Identification of patients with a high risk of osteoporosis. Analysis of risk factors, ultrasonography and DEXA, in a female population in the North East of Italy.

AIM: The aim of this observational study is the identification of women at high risk of osteoporosis by using the phalangeal quantitative ultrasound (QUS) value for osteoporosis screening. METHODS: The study population is composed of 1 152 women between 35 and 79 years old, both premenopausal and postmenopausal. Each woman underwent a questionnaire and phalangeal QUS. One hundred and forty-eight women also underwent dual energy X-ray absorptiometry (DEXA). Osteopenia and osteoporosis, as determined using the amplitude dependent speed of sound (AD-SoS) T-score, identified women at a high risk of fracture. Data were stored and analyzed using SPSS (Statistical Package for Social Science) for Windows. RESULTS: AD-SoS is significantly higher in premenopausal women than in postmenopausal women without history of hormone replacement therapy (HRT) (P<0.001), if they are over 50 years old. In women 50-59 years old, AD-SoS is significantly higher in premenopausal women than in postmenopausal women with or without HRT history (P<0.001). In postmenopausal women, discriminant analysis found that HRT and years of HRT are the only significant protective factors (P<0.001). In premenopausal and postmenopausal women with no history of HRT use, discriminant analysis demonstrated that early menopause and a family history of osteoporosis are the only significant risk factors (P<0.001). CONCLUSION: Early menopause and a family history of osteoporosis seem to be the greatest risk factors, while HRT seems to be a protective factor. The QUS technique, with DEXA as a secondary test, can be a screening test for the identification of postmenopausal women with a high risk of fracture.

The enzyme glutathione peroxidase in arachidonic acid metabolism of human platelets.

We investigated the possible regulatory role of glutathione peroxidase on thromboxane formation by reducing peroxides in platelets. Experiments carried out in platelet lysates demonstrated that the burst of the arachidonate metabolism was accompanied by a simultaneous burst of hydrogen transfer from glutathione to peroxides, catalyzed by endogenous glutathione peroxidase. The burst of hydrogen transfer was partially inhibited by acetylsalicylate concurrently with the complete inhibition of malondialdehyde formation, thus suggesting that the hydrogen acceptor peroxides were derived in part from the cyclooxygenase pathway. Moreover, increasing glutathione peroxidase activity by adding purified enzyme to the incubation media decreases thromboxane formation. Intact platelets, stimulated with arachidonic acid or thrombin, produced malondialdehyde and thromboxane in amounts roughly inversely related to the endogenous glutathione peroxidase activity. In contrast, no correlation was observed between glutathione peroxidase activity and agonist-induced platelet aggregation. Our experiments suggest that in normal platelets, glutathione peroxidase controls thromboxane formation.