NIH/National Digestive Diseases Information Clearinghouse[1] CDC Hepatitis C: Slide Set [2]
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Hepatitis C

Hepatitis C is a form of inflammatory disease of the liver caused by a virus, the hepatitis C virus (HCV). Almost always, Hepatitis C is spread by contact with an infected person's blood. The majority of the people with HCV infections have no symptoms. Therefore, they are unaware of the need to seek treatment. more...

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Hepatitis C infected 150 to 200 million people around the world and is now the leading cause of liver transplants, and a frequent cause of liver cancer. Co-infection with HCV is common for people with HIV/AIDS and often causes their death.

Signs and symptoms

Acute Hepatitis C

Hepatitis C is one of 6 viruses, called hepatitis A, B, C, D, E and G, that can cause an acute disease lasting several weeks. Most cases (between 60% and 70%), even those that develop chronic infection, are asymptomatic.

For persons with acute symptoms, abdominal pain, jaundice, itching and flu-like symptoms are the most prominent causes for seeking medical attention.

Chronic Hepatitis C

For persons with silent disease, some are diagnosed because of certain medical phenomena associated with the presence of hepatitis C virus, such as thyroiditis (inflammation of the thyroid), cryoglobulinemia (a form of vasculitis) and glomerulonephritis (inflammation of the kidney), specifically membranoproliferative glomerulonephritis (MPGN). Carriers of the virus may begin to develop symptoms after only a few years. Symptoms, when developed, are variable and dependent on individual carrier. They may include prolonged flu-like symptoms and any combination of the following: body aches, headaches, night sweats, loss of appetite, diarrhea, fatigue, nausea, mild abdominal pain, typically located in the upper right quadrant.

Diagnosis

Hepatitis C may be suspected on the basis of the medical history and symptoms, because of abnormal liver function tests or as part of routine blood tests in many situations. Occasionally, people are diagnosed as a result of targeted screening such as blood donation (for which every donor is screened for numerous blood-borne diseases) or as a result of contact tracing.

Presence of HCV is generally screened with serological blood tests, all based on ELISA testing (ELISA-1, 2 and 3 are in use). These tests have a strong positive predictive value for the presence of the virus, but may take 6 months to become positive (seroconversion); in the meanwhile, a patient may have a false-negative result. Confirmation of the presence of the virus is by reverse transcriptase-polymerase chain reaction (rtPCR). This test is more expensive and hence avoided when risk of infection is deemed low. It may come up positive much earlier after infection (sometimes several weeks). rtPCR can also confirm which genomic type (see below) of the virus is present, which may determine the treatment regimen best suited for the patient.

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Outcomes of Lung Transplant Recipients previously infected with hepatitis C virus
From CHEST, 10/1/05 by Hina Sahi

PURPOSE: Outcomes of Lung Transplant in Hepatitis C virus (HCV) positive Recipients is not known. We describe our experience with 5 such patients.

METHODS: Charts of LTR known to be HCV positive prior to transplantation were reviewed for demographics, HCV etiology, HCV RNA viral load pre and post transplantation, liver biopsy results, transaminase levels during various points post transplantation, the development of acute hepatitis and survival.

RESULTS: 454 lung transplants were performed during a 14 year period, only five patients (1%) [age (yrs [+ or -] SD): 48 [+ or -] 9.7, 3 females], were anti-HCV seropositive. Etiology of HCV infection included IVDA (n=l), unknown causes (n=4), and two patients had concomitant liver disease due to alpha-1-antitrypsin deficiency and cystic fibrosis. All patients were diagnosed with HCV prior to transplantation and confirmed with HCV qualitative RNA testing. All recipients had disease severity documented by liver biopsy (minimal peri portal fibrosis n=3, no cirrhosis n=5). The median duration from HCV diagnosis to transplantation was 2 years [inter quartile range, 1 to 8.2 yrs). Pre transplantation median quantitative HCV RNA levels were 50,300 IU/ml [inter quartile range, 16,897 to 200,780,000 IU/ml]. Post transplantation median quantitative HCV RNA level were noted to markedly increase [level (IU/ml): 2,470,000 IU/ml (inter quartile range, 646,825 to 2,897,500 IU/ml)]. There was no statistically significant increase in transaminase levels pre and post LTX despite increase in HCV RNA levels. The longest surviving_patient in this cohort is 5 yrs post transplantation, the shortest survival being 8 months. The patient died of respiratory complications with no evidence of hepatic failure at the time of death [mean survival (months [+ or -] SD): 32.6 [+ or -] 23.9].

CONCLUSION: Although viral loads tended to significantly increase post transplantation, there was no significant difference in the episodes of acute hepatitis, hepatic failure or cirrhosis during the duration of follow up. Post transplant monitoring of quantitative RNA HCV levels was not of any prognostic value.

CLINICAL IMPLICATIONS: Further studies are needed to provide guidelines for monitoring of this population post transplantation.

DISCLOSURE: Hina Sahi, None.

Hina Sahi MD * Marie Budev DO Holli Blazey Other Atul Mehta MBBS Cleveland Clinic Foundation, Cleveland, OH

COPYRIGHT 2005 American College of Chest Physicians
COPYRIGHT 2005 Gale Group

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