Case Presentation: A 19-year-old male with no significant past medical history presented with a three-week history of fever, fatigue, arthralgias, and new-onset left-sided sharp chest pain. The pain was constant, non-radiating, pleuritic, worse when supine, and associated with shortness of breath. He denied prior cardiac disease or family history of coronary artery disease. A malar rash was present, and a dermatologist had recently documented a positive ANA. On arrival, he was febrile and tachycardic. EKG showed sinus tachycardia. Labs demonstrated anemia (hemoglobin 9.8 g/dL), elevated troponin (279→394 ng/L), LDH 463 U/L, procalcitonin 0.53 ng/mL, ESR 92 mm/hr, CRP 7.28 mg/dL, ferritin 2346.9 ng/mL, transferrin 99 mg/dL, and iron < 12 µg/dL. Urinalysis showed 100 mg/dL protein, moderate hematuria, and a urine protein-to-creatinine ratio of ~2 g. CT angiography was negative for pulmonary embolism but showed left lower lobe consolidation and a moderate left pleural effusion. Echocardiogram showed an LVEF of 50–55% with normal wall motion and no valvular disease. Autoimmune workup revealed a strongly positive ANA (>1:1280), dsDNA (>1:640), and pANCA positivity. Renal biopsy was obtained due to proteinuria and hematuria, demonstrating Class IV lupus nephritis with ~15% crescents and no chronicity. Cardiac MRI was considered but not performed due to limited resources; therefore, myocarditis was diagnosed clinically. Given the presentation, labs, and imaging, a diagnosis of SLE with multi-organ involvement was made, including lupus myocarditis and nephritis. He was started on pulse-dose IV methylprednisolone (250 mg, increased to 500 mg daily), followed by oral prednisone 1 mg/kg. Prophylactic oscal and atovaquone were initiated. Empiric ceftriaxone and azithromycin were started for possible pneumonia.
Discussion: This case illustrates the diagnostic complexity of SLE in a young male presenting with overlapping cardiac, renal, and pulmonary involvement. Lupus myocarditis is an uncommon but serious complication, often presenting with non-specific symptoms such as chest pain, dyspnea, and elevated cardiac biomarkers. Diagnosis is challenging, especially where cardiac MRI is unavailable. In this patient, the diagnosis was supported by clinical presentation, labs, and echocardiographic findings. Significant proteinuria, hematuria, and biopsy-proven Class IV lupus nephritis underscore the aggressive nature of his disease. pANCA positivity raised concern for overlap with ANCA-associated vasculitis, though it may represent a false positive in the setting of high ANA titers. Multidisciplinary management with high-dose steroids and immunosuppressive therapy is critical to prevent irreversible organ damage.
Conclusions: This case highlights the need to consider lupus myocarditis in young SLE patients presenting with chest pain and elevated cardiac biomarkers, even without classic cardiac symptoms. Early recognition and prompt immunosuppression are essential for improved outcomes. It also emphasizes the importance of comprehensive, multidisciplinary care in severe, multi-organ SLE.