Mineral bone tissue density and risk factors for osteoporosis in patients with bronchial asthma


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Aim. To estimate mineral bone tissue density (MBTD) and risk factors for osteoporosis in patients with bronchial asthma (BA).
Material and Methods. A cross-sectional study included 119 patients (48 males and 71 females) aged 18 to 49 years who had no diseases or states that can induce MBTD, except BA. The patients were divided into 3 groups: 1) those untreated with glucocorticoids (GC); 2) those who received inhaled GC; and 3) those who permanently took oral and inhaled GC. The patients underwent questionnaire survey, double-power X-ray absorption of the lumbar vertebral column and proximal femur, and X-ray study; forced expiratory volume per sec and peak expiratory function were measured. Results. In Group J patients, there was a high incidence of osteopenia that Increased with the severity of BA. About 2.5-year therapy with inhaled GC in large and small doses had no impact on MBTD. The prolonged use of systemic GC caused a marked reduction in MBTD and led to the development of osteoporetic fractures. Changes were detected in both the lumbar spine and proximal femur. In males and females, MBTD decreases were equal. MBTD correlated with the duration of GC therapy and with age at its initiation, but not with the daily dose of GC. In 15.4% of the patients, MBTD remained in the normal range despite the prolonged use of GC in large doses. Osteoporetic fractures were observed at the values of MBTD, which had not reached the stage of osteoporosis according to the WHO criteria, which was indicative of qualitative GC-induced bone tissue changes.
Conclusion. GC is an important, but not alone, risk factor for osteoporosis in asthmatic patients. The high rate of low MBTD among the patients receiving no GC suggests that it is necessary to make an early diagnosis and to perform rational treatments.

参考

  1. Global initiative for asthma. Global strategy for asthfia management and prevention. NIH; 2002.
  2. Quanjer Ph. H., Tammeling G. L., Cotes J. E. et al. Lung volumes and forced ventilatory flows. Eur. Respir. J. 1993; 6 (suppl. 16): 5-40.
  3. Arts R. M., Lester G. E., Ontjes D. A. Bone loss physiology in critically ill patients. Chest 1998; 114 (4): 954-955.
  4. Wisniev/ski A. F., Lewis S. A., Green D. J. et al. Cross sectional investigation of the effects of inhaled corticosteroids on bone density and bone metabolism in patients with asthma. Thorax 1997; 52 (10): 853-860.
  5. Saito J. K., Davis J. W., Wasnich R. D., Ross P. D. Users of low dose glucocorticoids have increased bone rates, a longitudinal study. Calcif. Tissue Int. 1995; 57: 115-119.
  6. American college of rheumatology task force on osteoporosis guidelines. Recommendation for the prevention and treatment of glucocorticoid-induced osteoporosis. Arthr. & Rheum. 1996; 39(11): 1791-1801.
  7. Allen D. B. Growth suppression by glucocorticoid therapy. Endocrinol. Metab. Clin. N. Am. 1996; 25: 699-717.
  8. Backman K. S., Greenberg P. A., Paterson R. Airway obstruction in patients with long-term asthma consistent with irreversible asthma. Chest 1997; 112: 1234-1240.
  9. Dykman T. R., Gluck O. S., Murphy W. A. et al. Evaluation of factors associated with glucocorticoid-induced osteopenia in patients with rheumatic diseases. Arthr. and Rheum. 1985; 28: 361-368.
  10. Peck W. A., Gennari C., Raisz L. et al. Round table discussion. Corticosteroid and bone. Calcif Tissue Int. 1984; 36: 4-7.
  11. Als O. S., Gotfredsen A., Christiansen C. The effect of glucocorticoids on bone mass in rheumatoid arthritis patients. Arthr. and Rheum. 1985; 28: 369-375.
  12. Nagant de Deuxchaisnes C., Devogelaer J. P. et al. The effects of low dosage glucocorticoids on bone mass in rheumatoid arthritis: a cross-sectional and longitudinal studv usine sinolp photon absorbtiometry. Adv. Exp. Med. Biol. 1984; 171. 209- 239.
  13. Sambrook P., Birmingham J., Kelly P. et al. Prevention of corticosteroid osteoporosis. N. Engl. J. Med. 1993; 328 (24): 1747-1752.
  14. Morrison N. A., Shine J., Verkest V. et al. 1,25-Dihydroxyvitamin D responsive element and glucocorticoid repression in the osteocalcin gene. Science 1989; 246: 1158-1161.

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