Abstract

ABSTRACTHypomineralized matrix is a factor determining bone mineral density. Increased perilacunar hypomineralized bone area is caused by reduced mineralization by osteocytes. The importance of vitamin D in the mineralization by osteocytes was investigated in hemodialysis patients who underwent total parathyroidectomy (PTX) with immediate autotransplantation of diffuse hyperplastic parathyroid tissue. No previous reports on this subject exist. The study was conducted in 19 patients with renal hyperparathyroidism treated with PTX. In 15 patients, the serum calcium levels were maintained by subsequent administration of alfacalcidol (2.0 μg/day), i.v. calcium gluconate, and oral calcium carbonate for 4 weeks after PTX (group I). This was followed in a subset of 4 patients in group I by a reduced dose of 0.5 μg/day until 1 year following PTX; this was defined as group II. In the remaining 4 patients, who were not in group I, the serum calcium (Ca) levels were maintained without subsequent administration of alfacalcidol (group III). Transiliac bone biopsy specimens were obtained in all groups before and 3 or 4 weeks after PTX to evaluate the change of the hypomineralized bone area. In addition, patients from group II underwent a third bone biopsy 1 year following PTX. A significant decrease of perilacunar hypomineralized bone area was observed 3 or 4 weeks after PTX in all group I and II patients. The area was increased again in the group II patients 1 year following PTX. In group III patients, an increase of the hypomineralized bone area was observed 4 weeks after PTX. The maintenance of a proper dose of vitamin D is necessary for mineralization by osteocytes, which is important to increase bone mineral density after PTX for renal hyperparathyroidism. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.

Highlights

  • Accumulated evidence suggests that the osteocyte is a crucial determinant of bone strength

  • This figure was adopted to show the relationships between osteocytes and both osteoclasts and osteoblasts in HD patients with renal hyperparathyroidism (Figure 1).(1-3) there have been few clinical papers about the role of the osteocyte in patients with chronic kidney disease (CKD) (Figure 1).(4-7) It is likely that bone fragility in CKD patients suffering from renal hyperparathyroidism increases[8,9] as a result of increased hypomineralized bone area caused by impaired mineralization by osteocytes,(10,11) increased woven bone area,(12,13) and the reduced cortical bone area caused by cortical thinning and increased cortical porosity.[14,15] The long-term reduction of osteocyte number generally leads to increased fracture risk.[16]

  • Total parathyroidectomy (PTX) with immediate autotransplantation of 150 mg of diffuse hyperplastic parathyroid tissue is really important in patients with severe renal hyperparathyroidism.[7,19] Osteoblast surface (Ob.S/BS) increases 1 week after parathyroidectomy and low turnover osteomalacia with severe hypophosphatemia transiently develops 4 weeks after the surgery, thereafter, serum phosphorus level gradually increases

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Summary

Introduction

Accumulated evidence suggests that the osteocyte is a crucial determinant of bone strength. Total parathyroidectomy (PTX) with immediate autotransplantation of 150 mg of diffuse hyperplastic parathyroid tissue is really important in patients with severe renal hyperparathyroidism.[7,19] Osteoblast surface (Ob.S/BS) increases 1 week after parathyroidectomy and low turnover osteomalacia with severe hypophosphatemia transiently develops 4 weeks after the surgery, thereafter, serum phosphorus level gradually increases. The importance of vitamin D in the mineralization by osteocytes was investigated in hemodialysis patients who underwent total parathyroidectomy (PTX) with immediate autotransplantation of diffuse hyperplastic parathyroid tissue. In 15 patients, the serum calcium levels were maintained by subsequent administration of alfacalcidol (2.0 μg/day), intravenous calcium gluconate, and oral calcium carbonate for four weeks after PTX (Group I).

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