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A Journal on Internal Medicine
Indexed/Abstracted in: Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,236
Minerva Medica 2002 December;93(6):485-90
The usefulness of the quantitative ultrasound to diagnose glucocorticoids induced osteoporosis
Ponteggia M., Ponteggia F., Di Cato L., Puxeddu A., Coaccioli S.
Background. The aim of this study was to evaluate the utilization of heel ultrasonometry in the diagnosis of glucocorticoid induced osteoporosis.
Methods. The study group included 108 caucasian women, ranging in age from 30 to 81 years. They were all affected by inflammatory disorders (rheumatoid arthritis and other connective tissue diseases) and had been in chronic glucocorticoid therapy for at least 8 months, at an average daily dosage of not less than 7.5 mg of prednisolone. The control group was composed of 112 women. Every subject was evaluated by a heel ultrasonography (Hologic Sahara).
Results. The ultrasonometry data average values noted were: QUI (Quantitative Ultrasound Index) 71* (86); SOS (Speed of Sound) 1324 m/sec* (1541); BUA (Broadband Ultrasound Attenuation) 61 dB/MHz (62). The asterisk shows a statistically significant difference in comparison to the value in brackets. QUI/Stiffness and SOS had reached a significant statistic value in all the age groups, with regard to average values of patients not on glucocorticoid therapy. The BUA values did not demonstrate a significant difference, even if they always appeared inferior to the average observed (except in the range 60-70 years age group).
Conclusions. The concept that osteoporosis is a disease characterized exclusively to a reduction in bone density, now leaves room for consideration that corresponds with the concepts of quantitative and quality elements. Chronic glucocorticoid therapy is one of the major causes of osteoporosis. The use of glucocorticoids increases the risk of fractures, independently from the bone ùineral BMD in the various ages, which therefore cannot be explained solely by the reduced BMD. Ultrasound may provide information on the bone structure, and so its eventual modification, after chronic glucocorticoid therapy. Our results show that bone ultrasonometry is able to detect a population in chronic glucocorticoid therapy in comparison with those not treated. BUA and SOS are reduced in all the patients. Our experience derives that in the chronic glucocorticoid therapy patients, a major prevalence is noted of SOS which may provide information on the modification of the bone structure.