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Osteoporosis in Glucocorticoid-Dependent Asthmatic Patients

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Summary

Rib or vertebral fractures have been reported in 4.5 to 70% of glucocorticoid-treated patients with asthma, depending on the source of the data. Older age and postmenopausal status increase the risk of glucocorticoid-induced osteoporosis. The major pathogenetic mechanism appears to be direct glucocorticoid suppression of osteoblastic activity and bone formation. Other factors probably involved in the pathogenesis of glucocorticoid-induced osteoporosis include: (a) glucocorticoid inhibition of gastrointestinal absorption and urinary tubular reabsorption of calcium; (b) secondary hyperparathyroidism; and (c) sex hormone deficiency.

A number of drugs have been investigated in the prophylaxis and treatment of glucocorticoid-induced osteoporosis. Among the drugs studied, pamidronate and calcitonin appear to be most consistently effective in increasing bone density. Other bisphosphonates, such as etidronate, also appear to be effective, although less so than pamidronate. Vitamin D preparations increase calcium absorption, but do not necessarily improve bone density or decrease fracture rate, and they frequently cause hypercalciuria. Calcifediol or calcitriol appear to be more effective than vitamin D itself. Calcium alone may have beneficial effects, and fluoride has been reported to be effective in some but not all studies. Limited data have shown the promise of estrogen, progesterone and nandrolone.

Although optimal prophylaxis and therapy for glucocorticoid-induced osteoporosis have not been established, a number of recommendations can be made for glucocorticoid-dependent asthmatics. Oral calcium supplementation is recommended for all glucocorticoid-treated patients. Postmenopausal women receiving glucocorticoids should also receive cyclic estrogen and progesterone unless there are definite contraindications. Patients with hypercalciuria should be treated with hydrochlorothiazide. Until nasal calcitonin or oral pamidronate become available, patients with substantial bone loss should receive cyclic etidronate. Patients with an inadequate response should have calcifediol or calcitriol added or substituted, and for those not responding to the above therapy, parenteral calcitonin could be considered. Finally, fluoride or nandrolone could be used in patients whose bone loss does not respond to any of the previous therapies.

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Authors and Affiliations

  1. Department of Allergy, Kaiser Permanente Medical Center, San Diego, California, USA

    Michael Schatz

  2. Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado, USA

    Daniel Hamilos

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  1. Michael Schatz
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Schatz, M., Hamilos, D. Osteoporosis in Glucocorticoid-Dependent Asthmatic Patients. Clin. Immunother. 4, 180–196 (1995). https://doi.org/10.1007/BF03259284

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