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ZusammenfassungDiese DVO Leitlinien, die in erster Linie für Allgemeinmediziner und Spezialisten für Knochenerkrankungen bestimmt sind, sollten von allen im klinischen und ambulanten Bereich tätigen medizinischen Fachkräften angewendet werden. Ziel der Leitlinie ist die Verbesserung der Diagnose, Prävention und Behandlung von Osteoporose und der Folgen der Erkrankung auf der Grundlage evidenzbasierter Medizin.Klare Empfehlungen, welche Patienten zu diagnostizieren und behandeln sind (basierend auf Risikofaktoren [einschließlich sekundärer Osteoporose]) sowie Primär-, Sekundär- oder Tertiärprävention werden dargestellt, mit dem Schwerpunkt auf der postmenopausalen Osteoporose und der Osteoporose bei Männern.Die Identifizierung von Patienten mit einem hohen Risiko für Frakturen wird hervorgehoben, und spezifische Schwellenwerte für die Intervention sind definiert (20 % Hüftfrakturrisiko innerhalb von 10 Jahren diagnostischer Schwellenwert, 30 % Hüftfrakturrisiko innerhalb von 10 Jahren therapeutische Schwelle). Die Diagnose von Osteoporose basiert auf der Anamnese des Patienten, der körperlichen Untersuchung, dem Funktionstest (z. B. Timed Up and Go Test), konventionellen Röntgenaufnahmen der Brust- und Lendenwirbelsäule und der Bestimmung der Knochenmineraldichte (BMD) durch das DXA Verfahren.Die Anamnese ist entscheidend für die Abschätzung des Frakturrisikos auf der Grundlage von 40 wissenschaftlich überprüften Risikofaktoren, die das Frakturrisiko mindestens verdoppeln (z. B. Begleiterkrankungen, Hüftfrakturen in der Familie, prävalente Frakturen an jedem Ort, Lebensstil, Anwendung von Medikamenten, körperliche Aktivität und Stürze). Röntgenaufnahmen der Brust- und Lendenwirbelsäule sind wichtig, um prävalente Wirbelkörperfrakturen zu erkennen. Beim Fehlen eines großen Traumas kann jede Fraktur bei Erwachsenen über dem Alter von 50 Jahren eine Diagnose von Osteoporose nahelegen, mit dem höchsten Risiko für eine nachfolgende Fraktur innerhalb einer kurzen Zeit nach der ersten Fraktur. BMD-Messungen mit DXA sind wichtig, um das individuelle Frakturrisiko besser abschätzen zu können. Eine grundlegende Laboruntersuchung ist obligatorisch, um verschiedene Formen der sekundären Osteoporose ausschließen zu können.Der DVO-Patientenfindungs-Algorithmus basiert auf dem Geschlecht, Alter, Knochenmineraldichte und vorbestehenden Frakturen als wichtigste Informationen. Die Indikation für eine aktive anti-osteoporotische Therapie kann durch multiple Risikofaktoren modifiziert und verfeinert werden. Dieser Algorithmus wurde seit dem Richtlinien-Update 2006 verwendet und wurde entsprechend der internationalen Literatur zu Risikofaktoren für Osteoporose und osteoporotische Frakturen aktualisiert und angepasst.Die Behandlung der Osteoporose enthält viele Therapiepfeiler. Zusammen mit Empfehlungen für Bewegung, Physiotherapie und Sturzprävention sowie Ernährung (z. B. Calcium, Vit. D), werden pharmakologische Behandlungen basierend auf evidenzbasierter Medizin empfohlen. Die aktiven Anti-Osteoporose-Medikamente müssen für die Indikation postmenopausale Osteoporose und männliche Osteoporose in Deutschland, Österreich und der Schweiz zugelassen sein. Das Management und die Vorbeugung von häufigen oder seltenen Nebenwirkungen aufgrund von Anti-Osteoporose-Behandlungen, die in der klinischen Praxis angewendet werden, werden ebenfalls detailliert behandelt.

Objective-To evaluate bone mineral density and biochemical parameters of bone metabolism in ambulatory premenopausal female patients with systemic lupus erythematosus (SLE). Methods-30 women who fulfilled the ARA criteria for the classification of SLE were studied. Lumbar and femoral bone mineral density was determined by dual energy x ray absorptiometry. Various laboratory parameters including serum calcium, serum phosphorus, alkaline phosphatase, bone specific isoform of alkaline phophatase, propeptide of type 1 procollagen, deoxypyridinoline excretion, telopeptide of type 1 collagen, serum creatinine, osteocalcin, parathyroid hormone, 25-OH vitamin D, testosterone, progesterone, estradiol, follicle stimulating hormone and luteinotropic hormone were measured. Results-According to the WHO criteria 39% of all patients with SLE studied had normal bone mineral density, 46% had osteopenia and 15% had osteoporosis at the lumbar spine; at the femoral neck 38.5% had normal bone mineral density, 38.5% had osteopenia and 23% suVered from osteoporosis. Significantly lower osteocalcin levels were found in SLE patients. All other bone resorption and formation markers measured were not statistically diVerent, but higher serum albumin corrected calcium and lower phosphorus values were found in the SLE group. Of all sex hormones tested lower testosterone and higher follicle stimulating hormone concentrations were seen in patients with SLE. Conclusion-A high incidence was found of osteopenia and osteoporosis in premenopausal patients with SLE. Bone diminution in SLE seems to be attributable, at least in part, to decreased bone formation in SLE patients.

Because activity and regular exercise are important factors to maintain general good health in senior citizens, we investigated whether senior dancing has any effect on peripheral or lumbar bone density. We performed a prospective study over a12-mo period on bone density at a spinal and peripheral measuring site in 28 female senior members (mean age: 67 +/- 2 yr) of a dancing group in Vienna. Lumbar bone mineral density was assessed by quantitative computed tomography (qCT) and radial bone density by single photon absorptiometry of the distal forearm. The mean training time per week was 3.2 +/- 0.8 h. In the entire group of female dancers, no significant effects of dancing on radial or lumbar bone density could be observed. Linear regression analysis showed that the lower the qCT at the beginning of the observation period, the higher was the percentage increase of spinal qCT in the entire group during 12 mo of dancing (r = 0.52, P < 0.0001). For additional evaluation, females were divided into two subgroups, osteoporotic or nonosteoporotic, based on x-rays and lumbar bone mineral density (BMD) as measured by qCT. The group classified as dancers with osteoporosis (group I) showed a significant increase in lumbar bone density, whereas in the group of dancers without signs of osteoporosis (group II), BMD remained unchanged. Additionally, radial bone density did not show any changes in either group. Group I showed a significant correlation between basal spinal BMD and the percentage change of BMD during the observation period (r = 0.7, P < 0.001). Changes of the biochemical parameters were observed in the bone-specific isoenzyme of alkaline phosphatase, a marker of osteoblastic activity, in group I giving additional evidence of increased bone formation.

To assess the effect of chronically elevated plasma growth hormone (GH) levels on bone metabolism and bone mineral density (BMD), 16 patients (10 females and 6 males) with a mean age of 49.1 +/- 13.2 years (range 33-68) with active acromegaly were studied and compared to a control group of 16 sex- and age-matched subjects. BMD of the lumbar spine and two different sites of the proximal femur were measured by dual-energy x-ray absorptiometry (Norland XR-26). In the acromegalic patients the mean plasma GH concentration was 30.1 +/- 11.1 micrograms/liter, and the mean plasma somatomedin C (SMC) concentration was 6.5 +/- 1.5 U/liter. Mean serum osteocalcin (OC) levels (14.3 +/- 1.1 versus 7.2 +/- 0.4 ng/ml, p < 0.001) as well as the urinary hydroxyproline excretion (OHP; 8.8 +/- 1.4 versus 2.7 +/- 0.3 mg, p < 0.0001) were significantly higher in the acromegalic patients than in the control subjects. In the acromegalic patients BMD was significantly elevated in the two examined regions of the proximal femur, that is, the femoral neck (1.06 +/- 0.05 versus 0.86 +/- 0.03 g/cm2, p < 0.05) and Ward's triangle (0.92 +/- 0.06 versus 0.76 +/- 0.03 g/cm2, p < 0.02), whereas the BMD of the lumbar spine was not significantly different from that of control subjects. Among the patients with acromegaly a significant positive correlation between serum OC concentrations, on the one hand, and urinary OHP excretion (r = 0.7, p < 0.004) as well as BMD in the proximal femur (r = 0.64, p < 0.007), on the other hand, could be observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Reduced bone mineral density (BMD) and the prevalence for osteoporotic vertebral fractures are symptoms of growth hormone deficiency (GHD) syndrome, and GH replacement therapy is now available for GH-deficient adults. We investigated the long-term effects of GH replacement therapy on bone mineral density (BMD) and bone metabolism in 19 adult patients with GHD over a period of 18 months. In response to GH treatment, the initially decreased IGF-I concentrations rose significantly during 18 months of therapy to levels within the normal range (matched for sex and age) (mean change 158.1 +/- 50.8 ng/ml, P < 0.001). Parameters of bone formation such as osteocalcin (OC) and procollagen I-C-Peptide (PICP) showed a significant increase in the first 6 months of therapy, followed by a slight decrease in the next months. Markers of bone resorption (CrosslapsR and deoxypyridinoline (D-Pyr) also increased significantly with a peak value after 6 months and all parameters except PICP remained above baseline values after 18 months. BMD of the femoral neck (FN) showed an increase after 18 months of therapy (mean change 0.01 +/- 0.03 g/cm2 after 18 months, n.s.). However, the increase in BMD was significant only in the lumbar spine (LS) (mean change 0.03 +/- 0.04 g/cm2, P < 0.05 after 18 months). We conclude that GH replacement therapy in adult patients with GHD over a period of 18 months causes a pronounced increase in bone turnover mainly during the first 12 months of therapy and increases BMD of the lumbar spine and the femoral neck after 18 months.

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With advancing age both sexes have an increased incidence of osteoporotic fractures, although fractures are more common in women than in men. Whereas in women several potential risk factors have been identified, less is known about osteoporosis in men. A total of 27 Austrian men (mean age: 65 +/- 2 years) with atraumatic spine fractures were studied. In all patients, medical history gave no evidence of disease or medications causing osteoporosis. Peripheral bone mass was determined by single-photonabsorptiometry on the distal non-dominant forearm; lumbal bone density was measured by quantitative computed tomography. Serum levels of calcium, phosphate, alkaline phosphatase, osteocalcin, testosterone, estrogen, parathyroid hormone and 25-hydroxy-vitamin D as well as 2-h-urinary-OH proline and calcium excretion were measured. All data were compared with those of an age and sex matched control group consisting of 19 healthy males. A significant difference in mean peripheral and axial bone mass (SPA: P less than 0.004; QCT: P less than 0.0001) was observed between osteoporotic men and controls. When compared to controls, serum levels of alkaline phosphatase (P less than 0.012), urinary OH proline (P less than 0.05) and urinary calcium excretion (P less than 0.003) were significantly higher in the osteoporotic males. Additionally, there was a significant positive correlation between serum alkaline phosphatase and urinary OH proline excretion (r = 0.32; P less than 0.04) in the osteoporotics. All other biochemical parameters showed no significant differences. Our results may lead to the assumption that osteopenia in men is related to increased bone turnover.