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Regression of Skeletal Manifestations of Hyperparathyroidism with Oral Vitamin D

Calcium Metabolism and Osteoporosis Program (A.A., G.E.-H.F.), Division of Endocrinology, Department of Diagnostic Radiology (N.K.), Division of Nephrology, Hypertension and Vascular Medicine (A.B.), Department of Pathology and Laboratory Medicine (L.Z.), American University of Beirut-Medical Center, Beirut, Lebanon 113-6044

Address all correspondence and requests for reprints to: Asma Arabi, M.D., Calcium Metabolism and Osteoporosis Program, American University of Beirut-Medical Center, Bliss Street, Beirut, Lebanon 113-6044. E-mail: aa22{at}aub.edu.lb.

Context: Parathyroidectomy is the only effective therapy for osteitis fibrosa cystica in hyperparathyroidism.

Objective: The objective of this study was to describe the changes of skeletal and nonskeletal manifestations in a patient with hyperparathyroidism and renal failure after oral vitamin D therapy.

Design: This was a descriptive case report.

Setting: The patient was followed up in a referral center.

Patient: A 55-yr-old male patient with moderate renal failure was referred for expansile lytic lesions affecting several ribs and the spinous process of T12. His creatinine was 1.8 mg/dl; calcium, 8.9 mg/dl; PTH, 666 pg/ml; and 1,25 dihydroxy-vitamin D, 27 pg/ml. Bone mineral density (BMD) Z-scores by dual-energy x-ray absorptiometry were –4.1 at the spine, –1.7 at the hip, and –4.3 at the forearm.

Main Outcome Measures: The main outcome measures were the skeletal manifestations of hyperparathyroidism.

Results: At 10 months of therapy, calcium level was 10 mg/d, PTH level declined to 71 pg/ml, and BMD increased by 12% at the spine and 18% at the hip. Computerized tomography (CT) cuts revealed marked regression in the lytic lesions. At 2 yr, BMD increased by an additional 6% at the spine, and there were no further changes in the lytic lesions by CT. The vitamin D receptor genotype using the restriction enzymes Bsm1, Taq1, and Apa1 was Bb, tt, and AA.

Conclusions: We showed regression of severe skeletal abnormalities of hyperparathyroidism documented by serial CT images in response to oral vitamin D therapy. It is possible that the vitamin D receptor genotype of the patient modulated this response.

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