Increased 18F fluorodeoxyglucose uptake of a vertebral hemangioma responsible for oncogenic osteomalacia

We recently read with interest the article by Dupond et al. about a case of oncogenic osteomalacia (OO) [1]. The originality of this case lies in the fact that the tumor responsible for phosphatonin hyperproduction could only be detected by 18F fluorodeoxyglucose (FDG) PET-scan. An interesting feature of this case was that octreotide scintigraphy–like total body CT and MRI–was not able to localize the tumor. Cases of mesenchymal tumors responsible for OO, as evidenced by octreotide scintigraphy, have been reported in the literature. This finding supports successful treatment of OO in some cases with subcutaneous analogues of somatostatin [2]. We report herein a case of a 46-year-old man with dorsal vertebral hemangioma who was admitted to the Department of Neurosurgery of our hospital for exacerbation of paraparesia. This patient had undergone vertebral laminectomy for this hemangioma, located in the ninth dorsal vertebra, 2 years earlier. Recently, he had developed progressively increasing weakness, mainly of the lower limbs. Remarkable findings of the physical examination were hyporeflexia at the level of the lower limbs and the absence of Babinski sign. This was unexpected, given the suspicion of medullar compression by the hemangioma. The finding of a dramatic hypophosphoremia (0.6 mg/dl, normal range 2.5–4.5 mg/ dl), combined with an elevated phosphaturia (1380 mg/day) and increased phosphate clearance (64 ml/min, N