. The mean age at onset was 13.7 years and median follow-up 7.7 years. The initial presentation was generalised disease in 90% and ocular disease in the remaining patients. Sixty-five patients (82%) were thymectomised. In 14 of these, treatment consisted of a combination of azathioprine (2-3 mg/kg), corticosteroids (prednisolone up to 60 mg for a maximum duration of 12 months with subsequent tapering) and acetylcholinesterase (AChE) inhibitors, and of azathioprine and AChE inhibitors in 27 patients. One patient received azathioprine and 22 AChE inhibitors only; in another no further medication was necessary. In the severely affected group (n = 16), plasmapheresis was performed additionally before thymectomy and continued for some time after the operation. Treatment was started between 1 and 14 months (mean 2.4 months) after the onset of myasthenic symptoms. No thymectomy was done in 14 patients, and immunosuppressive treatment and AChE inhibitors were given in 9 of these cases. One patient received azathioprine only; 4 patients received AChE inhibitors only. The histology of the thymus gland showed follicular hyperplasia in 89% of the 65 thymectomised patients and normal findings in the remainder. Remission occurred in 60% of patients who underwent thymectomy and in 29% of those who were not thymectomised. Hyperthyroidism (6 patients, 8%), diabetes mellitus (2 patients, 3%) and rheumatoid arthritis (2 patients, 3%) were the most frequent associated immune-mediated diseases. Epileptic seizures and neoplasia were coincident diseases in 2 (3%) and 3 (4%) patients, respectively. There were no deaths from thymectomy or from immunosupression. This open, retrospective analysis suggests that juvenile-onset myasthenia gravis can be treated satisfactorily in most patients by the use of thymectomy and/or immunosupressive medication.

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“…A genetic predisposition seems to be a prerequisite for the development of drug-induced immunoglobulin A (IgA) deficiency (Fontana et al 1976). It has been suggested that patients with epilepsy with the human leucocyte antigen (HLA) A2 histocompatibility antigen are more likely to develop IgA deficiency when given phenytoin (Fontana et al 1978b;Shakir et al 1978). Furthermore, the finding of immunological abnormalities in relatives of patients with epilepsy supports the concept of an underlying genetically-determined immune imbalance (Eeg-Olofsson et al 1986;Fontana et al 1978a;Haldorsen & Aarli 1977).…”

Section: Discussionmentioning

confidence: 99%

Immunological Adverse Effects of Anticonvulsants

et al. 1993

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Long term administration of anticonvulsants is sometimes associated with impairment of the humoral and/or cellular immune response. Furthermore, certain well known adverse reactions to antiepileptics may have an immunotoxicological origin e.g. lymphadenopathy, pseudolymphoma and systemic lupus erythematosus. However, two important questions remain unresolved. First, the possibility that epilepsy per se might be primarily associated with immune alterations makes it difficult to assess the pathogenetic role of a specific drug, especially in a patient population usually on multiple drug therapy. Secondly, the clinical relevance of some of the observed immunological abnormalities is still highly controversial. This review is intended to give an outline of the present state of knowledge on the effects of anticonvulsants on humoral, cellular and nonspecific immunity, with particular regard to some of the major clinical conditions that have been ascribed to drug-induced immune dysregulation, such as pseudolymphoma and systemic autoimmune diseases. The immunotoxic potential of anticonvulsants appears to be low, and immunological monitoring is not usually required except in patients with known immune defects.

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Immunological abnormalities and HLA antigen frequencies in IgA deficient patients with epilepsy.

Cited by 46 publications

References 21 publications

Transient IgA and IgM deficiencies are frequent in children with ulcerative colitis

Transient IgA and IgM deficiencies are frequent in children with ulcerative colitis

Outcome in juvenile-onset myasthenia gravis: a retrospective study with long-term follow-up of 79 patients

Immunological Adverse Effects of Anticonvulsants

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