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1.
Acta Obstet Gynecol Scand ; 75(9): 843-8, 1996 Oct.
Article in English | MEDLINE | ID: mdl-8931510

ABSTRACT

OBJECTIVE: To evaluate whether thyroid stimulating hormone-suppressive thyroxine replacement therapy increases bone loss in postmenopausal women. MATERIALS AND METHOD: The study had a cross-sectional design. Fifty-four postmenopausal women on long-term treatment with thyroxine for primary hypothyroidism, who showed suppressed thyroid stimulating hormone levels were enrolled in our study. In these patients and in a control group of 54 healthy postmenopausal women we evaluated bone mineral density at distal radius and the main biochemical parameters of bone turnover. Student's t test, Wilcoxon signed rank-test, Chi-square test and the univariate linear regression in the statistical analysis of the data were employed. RESULTS: Bone mineral density values, expressed as z-scores, in the treated group were significantly decreased in comparison with the control group (p < 0.01). We did not detect a significant relationship between different L-thyroxine doses administered and bone mineral density z-scores. On the contrary, an inverse correlation was detected between length of treatment and bone mineral density z-scores. Treated patients showed a significantly higher concentration of serum alkaline phosphatase, osteocalcin, urinary calcium/creatinine and hydroxyproline/creatinine in comparison with the controls. CONCLUSIONS: Our study suggests that thyroxine replacement therapy in patients with suppressed thyroid stimulating hormone levels increases postmenopausal bone loss.


Subject(s)
Bone Density/drug effects , Bone Remodeling/drug effects , Hypothyroidism/drug therapy , Osteoporosis, Postmenopausal/chemically induced , Postmenopause , Thyroxine/adverse effects , Case-Control Studies , Cross-Sectional Studies , Female , Humans , Hypothyroidism/complications , Middle Aged , Osteoporosis, Postmenopausal/epidemiology , Risk Factors , Thyrotropin/blood , Thyroxine/therapeutic use , Time Factors
2.
Minerva Ginecol ; 45(5): 263-6, 1993 May.
Article in Italian | MEDLINE | ID: mdl-8351065

ABSTRACT

The co-existence of pelvic tumor, hydrothorax and ascites has been known since the last century. The features of this disease were described by Meigs and Cass in 1937; in the same year Roads named it Meigs syndrome. According to the original description this syndrome only included, as pelvic involvement, an ovarian neoplasm; at present it is accepted that hydrothorax and the ascites can also be associated with a uterine tumor, like a fibroma. The existence of either an ovarian or a uterine neoplasm distinguishes the typical Meigs syndrome from a pseudo-Meigs syndrome. The most likely pathogenesis of Meigs syndrome ascribes the formation of the peritoneal and pleural effusion to the filtration of interstitial fluid in the peritoneum through the tumor capsule, and the diffusion to the pleural space, generally at the right side, through the diaphragm lymphatic vessels and the foramen of Bochdalek. Dockerty reported that at least 40% of ovarian tumors had a diameter of more than 6 cm when associated with hydrothorax and ascites. The entity of pleural and peritoneal effusion can be moderate or massive. The effusions generally derive from a transudative process, but they can occasionally contain blood cells. The connection between the pelvic tumor and the effusion is demonstrated by the regression of the latter when the neoplasm is excised. When the pelvic tumor has an ovarian location it derives from the connective tissue of the hilus, it appears during fertile age and has a slow growth, the clinical signs becoming evident in elder age.


Subject(s)
Hydrothorax/etiology , Meigs Syndrome/complications , Ovarian Neoplasms/complications , Aged , Ascites/etiology , Ascites/radiotherapy , Drainage , Female , Humans , Hydrothorax/diagnosis , Hydrothorax/therapy , Meigs Syndrome/diagnosis , Meigs Syndrome/therapy , Ovarian Neoplasms/diagnosis , Ovarian Neoplasms/radiotherapy , Tetracycline/therapeutic use , Tomography, X-Ray Computed
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