Relation Between NAFLD, Carotid Intimal Thickness And Metabolic Syndrome

Abstract

Nonalcoholic fatty liver disease (NAFLD) has evolved as the world’s epidemic. NAFLD involves a spectrum of hepatic steatosis, nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC) that occurs in the absence of significant alcohol intake and absence of other viral, genetic and autoimmune components. Hepatic disorders are not the sole morbidity associated with NAFLD and several extra-hepatic manifestations including malignancies and cardiovascular events threaten patients’ lives. Cardiovascular disorders constitute major health threats in NAFLD .Thus, prediction of NAFLD at earlier stage is important in prevention of the inherent process of NAFLD and the associated fatal cardiovascular disorders. NAFLD frequently associated with the metabolic syndrome (MS), which has led many authors to suggest that NAFLD represents the hepatic component of this syndrome. The strong association between NAFLD and MS may explain the high cardiovascular mortality observed in NAFLD patients. Furthermore, NAFLD is by itself a risk factor for atherosclerosis and coronary artery disease independently of established risk factors. Increased carotid artery intima-media thickness (CIMT) is considered a surrogate marker of early generalized atherosclerosis and subclinical CVD so this study was designed to assess the relation between NAFLD, carotid intimal thickness and metabolic syndrome. It was conducted on 30 patients divided into two groups:  Group1: 15 Patients with NAFLD and metabolic syndrome.  Group2: 15 Patients with NAFLD without metabolic syndrome. Summary 87 The metabolic syndrome was defined according to the criteria established by the National Cholesterol Education Program Adult Treatment : Accordingly, participants with three or more of the following five criteria were defined as having metabolic syndrome: abdominal obesity by waist circumference (≥102 cm in men and ≥88 cm in women), high blood pressure (≥130/85mmHg) or on antihypertensive medication, elevated fasting blood glucose (≥ 100 mg/dL) or on antidiabetic medication, hypertriglyceridemia (≥ 150 mg/dL) or on drug treatment for elevated triglycerides, and low serum, HDL–cholesterol (< 40 mg/dL in men and < 50 mg/dL in women)or on drug treatment for reduced HDL-C.NAFLD was diagnosed by confirmation of hepatic steatosis by ultrasound and exclusion of other causes of fatty liver disease. All patients in this study were subjected to the following: Full history taking, full clinical examination, Anthropometric measures (weight, height and BMI), waist circumference measurement, laboratory tests: CBC, prothrombin activity, albumin, bilirubin, SGOT, SGPT, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, fasting blood sugar and HBA1C, virological marker: HCV Ab and HBs Ag, immune markers: ANA, AMA, anti-LKM-1 and ASMA, abdominal ultrasound and carotid US to detect CIMT and presence of plaques. Data were collected, tabulated and statistical analysis was done and revealed a significant increase in carotid IMT in patients of NAFLD in both groups with mean value in group 1 (1.011 + 0.126 cm) and mean value in group 2(1.012 + 0.139cm), although group 1 show a significant increase in metabolic risk factors (DM, HTN, TG, total cholesterol and LDL) than group 2 .This indicate that, NAFLD is by itself a risk factor for atherosclerosis and increased carotid artery intima-media thickness in subjects with or without metabolic syndrome.