Related Experiment Videos
[D-penicillamine induced myasthenic syndromes in rheumatoid arthritis. Two cases (author's transl)]
Abstract:
The authors report on 2 personal cases, and review 48 published cases of myasthenia induced by D-penicillamine (D-P) treatment in patients with rheumatoid arthritis. The clinical symptoms were not different from those of myasthenia gravis, and no correlation could be found between the total cumulative dose of D-P and the onset on the myasthenic syndrome. In 71% of the patients the neurological deficiency regressed after D-P was withdrawn, but in some cases anticholinesterase treatment had to be continued and thymectomy was contemplated. The most remarkable biological abnormalities were anti-striational antibodies (found in 58% of the cases) and anti-acetylcholine receptors antibodies (found in 4 out of 7 patients tested). These findings are in favour of a genuine myasthenia and against a myasthenic syndrome due to neuro-muscular blockade. While the mechanisms underlying the emergence of these antibodies remains unknown, their presence throws new light on immunological disorders in rheumatoid arthritis.
Insights
D-penicillamine (D-P) treatment can induce myasthenia gravis in rheumatoid arthritis patients. Symptoms resolved in most cases after stopping D-P, with antibody findings suggesting genuine myasthenia.
Area of Science:
- Neurology
- Immunology
- Rheumatology
Background:
- Rheumatoid arthritis patients treated with D-penicillamine (D-P) can develop myasthenia.
- This study reviews 50 cases of D-P-induced myasthenia.
Observation:
- Clinical symptoms were indistinguishable from classic myasthenia gravis.
- No correlation was found between D-P dose and symptom onset.
- Neurological deficits resolved in 71% of patients after D-P withdrawal.
Findings:
- Elevated anti-striational antibodies (58%) and anti-acetylcholine receptor antibodies (4/7 tested) were observed.
- These immunological markers support a diagnosis of genuine myasthenia.
- Findings suggest D-P-induced myasthenia is not due to neuromuscular blockade.
Implications:
- The presence of autoantibodies sheds light on immunological dysregulation in rheumatoid arthritis.
- Understanding these mechanisms may inform future treatment strategies.
- Further research is needed to elucidate the mechanisms behind antibody emergence.