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[A case of cyclosporin A-induced myopathy]
Y Yamanishi1, Y Ishibe, Y Taooka
1Immunology and Rheumatology Division, Saijo Central Hospital, Higashi-Hiroshima City.
Insights
Cyclosporine A (CYA) may cause myopathy in Behçet's disease patients. Increasing CYA dosage led to severe muscle pain and weakness, which resolved after discontinuing the drug.
Area of Science:
- Ophthalmology
- Rheumatology
- Clinical Pharmacology
Background:
- Behçet's disease is a multisystem inflammatory disorder.
- Ocular involvement, such as retinitis, is a common and severe manifestation.
- Immunosuppressive therapy, including cyclosporine A (CYA) and colchicine (Col), is a standard treatment.
Observation:
- A 40-year-old male with Behçet's disease experienced a severe decrease in visual acuity.
- Treatment intensification with higher doses of CYA and Col preceded the onset of symptoms.
- The patient presented with fever, myalgia, muscle weakness, fatigue, and significantly elevated creatine kinase levels.
Findings:
- The clinical presentation and laboratory findings strongly suggested drug-induced myopathy.
- Discontinuation of CYA and reduction of Col led to rapid resolution of myopathic symptoms and normalization of creatine kinase.
- CYA was identified as the likely causative agent for the myopathy.
Implications:
- Clinicians should be vigilant for myopathy in Behçet's disease patients treated with CYA, especially with dose escalation.
- Monitoring creatine kinase levels may be crucial for early detection of CYA-induced myotoxicity.
- This case highlights the importance of considering iatrogenic causes for new-onset systemic symptoms in patients with chronic inflammatory diseases.
Abstract:
A 40-year old man with Behçet's disease was admitted for severe decrease of visual acuity. Since 1987, he had suffered from oral aphtha, retinitis, erythema nodosum, genital ulcer and epididymitis. He was diagnosed as complete Behçet's disease and has been administered cyclosporin A (CYA) and colchicine (Col). Because of repeated ocular attacks and reduced visual acuity, CYA was increased from 3.49 mg/kg/day (220 mg/day) to 6.35 mg/kg/day (400 mg/day) and Col, 0.5 mg/day to 1.0 mg/day. 2 weeks later, he revealed fever, generalized myalgia, muscle weakness and general fatigue, accompanying marked elevation of creatine kinase (4962 IU/l). CYA was discontinued and Col was diminished to 0.5 mg/day. The myalgia disappeared in 4 days and general conditions including creatine kinase were normalized within 2 weeks. We concluded that CYA was highly suspected of the cause of myopathy considering his clinical course.