Antiphospholipid Syndrome Patient with Libman-Sacks Endocarditis

Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by recurrent arterial and venous thrombosis, often associated with complications such as pregnancy morbidity. Libman-Sacks Endocarditis (LSE), a form of nonbacterial thrombotic endocarditis, is commonly observed in APS patients. This case report presents a 29-year-old Javanese woman with APS and Libman-Sacks Endocarditis. The patient, previously diagnosed with a transient ischemic attack, was admitted to Dr. Soetomo General Hospital with progressive shortness of breath, leg swelling, and abdominal distension. Initial investigations revealed thrombocytopenia, anemia, pleural effusion, cardiomegaly, and valve abnormalities. Despite anticoagulant therapy and supportive measures, the patient’s condition worsened, and she developed signs of heart failure and neurological deficits. Blood cultures remained negative, ruling out bacterial endocarditis. Imaging studies confirmed the presence of sterile vegetations on the mitral valve, a hallmark of LSE. The patient was diagnosed with primary APS based on clinical and laboratory findings, including positive lupus anticoagulant. After 28 days of hospitalization, she was discharged in stable condition but was re-admitted two days later with neurological decline. Despite aggressive management, including corticosteroids, diuretics, and anticoagulants, the patient suffered multiple complications, including seizures and possible thrombotic stroke and eventually passed away. This case underscores the diagnostic challenges and complexity in managing APS with Libman-Sacks Endocarditis, highlighting the need for early diagnosis and comprehensive treatment. The objective of this case report is to highlight the diagnostic challenges and management complexities of APS with Libman-Sacks Endocarditis, emphasizing the importance of early recognition and comprehensive treatment to mitigate associated morbidity and mortality. LSE remains a rare but severe manifestation of APS, with potential for thromboembolic events and significant morbidity.