A precontrast computed tomography scan showed a diffusely hyperdense liver and a large amount of ascites (Panel A). Transjugular liver biopsy demonstrated cirrhosis with polymorphonuclear infiltrate, Mallory bodies (arrows), and ballooning degeneration (arrowheads) (Panel B). Electron microscopy showed lysosomal myeloid bodies with dense deposits

(asterisks) within hepatocytes (Panel C). On the basis of clinical history and histologic findings, amiodarone-induced liver cirrhosis was diagnosed, and the drug was replaced with another antiarrhythmic agent (propafenone). He was discharged with improved general condition with marked reduction of ascites. Although asymptomatic elevations of aminotransferases have been reported in up to 25% of the patients

treated with long-term amiodarone therapy, symptomatic liver dysfunction has been reported to occur in fewer than 1% of these patients.1, 2 However, amiodarone-induced Selleck PLX3397 hepatitis can progress to cirrhosis, resulting in decompensated hepatic failure, although this rarely happens.1, 2 Amiodarone is one of the cationic amphiphilic drugs (CADs) that can cause phospholipidosis in liver.3 In this case, the findings demonstrating intralysosomal myelin figures and electron-dense material on electron microscopy are compatible with the findings of CAD-induced phospholipidosis.4 However, the functional consequences of phospholipidosis on cellular or tissue function have not been well explained. Rather, liver damage is considered to be caused by amiodarone-induced find more inhibition of mitochondrial β-oxidation.5 “
“We read with great interest the article by Lange and coworkers.1 It is known that mitochondrial toxicity related to the nucleoside analogues can result in macrovesical hepatic steatosis and lactic acidosis. In vivo, these results were shown as side effects of long-term lamivudine use in patients with human immunodeficiency virus (HIV).2 It was noted that the amount of mitochondrial DNA

defects is a predictive marker for the clinical expression of mitochondrial toxicity.2 In case of the severity of the underlying liver dysfunction due to cirrhosis, or acute exacerbation of chronic liver disease, the function of mitochondria in hepatocytes declines immediately. In light of these data, severe mitochondrial 4-Aminobutyrate aminotransferase dysfunction leading to lactic acidosis can be aggravated by nucleoside analogues in patients with an underlying disease, as discussed above. Moreover, hepatic steatosis may be an additional risk factor for these patients with hyperlactatemia who are using entecavir. Obesity was reported as a possible risk factor for mitochondrial toxicity in patients with HIV who are undergoing highly active antiretroviral therapy.3 So, in spite of the small numbers of patients with lactic acidosis under entecavir, we worry about the effect of body mass index on treatment toxicity. Akif Altınbas MD*, Fuat Ekiz MD*, Osman Yuksel MD, Assoc. Prof.