Elevated creatine phosphokinase levels associated with linezolid therapy.

PURPOSE: A case of elevated creatine phosphokinase (CPK) levels associated with linezolid therapy in a patient on chronic antihyperlipidemic therapy is presented. SUMMARY: A 79-year-old Caucasian man with a primary diagnosis of acute hemoptysis secondary to pneumonia was admitted to the medical-surgical intensive care unit. A chest radiograph showed a large, right, lower-lobe infiltrate with alveolar consolidation. The patient's medical history included hyperlipidemia that was chronically treated with lovastatin and gemfibrozil. Methicillin-resistant Staphylococcus aureus (MRSA) pneumonia was suspected and confirmed. Vancomycin 1 g i.v. every 12 hours was administered for approximately 10 days into the admission and switched to linezolid 600 mg i.v. every 12 hours after a lack of response to vancomycin. On hospital day 11, the patient's CPK concentration was 47 units/L. Seven days later, his CPK concentration was 2584 units/L and his lovastatin and gemfibrozil were discontinued on that day. The patient's CPK concentration peaked at 5369 units/L on the following day, and linezolid was discontinued at that point. One week later, his CPK concentration was 28 units/L. Approximately two weeks after the patient's CPK levels normalized, he developed numerous complications. The patient died as a result of respiratory failure 11 days after being extubated, which occurred about 38 days after his admission. Although concomitant use of statins and gemfibrozil is known to increase the risk for CPK elevations, the continued rise in CPK levels after discontinuation of antihyperlipidemic therapy and the rapid time course for normalization after linezolid discontinuation are more consistent with an event associated with linezolid initiation. CONCLUSION: A patient on chronic antihyperlipidemic therapy developed elevated CPK levels after receiving linezolid for the treatment of MRSA pneumonia.

Lessons from Mycobacterium avium complex-associated pneumonitis: a case report.

INTRODUCTION: Mycobacterium avium complex (MAC) is an increasingly recognized cause of pulmonary disease in immunocompetent individuals. An acute form of MAC lung disease, MAC-associated pneumonitis, has generally been associated with the use of hot tubs. There is controversy in the literature about whether MAC-associated pneumonitis is a classic hypersensitivity pneumonitis or is a direct manifestation of mycobacterial infection. CASE PRESENTATION: We report the second case in the literature of MAC-associated pneumonitis not related to the use of hot tubs. The source of MAC in a 52-year-old immunocompetent patient was an intrapulmonary cyst containing numerous acid-fast bacilli. The patient developed disseminated miliary nodules throughout both lung fields. Histological examination of resected lung tissue revealed well-formed, acid-fast negative granulomas composed predominantly of CD4+ T-cells and CD68+ histiocytes. The granulomas were strongly positive for tumor necrosis factor-alpha, a pro-inflammatory cytokine. CONCLUSION: The attempt to classify MAC-associated pneumonitis as either a classic hypersensitivity pneumonitis or a direct manifestation of mycobacterial infection is not particularly useful. Our case demonstrates that MAC-associated pneumonitis is characterized by a vigorous T-helper 1-like, pro-inflammatory, immune response to pulmonary mycobacterial infection. The immunopathology provides a rationale for clinical studies of anti-MAC therapy with the addition of anti-inflammatory agents (for example, corticosteroids) to hasten the resolution of infection and symptoms.