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Journal of Postgraduate Medicine, Vol. 53, No. 4, October-December, 2007, pp. 274-275 Letter Risedronate induced transient ocular myasthenia Raja V, Sandanshiv P, Neugebauer M The Eye Care Centre, Leighton Hospital, Crewe, CW1 4QJ Code Number: jp07098 Sir, We present a case of ocular myasthenia gravis induced by risedronate therapy for osteoporosis which has not been reported elsewhere. An 81-year-old Caucasian lady was referred to the eye service for evaluation of vertical diplopia that appeared to be persistent though variable over a 2-week period. She had previously undergone cataract extraction with intraocular lens implantation in the right eye 5 years back. She was diagnosed as having osteoporosis 6 weeks earlier and was started on oral calcium and risedronate sodium (Actonel ® 35 mgs tablet once a week). Her medical history was otherwise not significant and she was on no other medications. Examination revealed right upper lid ptosis with marked variability and fatigability. An orthoptic assessment showed a right over left hypertropia of 8 prism dioptres increasing to 15 prism dioptres on right gaze with mild underaction of the right inferior rectus muscle. She demonstrated a positive Cogan′s lid twitch and an ice-pack test showed a marked improvement of ptosis. Fundus examination showed healthy fundi in both eyes. No weakness was elicited in any of the extremities. She underwent baseline investigations that included complete blood count, erythrocyte sedimentation rate and random blood sugar and was specifically investigated for anti-acetylcholine receptor antibodies. All investigations were normal but for a mildly elevated anti-acetylcholine receptor antibody at 0.06 nmol/L (normal 0.02 nmol/L). She was diagnosed with ocular myasthenia. She noted improvement of symptoms within 3 weeks of stopping risedronate sodium and was completely asymptomatic within 2 months. Examination showed good levator and orbicularis function along with normal ocular alignment and extra-ocular motility. All blood tests and antibody levels were subsequently normal. Many medications have been known to incite or aggravate myasthenia. These drugs may interfere with neuro-muscular transmission presynpatically or postsynpatically. Anti-convulsants, antiarrhythmics, beta-blockers, immunosuppressives and antibiotics have all been reported in association with myasthenia. [1] Many antibiotics like ciprofloxacin, erythromycin, clarithromycin and nitrofurantoin have been reported to be associated with myasthenia. [2],[3],[4] Risedronate is a pyridinyl bisphosphonate that inhibits osteoclast-mediated bone resorption and modulates bone metabolism and is widely used in patients with osteoporosis. On review of the safety information and side effects of Risedronate as provided by the manufacturer Proctor and Gamble in its package insert, it has been known to cause blurring of vision and generalised myasthenia in less than 3% of subjects. Applying the Naranjo′s adverse drug reactions (ADR) probability scale, a causality assessment was made which categorized this reaction as probable with a score of 7. The Naranjo′s algorithm categorises adverse reactions as definite (score > 9), probable (score between 5- and 8), possible (score 1-4) and doubtful (score < 1).[5] In our case, risedronate use was associated with variable ptosis and diplopia, which resolved completely on termination of the drug. The mechanism by which bisphosphonates cause myasthenia is not known. The review of literature showed a similar case report by Palin et al . [6] where they have deliberated whether treatment of hypercalcemia with a bisphosphonate Pamidronate might have caused myasthenia in a patient with primary hyperthyroidism. We are not aware of any previous reports of association of ocular myasthenia with risedronate usage and our case appears to be the first. References
Copyright 2007 - Journal of Postgraduate Medicine |
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