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Cytomegalovirus Infection in Decompensated Liver Failure

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A5186 - Cytomegalovirus Infection in Decompensated Liver Failure
Author Block: R. Butzko1, R. Ortiz Pacheco1, A. Berman2; 1Internal Medicine, Rutgers NJMS, Newark, NJ, United States, 2Pulmonary Medicine, Rutgers, New Jersey Medical School, Newark, NJ, United States.
Introduction: Cirrhosis is associated with numerous systemic complications, including decompensated renal, cardiovascular and lung function. Additionally, cirrhosis has been linked to immunosuppression. Ordinarily, cirrhosis-associated immune dysfunction (CAID) increases susceptibility to bacterial infections. Today, we present a case of severe cytomegalovirus (CMV) infection in decompensated liver failure.
Case: A 37-year-old male was transferred to our institution for management of alcoholic hepatitis. During the preceding hospitalization, his liver function deteriorated despite completing a two-week course of prednisone. MELD score on admission was 35. Hospital course was complicated by gastrointestinal bleeding requiring transfusions. Esophagogastroduodenoscopy was performed and revealed pathologic duodenal ulcers suspicious for infection. Biopsies were not performed due to coagulopathy; however serum studies for bacterial and viral etiologies were sent.
Several days later, the patient developed respiratory distress following blood transfusion. Chest X-ray revealed diffuse, bilateral infiltrates suspected to be secondary to transfusion-associated circulatory overload. The patient was given furosemide and placed on non-invasive positive pressure ventilation, but ultimately required intubation. HIV and herpes simplex returned negative, however serum CMV polymerase chain reaction (PCR) returned positive with 303,534 copies/mL. A bronchoalveolar lavage was performed, and CMV PCR returned positive with 897,120 copies/mL in the lavage fluid. Ganciclovir was initiated with decrease in serum CMV titers. Despite treatment, the patient’s hepatic function never improved and he eventually expired.
Discussion: Both liver-specific and systemic factors influence CAID. These include elevated serum prostaglandins, decreased immune surveillance from damaged hepatic reticulo-endothelial system, reduced synthesis of pattern recognition proteins, direct immune cell damage from persistent systemic inflammation, and constant immune activation from translocated intestinal bacteria. Many factors increase susceptibility to bacteria; however immune dysfunction extends beyond reduced bactericidal activity. Lymphopenia has been reported, secondary to decreased production and splenic sequestration. Impaired B-cell memory function has also been described. Additionally, CMV infection/reactivation can further compromise liver function. In immunocompetent hosts, CMV infection is generally limited and asymptomatic. Transplant recipients and AIDS patients can contract symptomatic CMV infection, although severe infection is still rare in cirrhosis. A retrospective analysis in Japan found that CMV reactivation was common in cirrhosis, and showed that liver function was more impaired in CMV-positive patients, however symptomatic infection was rare. Additionally, two case reports from Italy describe CMV as the sole precipitant for acute-on-chronic liver failure. To our knowledge, this is the third case of symptomatic CMV infection in cirrhosis. Further studies are needed to better characterize the level of immune dysfunction in cirrhosis.
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