الفهرس 
PATIENTSOnly 14 pages are availabe for public view
 |  | from | 97 |  |  |
| | | from | 97 | | |
Abstract
Hepatocellular carcinoma (HCC) is the fifth commonest cancer in the world in men and is the third highest contributor towards any cancer-related mortality(1). Although the highest number of cases relates to the Far East, Middle- East, and Africa, the last decades have seen nearly a doubling of the incidence of HCC in the western world, particularly in the United States with the trend still on the rise (2). The vast majority of HCC cases occur on a background of preexisting liver disease, and more recently NASH and HCV have emerged as the leading causes of cirrhosis and thereby, HCC (3). This majority may be mediated by metabolic disturbance (mediators of metabolic syndrome (MS)). The MS is a constellation of problems that includes insulin resistance (IR), obesity, hypertension, and hyperlipidemia. Increasingly, components of the MS are being linked to various forms of cancer with respect to both increased risk of disease and worsened outcome. A better understanding of the relation between these 2 diseases ultimately should lead to improved screening and treatment options for patients with HCC(4). IR is an important risk factor for metabolic syndrome and thereby HCC(5). There is evidence supporting the fact that by the time glucose tolerance or fasting glucose levels become impaired(6). Early identification of insulin resistant individuals is important for the prevention strategies of MS and thereby HCC. The euglycaemic insulin clamp method, intravenous glucose tolerance test (IVGTT) and minimal model approximation of the metabolism of glucose (MMAMG) are standard methods for the measurement of IR in research. However, they are impractical in clinical practice and are difficult to perform in population based research studies(7,~). In addition to these standard methods, there are indirect methods for the assessment of IR; Homeostasis Model Assessments (HOMA) (9), Quantitative Insulin Sensitivity Check Index (QUICKI) (lo) and McAuley index (McA) (11). HOMA and QUICKI indices are calculated using both the fasting insulin (FI) and fasting blood glucose levels. McA is calculated using fasting insulin and fasting triglyceride level. When confronted with the results obtained by the MMAMG (gold standard method), the sensitivity and specificity of diagnosis were higher by the indirect method as proposed by McAuley. It has been found that, fasting insulin (FI) is also accurate in predicting IR in the normoglycaemic population who have preparation for abnormal metabolism similar to HOMA, insulin to glucose ratio and the Bennett index. FI >12mu/l has been proposed as the limiting level for IR in non-diabetic population and has been considered as cut off points for diabetic population as well.