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Bone and Mineral Metabolism

MON-806 - Blood cell count parameter changes following PTH analog treatment in a real-world case series

Monday, June 15, 2026
9:00 AM - 2:00 PM CT


Background: In preclinical models, parathyroid hormone receptor (PTH1R) signaling in the osteoblast lineage regulates hematopoiesis. In limited human studies, observational data suggest that patients with hyperparathyroidism can recover from anemia, thrombocytopenia or leukopenia after parathyroidectomy. Additionally, teriparatide has been shown to increase circulating hematopoietic stem cells in in postmenopausal women with osteoporosis. Despite these findings, there remains a lack of large-scale clinical studies investigating changes in blood cell counts following parathyroid hormone (PTH) analog treatment in humans. This study aims to investigate the effects of PTH analog therapy on blood cell counts among patients with osteoporosis using real-world clinical data.

Method: We conducted a retrospective analysis using the Atropos Health Apollo (Ver 2.0.0) electronic health record dataset representing 161 million patients seen in community hospitals and academic medical centers across the US from January 2010 to October 2025. Eligible patients included those aged ≥50 years old with a diagnosis of osteoporosis who had received PTH analog therapy (either teriparatide or abaloparatide) for more than one year with available blood cell count data, including hematocrit (HCT), red blood cell (RBC) count, white blood cell (WBC) count, and platelets, at baseline (6 months to 1 day prior to start of PTH therapy) and 6 to 12 months after the initiation of PTH analog therapy. Changes in these parameters were analyzed statistically using a paired t-test.
Result: A total of 251 patients were analyzed, predominately female (87.3%) and white (66.1%) with a mean age of 68.5. Majority (76.9%) of patients received teriparatide while 23.1% received abaloparatide. Anemia was present in 21.9% of patients, and 18.3% had eGFR < 60. The most prevalent comorbidities were chronic pulmonary disease (43.0%) and peripheral vascular disease (27.9%). Significant findings included a decrease in platelet count from 265.1±84.6×10⁹/L at baseline to 253.9±71.5×10⁹/L at 6-12 months after initiation of PTH treatment (p=0.031). No significant differences were observed in HCT, RBC or WBC counts.

Conclusion: Over a treatment period of 6 to 12 months, PTH analog therapy was associated with a modest yet significant decrease in platelet count, which remained within the normal range. While earlier studies have suggested a possible influence of parathyroid hormone on platelet biology through modulation of bone marrow microenvironment, this study is the first to identify a decrease in platelet count during PTH analog treatment. Further studies are needed to elucidate the mechanism by which PTH analog impacts platelet levels in humans.

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