Risk factors for central pontine and extrapontine myelinolysis after liver transplantation: a single-center study.

BACKGROUND: Central pontine and extrapontine myelinolysis (CPM/EPM) are severe neurologic complications after liver transplantation. METHODS: The present work retrospectively evaluated single-center prevalence of CPM/EPM and associated risk factors: cause of liver disease, hepatic encephalopathy, preoperative, intraoperative, and perioperative blood components use, serum levels, and variation of Na, Cl, and K and immunosuppression were compared between CPM/EPM patients and control group of transplanted patients without neurologic complications. RESULTS: Among 997 transplants, CPM/EPM were diagnosed in 11 patients (1.1%), of whom four were CPM, one was EPM, and six were associated CPM and EPM. Control group consisted of 44 transplanted patients. Central pontine and extrapontine myelinolysis patients experienced higher intraoperative and perioperative serum Na/24 hr variations compared to controls (16.69 ± 5.17 vs. 9.8 ± 3.4 mEq/L, P = 0.001). Maximum peak of intraoperative or perioperative serum Na was significantly higher in patients compared to controls (151.5 ± 3.3 vs. 140.8 ± 6.2 mEq/L, P ≤ 0.001), but no difference in preoperative serum Na was detected. Three patients presented hypernatremia as isolated risk factor. CONCLUSION: Extrapontine myelinolysis can be found isolated or associated with CPM in up to two of three liver transplanted patients with myelinolysis. A marked variation of perioperative serum Na remains the main risk factor even in patients without preexisting hyponatremia; however, isolated hypernatremia may be solely responsible in some cases.

Neuropsychological alterations in hepatitis C infection: the role of inflammation.

About 50% of patients with hepatitis C virus (HCV) infection complain of neuropsychiatric symptoms, "brain fog", weakness, fatigue, and exhibit some degree of quality of life impairment, irrespective of the severity of liver disease. Since the first observation of HCV-related cognitive deficits, 10 studies have been published that have evaluated neuropsychiatric performance in patients with HCV infection and different degrees of hepatic impairment. Unfortunately, these have often included patients with cirrhosis, patients who had acquired the infection through previous intravenous drug misuse, who had a history of relatively recent treatment with interferon, or were on psychoactive medication. In addition, different neuropsychological batteries and tests that explored different cognitive domains were used, which makes the results of the studies difficult to compare. Finally, limited information is available on the pathogenesis of HCV-related cognitive impairment. Cerebral and/or systemic inflammation may be important players but their potential role has not been substantiated by experimental data. The present review outlines the available evidence of the presence of cognitive impairment in patients with HCV infection, with a focus on the potential relationship with cerebral and/or systemic inflammation.