Sandbox/HIV: Difference between revisions
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*Incidence of mother-to-child HCV transmission is increased when mothers are HIV-co-infected, reaching rates of 10% to 20%.28,29 | *Incidence of mother-to-child HCV transmission is increased when mothers are HIV-co-infected, reaching rates of 10% to 20%.28,29 | ||
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*'''Both acute and chronic HCV infections are usually minimally symptomatic or asymptomatic. | |||
*Fewer than 20% of patients with acute infection have characteristic symptoms, including low-grade fever, mild right upper quadrant pain, nausea, vomiting, anorexia, dark urine, and jaundice''' | |||
*Cirrhosis develops in approximately 20% of patients with chronic HCV infection within 20 years after infection, although the risk for an individual is highly variable | |||
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*All HIV-infected patients should undergo routine HCV screening | |||
* Initial testing for HCV should be performed using the most sensitive immunoassays licensed for detection of antibody to HCV (anti-HCV) in blood | |||
*Persons who test positive for HCV antibody should undergo confirmatory testing by using a sensitive quantitative assay to measure plasma HCV RNA level | |||
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*The goal of HCV therapy is to achieve a sustained virologic response (SVR). SVR is defined as the absence | |||
of detectable viremia ≥6 months after discontinuation of HCV treatment. | |||
*HCV treatment recommendations are genotype specific as HCV genotype is an important determinant of the likelihood of response to interferon (IFN)-based HCV treatment regimens (genotype 2 > 3 > 1 and 4). | |||
*Host genetic polymorphisms near the interleukin-28B gene (IL28B encoding an interferon lambda) are strongly linked to spontaneous clearance of acute HCV infection and to response to IFN-based therapy for chronic HCV infection | |||
*The combination of peginterferon alfa (PegIFN) plus ribavirin is the recommended backbone of therapy for HIV/HCV-co-infected patients regardless of HCV genotype (AI) | |||
* HCV-genotype-1-infected patients who are not co-infected with HIV, a HCV NS3/4A PI, either boceprevir or telaprevir, in combination with PegIFN/ribavirin is recommended on the basis of large clinical trials | |||
*Two formulations of PegIFN are available (alfa-2a and alfa-2b) for weekly subcutaneous injection. These agents are used for all HCV genotypes | |||
*Ribavirin is recommended for use with PegIFN for all HCV genotypes. | |||
*Telaprevir is approved for use in combination with PegIFN/ribavirin in HCV-genotype-1- monoinfected-patients. The approved regimen for HCV monoinfected patients is telaprevir 750 mg orally (with at least 20 grams of fat) every 7 to 9 hours plus PegIFN/ribavirin for the initial 12 weeks of treatment followed by the discontinuation of telaprevir and the continuation of PegIFN/ribavirin for an additional 12 or 36 weeks, according to the observed HCV response at the end of treatment week 4 (response guided therapy | |||
| style="padding: 5px 5px; background: #F5F5F5;" |*The primary route of HCV transmission is drug injection via a syringe or other injection paraphernalia (i.e., “cookers,” filters, or water) previously used by an infected person. HCV-seronegative injection drug users should be encouraged to stop using injection drugs by entering a substance abuse treatment program or, if they are unwilling or unable to stop, to reduce the risk of transmission by never sharing needles or injection equipment. | |||
*There is no vaccine or recommended post-exposure prophylaxis to prevent HCV infection. Following acute HCV infection, chronic infection may be prevented within the first 6 to 12 months after infection through treatment with peginterferon with or without ribavirin. | |||
*Relatively high rates of viral clearance have beenobserved with HCV treatment during the acute phase of infection | |||
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Revision as of 11:35, 17 October 2014
Coinfection | Epidemeology | Clinical features | Diagnosis | Treatment | Prevention |
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Hepatitis B |
through sexual contact and injection drug use, whereas perinatal and early childhood exposures are responsible for most HBV transmission in higher prevalence regions. Although the general modes of transmission are similar to HIV, HBV is transmitted more efficiently than HIV.[6] HBV has an average incubation period of 90 days (range 60–150 days) from exposure to onset of jaundice and 60 days (range 40–90 days) from exposure to onset of abnormal liver enzymes. Genotypes of HBV (A–H) have been identified with different geographic distributions. Genotype A is most common among patients in North America and Western Europe. |
portal hypertension (i.e., ascites, variceal bleeding, coagulopathy, jaundice, or hepatic encephalopathy).
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with chronic HBV infection should be further tested for HBV e-antigen (HBeAg), antibody to HBeAg (anti-HBe), and HBV DNA
negative HBeAg, normal ALT levels, and an HBV DNA level <2,000 international units/mL.
aminotransferase (AST), albumin and bilirubin levels, and prothrombin time monitored at baseline and every 6 months thereafter to assess severity and progression of liver disease
chronic hepatitis B and may provide important information in monitoring disease progression, guiding treatment, and excluding other diseases |
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Hepatitis C |
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of detectable viremia ≥6 months after discontinuation of HCV treatment.
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*The primary route of HCV transmission is drug injection via a syringe or other injection paraphernalia (i.e., “cookers,” filters, or water) previously used by an infected person. HCV-seronegative injection drug users should be encouraged to stop using injection drugs by entering a substance abuse treatment program or, if they are unwilling or unable to stop, to reduce the risk of transmission by never sharing needles or injection equipment.
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- ↑ Lee WM (1997). "Hepatitis B virus infection". N Engl J Med. 337 (24): 1733–45. doi:10.1056/NEJM199712113372406. PMID 9392700.
- ↑ Levine OS, Vlahov D, Koehler J, Cohn S, Spronk AM, Nelson KE (1995). "Seroepidemiology of hepatitis B virus in a population of injecting drug users. Association with drug injection patterns". Am J Epidemiol. 142 (3): 331–41. PMID 7631637.
- ↑ Armstrong GL, Wasley A, Simard EP, McQuillan GM, Kuhnert WL, Alter MJ (2006). "The prevalence of hepatitis C virus infection in the United States, 1999 through 2002". Ann Intern Med. 144 (10): 705–14. PMID 16702586. Check
|pmid=
value (help). - ↑ Blatt LM, Mutchnick MG, Tong MJ, Klion FM, Lebovics E, Freilich B; et al. (2000). "Assessment of hepatitis C virus RNA and genotype from 6807 patients with chronic hepatitis C in the United States". J Viral Hepat. 7 (3): 196–202. PMID 10849261. Check
|pmid=
value (help). - ↑ Staples CT, Rimland D, Dudas D (1999). "Hepatitis C in the HIV (human immunodeficiency virus) Atlanta V.A. (Veterans Affairs Medical Center) Cohort Study (HAVACS): the effect of coinfection on survival". Clin Infect Dis. 29 (1): 150–4. doi:10.1086/520144. PMID 10433578. Check
|pmid=
value (help). - ↑ Sherman KE, Rouster SD, Chung RT, Rajicic N (2002). "Hepatitis C Virus prevalence among patients infected with Human Immunodeficiency Virus: a cross-sectional analysis of the US adult AIDS Clinical Trials Group". Clin Infect Dis. 34 (6): 831–7. doi:10.1086/339042. PMID 11833007.
- ↑ Ohto H, Terazawa S, Sasaki N, Sasaki N, Hino K, Ishiwata C; et al. (1994). "Transmission of hepatitis C virus from mothers to infants. The Vertical Transmission of Hepatitis C Virus Collaborative Study Group". N Engl J Med. 330 (11): 744–50. doi:10.1056/NEJM199403173301103. PMID 8107740. Check
|pmid=
value (help).