Objective: Endogenous Cushing's syndrome (CS) is a known cause of secondary osteoporosis. Vertebral fractures (VFs) in endogenous CS may occur despite normal bone mineral density (BMD). Trabecular bone score (TBS) is a relatively new, noninvasive technique to assess bone microarchitecture. The objective of our study was to analyse the BMD and bone microarchitecture using TBS in endogenous CS and compare it with a group of age and sex-matched healthy controls, and also analyse the factors predicting BMD and TBS.Design: Cross-sectional study of cases and controls.Patients and measurements: We included 40 female patients with overt endogenous CS, out of which 32 were adrenocorticotropic hormone (ACTH)dependent CS and 8 were ACTH-independent. We also included 40 healthy, female controls. Both patients and controls were subjected to an assessment of biochemical parameters and BMD and TBS.Results: Patients with endogenous CS had significantly lower BMD at the lumbar spine, femoral neck, and total hip and significantly lower TBS than healthy controls (all p < .001), while no significant difference was noted in the distal radius BMD (p = .055). In endogenous CS, a large proportion of patients, n = 13 (32.5%) had normal BMD for age (BMD Z-score ≥ −2.0) with low TBS (L 1 -L 4 TBS ≤ 1.34). TBS correlated negatively with HbA1c (p = .006), and positively with serum T4 (p = .027).
Conclusion: TBS should be considered an important complementary tool in additionto BMD for the routine assessment of skeletal health in CS. K E Y W O R D S bone microarchitecture, bone mineral density, cortisol, Cushing's syndrome, trabecular bone score 1 | INTRODUCTION Endogenous Cushing's syndrome (CS) is a relatively rare endocrine disease with an incidence of 3.2 cases per million population per year. 1 Previous studies have shown that both exogenous and endogenous glucocorticoid excess leads to an increased risk of fragility fractures. 2 The underlying mechanisms include excess cortisol mediating negative calcium balance with decreased calcium re-absorption from the gut and impaired conversion of 25-hydroxyvitamin D [25(OH)D] to its active form, calcitriol. Excess cortisol also