A 42-year-old woman with systemic lupus erythematosus on chronic prednisone develops acute chest pain. Vital signs show BP 145/92 mmHg, HR 102/min, RR 18/min, temp 37°C, SpO2 98%. EKG reveals ST elevation. Laboratory studies show prolonged aPTT, false-positive RPR, LDL 180 mg/dL, HDL 28 mg/dL, and negative antiphospholipid antibodies. Which mechanism best explains her premature atherosclerosis and thrombotic complications?
- A)Corticosteroids directly increase hepatic HMG-CoA reductase expression
- B)Lupus anticoagulant increases HDL catabolism exclusively
- C)Chronic corticosteroid use induces apolipoprotein B mutations
- D)SLE causes primary lipoprotein lipase deficiency
- E)Antiphospholipid antibodies impair apolipoprotein-mediated LDL receptor recognitionGABARITO
Explicação
Antiphospholipid antibodies in SLE can interfere with the binding of apolipoprotein B and E to LDL receptors, impairing hepatic LDL clearance. This, combined with corticosteroid-induced dyslipidemia and inflammatory effects, accelerates atherosclerosis. Ver explicação completa e trilha adaptativa →