Trabecular bone density in premenopausal rheumatoid arthritis patients.

OBJECTIVE: This study was undertaken to compare trabecular bone mineral density (BMD) in premenopausal rheumatoid arthritis (RA) patients and normal age-matched controls. METHOD: A protocol was designed to record age, duration of disease, use of corticosteroids (CS) and/or slow-acting antirheumatic drug (SAARD) therapy together with duration of such therapy. BMD was measured using the Hologic QDR 1,000 dual energy X-ray absorptiometer. The first four lumbar vertebrae and the left femur were measured in 56 RA patients and 165 controls. Height and weight were measured. Comparisons were made between RA patients and controls, as well as between subgroups of RA patients based on CS therapy. RESULTS: Patients with RA had significantly lower BMD (P < 0.05) at all the sites than the normal controls. The mean duration of RA at the time of study was 60 months (standard deviation 58 months). Thirteen RA patients had used CS in doses less than 10 mg daily for 6 months or longer (mean 19 months), while 25 patients had been on SAARD for an excess of 6 months (mean 23 months). The CS-treated patients had significantly lower BMD than untreated subjects at the femoral neck and inter-trochanteric region (P < 0.05), but not at the lumbar spine. However, when compared with normal controls, the CS-treated subgroups had significantly lower BMD at the lumbar spine and all femoral areas. Trochanteric BMD was the best determinant of the RA group, with a sensitivity of 65% and specificity of 77%. The positive predictive value was 16%, while the negative predictive value was 10%. Using Bayes' theorem, the prevalence of osteopenia in RA was found to be 6%. CONCLUSION: We conclude that generalised bone loss is a systemic feature of RA and that loss at the spine and femur may be aggravated by CS therapy.

Assessment of age-related bone loss in normal South African women by means of the Hologic QDR 1000 system.

The aim of this study was to evaluate age-related changes in cortical and trabecular bone mineral density (BMD) in South African subjects, and to develop a local reference database for dual energy X-ray absorptiometry with the QDR 1000 densitometer. A questionnaire was used to recruit volunteers. Age, years since menopause, use of medications and medical diseases were recorded. Men were excluded. Only whites and coloureds were studied. Three hundred and eleven women had single measurements over a 2-year period. Seven sets of subjects were defined according to age (18-44; 45-49; 50-54; 55-59; 60-64; 65-69; > 70 years) (N = 163; 32; 35; 23; 25; 16; 17 respectively). Height and weight did not change significantly with age. There were significant differences in lumbar and femoral BMD (Ward's) compared with those of American subjects in the different age categories. Both the lumbar and total femoral BMD began to fall significantly between the ages of 60 and 65 years (P < 0.01). Ward's triangle showed a significant fall in BMD between 45 and 50 years of age (P < 0.01). Ward's BMD predicted 36% of the variation in lumbar BMD at 45 years but 10% at 70 years. Ward's triangle is a useful predictor of femoral bone loss in later years. The fracture threshold at the lumbar vertebrae was 0.822 g/cm2; at Ward's triangle it was 0.443 g/cm2. This gave a 16% prevalence of osteopenia in the lumbar region and a prevalence of 24% at Ward's area.

Loss of trabecular bone mineral density in systemic lupus erythematosus.

OBJECTIVE: To evaluate trabecular bone mineral density (BMD) in young ambulatory female patients with systemic lupus erythematosus (SLE). METHODS: Bone mineral density (gm/cm2) at the lumbar vertebrae (L1-L4) and at the left femur (neck, trochanter, intertrochanter, and Ward's triangle) was measured by dual x-ray absorptiometry in 46 SLE patients (mean age 31 years, mean disease duration 76 months) and in 108 healthy female controls (mean age 32 years). Twenty-two of the SLE patients were receiving corticosteroids (CS) at the time of the study. RESULTS: Lumbar BMD in the SLE patients was less severely reduced than was BMD at the femoral sites, but the SLE group was closer to the lumbar fracture threshold of 0.812 gm/cm2 than was the control group (P = 0.0009). There were no significant differences between the SLE patients currently being treated with corticosteroids and those who were not (P > 0.3). BMD at Ward's triangle and at the femoral neck was not significantly reduced in the SLE patients. Total femoral BMD had a sensitivity of 76% and specificity of 62% in differentiating the SLE group from the controls. The positive predictive value was 61% and the negative predictive value was 89%. The prevalence of osteopenia in the SLE patients was 25%. CONCLUSION: SLE causes significant trabecular bone loss, which is not due to corticosteroid therapy.