A 41-year-old man with hyperlipidemia and hypertension presents to the emergency department with severe diffuse myalgias, dark urine, and tea-colored urine for 3 days. He started atorvastatin 80 mg daily 8 weeks ago. Two weeks ago, he was prescribed clarithromycin for community-acquired pneumonia. Vital signs are stable. Physical examination reveals diffuse muscle tenderness. Laboratory studies show: creatine kinase 7,200 U/L (normal <200), myoglobin 380 ng/mL (normal <110), serum creatinine 1.8 mg/dL (baseline 1.0), urinalysis with brown granular casts and dipstick positive for blood without RBCs on microscopy. Which of the following best explains the mechanism of this patient's current clinical presentation?

1. A)Clarithromycin inhibits CYP3A4, reducing atorvastatin metabolism and increasing intramuscular statin accumulationGABARITO
2. B)Atorvastatin directly inhibits myofibrillar ATPase, causing dose-dependent myotoxicity independent of drug interactions
3. C)Clarithromycin competitively binds to HMG-CoA reductase, potentiating statin effects on muscle cholesterol depletion
4. D)Clarithromycin induces CYP2D6, accelerating atorvastatin metabolism and promoting formation of toxic metabolites
5. E)Combined atorvastatin and clarithromycin therapy causes myositis through direct immune-mediated muscle inflammation unrelated to drug metabolism