Abstract
This study evaluated the effects of LT4 administration on the bone mineral density (BMD) in physiological postmenopausal women after two years of continuative treatment. 110 postmenopausal women with nodular goiter aged between 50 and 55 years were examined before and after 2 years of therapy with a fixed dose of LT4 (1.6 mcg/kg/die) for the treatment of nodular thyroid disease. The results showed that the patients on treatment with LT4 have a slight, but significant reduction of the BMD after 2 years of treatment, associated with increased serum levels of alkaline phosphatase and urinary excretion of hydroxyproline, confirming our data conducted on the same group after one year of therapy. Comparison between patients receiving LT4 (group A) or not (group B) showed that group A patients had significantly lower BMD. We demonstrated the statistically significant influence of the following risk factors on BMD: (1) body mass index <19 kg/m2; (2) the onset of menarche after the age of 15 years; (3) positive history for period of amenorrhoea; (4) nulliparity.
Highlights
Bioavailable 17β-estradiol correlates with the bone mineral density (BMD)
The serum levels of alkaline phosphatase (AP) and the amount of hydroxyproline excreted with the 24 h urine increased significantly (P < 0.0001) during treatment with LT4 (Tables 1 and 2)
The impact of some risk factors for osteoporosis was evaluated on the BMD of the patients treated with LT4
Summary
Bioavailable 17β-estradiol correlates with the bone mineral density (BMD). On the contrary, an estrogenic lack determines a condition characterized by the prevalence of bone reabsorption phase over the bone formation phase. The biochemical indicators of increased osteoblastic activity are represented by the serum levels of osteocalcin and of alkaline phosphatase, while the urinary levels of hydroxyproline are expression of an increased osteoclastic activity. Thyroid hormones certainly determine an increase of both osteoblastic and osteoclastic activities over both cortical and trabecular bones [2, 3]. Studies in vitro suggest that thyroid hormones increase more the re-absorption than bone formation, determining a loss of bone mass [8, 9]. It has been reported how thyrotoxicosis increases the fracture risk in post-menopause women and in patients with low bone mass peak. A recent study has shown that endogenous subclinical hyperthyroidism
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