ホルモン受容体陽性乳がんの閉経後女性におけるがん治療誘発性骨量減少に対するロモソズマブ：症例シリーズ

UNLABELLED: Romosozumab was associated with increases in bone mineral density in postmenopausal women with hormone receptor-positive breast cancer and cancer treatment-induced bone loss (CTIBL). No clinical signals of fracture occurrence or cancer recurrence were observed; however, these findings are based on a small retrospective case series and require confirmation in larger prospective studies. BACKGROUND: Cancer treatment-induced bone loss (CTIBL) is a major complication in postmenopausal women with hormone receptor-positive breast cancer receiving aromatase inhibitor therapy. Although antiresorptive agents are commonly used, some patients continue to experience progressive bone loss or fragility fractures. Romosozumab, a monoclonal antibody against sclerostin, has demonstrated efficacy in postmenopausal osteoporosis; however, clinical data in patients with cancer remain limited. METHODS: We retrospectively analyzed 22 postmenopausal women with clinically non-metastatic (Stage I-III) hormone receptor-positive breast cancer who received romosozumab for CTIBL at a single institution. Romosozumab was administered for 12 months in patients with progressive bone loss, new fragility fractures, or high fracture risk. All patients received concomitant calcium and/or active vitamin D supplementation. Changes in bone mineral density (BMD), bone turnover markers, and tumor markers (CA15-3, CEA) were evaluated. Differences in skeletal response were also evaluated between treatment-naïve patients and those with prior exposure to bone-modifying agents. Clinical outcomes, including new fragility fractures and cancer recurrence, were assessed during follow-up. RESULTS: The mean age of the patients was 66.8 years, and the mean duration of aromatase inhibitor therapy prior to treatment was 35.3 months to 36.9 months. After 12 months of romosozumab treatment, lumbar spine BMD increased by 11.5% (P < 0.001), and total hip BMD increased by 4.1% (P = 0.002). Changes in bone turnover markers were observed, consistent with the known mechanism of action of romosozumab. No new fragility fractures were observed during the treatment period. During a mean follow-up period of 38.3 months (including the 12-month treatment period), tumor markers remained stable, and no clinical evidence of cancer recurrence was observed. CONCLUSIONS: In this small retrospective case series, romosozumab was associated with increases in BMD in postmenopausal women with hormone receptor-positive breast cancer and CTIBL. No clinical signals suggestive of short-term oncological deterioration were observed; however, given the limited sample size, retrospective design, and lack of a control group, these findings should be interpreted with caution. Further prospective studies with larger cohorts and longer follow-up are required to better define the efficacy and safety of romosozumab in this population.