Document Type

Conference Proceeding

Publication Date

5-2-2025

Abstract

Lupus myocarditis (LM) is a potentially fatal manifestation of systemic lupus erythematosus (SLE) occurring in 5-10% of SLE patientspatients with SLE (1). Lupus nephritis (LN) is a form of glomerulonephritis that constitutes one of the most severe organ manifestations of SLE (2). We present a unique case of a 27-year-old female with acute lower extremity edema secondary to LM with concomitant LN . This case report highlights LM as a rare manifestation of SLE and the importance of a thorough workup of acute bilateral lower extremity swelling in SLE patientspatients with SLE and glomerulonephritis. A 27-year-old female with a past medical history of SLE, antiphospholipid syndrome, present and SLE glomerulonephritis presented with acute bilateral lower extremity swelling. Initial workup demonstrated enlarged cardiomediastinal silhouette on chest x-ray, 1 hour troponin 99 ng/mL, 2-hour troponin 108 mg/mL, brain natriuretic peptide 768 pg/mL, Complement 3 59 ng/dL, Complement 4 21 mg/dL, total complement 30.3 mg/dL and urine protein >1,000 mg. An echocardiogram was ordered which demonstrated a newly reduced ejection fraction of 35%, previously 65%. Consultations to cardiology, rheumatology and nephrology were placed. Rheumatology recommended continuing patient’s home mycophenolic acid 500 mg twice daily (BID), hydroxychloroquine 500mg BID, & and prednisone 20mg daily. Nephrology recommended continuing patient’s home immunosuppressive therapy, 40 mg methylprednisolone every 8 hours (q8h) and prednisone taper on discharge (20 mg daily for 10 days, then 10mg for 30 days). Cardiology performed a right and left heart catheterization that revealed nonischemic cardiomyopathy, normal left ventricular end diastolic pressure, and no evidence for pulmonary hypertension. Lupus myocarditis was diagnosed with patient history, decreased complement levels, positive double-stranded DNA antibodies, high Erythrocyte Sedimentation RateSR and/ C-reactive protein ,CRP and new onset nonischemic cardiomyopathy. She was treated with mycophenolic acid 500mg BID, hydroxychloroquine 200mg BID, 40 mg methylprednisolone q8h, IV furosemide 40 mg BID, metoprolol 50mg daily, empagliflozin 10mg daily, spironolactone 25mg daily, and sacubitril-valsartan 49-51 mg BID. Home apixaban 5mg BID was continued for her history of anti-phospholipid syndrome. She was discharged on a prednisone taper as described above, empagliflozin 10mg daily, spironolactone 25mg daily, sacubitril-valsartan 49-51 mg, metoprolol 50mg daily, 5mg Eliquis BID, and furosemide 40 mg every Monday, Wednesday, and Friday. She was instructed to follow up with her Family Physician, Cardiology, Rheumatology and Nephrology. This case underscores the importance of recognizing LM as an etiology behind lower extremity edema in patients with SLE glomerulonephritis instead of solely attributing it to poor renal function. Although rare, it is important to consider LM as the culprit behind acute lower extremity edema since patients with high SLE disease activity have both LM and LN (3). LM Diagnosis is established through urinalysis, troponin, transthoracic echocardiogram, left and right heart catheterization, and specialty expertise. It is important to consider LM as an etiology behind acute lower extremity edema in SLE glomerulonephritis patients. Early recognition and diagnosis are key for optimizing patient outcomes through tailored medications, specialists’ recommendations, and close follow-up. In turn, early individualized treatment plans improve disease burden and patient quality of life.

Comments

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

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