Glucocorticoid-Induced Osteoporosis

The use of glucocorticoids (GC) in the medium and long term, causes several considerable side effects, being one of the main ones the reduction of bone mineral density (BMD). Prolonged corticosteroid therapy reduces BMD by up to 20% in trabecular bone and approximately 2–3% in cortical bone in the first year of use. This loss rate declines and stabilizes at approximately 2% in subsequent years. Therefore, there is a considerable increase in the incidence of pathological fractures, whether clinically symptomatic or asymptomatic (detected as a radiological finding), which varies between 30 and 50% of patients who use GC for more than three months. In view of the above, it is essential to prevent fractures and treat osteoporosis in patients using glucocorticoids for long periods (in particular, greater than or equal to 3 months), which may or may not be associated with clinical risk factors or previous fractures. The guidelines for the treatment and prevention of this comorbidity are well established for postmenopausal women and men over 50 years of age. However, for patients below this range, studies are still lacking

Beyond the metabolic syndrome: Visceral and marrow adipose tissues impair bone quantity and quality in Cushing's disease.

The present study was designed to evaluate the relationship between bone traits [bone mineral density (BMD) and trabecular bone score (TBS)] and the accumulation of fat in adipose tissues [abdominal subcutaneous (SAT), visceral (VAT), marrow (MAT) and intrahepatic lipids (IHL)], as well as insulin resistance, in subjects with Cushing's disease (CD). The study included control (C = 27), paired (P = 16) and Cushing's disease (CD = 10) groups, which underwent biochemical assessment, dual X-ray absorptiometry, TBS, and magnetic resonance imaging to determine fat deposits. The CD group showed higher serum levels of glucose and insulin, as well as HOMA-IR values, but lower circulatory levels of osteocalcin, in comparison to C and P. The CD group exhibited lower L1-L4 BMD than P (P = 1.059 ± 0.141 vs CD = 0.935 ± 0.093 g/cm2, p < 0.05) (Fig 1A). The lumbar spine BMD from the C group was similar to the other groups. TBS was lower in CD than in P and C (C = 1.512±0.077 vs P = 1.405±0.150 vs CD = 1.135±0.136; p<0.05); there was also significant difference between C and P (p<0.05). MAT, VAT, and IHL were higher in CD than in C and P (p<0.05). Considering all subjects, there was a positive association between TBS with both lumbar spine BMD (R2 = 0.45; p<0.0001) and osteocalcin (R2 = 0.44; p = 0.05). TBS was negatively associated with MAT (R2 = 0.49; p = 0.01), VAT (R2 = 0.55; p<0.05), and HOMA-IR (R2 = 0.44; p<0.01). MAT was positively related with VAT (R2 = 0.44; p<0.01) and IHL (R2 = 0.41; p<0.05). In CD, insulin resistance and adipose tissue dysfunction, including high MAT, are active players in bone deterioration, as confirmed by lower lumbar spine BMD and lower TBS. Thus, our findings point to an additional component of the already well-known complex mechanisms of osteoporosis associated with hypercortisolism