β Scribed by Frederick S Kaplan; Robert J Pignolo; Eileen M Shore
No coin nor oath required. For personal study only.
F ibrodysplasia ossificans progressiva (FOP) is one of the most disabling conditions known to humankind. Children with FOP succumb to episodes of inflammation-induced ectopic skeletogenesis that transform skeletal muscles and soft connective tissues into an immobilizing second skeleton of heterotopic bone. (1) Removal of heterotopic bone leads to additional episodes of new bone growth. (1) The recent discovery of the mutated gene that causes FOP, (2) an extraordinarily specific mutation in a highly conserved bone morphogenetic protein (BMP) receptor, (2) immediately predicted the mutant receptor and downstream pathway as an ideal target for drug therapy. (3) A recent case report by Gatti and colleagues from the University of Verona approaches the problem from a different perspective. (4) The report claims that rosiglitazone, an antiinflammatory and antidiabetic agent that alters the fate of marrow stromal cells, ''is associated with major clinical improvements in a patient with fibrodysplasia ossificans progressiva (FOP).'' (4) Gatti and colleagues describe a 48-year-old woman with FOP characterized by continuous flares that she was partially controlling with prednisone. She took rosiglitazone (initially 4 mg and then 8 mg daily) for 14 months. No new flares were observed during rosiglitazone therapy compared with five episodes observed during the previous year while she was on 20 to 25 mg of prednisone daily. ''The steroid dose was progressively lowered to 5 mg daily, the skin became softer, and the articular mobility improved impressively,'' according to the authors, who concluded that ''rosiglitazone therapy, possibly in association with small doses of prednisone, is associated with important clinical improvements in patients with FOP.'' (4) Rosiglitazone is an antidiabetic drug that is useful for the treatment of type 2 diabetes. (5) In addition, it appears to have a potent anti-inflammatory effect as well as an adverse effect on the skeleton. (6,7) Gatti and colleagues postulate that the adverse skeletal effects might be exploited therapeutically in diseases such as FOP. (4)
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