Association of bone microarchitecture with parathyroid hormone concentration and calcium intake in men: the STRAMBO study.

UNLABELLED: OBJECTVIE: In the elderly, vitamin D deficit, low calcium intake, and impaired bone microarchitecture are associated with higher risk of hip fracture. We assessed the association of bone microarchitecture with calcium intake and serum concentrations of 25-hydroxycholecalciferol (25OHD) and parathyroid hormone (PTH) in men. DESIGN: Cross-sectional analysis was performed in 1064 men aged 20-87 years not taking vitamin D or calcium supplements. METHODS: Daily calcium intake was assessed using a food frequency questionnaire. Bone microarchitecture was assessed at distal radius and tibia by high-resolution peripheral quantitative computed tomography. We measured serum and urinary levels of biochemical bone turnover markers (BTMs). Statistical models were adjusted for age, weight, height, and glomerular filtration rate. RESULTS: In 500 men aged <65 years, lower 25OHD levels and low calcium intake were associated with lower trabecular volumetric bone mineral density (Dtrab) at the distal tibia, due to lower trabecular number (Tb.N). Low calcium intake was associated with lower cortical thickness (Ct.Th). Higher PTH level was associated with higher BTM levels. In 563 men aged ≥65 years, the highest PTH quartile was associated with lower Ct.Th (tibia), lower Dtrab (both sites), and lower Tb.N (radius) compared with the lowest quartile. Low calcium intake was associated with lower Tb.N and more heterogenous trabecular distribution. BTM positively correlated with the PTH concentration. CONCLUSION: In older men, elevated PTH concentration is associated with high bone turnover, poor trabecular microarchitecture (radius and tibia), and, at the distal tibia, lower Ct.Th. Low calcium intake is associated with lower Tb.N and more heterogenous trabecular distribution.

[Adrenal cortex and avitaminosis A: II. Complementary in vivo and in vitro studies on inhibition of corticoidogenesis in moderate deficiency in the rat. III. In vivo criterion for activity: glycemic response to ACTH]. / Corticosurrénale et avitaminose A: II. Compléments a l'étude in vivo et in vitro; modalités d'inhibition de la corticoidogenèse en carence modérée chez le rat. III. Recherche d'un critère d'activité utilisable in vivo; réponse glycémique a l'ACTH

II. We set up new experiments, both in vivo and in vitro, in order to explain the impaired adrenal response to stress, of vitamin A middly deficient, male Wistar rats. Injections of progesterone, 6 mg s.c. or i.p. every other day, did not improve the deficiency curse in our rats. In agreement with these results, we have found that, in vitro, the delta5-3beta hydroxysteroide dehydrogenase is not altered in deficient glands; we confirmed it histochemically. On the other hand, the 11beta and 18 hydroxylase activities are lowered in vitro (and presumably in vivo). When conditions of hyperactivity are established, the conversion of deoxycorticosterone (DOC) to 18 OH-DOC or to corticosterone is reduced and DOC accumulates in the incubation medium. III. When middly deficient intact rats are injected with ACTH i.p. (2UI p. 100 g of body weight), only some of them are found to have normoglycemia or hyperglycemia, 45 or 60 minutes after injection, as the controls do. Many deficient rats become hypoglycemic as the adrenalectomised animals do. We think that the changes in the glycemia after ACTH injection could be used to discriminate between the more or less deficient rats.