Drug-induced
toxic myopathy is a complication of
familial Mediterranean fever in patients who receive
colchicine, especially when combined with
cyclosporine. Protracted febrile
myalgia syndrome is a severe form of
familial Mediterranean fever. A 34-year-old man who had
familial Mediterranean fever for > 15 years developed
kidney failure because of secondary
amyloidosis. He received living-unrelated-donor kidney transplant that functioned normally. He was on
colchicine prophylaxis that was continued after transplant, and he received immuno-suppression induction with
antithymocyte globulin and maintenance with
prednisolone,
mycophenolate mofetil, and
cyclosporine. After 2 months, he presented with severe
myopathy and elevated
creatine kinase. Muscle biopsy showed evidence of
drug-induced
toxic myopathy, most likely caused by
cyclosporine in combination with
colchicine.
Cyclosporine was replaced with
sirolimus and
colchicine was stopped. Symptoms partially improved and
creatine kinase decreased to normal. The
prednisolone dosage was reduced gradually to 5 mg daily. At 8 months after transplant, he was readmitted because of severe
arthralgia, prolonged
fever, pleuritic
chest pain, diffuse
abdominal pain, purpuric
rash, macroscopic
hematuria,
proteinuria, and
diarrhea. The
C-reactive protein and erythrocyte sedimentation rate were elevated. The clinical diagnosis was recurrent
familial Mediterranean fever presenting as protracted febrile
myalgia syndrome. Despite the history of
toxic myopathy, he was restarted on
colchicine (0.5 mg, twice daily), and
colchicine was well tolerated. There was marked improvement of most symptoms within several days. Follow-up 5 years later showed normal kidney graft function and no
familial Mediterranean fever activity on
colchicine prophylaxis. In summary,
familial Mediterranean fever reactivation and protracted febrile
myalgia syndrome after kidney transplant may be treated with
colchicine and modulation of immunosuppressive therapy.