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April 1986

Measures of Bone Loss in Rheumatoid Arthritis

Author Affiliations

From the Rheumatology Division and Endocrine Section, Department of Internal Medicine, University of California Medical Center—San Diego, and the Veterans Administration Medical Center, San Diego.

Arch Intern Med. 1986;146(4):701-704. doi:10.1001/archinte.1986.00360160115016

• Patients with rheumatoid arthritis (RA) are prone to develop osteoporosis, especially women receiving steroid hormone therapy. Inhibition of bone formation and/or excessive bone resorption may be responsible. Bone γ-carboxyglutamic acid—containing protein (BGP), the major noncollagen protein of bone and a plasma marker of bone formation, was measured in 81 consecutive RA patients and 79 age- and sex-matched control subjects, in addition to the hormone regulators of bone metabolism, calcitonin, parathyroid hormone, and 1,25-dihydroxyvitamin D. Mean (±SE) BGP levels (picomoles per milliliter) were lower for RA men (1.46 ± 0.14) and women (1.52 ± 0.2) compared with their respective controls (2.05 ± 0.17 for men, 2.47 ± 0.22 for women). Women taking steroids had the lowest levels (1.13 ± 0.22) and, in contrast to men, this value was lower than the nonsteriod-treated group. Steroid treatment appears to be a major determinant of low BGP levels; the effect of RA itself is suspected but not proved in this study. Calcitonin levels were lower in RA men as well as in all women. Diminution of BGP in these subjects supports the view that "low-dose" corticosteroid treatment may suppress bone formation, especially in women. Prevention or remediation of osteopenia may be monitored by BGP, if further studies validate this hypothesis with other measures of skeletal mass.

(Arch Intern Med 1986;146:701-704)

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