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Parathyroid Hormone‐Related Protein Induced Coupled Increases in Bone Formation and Resorption Markers for 7 Years in a Patient With Malignant Islet Cell Tumors
Author(s) -
Takeuchi Yasuhiro,
Fukumoto Seiji,
Nakayama Konosuke,
Tamura Yasuhiro,
Yanagisawa Akio,
Fujita Toshiro
Publication year - 2002
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1359/jbmr.2002.17.5.753
Subject(s) - endocrinology , medicine , bone resorption , primary hyperparathyroidism , parathyroid hormone , bone remodeling , hyperparathyroidism , parathyroid hormone related protein , calcium metabolism , calcium
Parathyroid hormone‐related protein (PTHrP) and PTH share the common PTH/PTHrP receptor. Although an elevated level of circulating PTHrP in patients with malignancies causes hypercalcemia as does PTH, chronic and systemic effects of PTHrP on bone metabolism in humans are not well understood because tumor‐burden patients showing hypercalcemia usually have a poor prognosis. We investigated bone and calcium metabolism in a patient with malignant islet cell tumors showing hypercalcemia due to the elevated plasma PTHrP level for 7 years. Hypercalcemia and hypercalciuria continued throughout the clinical course in spite of frequent infusions of bisphosphonates. Bone resorption markers and a bone formation marker were consistently elevated as seen in primary hyperparathyroidism, a disease caused by an autonomous hypersecretion of PTH. Based on biochemical measurements including bone markers and serum 1,25‐dihydroxyvitamin D, the clinical features of this case essentially are the same as those of primary hyperparathyroidism except for the elevated level of plasma PTHrP with suppressed intact PTH level. Therefore, it is suggested that chronic and systemic effects of PTHrP on bone as well as calcium metabolism are indistinguishable from those of PTH in human.