Document Type

Conference Proceeding

Publication Date

5-2-2025

Abstract

Systemic lupus erythematosus (SLE) is a complex, multisystem autoimmune that often presents with nonspecific symptoms, complicating diagnosis. Myopericarditis is a rare initial manifestation, mimicking infections or malignancies. We present a case underscoring the importance of considering SLE in refractory multisystem illness. A 26-year-old previously healthy male presented to an outside hospital with a one-week history of left-sided pleuritic chest pain, fever, chills, palpitations, fatigue, cough, sinus congestion, and headache. Initial evaluation revealed marked tachycardia (heart rate 180s/min on exertion). CT pulmonary angiography excluded pulmonary embolism but identified a large right-sided consolidation consistent with pneumonia. His initial troponin was 223 with no acute changes in the electrocardiogram (EKG). An echocardiogram was done, which revealed moderate pericardial effusion with normal ejection fraction. Coxsackie A antibodies were positive so he was diagnosed with myopericarditis. He received 7 days of ceftriaxone and doxycycline in the hospital and discharged with 5 more days of amoxicillin for the pneumonia. He was started on ibuprofen, colchicine, and metoprolol succinate for the myopericarditis, which he was instructed to continue taking outpatient and follow up with a cardiologist. Despite adherence to therapy, symptoms persisted, prompting evaluation at our institution two weeks later. At that time his chief complaints were fatigue, palpitations, and night sweats. His viral symptoms were also still present, but somewhat improved. In the emergency department his troponin was still elevated, but his EKG remained unremarkable. His labs were remarkable for low hemoglobin of 9.0 and elevated BNP of 136. Urinalysis showed non-infectious proteinuria (protein-tocreatinine ratio 1.5). Repeat CT angiography demonstrated bulky mediastinal, hilar, and axillary lymphadenopathy with splenomegaly. Physical exam confirmed generalized lymphadenopathy (cervical, axillary, and inguinal). Epstein-Barr infection was suspected, but IgM antibodies were negative. Given concern for lymphoma, an excisional lymph node biopsy was performed, revealing reactive hyperplasia. Echocardiography showed severely increased wall thickness of the left ventricle, moderately increased wall thickness of the intraventricular septum, and small to moderate pericardial effusion. Cardiology was consulted and a cardiac magnetic resonance imaging study was done which revealed global inflammation and edema, consistent with myocarditis. At this time, autoimmune serology returned positive antinuclear antibody (ANA, 1:280 titer), anti-double-stranded DNA (dsDNA), anti-Smith, anti-RNP, and anti-SS-A/Ro antibodies, strongly supporting systemic lupus erythematosus (SLE) or mixed connective tissue disease. During his hospitalization, the patient also started complaining of muscle pain in his quadriceps and his creatinine kinase was 3,791 indicating possible myositis. Nephrology consultation prompted a kidney biopsy due to proteinuria, revealing mesangial proliferative lupus nephritis (Class II). Rheumatology initiated high-dose methylprednisolone (60 mg daily) and mycophenolate mofetil (500 mg twice daily), with colchicine continued for pericarditis. Within 72 hours, his fatigue, myalgias, and tachycardia improved significantly. SLE should be considered in young patients with persistent, multisystem inflammation despite treatment, even when infections are present. Early serologic testing (ANA, anti-dsDNA, anti-Smith) and multidisciplinary collaboration are critical to avoid diagnostic delays. This case reinforces that myopericarditis, though uncommon, may herald underlying autoimmunity, warranting thorough evaluation for connective tissue diseases.

Comments

American College of Physicians Michigan Chapter and Society of Hospital Medicine Michigan Chapter Resident and Medical Student Day, May 2, 2025, Troy, MI

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