Effect of long-term L-thyroxine treatment on bone mineral density in young adults with congenital hypothyroidism.

OBJECTIVE: To evaluate whether long-term L-thyroxine therapy in young adults with congenital hypothyroidism may affect bone mineral density (BMD). DESIGN: Thirty-seven subjects with congenital hypothyroidism, detected by neonatal screening and longitudinally followed from the time of diagnosis and treatment (26+/-4 days) up to the age of 17.8+/-1.0 years, were studied. METHODS: Spinal (L2-L4) BMD, measured by dual-energy X-ray densitometry, and bone quality, measured as amplitude-dependent speed of sound (Ad-SoS) by quantitative ultrasound, were evaluated. RESULTS: Z-score mean values (+/-s.d.) of BMD (-0.3+/-0.7) and Ad-SoS (-0.7+/-1. 1) were slightly below the average but within the normal range. Ad-SoS resulted in a z-score below -1 in 38% of patients as compared with BMD which resulted in a z-score below -1 in only 13.5% of subject. No significant differences were observed between males (BMD, -0.3+/-0.7; Ad-SoS, -0.9+/-1.0) and females (BMD, -0.3+/-0.7; Ad-SoS, -0.5+/-1.2) or when dividing patients on the basis of aetiological defects; ectopic gland (BMD, -0.3+/-0.6; Ad-SoS, -0.8+/-0.9), athyreosis (BMD, -0.3+/-0.9; Ad-SoS, -0.8+/-1.0) and eutopic gland (BMD, -0.3+/-0.8; Ad-SoS, -0.4+/-1.3). No significant relationships were observed between BMD or Ad-SoS z-score and hormonal status or L-thyroxine dosages at the time of the study or during the pubertal period. CONCLUSIONS: The careful monitoring of serum thyroid-stimulating hormone and adjustment of l-thyroxine dosage avoided the significant deleterious effects of prolonged L-thyroxine replacement therapy on bone tissue in adolescents and young adults with congenital hypothyroidism treated from the neonatal period.

Reduced bone mass detected by bone quantitative ultrasonometry and DEXA in pre- and postmenopausal women with endogenous subclinical hyperthyroidism.

BACKGROUND: Although overt hyperthyroidism is a well known cause of bone loss, systemic effects of subclinical hyperthyroidism (SH) are still a matter of debate. OBJECTIVE: The aim of this cross-sectional study was to evaluate the effect of endogenous SH on bone in relation to the menopausal status. METHODS: Bone mass and turnover were assessed in a group of 60 patients with endogenous SH due to multinodular goitre; 30 of them were premenopausal and 30 early postmenopausal (mean age, 40.9 +/- 7.3 and 57.7 +/- 6.75, respectively). Sixty healthy women matched for age-, BMI- and menopausal status served as controls. Three different skeletal sites were evaluated using two different techniques: lumbar spine and femoral neck were assessed by DEXA whereas the proximal phalanges were evaluated by quantitative ultrasonometry (QUS), measuring the amplitude-dependent speed of sound (Ad-SoS). Serum osteocalcin and urinary deoxypyridinoline (DPD) were also determined as markers of bone turnover. RESULTS: A significant decrease was found in femoral BMD (P < 0.05) and phalangeal Ad-SoS (P < 0.001) in pre- and postmenopausal patients compared to controls, being greater in those postmenopausal. Lumbar BMD was decreased only in postmenopausal patients (P < 0.05). Bone turnover markers were higher in patients than in controls and in post- than in the premenopausal ones. A significant negative correlation was found between femoral BMD, Ad-SoS and serum free T3 levels, the latter considered a marker of disease activity. CONCLUSIONS: A significant increase in bone turnover markers and a decrease in bone mass was found in women affected by endogenous SH, being greater in early postmenopausal patients. Cortical rich bone was mainly affected. Both QUS and the conventional DEXA technique were equally able to determine bone density decrease related to mild thyroid hormone excess and sexual hormone decrease.

The lumbar bone mineral density is affected by long-term poor metabolic control in adolescents with type 1 diabetes mellitus.

AIM: To analyze whether bone mineral density (BMD) and bone resorption status are influenced by long-term metabolic control and duration of disease in adolescents with long-standing type 1 diabetes mellitus. METHODS: Twenty-seven adolescents (age 13.1 +/- 1.7 years, duration of diabetes 6.9 +/- 3.0 years) were studied. The BMD, expressed as z score, was measured at the lumbar spine (L1-L4) using dual-energy X-ray absorptiometry, while the urinary excretion of total deoxypiridinoline (Dpyd), a marker of bone resorption, was measured by immunoassay and was corrected by creatinine (Cr). Linear and multivariate correlations between lumbar BMD z score or Dpyd/Cr excretion and age and disease variables [short-term (Hb A(1c latest)) or long-term (Hb A(1c whole duration)) metabolic control, duration, 'diabetes impact index' (mean Hb A(1c whole duration) x duration of disease in months)] were sought. RESULTS: In diabetic subjects the mean BMD z score was -0.44 +/- (SD) 1.02 (95% CI: -0.03; -0.84), and the Dpyd/Cr excretion was not increased. A negative correlation was found between lumbar BMD z score and age (r -0.59; p = 0.001), duration (r -0.39; p = 0.04), and the diabetes impact index (r -0.4; p = 0.04). The Dpyd/Cr ratio correlated negatively with age (r -0.40; p = 0.04) and positively with height velocity (r 0.42; p = 0.04). By using multiple linear regression, age showed a significant inverse correlation with lumbar BMD z score (beta = -0.39; p = 0.0005). A negative correlation was found between lumbar BMD z score and Hb A(1c whole duration) (beta = -0.40; p = 0.02) or diabetes impact index (beta = -0.001; p = 0.01). CONCLUSIONS: Poor metabolic control may expose adolescents with long-standing type 1 diabetes to the risk of developing osteopenia in adult age. Optimization of metabolic control in growing diabetic children may prevent osteoporosis in later life.