Population group
Incidence of HCC
Surveillance recommended
Asian male hepatitis B carriers > age 40
0.4–0.6 %/year
Asian female hepatitis B carriers > age 50
0.3–0.6 %/year
Hepatitis B carrier with family history of HCC
Incidence higher than without family history
African/North American blacks with hepatitis B
HCC occurs at a younger age
Cirrhotic hepatitis B carriers
3–8 %/year
Hepatitis C cirrhosis
3–5 %/year
Stage 4 primary biliary cirrhosis
3–5 %/year
Genetic hemochromatosis and cirrhosis
Unknown, but probably >1.5 %/year
Alpha 1-antitrypsin deficiency and cirrhosis
Unknown, but probably >1.5 %/year
Other cirrhosis
Unknown
Surveillance benefit uncertain
Hepatitis B carriers <40 (males) or <50 (females)
<0.2 %/year
Hepatitis C and stage 3 fibrosis
<1.5 %/year
Noncirrhotic NAFLD
<1.5 %/year
Screening for esophageal varices . Patients with cirrhosis should be screened for the presence of esophageal varices by upper endoscopy, so that prophylactic therapy such as nonselective beta blocker (i.e., propranolol, nadolol) or carvedilol can be started in those with varices that are at increased risk for bleeding [26]. In those intolerant of beta blocker therapy, prophylactic band ligation of esophageal varices should also be considered. Identifying and treating patients with high-risk varices leads to improved clinical outcomes, including reduced risk of hemorrhage and decreased mortality [26].
Treatment of Underlying Liver Disease/ Hepatitis . Elimination of the underlying cause of ongoing inflammation can result in significant improvement in liver function and potentially avoidance of long-term complications. Anyone diagnosed with active chronic Hepatitis B (HBsAg positive, HBeAg positive, or HBeAg negative) should be evaluated for the treatment with antiviral medication [27]. The rationale for treatment in patients with chronic HBV is to reduce the risk of progressive chronic liver disease and hepatocellular carcinoma. The full recommendations of the American Association for the Study of Liver Diseases (AASLD) updated in 2009 regarding the treatment of chronic hepatitis B virus infection are available online (http://www.aasld.org/sites/default/files/guideline_documents/ChronicHepatitisB2009.pdf). Similarly, those with chronic hepatitis C virus (HCV) infection should be considered for treatment in order to eradicate HCV RNA as indicated by attainment of a sustained virologic response (SVR) indicating negative viral load at either 12 weeks (SVR12) or 24 weeks after cessation of therapy. The recent guidelines released jointly by the American Association for the Study of Liver Diseases (AASLD) and the Infectious Diseases Society of America (IDSA) regarding the diagnosis and management of HCV infection are available online (http://www.hcvguidelines.org/). Sustained viral response has been associated with regression of fibrosis and cirrhosis, a reduced rate of hepatic decompensation, a reduced risk for hepatocellular carcinoma, and reduced liver-related mortality [28]. Treatment of underlying autoimmune hepatitis has similarly resulted in enhanced outcomes including fibrosis as well as in those with nonalcoholic steatohepatitis with fibrosis who have undergone bariatric surgery with concomitant weight loss.
How Do I Know How Severe My Liver Disease Is?
Severity of liver disease can be determined by different modalities, like physical examination findings, various blood tests, imaging, portal pressure measurement, liver biopsy, and use of different prognostic models.
Signs/Symptoms. Physical changes such as development of spider nevi (swollen blood vessels looking like spider’s web), palmar erythema (reddening of the skin on the palmar aspect of the hands), gynecomastia (enlargement of breasts), caput medusa (distended veins, which are seen radiating from the umbilicus), Dupuytren’s contractures (hand deformity where fingers are bent and cannot be fully straightened), and testicular atrophy (shrunken testes) are usually indicative of advanced liver disease and are typically not present in the absence of cirrhosis and even those with early cirrhosis. Physical signs/symptoms can help in differentiating compensated from decompensated cirrhosis. Decompensated cirrhosis is defined by the presence of complications particularly development of ascites, variceal bleeding, and/or hepatic encephalopathy (mental changes from liver disease like confused thinking). Hepatocellular carcinoma, another complication of cirrhosis, can occur in the presence or absence of decompensation. Prognosis and survival is markedly worse in decompensated cirrhosis than that in compensated cirrhosis. Thus, any patient with decompensated cirrhosis should be evaluated urgently by a hepatologist and if appropriate, referred for transplant consideration.
Laboratory Tests. There is a battery of blood tests for assessment of liver disease like serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, direct and indirect bilirubin, serum albumin, and prothrombin time (PT). Although high elevations of aminotransferases (AST and ALT) usually over 1000 IU/L generally implement extensive hepatocellular injury, they can often be normal in patients with chronic liver disease or cirrhosis. Thus, serum aminotransferases and alkaline phosphatase do not reliably reflect disease severity but more likely reflect liver injury. On the other hand, serum bilirubin and prothrombin time, and serum albumin more so reflect liver function and the former two along with serum creatinine, are components of MELD Score, a tool used to assess the severity of liver disease and predict outcomes of interventions in patients with liver disease and to prioritize patients awaiting the liver transplant.
Imaging. Different imaging modalities are available including abdominal ultrasound, computed tomography scan, and magnetic resonance imaging. Abdominal ultrasound is typically the first radiologic study as it is widely available, less expensive, and does not expose patients to radiation or contrast hazards. Shrunken, coarsened, irregular, and nodular appearance and increased echogenicity of liver on ultrasound suggest advanced liver disease or cirrhosis. Milder changes such as fatty infiltration may also be identified. Abdominal ultrasound may reveal cirrhosis-related complications like ascites, varices, splenomegaly, and portal vein thrombosis. Ultrasound is also a screening modality for detection of hepatocellular carcinoma but CT and MRI scans are more sensitive for detection of lesions albeit at a higher monetary cost and potential complications.
Portal Pressure Measurement. Portal vein is the large vessel that carries blood from the digestive organs to the liver. In cirrhosis, resistance to the portal blood flow develops inside the liver, resulting in portal hypertension. The hepatic venous pressure gradient (HVPG) is measured to calculate the gradient (difference) in pressure between the portal vein and the inferior vena cava (large vein carrying blood from lower part of the body to the heart for purification). Portal hypertension is present if the HVPG is ≥6 mmHg. The risk of complications from cirrhosis and mortality rates increases as HVPG value increases. For example, with HVPG is ≥12 mmHg, people are at risk for variceal bleeding and the development of ascites (fluid collection in the abdomen).
Liver Biopsy. Liver biopsy remains an important tool of diagnosing some liver diseases which are otherwise not obvious from physical examination, laboratory data, and imaging. Since it is invasive, it is usually the last resort for diagnosing and assessing liver disease. Nevertheless, liver biopsy is the most accurate means of assessing severity of inflammation (grade) and degree of fibrosis (grade) of liver damage.
Prognostic Models . There are different prognostic models available for estimating disease severity and survival in patients with liver disease. Several prognostic models are currently used which are disease specific, such as the models for predicting survival in patients with primary biliary cirrhosis, primary sclerosing cholangitis, and alcoholic liver disease [29–32]. There are two models that are used commonly in the care of patients with cirrhosis in general. They are the Child–Turcotte–Pugh (CTP) score and the Model for End-stage Liver Disease (MELD) score. Similarly King’s College Hospital criteria are commonly used model for assessing prognosis in patients with acute liver failure [33].
Child–Turcotte–Pugh (CTP) Score : First developed in 1973, the Child–Pugh score was originally used to stratify the risk of portacaval shunt surgery in patients with cirrhosis, but the score has since been modified, and become a widely used tool to assess prognosis in patients with chronic liver disease and cirrhosis [34, 35]. Moreover, it was previously prior to implementation of the MELD in order to determine priority for liver transplantation. CTP Score incorporates five variables, namely the serum albumin, serum bilirubin, ascites, encephalopathy, and prothrombin time. The score ranges from 5 to 15. Depending on the score, patients can be categorized into Child–Pugh class A (5–6 points), class B (7–9 points), or class C (10–15 points). The higher the score, the more severe the liver disease is. CTP Score is a reliable predictor of survival in many liver diseases and also predicts major complications such as bleeding from varices.
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