Hepatitis C is an infection characterized by liver damage caused by the hepatitis C virus. It rarely has significant symptoms, but usually persists as a persistent infection, causing a progressive increase in liver scar tissue and eventually cirrhosis. Some patients with cirrhosis will progress to life-threatening hepatocellular carcinoma, liver failure and portal hypertension. Hepatitis C virus infects only humans and chimpanzees and is transmitted primarily through blood and blood products. Intravenous drug use is the main mode of transmission of hepatitis C, followed by manicures, pedicures, tattoos, and again sexual intercourse and childbirth; medical supplies that are not strictly sterilized can also cause infection. Kissing and breastfeeding do not cause hepatitis C virus infection. There are two clinical types of hepatitis C: acute and chronic. About 20% and 80% of people infected with hepatitis C virus will develop acute and chronic hepatitis C, respectively. Unlike hepatitis A, B, and E, only about 15% of patients with acute hepatitis C have mild or nonsignificant and vague or indeterminate symptoms, mainly malaise, muscle aches, nausea, and loss of appetite; most patients do not develop jaundice, and almost no patients develop liver failure. Of these, 10% to 50% of patients will recover spontaneously. Pre-sexual maturity and females are predictors of acute hepatitis C toward self-healing. Although chronic hepatitis C can have mild or nonsignificant malaise, most patients usually do not develop symptoms associated with liver disease until decades later. Once symptoms appear, most patients have developed cirrhosis. Chronic hepatitis C that persists for more than 30 years progresses to cirrhosis in 10-30% of patients. Co-infection with hepatitis B virus or human immunodeficiency virus, alcoholism, and being male are additional factors in the development of cirrhosis in chronic hepatitis C. Patients with chronic hepatitis C who have cirrhosis are 20 times more likely to develop hepatocellular carcinoma than patients without cirrhosis, and their annual incidence of hepatocellular carcinoma is 1 to 3 percent. Globally, about 27% of cirrhosis and 25% of hepatocellular carcinoma are caused by chronic hepatitis C. Cirrhosis and/or hepatocellular carcinoma are the leading causes of liver failure and/or portal hypertension. Hepatic decompensation and portal hypertension are the two main liver disease-related syndromes that lead to the inability of patients to live, work, study and eventually die, and are the main markers for patients requiring liver transplantation. The main manifestations of hepatic decompensation are persistent and recurrent hyperbilirubinemia (jaundice), hypoalbuminemia (swelling) and hepatic encephalopathy (mental-consciousness disorders); portal hypertension is mainly manifested by progressive esophagogastric varices (dilatation of veins and thinning of vessel walls), ascites (fluid in the abdominal cavity) and spontaneous bacterial peritonitis (peritonitis caused by bacterial components). Hepatitis C may also be associated with a number of extrahepatic diseases. To date, hepatitis C-related disorders reported in the literature include dry syndrome, lichen planus, nodular itchy rash, B-cell lymphoid tissue hyperplasia, thrombocytopenia, diabetes mellitus, glomerulonephritis, and cold sediment [precipitating] globulinemia.