Academic literature on the topic 'Hepatitis C Victoria'

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Journal articles on the topic "Hepatitis C Victoria"

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FAYYAZ, MOHAMMAD, Muhammad Ayub Khan, MASROOR ALI QAZI, Ghulam Mohyud Din `Chaudhary, and GULZAR AHMED. "HEPATITIS B, C & HIV." Professional Medical Journal 13, no. 04 (December 16, 2006): 632–36. http://dx.doi.org/10.29309/tpmj/2006.13.04.4941.

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Objective: To determine the prevalence of HBV, HCV and HIV in healthyblood donors in Blood Transfusion Services, Bahawal Victoria Hospital, Bahawalpur. Design: Prospective observationalstudy. Setting: Blood Transfusion Services, Bahawal Victoria Hospital (BVH), affiliated with Quaid-e-Azam medicalCollege Bahawalpur. Period: From 1 January t st o 31st December 2005. Methods and Materials: All the personscoming for blood donations , at the BVH facility, were included. Clinically anaemic, ill, past history of jaundice and ageof less than 18 or more than 50 years were excluded. All the donors (27938) from various areas of Bahawalpur,Bahawalnagar, Lodhran, Vehari and Rahim Yar Khan districts, were screened for hepatitis B surface antigen (HBs)Antigen, hepatitis C antibody (Anti HCV) & Human Immuno-deficiency Virus Antibody (Anti-HIV)on sera by one StepTest Device. All the positives cases were confirmed by Enzyme Linked Immunosorbant Assay. Results: Out of total27938, 25420(91%) were male. Mean age was 28 years with age range 18-50. No HIV positive case was detected.HBV was 2.69%, slightly more than HCV, 2.52%. Males were significantly (p<0.02) more infected than females.Conclusion: Risk of transmission of viral hepatitis is a major problem of blood transfusion. Frequency of viral hepatitisin blood donors is higher in our area as compared to rest of the world. HIV infection is very low. Preventive strategiesinclude good blood transfusion services along with safe sex and other measures.
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Fairley, Christopher K., David E. Leslie, Suellen Nicholson, and Ian D. Gust. "Epidemiology and hepatitis C virus in Victoria." Medical Journal of Australia 153, no. 5 (September 1990): 271–73. http://dx.doi.org/10.5694/j.1326-5377.1990.tb136899.x.

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NAEEM, MUHAMMAD, AMEER AHMAD, IMRAN QAISAR, and Fiaz Ahmad. "STATUS OF HEPATITIS C VIRUS (HCV) INFECTION." Professional Medical Journal 18, no. 03 (September 10, 2011): 445–49. http://dx.doi.org/10.29309/tpmj/2011.18.03.2364.

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Objective: To know the status of hepatitis C virus (HCV) infection in children admitted in Pediatric ward of Bahawal Victoria Hospital Bahawalpur. Study design: Cross-sectional descriptive study. Place and duration of study: Pediatric unit-1 Bahawal Victoria Hospital Bahawalpur over a period of 2 months and 15 days. Material and methods: This study was conducted over 500 children admitted in children ward-1 of Bahawal Victoria Hospital Bahawalpur. Children of 1-15 years of age were included in the study. The blood samples of these children were taken at the time of admission and serum was tested for HCV with ICT method and later on confirmed by ELISA. Children having HCV infection were tested for SGPT level. Different risk factors for transmission of HCV infection were also studied. Results: Out of 500 children 43 were HCV positive by ICT method. Out of these 43 ICT positive children 38 were confirmed by ELISA. In this way 7.6% children were found positive for HCV. In 23 cases (60.5%) SGPT was raised (>40). Statistically significant risk factors for transmission of HCV infection found in this study were past history of blood transfusion and history of injections in past. Conclusions: HCV infection is quite common in children. Safe blood transfusions and use of disposable and sterilized syringes is important for prevention of this infection.
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Wong, Dodd, Kiely, Carroll, and Whyte. "Characteristics of hepatitis C-positive blood donors in Victoria, Australia." Transfusion Medicine 9, no. 1 (January 1999): 15–19. http://dx.doi.org/10.1046/j.1365-3148.1999.009001015.x.

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Rawson, S. L., C. El-Hayek, J. Asselin, J. Howell, M. Stoové, W. Dimech, R. Guy, B. Donovan, J. S. Doyle, and M. Hellard. "P53 Hepatitis C diagnostic testing trends in Victoria, 2010–2015." Journal of Virus Eradication 3 (August 2017): 30. http://dx.doi.org/10.1016/s2055-6640(20)30794-9.

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Glenister, Kristen, William Kemp, Dunya Tomic, David Simmons, and Stuart Roberts. "Prevalence of Hepatitis C and treatment uptake in regional Victoria." Australian and New Zealand Journal of Public Health 44, no. 6 (November 30, 2020): 514–16. http://dx.doi.org/10.1111/1753-6405.13040.

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C.Trasancos, Claudia, Marion A. Kainer, Paul V. Desmond, and Heath Kelly. "Investigation of potential iatrogenic transmission of hepatitis C in Victoria, Australia." Australian and New Zealand Journal of Public Health 25, no. 3 (June 2001): 241–44. http://dx.doi.org/10.1111/j.1467-842x.2001.tb00569.x.

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Thompson, S. C., R. E. Goudey, A. M. Breschkin, J. Carnie, and M. Catton. "Exposure to hepatitis B and C of tattooists in Victoria in 1984." Journal of Viral Hepatitis 4, no. 2 (March 1997): 135–38. http://dx.doi.org/10.1111/j.1365-2893.1997.tb00216.x.

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Street, Alison M., and Jennifer L. Williams. "Prevalence of hepatitis C antibodies in patients with clotting disorders in Victoria." Medical Journal of Australia 157, no. 4 (August 1992): 284. http://dx.doi.org/10.5694/j.1326-5377.1992.tb137156.x.

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Pedrana, A., J. Doyle, M. Stoove, J. Richmond, J. Gold, P. Dietze, P. Higgs, et al. "P48 Implementing an elimination program for hepatitis C: a partnership approach from Victoria." Journal of Virus Eradication 3 (August 2017): 28. http://dx.doi.org/10.1016/s2055-6640(20)30789-5.

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Book chapters on the topic "Hepatitis C Victoria"

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Frank, Yitzchak. "Cognitive and Behavioral Abnormalities Associated with Liver Disease and Wilson Disease." In Cognitive and Behavioral Abnormalities of Pediatric Diseases. Oxford University Press, 2010. http://dx.doi.org/10.1093/oso/9780195342680.003.0021.

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Liver diseases may be associated with neurological abnormalities, more commonly with central nervous system (CNS) dysfunction (Lewis and Howdle 2003; Lockwood 1995; Raskin and Rowland 1995; Steinberg and Frank 1993; Victor and Rothstein 1992). Consequently, cognitive and behavioral abnormalities are commonly present in patients with acute and chronic liver disease. Cognitive impairment may include impairments of memory, attention, and executive and motor functions, can be initially mild and then progress into overt hepatic encephalopathy (HE) (Collie 2005; O’Carroll 2007). Specific patterns of cognitive dysfunction have been investigated. Selective attention deficits and abnormalities of motor skills in the absence of impairment in general intellect, language, or visuospatial skills have been described, suggesting abnormalities of the basal ganglia as the pathophysiology for cognitive dysfunction in cirrhotic patients, at least in the early stages of HE (McCrea et al. 1996). We need to be aware of the fact that cognitive abnormalities may also be related to the etiology of liver disease (hepatitis C virus, Wilson disease, alcoholic liver disease [ADL]). Chronic alcoholism, a common etiology for liver disease in adults, may cause cognitive impairment of executive functions, including working memory, independent of the effect of the liver disease or impairment in the formation and retrieval of new memory in the case of Wernicke- Korsakoff disease. When ALD is present in addition to alcoholism, the result may be an increased severity of the same profile of deficits. Central and peripheral nervous system manifestations can be part of an infection with hepatitis virus. Encephalitis, myelitis, Guillain-Barré syndrome (GBS), and polymyositis are infrequent complications of hepatitis A and B (Peters 1989). Central nervous system manifestations of these diseases include encephalopathy, pyramidal signs, and myoclonus. Similarly, hepatitis C (HCV) virus infection may be associated with extrahepatic syndromes including those affecting the nervous system (Hilsabek 2003). Circulating immune complexes containing hepatitis B antigens have been detected in the serum and cerebrospinal fluid (CSF) of adult patients at the height of neurologic symptoms, but it is unclear whether this is due to intrathecal synthesis or whether it reflects blood–brain barrier dysfunction (Peters 1989).
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