Abstract Introduction Libman-Sacks endocarditis is noninfectious endocarditis marked by sterile platelet thrombi on heart valves. It is a rare cardiac manifestation of systemic lupus erythematosus (SLE). Differentiating its vegetations from culture-negative infective endocarditis (IE) is difficult, especially in patients with risk factors for both, as seen in our case. Case Presentation A 51-year-old female with type 2 diabetes mellitus, hypertension, and end-stage renal disease on peritoneal dialysis was recently treated with antibiotics for multifocal pneumonia. Six days post-discharge, she presented with dyspnea, cough, hemoptysis, fever, and hypoxia. Chest CT revealed diffuse ground-glass opacities and pulmonary edema. Transthoracic echocardiography (TTE) showed a large (39 × 10 mm), mobile vegetation on the posterior mitral leaflet with moderate mitral regurgitation. Autoimmune serologies were positive for ANA, anti-dsDNA, lupus anticoagulant, anticardiolipin, and β2-glycoprotein antibodies. The initial bronchoscopy was not favorable for diffuse alveolar hemorrhage (DAH), and blood cultures were negative. A prior kidney biopsy (2021) showed diabetic glomerulosclerosis with resolved immune complex glomerulonephritis. Given the vegetation’s size and mobility, lack of clinical SLE features, elevated WBC, CRP, and procalcitonin, and negative DAH, a multidisciplinary team favored culture-negative IE over Libman-Sacks. Empiric vancomycin and ceftriaxone were initiated. The hospital course was complicated by embolic strokes and DRESS syndrome. Antibiotics were stopped, high-dose prednisone and anticoagulation were started. Repeat TTE showed smaller vegetation and improved mitral regurgitation. She was discharged in stable condition. Ten days later, she returned with hypoxic respiratory failure from DAH (confirmed on bronchoscopy), hemorrhagic toe bullae, and anterior tibial artery occlusion. Lupus flare or catastrophic antiphospholipid syndrome (CAPS) was suspected. She improved with plasmapheresis, rituximab, and corticosteroids, and was discharged on immunosuppressants and warfarin. Discussion and Conclusion Several factors help differentiate Libman-Sacks from IE. Libman-Sacks is more commonly associated with high prevalence of antiphospholipid antibodies but a lower prevalence of SLE-specific autoantibodies. IE typically presents with high WBC, markedly elevated CRP, and procalcitonin, whereas Libman-Sacks may show low WBC and strongly positive antiphospholipid antibodies. Valvular pathology also differs: Libman-Sacks shows small to medium vegetations on either or both sides of the leaflets, while IE typically has large, irregular masses on the valve cusps, often extending to the cords. Our patient’s inflammatory markers and valve findings favored infection initially. This case highlights the diagnostic challenge in patients with risk factors for both. Early multidisciplinary evaluation is essential in guiding management. This abstract is funded by: None
Farouji et al. (Fri,) studied this question.