Osteoporosis and sarcopenia · 2026
Effect of genetic polymorphisms of aldehyde dehydrogenase 2 on the efficacy of intermittent parathyroid hormone treatment and bone mineral density: A retrospective multicenter study.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Obara Hinako, Tajima Takafumi, Tsukamoto Manabu, Yamanaka Yoshiaki, Suzuki Hitoshi, Nagashima Masato, Nishida Satoshi, Ikeda Satoshi, Maekawa Kazumichi, Sakai Akinori
Аннотация
OBJECTIVES: In a mouse model, aldehyde dehydrogenase 2 (ALDH2) knockout resulted in lower bone mineral density; however, higher parathyroid hormone receptor expression than wild-type mice. This study aimed to investigate whether ALDH2 polymorphisms influence efficacy of intermittent parathyroid hormone therapy and bone mineral density changes in humans.
METHODS: Eighty-two patients with primary osteoporosis treated with parathyroid hormone for > 1 year were divided into wild-type ALDH2 (ALDH2∗1) and variant (ALDH2∗2) groups. Bone mineral densities were measured by dual-energy X-ray absorptiometry. Changes in bone mineral density, treatment response, bone turnover markers, and new fracture incidence were evaluated. Furthermore, bone mineral density was analyzed using a mixed-effects model.
RESULTS: Femoral neck bone mineral density increased by 1.0 ± 7.4% in the ALDH2∗1 group and 4.3 ± 8.1% in the ALDH2∗2 group (P < 0.05), whereas lumbar spine bone mineral density increased by 5.7 ± 8.2% and 9.4 ± 9.1% without significance. Treatment success rates were higher in ALDH2∗2 group (femoral neck 38.7%, lumbar spine 68.8%) compared with ALDH2∗1 (16.3%, 51.0%). Statistical significance was observed only at the femoral neck. Bone turnover markers and fracture incidence were comparable between groups. Mixed-effects analysis adjusting for confounders showed a significant ALDH2 genotype × duration interaction for femoral neck, indicating genotype-related differences in the rate of bone mineral density increase over time. For lumbar spine, the genotype main effect was significant, whereas the interaction was not.
CONCLUSIONS: These findings suggest that ALDH2 polymorphisms may influence the therapeutic response to PTH treatment and highlight the need for larger future studies.
METHODS: Eighty-two patients with primary osteoporosis treated with parathyroid hormone for > 1 year were divided into wild-type ALDH2 (ALDH2∗1) and variant (ALDH2∗2) groups. Bone mineral densities were measured by dual-energy X-ray absorptiometry. Changes in bone mineral density, treatment response, bone turnover markers, and new fracture incidence were evaluated. Furthermore, bone mineral density was analyzed using a mixed-effects model.
RESULTS: Femoral neck bone mineral density increased by 1.0 ± 7.4% in the ALDH2∗1 group and 4.3 ± 8.1% in the ALDH2∗2 group (P < 0.05), whereas lumbar spine bone mineral density increased by 5.7 ± 8.2% and 9.4 ± 9.1% without significance. Treatment success rates were higher in ALDH2∗2 group (femoral neck 38.7%, lumbar spine 68.8%) compared with ALDH2∗1 (16.3%, 51.0%). Statistical significance was observed only at the femoral neck. Bone turnover markers and fracture incidence were comparable between groups. Mixed-effects analysis adjusting for confounders showed a significant ALDH2 genotype × duration interaction for femoral neck, indicating genotype-related differences in the rate of bone mineral density increase over time. For lumbar spine, the genotype main effect was significant, whereas the interaction was not.
CONCLUSIONS: These findings suggest that ALDH2 polymorphisms may influence the therapeutic response to PTH treatment and highlight the need for larger future studies.