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Dramatic mitigation of bone pain after phosphorus replacement therapy in a subject with FGF23-related hypophosphatemic osteomalacia.

Tatsumi, Fuminori; Horiya, Megumi; Tanabe, Akihito; Nishioka, Momoyo; Fushimi, Yoshiro; Sanada, Junpei; Hirata, Yurie; Irie, Shintaro; Kinoshita, Tomoe; Kamei, Shinji; Shimoda, Masashi; Mune, Tomoatsu; Kaku, Kohei; Kaneto, Hideaki.
Springerplus; 5(1): 1904, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27867811

INTRODUCTION:

Fibroblast growth factor 23 (FGF23) is secreted from bone and suppresses the absorption of phosphorus in renal proximal tubule and in intestinal tract. Therefore, the increase of serum FGF23 levels leads to hypophosphatemic situations. Tumor-induced osteomalacia is often induced by various tumors, but it is often difficult to identify the localization of tumor, because most of the FGF23-producing tumors are small and could be observed in any part of the body.CASE DESCRIPTION: Here we report a case of elderly female subject with FGF23-related hypophosphatemic osteomalacia who repeatedly experienced severe bone pain and fragility fracture in various parts of the body. Although we failed to identify the localization of tumor in this subject even with various examination, after starting phosphorus replacement therapy with relatively small amounts of calcium phosphate (1.5 g/day) (phosphorus content: 270 mg), hypophosphatemia was ameliorated and repeated bone pain was dramatically mitigated without any surgical operation.

DISCUSSION AND EVALUATION:

Even when we fail to identify the localization of tumor in subjects with FGF23-related hypophosphatemic osteomalacia, phosphorus replacement therapy for hypophosphatemia could reduce the bone pain.

CONCLUSIONS:

We should be aware of the possibility that phosphorus replacement therapy exert marked beneficial effects for the reduction of bone pain in subjects with FGF23-related hypophosphatemic osteomalacia even when we fail to identify tumor localization.
Selo DaSilva