Changes in serum receptor activator of nuclear factor-κb ligand, osteoprotegerin, and interleukin-6 levels in patients with glucocorticoid- induced osteoporosis treated with human parathyroid hormone (1-34)

Eric C. Buxton, Wei Yao, Nancy E Lane

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    Abstract

    Changes in biochemical markers of bone turnover following intermittent injections of human (h)PTH (1-34) suggest that bone formation is initially favored over bone resorption. hPTH (1-34) is also known to influence osteoclast maturation and activity through modulation of osteoblast-derived cytokines, such as receptor activator of nuclear factor-κB ligand (RANKL), osteoprotegerin (OPG), IL-6, and IL-6 soluble receptor (IL-6sR). In this experiment, we investigated the changes in serum levels of soluble RANKL (sRANKL), OPG, IL-6, and IL-6sR in patients with glucocorticoid-induced osteoporosis treated with hPTH (1-34). Fifty-one postmenopausal women with glucocorticoid-induced osteoporosis were randomized to receive 12 months of 400 U hPTH (1-34) (∼40 μg) daily and standard hormone replacement therapy, or hormone replacement therapy alone. Serum levels of sRANKL, OPG, IL-6, and IL-6sR were measured at baseline, 1 month, and every 3 months thereafter for a total of 24 months. hPTH (1-34) caused a rapid and significant increase in sRANKL within 1 month, and the levels remained elevated throughout the duration of therapy. IL-6 and IL-6sR increased significantly within 1 month, but returned to baseline levels more rapidly. In contrast, OPG was mildly suppressed beginning 6 months after hPTH therapy. These data support the hypothesis that hPTH (1-34) initially stimulates osteoblast maturation and function, which in turn leads to osteoclast activation and a gradual rebalancing of bone formation and resorption.

    Original languageEnglish (US)
    Pages (from-to)3332-3336
    Number of pages5
    JournalJournal of Clinical Endocrinology and Metabolism
    Volume89
    Issue number7
    DOIs
    StatePublished - Jul 2004

    Fingerprint

    Teriparatide
    RANK Ligand
    Interleukin-6 Receptors
    Cytoplasmic and Nuclear Receptors
    Glucocorticoids
    Osteoporosis
    Interleukin-6
    Osteoprotegerin
    Serum
    Hormone Replacement Therapy
    Osteoclasts
    Bone Resorption
    Bone
    Osteoblasts
    Osteogenesis
    Bone Remodeling
    Parathyroid Hormone
    Hormones
    Biomarkers
    Cytokines

    ASJC Scopus subject areas

    • Biochemistry
    • Endocrinology, Diabetes and Metabolism

    Cite this

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    abstract = "Changes in biochemical markers of bone turnover following intermittent injections of human (h)PTH (1-34) suggest that bone formation is initially favored over bone resorption. hPTH (1-34) is also known to influence osteoclast maturation and activity through modulation of osteoblast-derived cytokines, such as receptor activator of nuclear factor-κB ligand (RANKL), osteoprotegerin (OPG), IL-6, and IL-6 soluble receptor (IL-6sR). In this experiment, we investigated the changes in serum levels of soluble RANKL (sRANKL), OPG, IL-6, and IL-6sR in patients with glucocorticoid-induced osteoporosis treated with hPTH (1-34). Fifty-one postmenopausal women with glucocorticoid-induced osteoporosis were randomized to receive 12 months of 400 U hPTH (1-34) (∼40 μg) daily and standard hormone replacement therapy, or hormone replacement therapy alone. Serum levels of sRANKL, OPG, IL-6, and IL-6sR were measured at baseline, 1 month, and every 3 months thereafter for a total of 24 months. hPTH (1-34) caused a rapid and significant increase in sRANKL within 1 month, and the levels remained elevated throughout the duration of therapy. IL-6 and IL-6sR increased significantly within 1 month, but returned to baseline levels more rapidly. In contrast, OPG was mildly suppressed beginning 6 months after hPTH therapy. These data support the hypothesis that hPTH (1-34) initially stimulates osteoblast maturation and function, which in turn leads to osteoclast activation and a gradual rebalancing of bone formation and resorption.",
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    AU - Lane, Nancy E

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