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Biotech / Medical : Indications -- Hepatitis -- Ignore unavailable to you. Want to Upgrade?

To: zeta1961 who wrote (65)	4/25/2004 4:16:14 PM
From: zeta1961	Respond to of 312

DDW...nosocomial HepC breakout in oncology clinic...ouch... Outcomes of a Large, Point-Source Genotype 3a Hepatitis C Outbreak in an Oncology Clinic Mark Mailliard, Matthew Hrnicek, Mary Capadano, Richard Gilroy, James Gulizia, John Gollan Background and Methods: Between March, 2000 and June, 2001, at least 95 adults acquired chronic infection with genotype 3a hepatitis C (HCV-3a) in an oncology clinic in Fremont, Nebraska. Infection occurred through the flushing of their intravenous access with HCV-contaminated saline. Following recognition in 2002 of transmission in a health-care setting, screening of 486 at-risk patients revealed 77 with serum HCV antibody/HCV RNA, 18 HCV antibody negative/HCV RNA positive individuals, and four HCV antibody positive/HCV RNA undetectable persons. None of the patients had other risk factors for HCV. At the time of HCV exposure, all but four were being or had recently been treated for malignancy. This HCV-3a cluster is the largest known nosocomial, non-concurrent, point-source transmission of HCV in the United States. We report the clinical outcomes, with and without antiviral treatment, of 55 of the 95 HCV-3a patients. Results: The mean age of our HCV-3a cohort at infection was 59 years (range: 19-82) with slightly more women. The most common malignant diagnoses were colorectal (11) or breast (10) cancer and non-Hodgkins lymphoma (6). Symptoms had occurred in 18% of patients. Liver histology was available for 30 of the HCV-3a patients. The inflammation grade, fibrosis stage, and steatosis grade and distribution were determined. Grade 1 or 2 inflammation was observed in 88%; no patient had severe inflammation. Ten patients (33%) had steatosis present in greater than 30% of hepatocytes. Eight patients (27%) had stage 3 or 4 fibrosis in liver biopsy specimens obtained within two years of HCV-3a acquisition. Of nine patients with clinical evidence of portal hypertension or histologically advanced fibrosis, only one had evidence of a co-factor that predicted liver disease (iron overload). One HCV-3a patient died awaiting liver transplantation. Only one HCV-3a patient has died from pre-existing malignancy (metastatic adenocarcinoma of the prostate). Combination antiviral therapy with pegylated interferon plus ribavirin is underway or has been completed in 15 HCV-3a patients. Conclusions: The high rate of chronic infection, relative lack of HCV antibody and advanced liver injury indicate that co-factors exist in this HCV-3a cohort that lead to susceptibility to chronicity, atypical immune reponse and rapid progression of fibrosis. In addition to older age; immunosuppression, concurrent malignancy and its associated chemotherapy are potential co-factors that may accelerate the progression of chronic HCV infection.