Key result
Prednisone in SLE is linked to a 43% rate of elevated apoB versus untreated patients.
Why the study?
Does prednisone treatment increase apolipoprotein-B levels and alter triglyceride lipase activities in women with systemic lupus erythematosus?
Cross-Sectional (n=53)
Does prednisone treatment increase apolipoprotein-B levels and alter triglyceride lipase activities in women with systemic lupus erythematosus?
Absolute Event Rate: 43% vs 0%
p-value: p=<0.05
Prednisone therapy in patients with systemic lupus erythematosus is associated with elevated apolipoprotein-B levels, potentially explaining their increased risk of atherosclerosis.
May warrant apolipoprotein-B monitoring in prednisone-treated SLE; leaves open causal role in atherosclerosis.
Patients treated with corticosteroids often have a dyslipoproteinemia characterized by elevated plasma levels of triglyceride and low density lipoprotein cholesterol and/or decreased levels of the high density lipoprotein2 fraction of high density lipoprotein cholesterol. This study was undertaken to determine if such patients also have elevated apolipoprotein-B (apoB) levels and/or abnormalities of the activities of the triglyceride lipases in postheparin plasma. Plasma lipoprotein levels and the postheparin activities of hepatic lipase and lipoprotein lipase were measured in 28 women with systemic lupus erythematosus (SLE) who were treated with prednisone, 10 women with SLE not treated with prednisone, and 15 normal women. The prednisone-treated group had higher mean plasma levels of triglyceride [2.06 +/- 1.3 (+/- SD) vs. 1.15 +/- 0.35 and 0.95 +/- 0.46 mmol/L; P less than 0.01], low density lipoprotein cholesterol [3.41 +/- 1.4 (+/- SD) vs. 2.79 +/- 0.67 and 2.84 +/- 0.70 mmol/L; P less than 0.01], and apoB [1.16 +/- 0.35 (+/- SD) vs. 0.82 +/- 0.13 and 0.76 +/- 0.22 g/L] than the other 2 groups. Forty-three percent of the prednisone-treated group had apoB levels of 1.20 g/L or more compared to 7% of normal subjects and none of the untreated SLE group (P less than 0.05). However, of the 12 prednisone-treated patients with elevated plasma apoB levels 5 had normal plasma lipid levels. There were no differences in the postheparin lipase activities among the 3 groups. These data indicate that corticosteroid-treated patients have elevations in apoB as well as hyperlipidemia. The lipoprotein abnormalities may explain the increased risk of atherosclerosis reported in these patients.
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Ettinger et al. (1988) conducted a cross-sectional in Systemic lupus erythematosus (n=53). Prednisone vs. Untreated SLE patients and normal women was evaluated on Apolipoprotein-B (apoB) levels ≥ 1.20 g/L (p=<0.05). Prednisone treatment in women with SLE was associated with higher rates of elevated apolipoprotein-B levels (≥1.20 g/L) compared to untreated SLE patients (43% vs 0%; P<0.05).
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