ABSTRACT
Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases worldwide, with a global prevalence of approximately 30%. However, the prevalence of NAFLD has been variously reported depending on the comorbidities. The rising prevalence of obesity in both the adult and pediatric populations is projected to consequently continue increasing NAFLD prevalence. It is a major cause of chronic liver disease worldwide, including cirrhosis and hepatocellular carcinoma (HCC). NAFLD has a variety of clinical phenotypes and heterogeneity due to the complexity of pathogenesis and clinical conditions of its occurrence, resulting in various clinical prognoses. In this article, we briefly described the basic definition of NAFLD and classified the subtypes based on current knowledge in this field.
ABSTRACT
Portal hypertension is a clinical syndrome defined by an increased portal venous pressure. The most frequent cause of portal hypertension is liver cirrhosis, and many of the complications of cirrhosis, such as ascites and gastroesophageal variceal bleeding, are related to portal hypertension. Portal hypertension is a pathological condition caused by the accumulation of blood flow in the portal system. This blood flow retention reduces the effective circulation volume. To compensate for these changes, neurotransmitter hormone changes and metabolic abnormalities occur, which cause complications in organs other than the liver. A hepatic hydrothorax is fluid accumulation in the pleural space resulting from increased portal pressure. Hepatopulmonary syndrome and portopulmonary hypertension are the pulmonary complications in cirrhosis by deforming the vascular structure. Symptoms, such as dyspnea and hypoxia, affect the survival and the quality of life of patients. These lung complications are usually underestimated in the management of cirrhosis. This review briefly introduces the type of lung complications of cirrhosis.
ABSTRACT
Background@#This study aimed to determine whether serum uric acid (SUA) levels are associated with various indices of liver damage in the adult Korean population. @*Methods@#We used the Seventh (VII) Korean National Health and Nutritional Examination Surveys. Our study population comprised 6,007 men and 8,488 women. Levels of SUA were divided into four groups (≤ 5.3, 5.3–6.0, 6.0–7.0, and > 7.0 mg/dL for men and ≤ 4.0, 4.0–4.8, 4.8–6.0, and > 6.0 mg/dL for women). Elevated liver enzyme levels were defined as > 35 (men) and > 31 (women) IU/L for aspartate aminotransferase (AST), > 45 (men) and > 34 (women) IU/L for alanine aminotransferase (ALT). Hepatic steatosis index and fibrosis (FIB)-4 index was used to determine nonalcoholic fatty liver disease (NAFLD) and liver FIB, respectively. Adjusted odds ratios (aORs) were calculated by logistic regression analysis for liver enzymes, NAFLD, and liver FIB, according to the SUA level. @*Results@#Among women, the 4.8–6.0 and > 6.0 mg/dL SUA groups showed higher ORs of elevated AST (aOR, 1.78 and 2.03; 95% confidence interval [CI], 1.37–2.32 and 1.40–2.96, respectively; P 6.0 mg/dL SUA groups showed a higher ORs of ALT elevation (aOR, 1.35, 2.26, and 2.37; 95% CI, 1.02–1.79, 1.72–2.97, and 1.60–3.50, respectively; P 6.0 mg/dL SUA group showed higher OR of NAFLD status (aOR, 1.52; 95% CI, 1.06–2.19). Among men and women with NAFLD, hyperuricemia showed higher ORs of liver FIB (aOR, 2.25 and 1.89; 95% CI, 1.21–4.19 and 1.09–3.27, respectively) than the lowest level SUA group. @*Conclusion@#High SUA levels may be associated with elevated liver enzymes and NAFLD, mainly in women. Even in women with normal ALT levels, SUA levels may predict the NAFLD status. Hyperuricemia may predict advanced liver FIB in both men and women with NAFLD. Further studies investigating the causal effects of SUA on liver damage are required.