PubMed · 11668401
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P Connor, R H Hawes. 2001. ERCP topics.. https://doi.org/10.1055/s-2001-17924
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Imaging studies are becoming essential in the management of orthotopic liver transplantation (LT). They have a very important role in the preoperative evaluation and selection of suitable candidates. At the same time, they are essential in the early detection of postoperative complications, the recognition of which allows the prompt institution of appropriate therapeutic measures. Timely recognition of complications improves the success of LT; furthermore, some complications can be treated with interventional radiologic procedures, avoiding additional surgery. This article reviews the current application of diagnostic and interventional imaging in liver transplantation, both for cadaveric and living donor transplants.
Hepatic transplantation has become the treatment of choice for advanced irreversible liver disease. More than 4,000 hepatic transplantations were performed in the United States in 1997 and more than 11,000 are awaiting transplantation. Graft endurance and overall patient survival has been steadily improving, and between 1992 and 1994, 82% of the patients who received a liver transplant survived for at least a year. Today, liver transplant patients have a five-year survival rate of approximately 75%. The improvement in survival can be attributed to better patient selection and preparation, advances in organ preservation, improved immunosuppressive therapy agents and refinement of surgical techniques. In this article, we will address the hepatic parenchyma and vascular structures that should be evaluated prior to and following liver transplantation, the range of expected anomalies and abnormalities, and the utility of each of the three main imaging modalities, namely ultrasonography, computed tomography and magnetic resonance imaging in this assessment.
NAD(P)H:quinone oxidoreductase (NQO1) and dihydronicotinamide riboside:quinone oxidoreductases (NQO2) are cytosolic flavoproteins that catalyze the two-electron reduction of quinones and quinoid compounds to hydroquinones, thereby promoting detoxification and preventing the formation of highly reactive oxygen species, which lead to DNA and cell damage. Two NQO isoforms, designated NQO1 and NQO2, have been cloned and sequenced. To elucidate their role in carcinogenesis, the gene expression of human NQO1 and NQO2 in paired normal and tumor tissue samples was examined. Quantitative triplex reverse transcriptase polymerase chain reaction was employed to analyze NQO1 and NQO2 mRNA expression in normal hepatic and biliary tissue as well as in cholangiocellular carcinomas (CCC), hepatocellular carcinomas (HCC), and focal nodular hyperplasias (FNH). Coexpression of beta-actin RNA was used as an internal reference standard and linear ranges of transcript amplification were established for each sample. In normal hepatocellular tissue, the two NQO isoforms were differentially regulated, with a higher expression of NQO2 than NQO1. Malignant hepatocellular tissue (HCC), however, displayed up-regulation of NQO1 and down-regulation of NQO2. Regulation of either transcript was not seen in benign hepatocellular tumor tissue (FNH), which indicates a reciprocal control of NQO genes in hepatocarcinogenesis. Normal biliary tissue expressed a significantly higher level of NQO1 transcripts compared with normal liver, whereas biliary NQO2 levels were significantly lower than in hepatocellular tissue. Comparing the levels of expression in normal and malignant biliary tissue (CCC), no significant differences were noted between the expression levels of either transcript. Thus, this study provides evidence for differential hepatic and biliary regulation of both NQO1 and NQO2.