Prognosis

As with other types of viral hepatitis, (decompensated) cirrhosis, hepatocellular carcinoma (HCC), and liver-related mortality are potential complications of hepatitis D virus (HDV) infection.[67]

Patients with chronic HDV infection who have a higher risk of progression of liver disease include those with any of:[1]

  • Elevated aminotransferases

  • Elevated gamma-glutamyl transpeptidase (GGT) levels

  • Advanced stage of liver disease

  • Persistent HDV viremia

  • High serum hepatitis B virus (HBV) DNA levels

  • Viral coinfection

  • A history of other conditions associated with chronic liver disease (e.g., obesity, alcohol abuse, diabetes).

HDV infects susceptible hosts via simultaneous coinfection with HBV or via superinfection of an individual already infected with HBV. Very early studies suggest that both superinfection and coinfection with HDV increase the risk of fulminant hepatitis twofold compared with acute HBV infection alone.[68]

The natural history of HDV infection is likely more severe than that of HBV infection alone and appears to be related to the degree of HDV replication.[18][69][70]

An Italian study followed 299 patients with chronic HDV infections for almost 30 years and noted that 46 patients (15.4%) developed HCC, 43 (14.4%) developed ascites, 63 (21.1%) died, and 29 (9.7%) received liver transplantation. HDV replication was the only independent predictor of mortality.[18] Similar findings were noted in a Greek study of almost 5000 patients with chronic HBV infection. Patients with a positive anti-HDV (4.2%) had more active and advanced disease at baseline, were more likely to have cirrhosis at a younger age, and were more likely to develop a liver related event (20.0% vs. 8.5%) over a median follow-up of 4.2 years, compared with patients negative for anti-HDV.[70] After adjusting for clinical and serologic differences, the increased risk of complications in patients with compensated cirrhosis with HDV/HBV coinfection compared with HBV infection alone were 3.2-fold for HCC, 2.2-fold for any decompensation, and 2.0-fold for mortality.[69]

There are some geographic differences in the risk of complications, with studies in Taiwan, where genotype 2 HDV predominates, suggesting that the risk of fulminant liver failure and cirrhosis or HCC is decreased compared with genotype 1 disease (found mainly in North America, Europe, the Middle East, and north Africa).[7][8] Conversely, genotypes 1 and 3 (which predominate in South America) lead to more severe disease and genotype 5 is associated with better response to therapy.[5][6]

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