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Cirrhosis and chronic liver failure rank as the 12th leading cause of death in the United States, accounting for 27,555 deaths (9.2 per 100,000 population) in 2006, with a slight male predominance (NCHS, 2009). The vast majority of cirrhosis-related morbidity and mortality is secondary to excessive alcohol consumption, hepatitis B and C, and obesity (nonalcoholic fatty liver disease [NAFLD]), and is theoretically preventable. The term cirrhosis refers to a progressive diffuse, fibrosing, and nodular condition that disrupts the entire normal architecture of the liver. Portal hypertension ensues with multiple long-term complications. Approximately 40% of patients are asymptomatic, with cirrhosis often discovered during a routine examination, including laboratory and radiographic studies (Figs. 38-13 and 38-14), or often at autopsy. Mortality rates in patients with alcoholic liver disease are considerably higher than in those with other forms of cirrhosis.

The major complications of cirrhosis that affect HRQOL and survival include ascites formation, spontaneous bacterial peritonitis, hepatorenal syndrome, encephalopathy, and GI bleeding secondary to portal hypertension and varices. Another serious complication of cirrhosis is the development of hepatocellular carcinoma, for which screening protocols with ultrasound and serum alpha-fetoprotein testing are cost-effective (Marrero, 2005). All patients with ascites

Table 38-3 Viral Hepatitis Serologic Tests and definitions



Hepatitis A virus (HAV)

Anti-HAV IgM

Immunoglobulin M (IgM) antibody to hepatitis antigen. Antibody of IgM class signifies recent acute infection. This develops at onset of symptoms and resolves in less than 1 year.

Anti-HAV IgG

Immunoglobulin G (IgG) antibody to hepatitis A antigen. With negative anti-HAV IgM, this indicates past HAV infection, and that patient is immune. It appears 1 to 2 weeks after IgM antibody.

Hepatitis B virus (HBV)


Hepatitis B surface antigen is earliest indicator of acute infection. It can be present for several months before symptoms and may remain detectable for up to 6 months. Persistence after 6 months may indicate a chronic carrier state.


Antibody to hepatitis B surface antigen is indicator of clinical recovery and subsequent immunity. It appears 1 to 2 months after HBsAg disappears, and it may be present for life.


No clinical significance, not readily available.

Anti-HBc IgG

Antibody to hepatitis B core antigen is early indicator of acute infection. It is also a lifelong marker that represents past exposure. It may precede the detection of HBsAg. This persists for years but does not necessarily confer immunity.

IgM Anti-HBc

Early indicator of acute active infection; usually short-lived (3-6 wk). Persistence of e antigen suggests progression to chronic carrier state.

HBe g

Active infection is present, and patient is highly contagious.


Seroconversion from antigen to antibody is prognostic for resolution of infection and, in a carrier, means very low infectivity.

IgM anti-HBc

IgM fraction of antibody to hepatitis B core antigen is test of choice to rule out acute HBV infection. IgM fraction disappears in first few months.

Hepatitis C


An antibody to HCV that appears 3 to 12 months after exposure.

Hepatitis D


This antibody to HDV may appear late and may be short-lived.

Hepatitis E

(non-A, non-B)

No markers detectable, epidemiology parallels that of hepatitis B.

Modified from: Rodney WM. Gastrointestinal disorders. In Rakel RE (ed). Textbook of Family Medicine, 6th ed. Philadelphia, Saunders, 2002.

Subchorionic Abruption

Map 3 170dB/C 3 Persist Off 2D Qpt:HSCT Fr Rate:Surv SonoCT®



Figure 38-13 Cirrhosis. Ultrasound shows lobulated shrunken liver with ascites and splenomegaly. (CourtesyDr. PerryPernicano.)

Figure 38-13 Cirrhosis. Ultrasound shows lobulated shrunken liver with ascites and splenomegaly. (CourtesyDr. PerryPernicano.)

Tuberculosis Colon Liver Metastasis

should be evaluated for liver transplantation because of poor 5-year survival (30%-40%) (Gines et al., 2004) (Fig. 38-15).

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