Abstract Introduction Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by antibodies against phospholipids and phospholipid-binding proteins, leading to a prothrombotic state that causes venous and arterial thromboses. APS can occur independently or alongside other autoimmune conditions, most commonly lupus. Its manifestations extend beyond thrombotic and obstetric events to include thrombocytopenia, valvular disease, nephropathy, and, rarely, pulmonary complications such as diffuse alveolar hemorrhage (DAH). DAH, a severe manifestation occurring in approximately 0.7-2% of APS patients, results from immune-mediated damage to the pulmonary microvasculature and presents with dyspnea, cough, hemoptysis, and hypoxemia. Diagnosis is challenging due to nonspecific clinical and radiographic findings, and management requires balancing the dual risks of bleeding and thrombosis. Case Presentation This case describes a 59-year-old woman with a history of COPD, recurrent sinus infections, and APS complicated by prior stroke and miscarriages, on a home regimen of daily low-dose aspirin and hydroxychloroquine, who presented with acute hemoptysis lasting 24 hours. Imaging revealed multifocal ground glass opacities concerning for DAH without pulmonary embolism, and she was admitted to the ICU for close monitoring. Her management included tranexamic acid nebulizers, high-dose intravenous steroids, and supportive measures; her home aspirin was discontinued and prophylactic anticoagulation was not pursued due to active bleeding. An infectious workup was negative, and rheumatologic evaluation supported an autoimmune etiology related to APS. Her hemoptysis improved after initiation of pulse-dose steroids. She was discharged on a steroid taper with pulmonology and rheumatology follow-up, during which she underwent repeat imaging which revealed new ground glass opacities with resolution of previous areas. Given these findings, she underwent bronchoscopy with biopsy which revealed intra-alveolar hemosiderin without evidence of thrombosis, capillaritis, or vasculitis, confirming her diagnosis of DAH. She remained asymptomatic and later resumed low dose aspirin, hydroxychloroquine, and was started on mycophenolate mofetil. Discussion This case underscores the importance of recognizing DAH as a potential pulmonary manifestation of APS, particularly in patients presenting with hemoptysis, as APS-associated DAH remains an underrecognized but critical clinical entity. It highlights the diagnostic value of bronchoscopy and the therapeutic role of early, aggressive corticosteroid therapy. It also illustrates the delicate balance of anticoagulation management in APS, emphasizing that inconsistent or suboptimal anticoagulation may predispose to severe thrombotic complications. This case adds to the limited literature describing pulmonary hemorrhage in APS and reinforces the need for prompt multidisciplinary management, judicious anticoagulation strategies, and continued research into optimizing therapy for this complex condition. This abstract is funded by: None
Ivanov et al. (Fri,) studied this question.
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