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A 35-year-old woman was admitted to our hospital with hip pain. She has no family history of primary hyperparathyroidism. Serum calcium, phosphate, creatinine, alkaline phosphatase, and intact PTH levels were 3.14 mmol/liter (range, 2.23–2.65), 0.55 mmol/liter (range, 0.74–1.49), 68.95 μmol/liter (range, 39.78–70.72), 5112 U/liter (range, 110–360), and 1100 pg/ml (range, 10–65), respectively. We found a 99mTc-hexakis 2-methoxy 2-methyl propyl isonitrile (MIBI) avid 18F-fluorodeoxyglucose (18F-FDG) negative posterior mediastinal tumor 7.0 cm in diameter. 18F-FDG positron emission tomography (PET)/computed tomography (CT) showed multiple 18F-FDG-avid osteolytic lesions (Fig. 1). Biopsy of the left iliac bone revealed an osteolytic lesion replaced by proliferating fibroblastic cells and multinucleated giant cells. At the periphery, osteoid formation and osteoblastic proliferation were observed. Resection of the mediastinal tumor was performed, and pathological diagnosis confirmed parathyroid adenoma. Six months later, 18F-FDG PET/CT showed sclerotic changes of bones with no focal 18F-FDG uptake (Fig. 2). Although increased 18F-FDG uptake in brown tumors has been reported (1), this is the first report to describe the clinical course and postoperative 18F-FDG PET/CT. Osteoclast-like giant cell-containing lesions, such as giant cell reparative granuloma, aneurysmal bone cyst, and giant cell tumor, show increased 18F-FDG uptake despite benign characteristics. Interestingly, many 18F-FDG-avid benign lesions can reportedly be categorized as giant cell- or histiocyte-containing lesions (2). These cells are in the monocyte-macrophage lineage, with energy predominantly supplied by intracellular glucose metabolism (3, 4). However, fibroblasts are also frequently observed within the lesions (5) and known to show a high accumulation of FDG. Further investigations are necessary to elucidate the mechanism of 18F-FDG accumulation in brown tumor.
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Kuwahara et al. (2007) studied this question.
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