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Viral Hepatitis

Background

Hepatitis, a general term referring to inflammation of the liver, may result from various causes, both infectious (ie, viral, bacterial, fungal, and parasitic organisms) and noninfectious (eg, alcohol, drugs, autoimmune diseases, and metabolic diseases); this article focuses on viral hepatitis, which accounts for more than 50% of cases of acute hepatitis in the United States, primarily in the emergency department setting.

In the United States, viral hepatitis is most commonly caused by hepatitis A virus (HAV), hepatitis B virus (HBV), and hepatitis C virus (HCV). These three viruses can all result in acute disease with symptoms of nausea, abdominal pain, fatigue, malaise, and jaundice.
Additionally, acute infection with HBV and HCV can lead to chronic infection. Patients who are chronically infected may go on to develop cirrhosis and hepatocellular carcinoma (HCC).
Furthermore, chronic hepatitis carriers remain infectious and may transmit the disease for many years.

Other hepatotropic viruses known to cause hepatitis include hepatitis D virus (HDV) and hepatitis E virus (HEV). However, the term hepatotropic is itself a misnomer. Infections with hepatitis viruses, especially HBV and HBC, have been associated with a wide variety of extrahepatic manifestations. Infrequent causes of viral hepatitis include adenovirus, cytomegalovirus (CMV), Epstein-Barr virus (EBV) and, rarely, herpes simplex virus (HSV). Other pathogens (eg, virus SEN-V) may account for additional cases of non-A/non-E hepatitis.

Acute versus chronic viral hepatitis

The term viral hepatitis can describe either a clinical illness or the histologic findings associated with the disease. Acute infection with a hepatitis virus may result in conditions ranging from subclinical disease to self-limited symptomatic disease to fulminant hepatic failure. Adults with acute hepatitis A or B are usually symptomatic. Persons with acute hepatitis C may be either symptomatic or asymptomatic (ie, subclinical).

Typical symptoms of acute hepatitis are fatigue, anorexia, nausea, and vomiting. Very high aminotransferase values (>1000 U/L) and hyperbilirubinemia are often observed. Severe cases of acute hepatitis may progress rapidly to acute liver failure, marked by poor hepatic synthetic function. This is often defined as a prothrombin time (PT) of 16 seconds or an international normalized ratio (INR) of 1.5 in the absence of previous liver disease.

Fulminant hepatic failure (FHF) is defined as acute liver failure that is complicated by hepatic encephalopathy. In contrast to the encephalopathy associated with cirrhosis, the encephalopathy of FHF is attributed to increased permeability of the blood-brain barrier and to impaired osmoregulation in the brain, which leads to brain-cell swelling. The resulting brain edema is a potentially fatal complication of fulminant hepatic failure.

FHF may occur in as many as 1% of cases of acute hepatitis due to hepatitis A or B. Hepatitis E is a common cause in Asia; whether hepatitis C is a cause remains controversial. Although FHF may resolve, more than half of all cases result in death unless liver transplantation is performed in time.

Providing that acute viral hepatitis does not progress to FHF, many cases resolve over a period of days, weeks, or months. Acute HBV infection is generally considered resolved once an individual has developed antibodies to the hepatitis B surface antigen (anti-HBs) and has cleared hepatitis B surface antigen (HBsAg) from their serum.
 Alternatively, acute viral hepatitis may evolve into chronic hepatitis. HBV infection is considered to have progressed to chronic infection when HBsAg, hepatitis B e antigen (HBeAg), and high titers of hepatitis B viral DNA are found to persist in the serum for longer than 6 months.
 Hepatitis C infection is considered to have progressed to chronic infection when HCV RNA persists in the blood for longer than 6 months.
 Hepatitis A and hepatitis E never progress to chronic hepatitis, either clinically or histologically.

The likelihood of progressing to chronic hepatitis B infection varies with the age at the time of infection. Chronic hepatitis B infection develops in up to 90% of individuals infected as neonates; however only 1-5% of individuals infected with HBV as adults develop chronic hepatitis B infection.
Chronic hepatitis C infection develops in 75-85% of patients infected with hepatitis C.
Individuals infected with HCV at a younger age are less likely to develop chronic hepatitis C infection.
Some patients with chronic hepatitis remain asymptomatic for their entire lives. Other patients report fatigue (ranging from mild to severe) and dyspepsia.

Individuals with chronic hepatitis B or hepatitis C infection may go on to develop cirrhosis, with histologic changes of severe fibrosis and nodular regeneration. In their study of serologic markers in patients with cirrhosis and hepatocellular carcinoma, Perz et al estimated that 57% of cirrhosis and 78% of hepatocellular carcinoma worldwide was attributable to chronic infection with either hepatitis B or C.

Although some patients with cirrhosis are asymptomatic, others develop life-threatening complications. The clinical illnesses of chronic hepatitis and cirrhosis may take months, years, or decades to evolve.

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