Abstract
At present, the questions of influence of the main characteristics of type 2 diabetes mellitus (T2DM) (carbohydrate metabolism parameters, duration of disease, especially glucoselowering therapy) on bone tissue, especially during menopause, are poorly studied and remain controversial requiring further studiesy. The purpose — an evaluation of T2DM effect on the state of bone remodelling in women, depending on age, duration of postmenopause, type of hypoglycemic therapy. Materials and methods. The state of bone metabolism was evaluated by the content of serum β-CrossLaps with an automated immunoassay analyzer «Cobas e 411 ROSHE HITACHI» (Germany) by immunoenzymatic method using β-CrossLaps/ serum ROSHE reagents. The study involved 101 women who were divided into three groups: 14 healthy women of late reproductive age without menstrual dysfunction, 56 practically healthy postmenopausal women, 31 postmenopausal women with T2DM. The evaluation of β-CrossLaps in postmenopausal women with T2DM was performed in 37 patients, divided into 2 subgroups, depending on the type of hypoglycemic therapy. Women of first subgroup were received oral hypoglycemic agents (22 patients). Women of second subgroup were taken insulintherapy (12 patients). Results. The concentration of serum β-CrossLaps in postmenopausal women with T2DM was significantly lower compared with postmenopausal women without diabetes mellitus (0.647±0.039 ng/mL, 0.388±0.031 ng/ml, р<0,001). Identified changes in the bone remodelling do not depend on age, duration of postmenopause, the degree of compensation of carbohydrate metabolism and type of hypoglycemic therapy. Conclusions. The level of bone remodelling in women of late reproductive age and in healthy postmenopausal women does not differ. T2DM slows down the process of bone remodelling in women of different age and is not dependent on menopausal duration. The intensity of bone remodelling processes in postmenopausal women with T2DM is not dependent on type of treatment (insulin therapy or oral hypoglycemic agents).