Decreased blood lead levels after calcitriol treatment in hemodialysis patients with secondary hyperparathyroidism. 2011

Kuo-Cheng Lu, and Chia-Chao Wu, and Wen-Ya Ma, and Chun-Chi Chen, and Hsin-Chi Wu, and Pauling Chu
Division of Nepheology, Department of Medicine, Cardinal Tien Hospital, School of Medicine, Fu-Jen Catholic University, New Taipei, Taiwan. kuochenglu@gmail.com

OBJECTIVE Secondary hyperparathyroidism (SHP) is characterized by high bone turnover, which may, in turn, result in increased release of lead from bone stores. This study investigated the effects of intravenous calcitriol on blood lead (BL) levels in patients with SHP. METHODS Intravenous calcitriol therapy was administered for 16 wk to 28 patients who were on maintenance hemodialysis (HD) and had intact parathyroid hormone (iPTH) plasma levels of >300 pg/mL. Blood was drawn at baseline and every 4 wk for 16 wk to determine the levels of iPTH; bone remodeling markers, including bone-specific alkaline phosphatase (bAP) and type 5b tartrate-resistant acid phosphatase (TRAP); and BL. RESULTS Of the 28 patients, 25 responded to calcitriol therapy; they exhibited significant decrements in serum iPTH levels by the end of 4 wk of therapy and thereafter. After 16 wk of therapy, these patients had significant reductions in serum iPTH levels (p<0.01) and significant and parallel decreases in the levels of bAP (p<0.01), TRAP (p<0.01), and BL (p<0.01). Further analysis showed a significant positive correlation between the levels of BL and serum iPTH (r=0.34, p<0.01) and BL and serum TRAP (r=0.22, p<0.05). However, there was no significant correlation between the levels of BL and serum bAP. CONCLUSIONS Elevated levels of BL and serum bone remodeling markers, which are common features of SHP, can be effectively suppressed by calcitriol therapy. This indicates that hyperparathyroidism not only accelerates bone remodeling but may also enhance bone lead mobilization in patients on maintenance HD.

UI MeSH Term Description Entries
D006962 Hyperparathyroidism, Secondary Abnormally elevated PARATHYROID HORMONE secretion as a response to HYPOCALCEMIA. It is caused by chronic KIDNEY FAILURE or other abnormalities in the controls of bone and mineral metabolism, leading to various BONE DISEASES, such as RENAL OSTEODYSTROPHY. Secondary Hyperparathyroidism,Hyperparathyroidisms, Secondary,Secondary Hyperparathyroidisms
D007527 Isoenzymes Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics. Alloenzyme,Allozyme,Isoenzyme,Isozyme,Isozymes,Alloenzymes,Allozymes
D007854 Lead A soft, grayish metal with poisonous salts; atomic number 82, atomic weight 207.2, symbol Pb.
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D010281 Parathyroid Hormone A polypeptide hormone (84 amino acid residues) secreted by the PARATHYROID GLANDS which performs the essential role of maintaining intracellular CALCIUM levels in the body. Parathyroid hormone increases intracellular calcium by promoting the release of CALCIUM from BONE, increases the intestinal absorption of calcium, increases the renal tubular reabsorption of calcium, and increases the renal excretion of phosphates. Natpara,PTH (1-84),PTH(1-34),Parathormone,Parathyrin,Parathyroid Hormone (1-34),Parathyroid Hormone (1-84),Parathyroid Hormone Peptide (1-34),Hormone, Parathyroid
D001842 Bone and Bones A specialized CONNECTIVE TISSUE that is the main constituent of the SKELETON. The principal cellular component of bone is comprised of OSTEOBLASTS; OSTEOCYTES; and OSTEOCLASTS, while FIBRILLAR COLLAGENS and hydroxyapatite crystals form the BONE MATRIX. Bone Tissue,Bone and Bone,Bone,Bones,Bones and Bone,Bones and Bone Tissue,Bony Apophyses,Bony Apophysis,Condyle,Apophyses, Bony,Apophysis, Bony,Bone Tissues,Condyles,Tissue, Bone,Tissues, Bone
D002117 Calcitriol The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption. 1 alpha,25-Dihydroxycholecalciferol,1 alpha,25-Dihydroxyvitamin D3,1, 25-(OH)2D3,1,25(OH)2D3,1,25-Dihydroxycholecalciferol,1,25-Dihydroxyvitamin D3,1 alpha, 25-dihydroxy-20-epi-Vitamin D3,1,25(OH)2-20epi-D3,1,25-dihydroxy-20-epi-Vitamin D3,20-epi-1alpha,25-dihydroxycholecaliferol,Bocatriol,Calcijex,Calcitriol KyraMed,Calcitriol-Nefro,Decostriol,MC-1288,MC1288,Osteotriol,Renatriol,Rocaltrol,Silkis,Sitriol,Soltriol,Tirocal,1 alpha,25 Dihydroxyvitamin D3,1,25 Dihydroxycholecalciferol,1,25 Dihydroxyvitamin D3,1,25 dihydroxy 20 epi Vitamin D3,Calcitriol Nefro,D3, 1 alpha,25-Dihydroxyvitamin,D3, 1,25-Dihydroxyvitamin,D3, 1,25-dihydroxy-20-epi-Vitamin,KyraMed, Calcitriol,MC 1288
D005260 Female Females
D006435 Renal Dialysis Therapy for the insufficient cleansing of the BLOOD by the kidneys based on dialysis and including hemodialysis, PERITONEAL DIALYSIS, and HEMODIAFILTRATION. Dialysis, Extracorporeal,Dialysis, Renal,Extracorporeal Dialysis,Hemodialysis,Dialyses, Extracorporeal,Dialyses, Renal,Extracorporeal Dialyses,Hemodialyses,Renal Dialyses

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