S. population. Approximately 20% of HIV-infected individuals are unaware of infection and account for half of all new infections in others. Though effective treatment for HIV is available and highly efficacious, linkage to appropriate care remains a significant barrier.[3] Figure 1 clearly illustrates the magnitude of this public health problem
in the United States. In the HIV-infected patient, there is a complex, multifactorial interaction between common etiologies of liver disease. These include viral hepatitis, drug-associated hepatotoxicity, drug-associated and -unassociated nonalcoholic steatohepatitis (NASH), alcohol, and liver involvement buy GSI-IX with systemic infections and malignancies. In addition, HIV-infected patients have the same risk as the general population of having the spectrum of liver diseases noted in the general population, including genetic hemochromatosis, alpha-1 antitrypsin deficiency, Wilson’s disease, and so on. Estimates of the worldwide burden of viral hepatitis in those with HIV are illustrated in Fig. 2. In addition, hepatitis D is quite prevalent among
hepatitis B virus (HBV)/HIV-coinfected patients in Europe, though it is diagnosed with far less frequency in the United States. The overall prevalence of delta hepatitis among hepatitis B surface antigen-positive patients in Europe is 14.5%, with peak prevalence observed in Russia (25%) and Spain and Italy (21%).[4] A EUROSIDA multivariable model suggests that the presence
of hepatitis D is the most important factor in progression Regorafenib purchase to liver-related death. The role of long-term exposure to nucleoside analogs with dual viral activity on natural history remains unknown. Recognition of hepatitis E as a cause of both acute hepatitis and as an agent associated with the development of chronic liver disease MCE公司 in immunosuppressed individuals is increasing. There are many critical research questions regarding incidence, prevalence, and risk of chronicity in HIV-infected patients.[5-7] The role of drugs in liver injury in those with HIV remains a persistent issue. Overall, acute toxicity associated with antiretroviral agents has decreased with the development and increased use of newer, less toxic medications. Liver injury may be idiosyncratic and may present as either an acute hepatotoxicity process or with chronic hepatotoxicity. In the chronic state, medications may represent an important factor in metabolic syndrome with nonalcoholic fatty liver disease or NASH. Liver injury, as evidenced by transaminase abnormalities, is highly variable and has been reported in all classes. Some antiretrovirals, such as the protease inhibitors, tipranavir or high-dose ritonavir, are strongly associated with hepatotoxicity. In all classes, the presence of concurrent coinfection with hepatitis C virus (HCV) increases the risk of liver injury.