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Losing Fat or Muscle? A Case of Rhabdomyolysis Following Initiation of Semaglutide (Wegovy)
Abstract Title Losing Fat or Muscle? A Case of Rhabdomyolysis Following Initiation of Semaglutide (Wegovy) Background GLP-1 receptor agonist semaglutide has gained popularity due to its glycemic control, positive cardiovascular effects, and role in weight management. Common side effects include fatigue, headache, injection site reactions, and gastrointestinal symptoms, like abdominal pain, nausea, and gastroparesis. Case Presentation A 56-year-old female with past medical history of systemic lupus erythematosus (SLE) on hydroxychloroquine (HCQ) for 30 years, gastroesophageal reflux disease, autoimmune hepatitis on budesonide, asthma, and fibromyalgia presented to the emergency department (ED) with five days of worsening fatigue, bilateral lower extremity weakness, and pain. One week prior, she experienced nausea, heartburn, and pruritus of the breast, back, and buttocks. Primary care visit labs revealed a creatine kinase (CK) above 27,000 u/L (n=30-184 u/L) prompting ED evaluation. On admission, she endorsed worsening pain, weakness, and decreased appetite. She denied new excessive exertion, foods or supplements, trauma, or statin use but did disclose starting semaglutide (Wegovy) 0.25 mg injections two weeks prior for weight loss. Family history includes polymyositis in her father. Admission vital signs were notable for pulse 113 beats per minute, blood pressure 137/99 mmHg, and BMI 36.85 kg/m2. Physical exam demonstrated bilateral calf tenderness, positive Homan’s sign, hip flexor weakness, normal range of motion, and no joint tenderness. Serum studies demonstrated CK above 34,000 u/L, aspartate aminotransferase (AST) 1018 u/L, alanine aminotransferase (ALT) 297 u/L, creatinine 0.60 mg/dL, estimated glomerular filtration rate (eGFR) >90 mL/min/1.73m2, and no leukocytosis. Rheumatological studies including C3/C4, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), urine protein-creatinine ratio, and double-stranded DNA (dsDNA) were within normal limits. Aldolase was elevated to 176.5 u/L (normal <7.7 u/L). Duplex doppler ultrasonography showed no venous thromboembolism bilaterally. She was diagnosed with rhabdomyolysis and admitted for three days during which her HCQ was held, and she received aggressive IV fluids. CK levels dropped nearly 10,000 u/L daily. At discharge, CK was below 6,000 u/L with no renal injury and improved liver enzymes; she reported near resolution of symptoms. Repeat CK four days post-discharge was 192 u/L. Discussion Limited information exists on the association between semaglutide and rhabdomyolysis; one case report details a similar presentation, both in timing and symptomology. This patient had significantly elevated CK levels and liver enzymes. Despite stable autoimmune conditions on long-term treatment, laboratory results suggest her rhabdomyolysis is attributable to recent semaglutide initiation instead of another etiology.