Recombinant parathyroid hormone(Beijing SL Pharmaceutical Co., Ltd.)

Accumulating evidence highlights the critical role of circadian rhythms in regulating bone turnover. Bone turnover markers, including parathyroid hormone, C-terminal telopeptide of type I collagen, and N-terminal propeptide of type I procollagen, all exhibit distinct diurnal variations. Teriparatide, a recombinant parathyroid hormone analog, demonstrates time-dependent efficacy influenced by these endogenous rhythms. However, the impact of administration timing on bone metabolism remains underexplored.

This randomized, open-label, exploratory trial investigates the impact of teriparatide administration timing by comparing subcutaneous injection at 08:00 versus 20:00 on bone turnover markers in postmenopausal women with osteoporosis.

Twenty-eight participants (aged 60-70 years, lumbar spine T-score ≤ -3.0) will be randomized in a 1:1 ratio to receive 20 µg/day of teriparatide via subcutaneous injection at either 08:00 or 20:00 for 12 weeks. All participants will receive standardized calcium (1000-1500 mg/day) and cholecalciferol (800-1200 IU/day) supplementation throughout the study period. The primary outcomes are the between-group differences in serum parathyroid hormone, C-terminal telopeptide of type I collagen, and N-terminal propeptide of type I procollagen profiles, which will be assessed at baseline, 4 weeks, and 12 weeks. Secondary outcomes will evaluate the safety profile during the trial.

This trial is expected to provide crucial insights into optimizing teriparatide administration timing, potentially guiding personalized dosing strategies to enhance bone formation and reduce fracture risk in osteoporosis. The findings may inform future research on circadian rhythm-aligned therapies.

ClinicalTrials.gov ID NCT06951776.

Glucocorticoid use is ubiquitous and is associated with multiple adverse reactions. Among them, osteoporosis and bone fractures are of our concern. In this review, we present current evidence on the effect of glucocorticoids on bone mineral density and the risk of fractures, the mechanisms underlying those effects, and the recommendations for monitoring and treating patients who take them. The bone mineral density of the lumbar spine and total hip is lower, and the risk of fractures is higher in glucocorticoid users than non-users. These effects have a rapid onset, are dose-dependent, and improve soon after discontinuation of glucocorticoids. They also appear to occur even with non-systemic routes of administration and with low doses. Glucocorticoids reduce bone mineral density by increasing osteoclast activity and decreasing osteoblast and osteocyte activity. Calcium metabolism and parathyroid hormone activity are less important than was initially thought. Treatment decisions are on risk stratification using clinical, radiographic, and prediction tools. Our armamentarium for the treatment and prevention of glucocorticoid-induced osteoporosis includes calcium and vitamin D, bisphosphonates, recombinant parathyroid hormone, monoclonal antibodies against receptor activator of nuclear factor kappa-B ligand, and hormone treatments.