C

• Child-Turcotte-Pugh Classification System: Widely used and published scoring system for liver disease severity. Based on clinical and lab criteria, patients are classified as Class A, B, or C. Those with class C have the most severe liver disease.
• Chronic “active” or “immune active” hepatitis B: Stage of hepatitis B infection characterized by an elevated serum ALT (usually defined as exceeding twice the upper limit of normal) and thought to reflect immune-mediated lysis of infected hepatocytes, often in the setting of HBV DNA level >2000 IU/mL; possibly triggered and maintained by ongoing viral replication.
• Cirrhosis: Describes a condition of the liver characterized by prominent and irreversible scarring. Physical examination or ultrasound findings may suggest a diagnosis of cirrhosis, and some non-invasive tests provide moderately accurate assessment of whether cirrhosis is present. However, ultimately the diagnosis of cirrhosis is based on liver histology and the presence the bridging fibrosis (see above).
• Compensated versus decompensated cirrhosis: Patients with cirrhosis can be categorized as having compensated or decompensated cirrhosis. From a clinical standpoint, patients with compensated cirrhosis have no clinical manifestations of portal hypertension.  Some experts divide compensated cirrhosis into two categories:  stage 1 (absence of varices) and stage 2 (presence of varicies without bleeding and abscence of acites).  Decompensated cirrhosis is characterized by the development of clinically-evident complications of portal hypertension (ascites, esophageal variceal bleeding, or encephalopathy) or liver insufficeincy (manifested by jaundice). Some experts categorize decompensated cirrhosis as stage 3 and stage 4, with satege 4 considered as severe decompensated cirrhosis and characterized by recurrent variceal hemorrhage, refractory ascites, hyponatremia, and/or hepatorenal syndrome.  The prognosis and survival with decompensated cirrhosis is dramatically worse than those with compensated cirrhosis. 
• Core antibody (anti-HBc): Hepatitis B core antigen (HBcAg) is an intracellular antigen expressed by infected hepatocytes that is not detectable in serum, but antibodies are produced in response to HBcAg peptides (smaller fragments of the HBcAg). These antibodies (anti-HBc) can be detected throughout the course of HBV infection and are a marker of natural exposure to HBV; anti-HBc is absent in those who have been vaccinated. Core antibody is generally in the form of IgM during acute infection or flares of HBV and predominantly in the form of IgG during chronic or resolved infection.
• Core promoter mutations: These mutations in the hepatitis B DNA core region can emerge spontaneously or under drug pressure resulting nucleotide substitutions in the core promoter region that effectively decrease the production of HBeAg. Patients who have these mutations can have active liver disease with high HBV DNA levels after HBeAg seroconversion. See case, “Approach to Hepatitis B e Antigen Negative Patients with Increased Hepatic Aminotransferase Levels.”