Effects of sex steroids on bone in women with subclinical or overt endogenous hypercortisolism.
OBJECTIVE
Glucocorticoid-induced osteoporosis is the most frequent cause of secondary osteoporosis. Nevertheless, limited data are available on bone status in patients with endogenous cortisol excess. This study is aimed at investigating the role of sex steroids and severity of hypercortisolism on bone mineral density (BMD) and prevalence of vertebral fractures in female patients.


METHODS
Cross-sectional, case-control study.


METHODS
Seventy-one consecutive women were enrolled: 36 with overt hypercortisolism (26 with ACTH-secreting pituitary adenoma and 10 with cortisol-secreting adrenal tumor) and 35 with subclinical hypercortisolism due to adrenal incidentalomas. They were compared with 71 matched controls.


METHODS
At diagnosis, we measured serum cortisol, FSH, LH, estradiol, testosterone, androstenedione and DHEAS, and urinary cortisol excretion. BMD was determined by dual energy X-ray absorptiometry at the lumbar spine and femoral neck. Vertebral fractures were investigated by a semiquantitative scoring method.


RESULTS
Between women with overt and subclinical hypercortisolism BMD values and prevalence of any vertebral (69 vs 57%, P = 0.56), clinical (28 vs 11.4%, P = 0.22), and multiple vertebral fractures (36 vs 31%, P = 0.92) did not differ. Among patients with subclinical hypercortisolism, amenorrhoic women had a lower BMD (P = 0.035) and more frequent vertebral fractures (80 vs 40%; P = 0.043) when compared with the eumenorrhoic ones. Among women with overt hypercortisolism, there was no difference in lumbar BMD (P = 0.37) and prevalence of fractures (81 vs 60%; P = 0.26) between those amenorrhoic and eumenorrhoic. By logistic regression analysis, lumbar spine BMD values and cortisol-to-DHEAS ratio were the best predictors of vertebral fractures (P < 0.01).


CONCLUSIONS
Vertebral fractures are very common in women with endogenous cortisol excess, regardless of its severity. The deleterious effects of hypercortisolism on the spine may be partly counterbalanced by DHEAS increase at any degree of cortisol excess, and by preserved menstrual cycles in women with subclinical but not in those with overt hypercortisolism.
Tauchmanovà
Libuse
L
Department of Molecular and Clinical Endocrinology and Oncology, Federico II University of Naples, Naples, Italy. tauchman@unina.it
Pivonello
Rosario
R
De Martino
Maria Cristina
MC
Rusciano
Andrea
A
De Leo
Monica
M
Ruosi
Carlo
C
Mainolfi
Ciro
C
Lombardi
Gaetano
G
Salvatore
Marco
M
Colao
Annamaria
A
D015502:Absorptiometry, Photon; D000328:Adult; D000368:Aged; D000735:Androstenedione / Q000097:blood; D015519:Bone Density; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D003480:Cushing Syndrome / Q000453:epidemiology* / Q000378:metabolism*; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D012739:Gonadal Steroid Hormones / Q000097:blood*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008875:Middle Aged; D010024:Osteoporosis / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000378:metabolism*; D012720:Severity of Illness Index; D016103:Spinal Fractures / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000378:metabolism*; D013739:Testosterone / Q000097:blood
D012739:Gonadal Steroid Hormones; D013739:Testosterone; D000735:Androstenedione; D004958:Estradiol; D019314:Dehydroepiandrosterone Sulfate; D005640:Follicle Stimulating Hormone; D006854:Hydrocortisone