Impact of aromatase inhibitor treatment on vertebral morphology and bone mineral density in postmenopausal women with breast cancer.

OBJECTIVE: The aim of this study was to evaluate the impact of aromatase inhibitor (AI) treatment on vertebral morphology by vertebral fracture assessment in postmenopausal women with early-stage breast cancer. METHODS: A clinical cross-sectional study was conducted. A group of 156 postmenopausal women with breast cancer (mean [SD] age, 60.4 [10.1] y; mean [SD] time since menopause, 11.7 [9.2] y) was included in the study. Eighty-two women received AI treatment, whereas 74 women did not. Women underwent extensive medical history check and risk factor assessment together with vertebral morphology and bone mineral density (BMD) evaluation. RESULTS: In the studied population, the prevalence of vertebral fractures identified by vertebral fracture assessment was 16.6%. Multivariate analysis showed that AI treatment was significantly associated with vertebral fractures (adjusted P < 0.04). Women receiving AI treatment had a higher prevalence of vertebral fractures than women not treated with AIs (25.6% vs. 4%). The risk of vertebral fractures in women treated with AIs was significantly higher than in non-AI-treated women (adjusted odds ratio, 4.7; P < 0.005). Vertebral fractures of the highest grade were identified at the lumbar spine. Women treated with AIs had a significantly lower BMD than women not treated with AIs (P < 0.01). Reduction of BMD was significantly associated with length of therapy, whereas there was no association between length of treatment and risk of vertebral fractures. CONCLUSIONS: AI treatment severely impacts vertebral morphology. Our study demonstrates a high prevalence of asymptomatic vertebral fractures in women treated with AIs.

Glucocorticoid therapy as a significant risk factor for osteoporosis and fractures in an Italian postmenopausal population.

OBJECTIVE: To analyze the potential effects of glucocorticoid treatment without an osteoporosis prevention strategy and to precociously identify patients at high risk of osteoporosis and fragility fractures in the postmenopausal period. METHODS: A total of 382 postmenopausal patients, 177 exposed and 205 not exposed to glucocorticoid therapy, were studied using a standard questionnaire. Epidemiological as well as clinical data that included the most recent absorptiometry test results were examined. RESULTS: Osteoporosis and fractures were frequent in the postmenopausal glucocorticoid-treated patients. Fragility fractures occurred more frequently in glucocorticoid-treated patients (vertebral fractures represented 45% of all fractures) than in the non-glucocorticoid-treated patients. In particular, the highest fracture percentage was found in 50- to 65-year-old glucocorticoid-treated patients, a subset of patients showing a prevalence of osteoporosis similar to that of non-exposed menopausal subjects older than 65. Glucocorticoid therapy increases the risk of fragility fractures fivefold and doubles the risk of osteoporosis in menopausal patients. CONCLUSIONS: Glucocorticoid treatments put menopausal patients at a high risk of incurring fragility fractures even in the early postmenopausal period. The management of strategies for fracture prevention must take into consideration early intervention in patients undergoing or about to undergo glucocorticoid treatment.

High-normal TSH values in obesity: is it insulin resistance or adipose tissue's guilt?

OBJECTIVE: Clinical evidences reported subclinical alterations of thyroid function in obesity, although the relationship between thyroid status and obesity remains unclear. We cross-sectionally investigated the influence of metabolic features on hypothalamic-pituitary-thyroid axis in obesity. DESIGN AND METHODS: We enrolled 60 euthyroid subjects with no history of type 2 diabetes mellitus and assessed the relationship of thyroid function with insulin resistance, measured using euglycemic clamp, and abdominal fat volume, quantified by computed tomography scan (CT scan). Thyroid stimulating hormone (TSH) correlated with BMI (r = 0.46; P = 0.02), both visceral (r = 0.58; P = 0.02) and subcutaneous adipose tissue volumes (r = 0.43; P = 0.03) and insulin resistance (inverse relationship with insulin sensitivity-glucose uptake: r = -0.40; P = 0.04). RESULTS: After performing multivariate regression, visceral adipose tissue volume was found to be the most powerful predictor of TSH (ß = 3.05; P = 0.01), whereas glucose uptake, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, subcutaneous adipose tissue volume, and triglycerides were not. To further confirm the hypothesis that high-normal TSH values could be dependent on adipose tissue, and not on insulin resistance, we restricted our analyses to moderately obese subjects' BMI ranging 30-35 kg/m(2). This subgroup was then divided as insulin resistant and insulin sensitive according to the glucose uptake (≤ or >5 mg · kg(-1) · min(-1), respectively). We did not find any statistical difference in TSH (insulin resistant: 1.62 ± 0.65 µU/ml vs. insulin sensitive: 1.46 ± 0.48; P = not significant) and BMI (insulin resistant: 32.2 ± 1.6 kg/m(2) vs. insulin sensitive: 32.4 ± 1.4; P = not significant), thus confirming absence of correlation between thyroid function and insulin sensitivity per se. CONCLUSION: Our study suggests that the increase in visceral adipose tissue is the best predictor of TSH concentration in obesity, independently from the eventual concurrent presence of insulin resistance.