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      Osteopenia in Patients with Glomerular Diseases Requiring Long-Term Corticosteroid Therapy

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          Background: Chronic corticosteroid (CS) use is associated with bone mass loss. Methods: Bone mineral density (BMD) was assessed in 72 patients (25 males/47 premenopausal females) with glomerular diseases, primary (n = 35) or secondary to systemic lupus erythematosus (n = 37) with normal renal function, who were taking CS, as prednisone and/or methylprednisolone, in doses ≧7.5 mg/day, for a period of at least 6 months. Cumulative dose and duration of prior CS therapy, as well as biochemical parameters and other factors contributing to bone loss were evaluated. Results: We found 37 (52%) patients with low BMD (29 with osteopenia and 8 with osteoporosis). The low BMD group presented a lower mean weight and body mass index (BMI) versus the normal BMD group (62 ± 15 vs. 70 ± 10 kg and 25 ± 4 vs. 27 ± 5, mean ± SD, p < 0.05). The estimated calcium intake was lower than 400 mg/day in all patients with low BMD, and they had taken furosemide as a concomitant drug for a longer mean period of time when compared to normal BMDpatients (30 ± 29 vs. 16 ± 27 months, p < 0.05). A higher mean number of pulses per patient and mean cumulative dose of methylprednisolone were observed in the low versus normal BMD group (7.7 ± 4.0 vs. 5.6 ± 4.0 pulses and 6.5 ± 3.9 vs. 3.9 ± 2.7 g, p < 0.05). Conclusions: These findings suggest a high frequency of osteopenia among young and premenopausal patients with glomerular diseases given long-term corticosteroid therapy. The lower BMI and calcium intake, as well as the concomitant furosemide use, might have contributed to such a bone loss. The higher number of pulse therapies leading to higher cumulative intravenous doses of corticosteroid mainly in lupus nephritis patients shows that pulse therapy may be deleterious to bone.

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          Damage in systemic lupus erythematosus and its association with corticosteroids.

          To evaluate the association between corticosteroid use and organ damage in patients with systemic lupus erythematosus (SLE). The occurrence and date of organ damage, as measured by the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index, were determined for 539 patients enrolled in the Hopkins Lupus Cohort Study. The risk of damage associated with the cumulative prednisone dose, high-dose prednisone (> or =60 mg/day for > or =2 months), and pulse methylprednisolone (1,000 mg intravenously for 1-3 days) was estimated using Cox proportional hazards regression analyses, controlling for age, race, and sex. Risk estimates for the cumulative prednisone dose were based on a reference dose of 36.5 gm (e.g., 10 mg of prednisone daily for 10 years [or equivalent]). The cumulative prednisone dose was significantly associated with the development of osteoporotic fractures (relative risk [RR] 2.5, 95% confidence interval [95% CI] 1.7, 3.7), symptomatic coronary artery disease (RR 1.7, 95% CI 1.1, 2.5), and cataracts (RR 1.9, 95% CI 1.4, 2.5). Each intravenous pulse was associated with a small increase in the risk of osteoporotic fractures (RR 1.3, 95% CI 1.0, 1.8); however, this result failed to reach statistical significance (P = 0.07). Each 2-month exposure to high-dose prednisone was associated with a 1.2-fold increase in the risk of both avascular necrosis (95% CI 1.1, 1.4) and stroke (95% CI 1.0, 1.5). SLE patients receiving long-term prednisone therapy were at significant risk of morbidity due to permanent organ damage. Additional research is required to determine the relative contributions of SLE disease activity and corticosteroids to the pathogenesis of specific types of organ damage. Furthermore, new steroid-sparing therapies are needed in order to treat disease activity and minimize cumulative and high-dose prednisone exposure.
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            NIH Consensus conference. Optimal calcium intake. NIH Consensus Development Panel on Optimal Calcium Intake.

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              Bone mineral density and biochemical parameters of bone metabolism in female patients with systemic lupus erythematosus.

              To evaluate bone mineral density and biochemical parameters of bone metabolism in ambulatory premenopausal female patients with systemic lupus erythematosus (SLE). 30 women who fulfilled the ARA criteria for the classification of SLE were studied. Lumbar and femoral bone mineral density was determined by dual energy x ray absorptiometry. Various laboratory parameters including serum calcium, serum phosphorus, alkaline phosphatase, bone specific isoform of alkaline phophatase, propeptide of type 1 procollagen, deoxypyridinoline excretion, telopeptide of type 1 collagen, serum creatinine, osteocalcin, parathyroid hormone, 25-OH vitamin D, testosterone, progesterone, estradiol, follicle stimulating hormone and luteinotropic hormone were measured. According to the WHO criteria 39% of all patients with SLE studied had normal bone mineral density, 46% had osteopenia and 15% had osteoporosis at the lumbar spine; at the femoral neck 38.5% had normal bone mineral density, 38.5% had osteopenia and 23% suffered from osteoporosis. Significantly lower osteocalcin levels were found in SLE patients. All other bone resorption and formation markers measured were not statistically different, but higher serum albumin corrected calcium and lower phosphorus values were found in the SLE group. Of all sex hormones tested lower testosterone and higher follicle stimulating hormone concentrations were seen in patients with SLE. A high incidence was found of osteopenia and osteoporosis in premenopausal patients with SLE. Bone diminution in SLE seems to be attributable, at least in part, to decreased bone formation in SLE patients.

                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                July 2003
                17 November 2004
                : 94
                : 3
                : c69-c74
                Nephrology Division, Escola Paulista de Medicina, UNIFESP, São Paulo, Brazil
                72023 Nephron Clin Pract 2003;94:c69–c74
                © 2003 S. Karger AG, Basel

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