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Thyroid hormones are key regulators of skeletal development in childhood and bone homeostasis in adulthood, and thyroid diseases have been associated with increased osteoporotic fractures. Hypothyroidism in children leads to an impaired skeletal maturation and mineralization, but an adequate and timely substitution with thyroid hormones stimulates bone growth. Conversely, hyperthyroidism at a young age accelerates skeletal development, but may also cause short stature because of a premature fusion of the growth plates. Hypothyroidism in adults causes an increase in the duration of the remodeling cycle and, thus, leads to low bone turnover and enhanced mineralization, but an association with a higher fracture risk is less well established. In adults, a surplus of thyroid hormones enhances bone turnover, mostly due to an increased bone resorption driven by osteoclasts. Thus, hyperthyroidism is a well-recognized cause of high-bone turnover secondary osteoporosis, resulting in an increased susceptibility to fragility fractures. Subclinical hyperthyroidism, especially resulting from endogenous disease, also has an adverse effect on bone mineral density and is associated with fractures. In most patients with overt or subclinical hyperthyroidism restoration of the euthyroid status reverses bone loss. In postmenopausal women who receive thyroid-stimulating hormone suppression therapy because of thyroid cancer, antiresorptive treatments may be indicated. Overall, extensive data support the importance of a euthyroid status for bone mineral accrual and growth in childhood as well as maintenance of bone health in adulthood.

Die osteologische Diagnostik beinhaltet ein breites Spektrum an komplementaren Verfahren von der Anamnese und korperlichen Untersuchung bis hin zur molekularen Bildgebung. Entsprechend den vielfaltigen Wechselwirkungen des Knochens mit anderen Organsystemen ist die Versorgung der Patienten interdisziplinar. Die Diagnostik der Osteoporose wird unterstutzt durch hochwertige Leitlinien. Die Knochendichte hat sich in ihrer Wertigkeit vom bestimmenden Diagnosekriterium zum Risikofaktor gewandelt. Das stellt einen wichtigen Paradigmenwechsel dar und starkt die klinischen Risikofaktoren im Rahmen des Risikoassessments. Parameter der Muskelmasse, -struktur und -funktion gehen in allen Altersgruppen zunehmend in die Diagnostik ein. Die allgemeine Labordiagnostik dient der Erkennung von Organerkrankungen, die den Knochenstoffwechsel beeintrachtigen. Spezielle Laborparameter sind die Marker fur den Knochenanbau und -abbau sowie den Kalzium- und Phosphatstoffwechsel. Die Praanalytik und Interpretation dieser Parameter erfordern Erfahrung und gehoren in die Hand des Spezialisten. Die humangenetische Diagnostik ist in der Diagnostik seltener Knochenerkrankungen mittlerweile gut etabliert, jedoch noch nicht in der Routinediagnostik polygenetischer Krankheiten wie der Osteoporose. Konventionelle radiologische Verfahren haben in der osteologischen Diagnostik einen hohen Stellenwert; sie dienen der Identifizierung von Frakturen, osteolytischen und osteoblastischen Lasionen sowie extraossaren Verkalkungen. Zunehmende Bedeutung erlangt die Kombination der Szintigraphie (Einzelphotonenemissionscomputertomographie [SPECT]) und der Positronenemissionstomographie (PET) mit der anatomischen Bildgebung (Computertomographie). Die osteologische Diagnostik verlangt ein breites Wissen und unterliegt einer dynamischen Weiterentwicklung.

OBJECTIVE: Polycystic ovary syndrome (PCOS) is characterized by obesity and insulin resistance (IR), which result in elevated plasminogen activator inhibitor-1 (PAI-1) levels. We aimed to assess the changes in PAI-1 levels in PCOS during treatment with metformin and during weight loss. DESIGN: Twenty-three normal weight women with PCOS were given metformin 850 mg bid for 6 months. Fifty overweight/obese women with PCOS were prescribed an energy-restricted diet, were instructed to exercise and were randomized to orlistat 120 mg tid or sibutramine 10 mg qd for 6 months. RESULTS: In normal weight women, treatment with metformin reduced the body mass index (BMI) and circulating androgens, improved markers of IR and lowered PAI-1 levels. In overweight/obese women, sibutramine and orlistat yielded comparable reductions in BMI and markers of IR. In contrast, the effects on the free androgen index (FAI) differed (p=0.027): sibutramine reduced the FAI (p=0.005), whereas orlistat had no effect. The effects of sibutramine and orlistat on PAI-1 levels also differed (p=0.042): sibutramine reduced PAI-1 levels (p

Limited data suggest that menstrual cycle abnormalities are more pronounced in younger and more obese patients with polycystic ovary syndrome (PCOS). We aimed to evaluate the association between menstrual cycle pattern and age, obesity and PCOS phenotype in a large population of women with PCOS.We studied 1,297 women with PCOS and divided them according to: a) age in ≤ 20, 21-30 and30 years old, b) body mass index in normal weight, overweight and obese and c) PCOS phenotype in phenotype 1 (anovulation, hyperandrogenemia and polycystic ovaries), 2 (anovulation and hyperandrogenemia without polycystic ovaries), 3 (hyperandrogenemia and polycystic ovaries without anovulation) and 4 (anovulation and polycystic ovaries without hyperandrogenemia).The proportion of women with regular menstrual cycles progressively increased in the older age groups, being 8.1, 10.5 and 12.7% in women ≤ 20, 21-30 and30 years old, respectively (p = 0.037). The proportion of women with regular menstrual cycles did not differ between normal weight and obese women but was higher in overweight women (9.3, 9.4 and 13%, respectively; p = 0.020). The proportion of women with regular cycles alternating with irregular cycles was highest in women with phenotype 4, intermediate in women with phenotype 2 and lowest in women with phenotype 1 (74.3, 69.4 and 61.7%, respectively; p = 0.027).Menstrual cycle pattern is more irregular in women with the "classic" PCOS phenotypes than in phenotype 4 but appears to normalize with ageing. On the other hand, obesity does not appear to have an important effect on menstrual cycle pattern in PCOS.

Background Lipocalin-2 is a novel adipokine that appears to play a role in the development of insulin resistance. Serum lipocalin-2 levels are elevated in obese patients. Obesity and insulin resistance are cardinal characteristics of the polycystic ovary syndrome (PCOS). However, there are limited data on serum lipocalin-2 levels in patients with PCOS. The aim of the present study was to assess serum lipocalin-2 levels in PCOS. Methods We studied 200 patients with PCOS and 50 healthy female volunteers. Results Serum lipocalin-2 levels were slightly higher in women with PCOS compared with controls (65.4 +/- 34.3 vs. 60.3 +/- 26.0 ng/ml, respectively) but this difference did not reach statistical significance. In contrast, lipocalin-2 levels were higher in overweight/obese women with PCOS than in normal weight women with the syndrome (76.2 +/- 37.3 vs. 54.5 +/- 27.2 ng/ml, respectively; p < 0.001). Serum lipocalin-2 levels were also higher in overweight/obese controls compared with normal weight controls (70.1 +/- 24.9 vs. 50.5 +/- 23.7 ng/ml, respectively; p = 0.004). In the total study population (patients with PCOS and controls), lipocalin-2 levels were independently correlated with the body mass index (p < 0.001). In women with PCOS, lipocalin-2 levels were independently correlated with the waist (p < 0.001). Conclusions Obesity is associated with elevated serum lipocalin-2 levels. In contrast, PCOS does not appear to affect lipocalin-2 levels.