Open AccessJournal Article
Hepatotoxicity of antiretroviral therapy.
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TLDR
Patients must be closely observed with regular liver function tests and a hypersensitivity type drug reaction should be excluded, and the less hepatotoxic drugs such as lamivudine and abacavir should be preferred in patients at high risk for hepatotoxicity.Abstract:
Hepatotoxicity is a serious complication in patients taking HAART. Coinfection with hepatitis viruses increases the risk of liver toxicity while taking antiretroviral therapy. Baseline transaminases should be checked before beginning antiretorviral therapy and all patients should be screened for pre-existing liver disease, most notably hepatitis B and C infections. Regular monitoring of transaminases is mandatory when commencing antiretroviral therapy. In patients with normal liver function, transaminases may be checked monthly after commencing HAART for the first 3 months. If stable this can be broadened to 3 month intervals. In patients with pre-existing liver disease monitoring should be performed more frequently (every 2 weeks) when initiating therapy. Once stable liver enzymes should be checked monthly. The less hepatotoxic drugs such as lamivudine and abacavir should be preferred in patients at high risk for hepatotoxicity. Risks include co-infection with hepatitis B and C viruses, a previous record of hepatotoxicity, cirrhosis, obesity and female gender. Minor enzyme elevations (< 5-fold upper normal limit) are generally safe to tolerate and usually resolve. Patients must be closely observed with regular liver function tests and a hypersensitivity type drug reaction should be excluded. The onset of clinical symptoms, elevated serum lactate or evidence of severe hepatic dysfunction (coagulopathy or elevation of ammonia levels) are suggestive of severe toxicity and HAART should be withheld. Treatment of suspected HAART related hepatotoxicity should first involve withdrawal of therapy. Hypersensitivity reactions may be treated with corticosteroids. Nucleoside-induced mitochondrial damage may improve with riboflavin or thiamine therapy.read more
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Guidelines for prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: recommendations from CDC, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America.
TL;DR: The most recent version of the guidelines for the prevention and treatment of opportunistic infections (OI) in HIV-infected adults and adolescents was published in 2002 and 2004, respectively as mentioned in this paper.
Journal ArticleDOI
Hepatotoxicity of antiretrovirals: Incidence, mechanisms and management
TL;DR: One of the toxicities linked to the use of antiretrovirals is the elevation of transaminases, a cause of morbidity, mortality, and treatment discontinuation in HIV-infected patients.
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Guidelines for prevention and treatment of opportunistic infections in HIV-infected adults and adolescents
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Drug-induced liver injury
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TL;DR: Drug-induced liver injury (DILI) is an adverse reaction to drugs or other xenobiotics that occurs either as a predictable event when an individual is exposed to toxic doses of some compounds or as an unpredictable event with many drugs in common use as discussed by the authors.
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Incidence and predictors of severe liver fibrosis in human immunodeficiency virus-infected patients with chronic hepatitis C: a European collaborative study.
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TL;DR: Severe liver fibrosis is frequently found in HCV-HIV-coinfected patients with elevated serum ALT levels, and its severity increases significantly with age, and the rate of complications due to end-stage liver disease will inevitably increase in this population, for whom anti-HCV therapy should be considered a priority.
References
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Journal ArticleDOI
A syndrome of peripheral lipodystrophy, hyperlipidaemia and insulin resistance in patients receiving HIV protease inhibitors.
Andrew Carr,Katherine Samaras,Samantha Burton,Matthew Law,Judith Freund,Donald J. Chisholm,David A. Cooper +6 more
TL;DR: A syndrome of peripheral lipodystrophy, hyperlipidaemia and insulin resistance is a common complication of HIV protease inhibitors and diabetes mellitus is relatively uncommon.
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Pathogenesis of HIV-1-protease inhibitor-associated peripheral lipodystrophy, hyperlipidaemia, and insulin resistance.
TL;DR: It is hypothesised that protease inhibitors inhibit CRABP-1-modified, and cytochrome P450 3A-mediated synthesis of cis-9-retinoic acid, a key activator of the retinoid X receptor; and peroxisome proliferator activated receptor type gamma (PPAR-gamma) heterodimer, an adipocyte receptor that regulates peripheral adipocyte differentiation and apoptosis.
Journal ArticleDOI
A syndrome of lipoatrophy, lactic acidaemia and liver dysfunction associated with HIV nucleoside analogue therapy: contribution to protease inhibitor-related lipodystrophy syndrome.
TL;DR: The NRTI-LD syndrome differed from protease inhibitor-related LD syndrome by the presence of recent onset symptoms and weight loss, higher lactate and alanine aminotransferase, and lower albumin, cholesterol, triglycerides, glucose and insulin.
Journal ArticleDOI
The mechanism of insulin resistance caused by HIV protease inhibitor therapy.
TL;DR: It is concluded that HIV protease inhibitors as a class are capable of selectively inhibiting the transport function of Glut4 and that this effect may be responsible for a major iatrogenic complication frequently observed in HIV patients.
Journal ArticleDOI
Mortality from liver cancer and liver disease in haemophilic men and boys in UK given blood products contaminated with hepatitis C
Sarah C. Darby,D. W. Ewart,Paul L. F. Giangrande,R. J. D. Spooner,Charles R. Rizza,Geoffrey Dusheiko,Christine A. Lee,Christopher A. Ludlam,F. Eric Preston +8 more
TL;DR: There is an emerging risk of mortality from liver disease and liver cancer in the UK haemophilia population in individuals both infected and uninfected with HIV-1, which probably results from infection with hepatitis C.