Observation of bone mineral density in Cushing syndrome

G. Narimova*^a (Dr), S. Ergashova^a (Dr), M. Narimova^b (Dr)

^a Republican Specilized-Scientific medical center of endocrinology, Uzbekistan, Tashkent, UZBEKISTAN ; ^b Republican Scientific Center of Emergency Medical Care, Tashkent, UZBEKISTAN

* Narimova71@mail.ru

One of the systemic manifestations of excess glucocorticoids (GC) is the development of glucocorticoid osteoporosis, accompanied by a decrease in bone mineral density (BMD) and fractures with minimal injury. Clinically, a slight decrease in BMD is observed, mainly in the lumbar spine, which indicates the greatest effect of GC on trabecular bone tissue.
Purpose: To analyze the mineral density of bone tissue in patients with Cushing syndrome (CS) condition registered in the CS register in Uzbekistan from 2000-2021.
Materials and methods: Analysis of BMD was carried out in patients with CS condition registered in the CS register in Uzbekistan from 2000-2021. All patients underwent hormonal blood tests (determination of the level of adrenocorticotropic hormone (ACTH), the rhythm of cortisol secretion, cortisol of daily urine) and biochemical studies (calcium). For the determination of BMD bone densitometry.
Results: BMD was analyzed in 235 patients with various types of SC, who were examined and treated at the Republican Specialized Scientific and Practical Medical Center of Endocrinology (Tashkent) in the period 2000-2021. The average age of patients is 33.25 ± 1.02 years. All complications of bone mineral density disorder were reported in 87.9%, of which osteopenia was detected in 29.6 % and osteoporosis in 58.3%. Pathological fractures were diagnosed in 12 (5.1%) patients, of which 75% had a compression fracture of the thoracic or lumbar spine. Pre-treatment hormonal spectrum analysis: morning and nocturnal cortisol 895.9±43.2 and 697.4±39.7 nmol/L; daily urine cortisol 368.1±20.9; ACTH 66.8±4.6 ng/mL; insulin 15.5±0.6 mMe/ml. The blood calcium level was 2.14±0.12 mmol/L.
Conclusion: Structural and functional changes in bone tissue lead to disability of patients and a decrease in the quality of life in the active stage of endogenous hypercortisolism. Early detection of characteristic bone mass changes in hypercortisolism contributes to early detection of bone loss and timely treatment, thereby reducing the occurrence of side effects such as fractures.

The author has declared no conflict of interest.