Books: 'HIV/Hepatitis C'

1

Ireland. Hepatitis C Compensation Tribunal. Annual report of the Hepatitis C Compensation Tribunal. Dublin: Stationery Office, 2003.

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2

Saskatchewan Subcommittee on HIV/AIDS. Guidelines for the management of potential exposures to Hepatitis B, Hepatitis C, HIV, and recommendations for post-exposure prophyalxis. Saskatchewan: Saskatchewan Health, 2004.

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3

Dublin, Ireland. Minister for Justice, Equality, and Law Reform. and Trinity College (Dublin, Ireland). Dept. of Community Health and General Practice., eds. Hepatitis B, hepatitis C and HIV in Irish prisoners: Prevalence and risk. Dublin: Stationery Office, 1999.

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4

Musharraf, Husain, and Population Council (Bangladesh), eds. Prevalence of HIV, HBV, HCV and syphilis markers in pregnant women of Bangladesh. Dhaka, Bangladesh: Population Council, 1997.

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5

San Francisco (Calif.). Dept. of Public Health. Communicable Disease Control Unit. Registry match: Chronic hepatitis B, hepatitis C infection and HIV : 2010, San Francisco, California. San Francisco, Calif: San Francisco Department of Public Health, 2011.

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6

Association, American Nurses. HIV, Hepatitis-B, Hepatitis-C: Blood-borne diseases; nurses' risks, rights, and responsibilities. Washington, DC: ANA, 1993.

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7

Dias, Giselle. Hard time: HIV and hepatitis C prevention programming for prisoners in Canada. Toronto: Canadian HIV/AIDS Legal Network = Râeseau juridique canadien VIH/Sida, 2007.

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8

Thiemann, Lillian. Double jeopardy: The HIV/HCV co-infection handbook. New York: Community Prescription Service, 1999.

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9

Ruiz, Juan D. Seroprevalence of HIV, hepatitis B, hepatitis C, and risk behaviors among inmates entering the California correctional system. [Sacramento]: California Dept. of Health Services, Office of Aids, HIV/AIDS Epidemiology Branch, 1996.

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10

Tribunal of Inquiry into the Infection with HIV and Hepatitis C of Persons with Haemophilia and Related Matters. Report of the Tribunal of Inquiry into the Infection with HIV and Hepatitis C of Persons with Haemophilia and Related Matters. Dublin: Stationery Office, 2002.

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11

Trinity, College (Dublin Ireland) Dept of Community Health and General Practice. Hepatitis B, hepatitis C, and HIV in Irish prisoners, part II: Prevalence and risk in committal prisoners 1999 : report prepared for the Minister for Justice, Equality, and Law Reform. [Dublin?: Stationary Office?, 2000.

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12

Jürgens, Ralf. HIV/AIDS and HCV in prisons: A select annotated bibliography. Ottawa, Ont: International Affairs Directorate, Health Canada, 2005.

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13

Association, Canadian Hospital, ed. Guide to policies for health care facilities and agencies: Bloodborne pathogens, especially Human Immunodeficiency Virus (HIV), Hepatitis B Virus, (HBV) and Hepatitis C Virus (HCV). Ottawa, Ont: Canadian Hospital Association, 1994.

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14

Cook, Catherine. The global state of harm reduction 2008: Mapping the response to drug-related HIV and hepatitis C epidemics. London: International Harm Reduction Association, 2008.

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15

Swan, Tracy. Care and treatment for hepatitis C and HIV coinfection: Expanding access through the Ryan White CARE Act. Rockville, MD: U.S. Department of Health and Human Services, Health Resources and Services Administration, HIV/AIDS Bureau, 2006.

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16

Health, New York (State) Legislature Assembly Committee on. Public hearing, health care in New York State prisons. [New York?]: EN-DE Reporting, Inc., 2004.

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17

New York (State). Legislature. Assembly. Committee on Health. Public hearing, health care in New York State prisons. [Albany, N.Y.?]: Associated Reporters Int'l., 2003.

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18

Duncan, Tim. Conquering Hepatitis C and surviving treatment: An essential guide through every step of the HCV treatment process. [Place of publication not identified]: T. Duncan, 2010.

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19

Network, Canadian Harm Reduction. Learning from each other: Enhancing community-based harm reduction programs and practices in Canada. Ottawa, Ont: Canadian AIDS Society, 2008.

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20

Kiwamu, Okita, ed. HCV/oxidative stress and liver disease. Tokyo: Springer, 2003.

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21

Dammacco, Franco. HCV Infection and Cryoglobulinemia. Milano: Springer-Verlag Italia, 2012.

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22

Giulio, Pisani, ed. Nucleic acid amplification technology (NAT) for the detection of Hepatitis C Virus (HCV) in plasma pools: Validation report. Roma: Istituto superiore di sanità, 2000.

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23

Mohamed Hatem Fathi El-Saied Wali. Natural history, factors affecting severity and progression rate of hepatitis c virus (HCV) infection in liver transplanted and non-transplanted patients. Birmingham: University of Birmingham, 2002.

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24

Price, Jennifer Cohen, Priyanka Amin, and Antoine Douaihy. Hepatitis C and HIV Co-Infection. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0043.

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Chronic infection with hepatitis C virus (HCV) is a leading cause of end-stage liver disease and is the most common indication for liver transplantation in the United States. Because of shared risk factors, individuals living with HIV infection are disproportionately affected by HCV. Moreover, co-infection with HIV accelerates the natural history of chronic HCV infection, increasing the risk of cirrhosis, hepatocellular carcinoma, hepatic decompensation, and death. Highly effective medications such as direct-acting antivirals (DAA) to cure HCV are now available and have the potential to profoundly improve the health of HIV-HCV-co-infected individuals. However, addressing the many gaps in the HCV care cascade is necessary to fully achieve the benefits of these drugs. This chapter reviews the natural history of HIV-HCV co-infection, the psychiatric comorbidities associated with HCV infection, the evolution of HCV treatment, and the barriers to care that HIV-HCV-co-infected individuals continue to face.

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25

HIV, STIs, HEPATITIS B (HBV) and HEPATITIS C (HCV) ISSUES for MEDICARE LOCALS. Australasian Society for HIV, Viral Hepatitis and Sexual Health Medicine (ASHM), 2012.

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26

The national policy guidelines on post exposure prophylaxis for HIV, hepatitis B and hepatitis C. [Kampala]: Ministry of Health, 2013.

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27

Northcott, Herbert C. HIV/hepatitis C issues in Alberta: The 2000 survey of adults. Alberta health and Wellness, 2001.

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28

McBride, Andrew, Karin Arnold, and Richard Pates. Injecting Illicit Drugs. Wiley & Sons, Incorporated, John, 2008.

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29

McBride, Andrew, Karin Arnold, and Richard Pates. Injecting Illicit Drugs. Wiley & Sons, Incorporated, John, 2008.

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30

McBride, Andrew, Karin Arnold, and Richard Pates. Injecting Illicit Drugs. Wiley & Sons, Limited, John, 2008.

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31

Lions, Rick. Call for Action, A: HIV/AIDS and Hepatitis C in Irish Prisons. Irish Penal Reform Trust, 2002.

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32

Schramm, Wolfgang, and Inge Scharrer. 25. Hämophilie-Symposium Hamburg 1994 : Verhandlungsberichte : HIV-Infektion Pädiatrische Hämostaseologie Synovitis Thrombophilie: APC-Cofaktor Hepatitis C. Springer London, Limited, 2013.

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33

Schramm, Inge Scharrer Wolfgang. 25. Hämophilie-Symposion Hamburg 1994 : Verhandlungsberichte : HIV-Infektion Pädiatrische Hämostaseologie Synovitis Thrombophilie: APC-Cofaktor Hepatitis C. Springer, 1995.

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34

Wilson, Deanna. Hepatitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0035.

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Hepatitis A (HAV) and E (HEV) viruses are spread via the fecal-oral route. Hepatitis B virus (HBV) exposure is via occupational or recreational activities. Hepatitis D virus (HDV; also spread parentally) can only coinfect or superinfect those with chronic HBV. Hepatitis C (HCV) transmission is predominantly parenteral; the highest risk group is injection drug users. Prodromal-period patients with acute hepatitis present with vague constitutional symptoms when serum transaminases peak, with elevated serum bilirubin and varying levels of hepatic protein synthesis impairment; during the icteric phase, patients develop abdominal pain, hepatomegaly, and jaundice. Acute hepatitis has limited therapy; treatment is predominantly supportive. However, most adults with acute phase HAV, HBV, HDV, and HEV spontaneously clear the virus. Most individuals with HCV develop chronic hepatitis. Patients with known HAV, HBV, or HEV exposures may be eligible for post-exposure prophylaxis to reduce their risk of infection.

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35

Gordon, Bruce, and Daniel Farb. OSHA Bloodborne Pathogens Manual and CD, Introductory But Comprehensive OSHA (Occupational Safety and Health) Training for the Managers and Employees in ... to AIDS, HIV, Hepatitis B, and Hepatitis C. UniversityOfHealthCare, 2003.

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36

Lopes, Eurides, and Jennifer Husson. Solid Organ Transplantation in HIV-Infected Individuals. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0025.

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End-organ disease has become a major cause of morbidity and mortality in HIV-infected patients due to increased life expectancy, increasing the demand for organ transplantation in these patients. The care of HIV-infected transplant recipients warrants a multidisciplinary team approach, including the transplant team, pharmacists, infectious disease specialists, nurses, and patients and their families. The immunosuppression of HIV-infected recipients post-transplant does not appear to further advance HIV disease. The post-transplant risk for HIV-infected recipients of opportunistic infections does not appear to be increased by immunosuppression. However, the overall rate of infections is high, and it is even higher in hepatitis C virus (HCV) co-infected transplant recipients. HIV/HCV co-infected recipients have worse outcomes compared to both liver and kidney HIV-infected recipients.

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37

Farb, Daniel. OSHA Bloodborne Pathogens 5 Users: Introductory but Comprehensive OSHA (Occupational Safety and Health) Training for the Managers and Employees in a Worker ... to AIDS, HIV, Hepatitis B, and Hepatitis C. UniversityOfHealthCare, 2005.

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38

Huyghebaert, Trudy. Is the Child-Pugh classification or other factors useful to predict hepatotoxicity following HAART in patients co-infected with HIV and hepatitis C? 2000.

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39

Keshav, Satish, and Palak Trivedi. Viral hepatitis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0212.

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Hepatitis means ‘inflammation of the liver’ and is manifest with symptoms that include malaise, anorexia, fever, flu-like symptoms, and pain in the right upper quadrant of the abdomen, with the pain being caused by swelling of the liver and its capsule. Elevations in circulating hepatic enzymes, particularly aspartate transaminase and alanine transaminase, are common, with jaundice occurring some time after the onset of other symptoms and signs. There are five viruses that primarily cause viral hepatitis: hepatitis A, B, C, D, and E viruses, abbreviated HAV, HBV, HCV, HDV, and HEV, respectively. These viruses are all hepatotrophic, in that the liver is the primary site of infection. HAV, HBV, and HEV are usually acute, self-limiting infections that may, nonetheless, cause morbidity and, in the case of HEV, fatality. However, HBV and, more so, HCV can cause chronic carriage of the virus over many years, as well as the development of chronic hepatitis. HDV is only pathogenic in conjunction with HBV. After recovery from acute infection with HAV, individuals have long-lasting immunity against further infection. The same holds true for the majority of individuals with acute HBV infection. There seems to be little natural immunity to HCV infection, and a significant proportion of cases result in chronic hepatitis. Immunity to HEV is not long-lasting, and repeated infections are possible. Many other viruses can cause hepatitis, of which cytomegalovirus, herpes simplex virus, Epstein–Barr virus, and flaviviruses such as dengue and yellow fever are the most important. The liver, however, is not their primary site of replication or cellular damage.

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40

Winston, Jonathan, Etti Zeldis, John A. Grimaldi, and Esteban Martínez. HIV-Associated Nephropathy, End-Stage Renal Disease, Dialysis, and Kidney Transplant. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0044.

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Antiretroviral therapy has changed the phenotype of HIV-related kidney disease to a more chronic disease model. In addition to HIV-associated nephropathy (HIVAN), patients with HIV may experience kidney dysfunction related to other chronic illnesses, such as diabetes, hypertension, and hepatitis C. Patients with HIV should be monitored for the development of chronic kidney disease and the potential nephrotoxicity of antiretroviral therapy. For patients with HIV who progress to end-stage renal disease, the outcomes on dialysis and management of the dialysis procedure are similar to the outcomes of patients without HIV. Renal transplantation is a promising treatment option for HIV patients with end-stage renal disease, despite certain barriers inherent in the transplant evaluation process. Concomitant HIV and end-stage renal disease, with the stress of dialysis, can exacerbate psychiatric illness.

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41

Bulterys, Marc, Julia Brotherton, and Ding-Shinn Chen. Prevention of Infection-Related Cancers. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0066.

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This chapter discusses primary prevention measures that disrupt transmission of oncogenic infections. It begins by discussing vaccination against hepatitis B virus (HBV) and human papillomavirus (HPV), two major causes of cancer for which safe and effective vaccines are currently available. It briefly discusses the importance of treatment and prophylaxis against human immunodeficiency virus type 1 (HIV-1), which potentiates the virulence of other viral infections as well as directly increasing the incidence of non-Hodgkin lymphoma. It does not discuss the treatment of HBV or hepatitis C virus (HCV) infection, since these are considered in Chapters 25 and 33. Also beyond the scope of this chapter are the randomized clinical trials currently underway to assess the efficacy and feasibility of eradication of Helicobacter pylori (Chapters 24, 31), vaccination against Epstein-Barr virus (EBV) (Chapters 24, 26, 39), or the prevention of schistosomiasis and liver flukes (Chapters 24, 33, and 52).

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42

Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Hepatitis C. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0058.

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Epidemiology 424Risk of transmission 424Clinical features 424Specific viral tests 425Diagnosis of HCV infection in infants born to HCV +ve mother 425Management 425• Hepatitis C virus (HCV) is an RNA virus of the flaviviride family.• More than 150 million people are infected with HCV worldwide....

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43

Fabrizi, Fabrizio. Hepatitis C. Edited by Vivekanand Jha. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0186.

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Hepatitis C virus (HCV) is associated with a large spectrum of histopathological lesions in both native and transplanted kidneys. The exact frequency of kidney damage in HCV-infected patients remains unknown, but the most frequent associated renal lesion is membranoproliferative glomerulonephritis (MPGN) with deposition of immunoglobulin and complement (MPGN type 1), usually in the context of type II mixed cryoglobulinaemia associated with a monoclonal IgM which binds IgG.Various approaches have been tried for the treatment of HCV-related glomerulonephritis, including immunosuppressive therapy (corticosteroids and cytotoxic agents), plasma exchange, and antiviral agents. Use of antiviral drugs for treatment of HCV-associated glomerulonephritis has shown encouraging results. Immunosuppressive therapy is recommended for cryoglobulinaemic kidney disease. Two distinct approaches should be considered for the treatment of HCV-associated cryoglobulinaemic glomerulonephritis according to the level of proteinuria and kidney failure. Preliminary evidence on rituximab therapy for HCV-related cryoglobulinaemic glomerulonephritis exists but several questions related to its use remain unclear.

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44

(Editor), I. Scharrer, and W. Schramm (Editor), eds. 30th Hemophilia Symposium Hamburg 1999: HIV Infection and Epidemiology in Hemophilia; Gene Therapy in Hemophilia A and B; Therapy of Hepatitis C; Inhibitors ... Pediatric Hemostasiology; Case Reports. Springer, 2000.

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45

Honegger, Jonathan R. Hepatitis C Virus. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190604813.003.0005.

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An estimated 185 million individuals have been infected with hepatitis C virus (HCV) worldwide. Although often clinically silent for decades, chronic HCV infection predisposes to late-onset complications, including liver cirrhosis and hepatocellular carcinoma. Mother-to-child transmission (MTCT) of HCV affects approximately 5% of children born to viremic mothers and is the primary route of HCV infection in young children. While some vertically acquired HCV infections are resolved during the first years of life, many persist indefinitely. Chronically infected children tend to be asymptomatic and have mild liver disease, but they face a risk of progression to advanced liver disease in adulthood. Current diagnostic and management strategies leave most infected children undiagnosed and untreated. Widespread use of newly-available direct-acting antiviral therapies has the potential to substantially reduce the global burden of HCV, including vertically acquired HCV, but an effective vaccine likely will be required to achieve this ultimate goal.

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46

Franceschi, Silvia, Hashem B. El-Serag, David Forman, Robert Newton, and Martyn Plummer. Infectious Agents. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0024.

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Eleven infectious agents (seven viruses, three parasites, and one bacterium) have been classified by the International Agency for Research on Cancer as carcinogenic to humans for one or more cancer sites: hepatitis B virus; hepatitis C virus; thirteen types of human papillomavirus (HPV); human immunodeficiency virus type 1 (HIV-1); human T-cell leukemia virus type 1; Epstein-Barr virus; Kaposi sarcoma herpesvirus; Helicobacter pylori; Opisthorchis viverrini; Clonorchis sinensis; and Schistosoma haematobium. Other infectious agents, such as Merkel cell polyomavirus, Plasmodium falciparum, and cutaneous HPVs, have been classified as “probably carcinogenic” or “possibly carcinogenic.” Accurate biomarkers of chronic infection have been essential for estimating risk and ascribing a causal role to infectious agents in cancer. Of the 14 million cases of cancer estimated to have occurred worldwide in 2012, 2.2 million were caused by infectious agents. Vaccination and screen-and-treat programs have the potential for greatly reducing the burden of cancer caused by infections.

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47

Vlachakis, Dimitrios. Computer-Aided Drug Design the Hcv Family Example. Lulu Press, Inc., 2011.

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48

Russi, Mark. Biological Hazards. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0016.

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This chapter describes various biological hazards and their impact on workers and others. A major focus of the chapter is biological hazards in healthcare and laboratory settings, including exposure to bloodborne pathogens and prevention of diseases related to them. Sections deal with sharps injuries, HIV/AIDS, hepatitis B virus, hepatitis C virus, tuberculosis, and other infectious diseases that can be acquired in the work environment via direct contact, droplet or airborne spread, or fecal-oral transmission. In addition, infectious agents spread by animal contact or arthropod vectors in a broad range of settings will be addressed. Newly emerging infectious or re-emerging infections, such as those due to H5N1 and novel H1N1 influenza, Middle Eastern respiratory syndrome (MERS), and Ebola Virus Disease (EVD) as well as agents associated with bioterrorism are discussed.

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49

Leung, Doris G. Neuropathies Associated with Infection or Toxic Exposure. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0113.

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Among the many causes of peripheral neuropathy are those mediated by environmental exposure to infectious and toxic agents. The most common neuropathy associated with HIV is HIV-associated distal sensory polyneuropathy (HIV-DSP). The clinical presentation of HIV-DSP is one of a distal, symmetric, often painful, small-fiber sensory axonal polyneuropathy. Other infectious causes of neuropathy include hepatitis C, leprosy, Lyme disease, rabies, and diphtheria, and antibiotic drugs such as isoniazid can also cause neuropathy. Heavy metals and a variety of other toxins including chemotherapeutic agents such as platinum, vincristine, and thalidomide disrupt peripheral nerve function. High doses of pyridoxine can cause damage to the dorsal root ganglia and foodbourne toxins such as saxitoxins found in shellfish.

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50

Matthews, Philippa C. Infections caused by RNA viruses. Edited by Philippa C. Matthews. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198737773.003.0009.

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This chapter consists of short notes, diagrams, maps, and tables to summarize RNA viruses that are significant causes of disease in the tropics and subtropics. This includes measles, polio, hepatitis A, C, and E viruses, rabies, arboviruses, and viral haemorrhagic fevers. The chapter also includes sections on important retroviruses, HIV, and human T-lymphotropic virus. For ease of reference, each topic is broken down into sections, including classification, epidemiology, microbiology, pathophysiology, clinical syndromes, diagnosis, treatment, and prevention.

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Books on the topic 'HIV/Hepatitis C'

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