Artículos de revistas: "Antiretroviral agents"

1

Chaudry, Muddasar N. y David H. Shepp. "ANTIRETROVIRAL AGENTS". Dermatologic Clinics 15, n.º 2 (abril de 1997): 319–30. http://dx.doi.org/10.1016/s0733-8635(05)70440-x.

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Kraus, George A., Alex Melekhov, Susan Carpenter, Yvonne Wannemuhler y Jacob Petrich. "Phenanthrenequinone antiretroviral agents". Bioorganic & Medicinal Chemistry Letters 10, n.º 1 (enero de 2000): 9–11. http://dx.doi.org/10.1016/s0960-894x(99)00589-2.

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Siegel, Lawrence y Roy M. Gulick. "New antiretroviral agents". Current Infectious Disease Reports 9, n.º 3 (27 de abril de 2007): 243–51. http://dx.doi.org/10.1007/s11908-007-0038-8.

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Cambou, Mary C. y Raphael J. Landovitz. "Novel Antiretroviral Agents". Current HIV/AIDS Reports 17, n.º 2 (12 de febrero de 2020): 118–24. http://dx.doi.org/10.1007/s11904-020-00486-2.

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5

Harris, Marianne. "Raltegravir: Its use in the Treatment of HIV Infection". Clinical Medicine. Therapeutics 1 (enero de 2009): CMT.S32. http://dx.doi.org/10.4137/cmt.s32.

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Raltegravir is the first integrase strand transfer inhibitor to be approved for the treatment of HIV infection. Administered orally in doses of 400 mg twice daily, it is well-tolerated and has minimal drug-drug interactions with coadministered antiretrovirals and other agents. In clinical trials including treatment-experienced and treatment-naïve HIV-infected adults, raltegravir in combination with other antiretroviral agents has demonstrated a rapid and potent virologic effect and a generally benign safety profile. Like other antiretrovirals, raltegravir should ideally be given with two additional agents to which the patient's virus is susceptible based on results of resistance testing. In this context, raltegravir offers a safe and effective option as a component of combination therapy in treatment-experienced patients who are infected with HIV-1 strains showing evidence of resistance to other antiretroviral agents. Pending the availability of longer-term efficacy and safety data, raltegravir cannot currently be recommended as part of first-line therapy for treatment-naïve patients.

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&NA;. "GUIDELINES FOR ANTIRETROVIRAL AGENTS". American Journal of Nursing 100, n.º 5 (mayo de 2000): 17. http://dx.doi.org/10.1097/00000446-200005000-00019.

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Collura, Jennifer M. y Donna M. Kraus. "New pediatric antiretroviral agents". Journal of Pediatric Health Care 14, n.º 4 (julio de 2000): 183–92. http://dx.doi.org/10.1067/mph.2000.107924.

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8

Owen, Andrew y Saye H. Khoo. "Pharmacogenetics of antiretroviral agents". Current Opinion in HIV and AIDS 3, n.º 3 (mayo de 2008): 288–95. http://dx.doi.org/10.1097/coh.0b013e3282f7cda4.

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COLLURA, J. y D. KRAUS. "New pediatric antiretroviral agents". Journal of Pediatric Health Care 14, n.º 4 (julio de 2000): 183–92. http://dx.doi.org/10.1016/s0891-5245(00)27765-1.

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10

Struble, Kimberly A., R. Douglas Pratt y Steven R. Gitterman. "Toxicity of antiretroviral agents". American Journal of Medicine 102, n.º 5 (mayo de 1997): 65–67. http://dx.doi.org/10.1016/s0002-9343(97)00065-x.

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Ghebremedhin, Beniam. "Maraviroc in Antiretroviral-Naïve HIV-1 Patients". Infectious Diseases: Research and Treatment 5 (enero de 2012): IDRT.S7597. http://dx.doi.org/10.4137/idrt.s7597.

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New antiretroviral agents that are better tolerated with less side effects and novel resistance patterns are needed at all lines of human immunodeficiency virus (HIV) therapeutic strategies. The CC-chemokine receptor 5 (CCR5) antagonist maraviroc is a member of the novel class of “antiretroviral agents” that prevents the entry of HIV-1 into host cells by blocking the CCR5 coreceptor. In the MERIT (Maraviroc versus Efavirenz in Treatment-Naïve Patients) study in antiretrovial-naïve patients aged ≥16 years with CCR5-tropic HIV-1 infection, maraviroc showed noninferiority to efavirenz for virological endpoints. Evidences from trials suggest that maraviroc is effective at reducing HIV-1 viral load in antiretroviral-experienced and -naïve patients with CCR5-tropic virus, as well as in those with CCR5-tropic virus who have developed HIV-1 resistance to existing antiretroviral regimens. Recent in vitro study demonstrated that maraviroc was also active against CCR5-tropic HIV-2 strains.

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12

Yakiwchuk, Erin M., Michelle M. Foisy y Christine A. Hughes. "Complexity of Interactions Between Voriconazole and Antiretroviral Agents". Annals of Pharmacotherapy 42, n.º 5 (15 de abril de 2008): 698–703. http://dx.doi.org/10.1345/aph.1k530.

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Objective: To evaluate and summarize pertinent aspects of the literature on interactions between voriconazole and antiretroviral agents. Data Sources: Primary literature was identified through MEDLINE (1950-February 2008), EMBASE (1988-February 2008), and International Pharmaceutical Abstracts (1970-February 2008) using the search terms voriconazole, ritonavir, protease inhibitors, nonnucleoside reverse transcriptase inhibitors, raltegravir, maraviroc, and drug interactions. Additionally, relevant abstracts from infectious diseases and HIV conferences (2004-February 2008), reference citations from relevant publications, and product information monographs were reviewed. Study Selection And Data Abstraction: All articles identified from the data sources and published in English were reviewed. Of these, studies and reports addressing voriconazole pharmacokinetics or interactions with antiretroviral agents were evaluated. Data Synthesis: The interactions between voriconazole and antiretroviral drugs are complex. Voriconazole and ritonavir exhibit a time- and dose-dependent interaction. Ritonavir initially inhibits voriconazole metabolism, but, with chronic administration, subsequently induces voriconazole metabolism. This interaction is more pronounced with high doses of ritonavir. Coadministration of voriconazole and efavirenz at usual doses is contraindicated because of a 2-way interaction resulting in efavirenz toxicity and decreased therapeutic effect of voriconazole. Dosage adjustments of both drugs are required. Based on pharmacokinetic characteristics, interactions between voriconazole and other protease inhibitors, nonnucleoside reverse transcriptase inhibitors (including etravirine), and maraviroc are likely but have not been well characterized in the literature. Interactions between voriconazole and nucleoside reverse transcriptase inhibitors or raltegravir are not anticipated. Conclusions: Interactions between voriconazole and antiretrovirals have the potential for serious consequences. However, because there is limited information available, further studies are warranted to establish these interactions and clarify their appropriate management. Until then, clinicians should be aware of the potential for interactions between voriconazole and antiretroviral agents and how to monitor for these interactions in clinical practice.

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Abu-Awwad, Simona-Alina, Ahmed Abu-Awwad, Madalina-Ianca Suba, Voichita Elena Lazureanu, Andrei-Daniel Bolovan, Ovidiu Rosca, Mirela-Mădălina Turaiche, Adela-Teodora Benea y Bogdan Hogea. "Evaluating Hepatotoxicity: A Comparative Analysis of New Generation versus Historical Antiretroviral Agents". Infectious Disease Reports 16, n.º 3 (24 de abril de 2024): 423–34. http://dx.doi.org/10.3390/idr16030031.

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(1) Background: Since the advent of zidovudine in 1987, antiretroviral therapy has undergone significant evolution, marked by the introduction of 34 antiretroviral drugs and 24 fixed-dose combinations. Despite these advances, hepatotoxicity remains a formidable challenge, influencing morbidity, mortality, and treatment adherence in HIV-infected patients. This study aims to compare the hepatotoxic effects of latest-generation antiretroviral medications with those of older-generation therapies, assessing their long-term impact on liver health in HIV patients. (2) Methods: This retrospective study analyzed data from 304 HIV patients treated with either latest-generation or older-generation antiretroviral drugs over four years. Patients were monitored for hepatotoxicity through liver function tests at diagnosis, six months, and one-year post-treatment initiation. (3) Results: Initial and six-month liver function tests showed no significant differences between the two groups. However, at one-year post-treatment, patients on latest-generation antiretrovirals exhibited significant improvements in ALT, AST, and ALP levels, suggesting a better safety profile regarding hepatotoxicity. Additionally, a significantly lower incidence of splenomegaly was observed in patients treated with newer medications. (4) Conclusions: The findings suggest that the latest-generation antiretroviral medications may offer a safer profile in terms of hepatotoxicity compared to older therapies, with potential benefits for long-term liver health. This study underscores the importance of continuous monitoring and further research to optimize ART strategies, ensuring improved patient outcomes and quality of life for individuals living with HIV.

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14

Sutherland, David C. "Antiretroviral agents in the nineties". Medical Journal of Australia 157, n.º 2 (julio de 1992): 135–38. http://dx.doi.org/10.5694/j.1326-5377.1992.tb137049.x.

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15

Barber, Tristan J. y Alan Winston. "Pharmacokinetics of experimental antiretroviral agents". Future Virology 2, n.º 1 (enero de 2007): 39–48. http://dx.doi.org/10.2217/17460794.2.1.39.

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16

Bang, Ji Hwan. "Recent Advances of Antiretroviral Agents". Korean Journal of Medicine 90, n.º 6 (1 de junio de 2016): 481–86. http://dx.doi.org/10.3904/kjm.2016.90.6.481.

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17

Kraus, George A., Alex Melekhov, Susan Carpenter, Yvonne Wannemuhler y Jacob Petrich. "ChemInform Abstract: Phenanthrenequinone Antiretroviral Agents." ChemInform 31, n.º 18 (8 de junio de 2010): no. http://dx.doi.org/10.1002/chin.200018174.

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18

Mascolini, Mark, Douglas Richman, Brendan Larder, John Mellors y Charles AB Boucher. "Clinical Implications of Resistance to Antiretrovirals: New Resistance Technologies and Interpretations". Antiviral Therapy 13, n.º 2 (febrero de 2008): 319–34. http://dx.doi.org/10.1177/135965350801300211.

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Understanding resistance to antiretroviral therapy plays an ever more crucial role in managing HIV infection as new agents – including several in new antiretroviral classes – promise better control of multidrug-resistant virus in the developed world. Yet these new drugs have different, and often complex, resistance profiles. At the same time, resistance has assumed a key role in developing countries as access to additional antiretrovirals expands in the face of first-line regimen failures. Every year the International HIV Drug Resistance Workshop gathers leading investigators and resistance-savvy clinicians to share unpublished, peer-reviewed research on the mechanisms, pathogenesis, epidemiology, and clinical implications of resistance to licensed and experimental antivirals. The 2007 workshop, held on 12–16 June, proved particularly notable for its exploration of resistance to two new antiretroviral classes, integrase inhibitors and CCR5 antagonists, as well as to agents that control hepatitis C virus (HCV) infection. This report summarizes most oral presentations from the workshop and many posters.

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19

Schnittman, Steven M. "Treatment of HIV-1 Infection with Combination Therapy: Antiretroviral Agents and Biological Response Modifiers". Canadian Journal of Infectious Diseases 5, suppl a (1994): 42A—46A. http://dx.doi.org/10.1155/1994/134340.

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While nucleoside antiretroviral agents are effective in delaying disease progression in human immunodeficiency virus (HIV - infected individuals. their activity is limited in magnitude and duration. Therefore, approaches to attacking HIV via combination therapies have recently been under investigation. In particular, since HIV infection dysregulates and destroys the immune system. it is logical to develop therapeutic approaches that would both restore the immune response and have direct antiviral activity. Preliminary evaluations of the combination of zidovudine wilh interferon alpha (IFN-α) have demonstrated enhanced antiviral. antitumour and immunomodulatory activity. Other promising approaches include antiretroviral therapy with interleukin (IL) -2, and IFN-α wilh IL-2. The clinical research pertaining to these combinations of antiretrovirals and biological response modifiers is reviewed.

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20

Mouradjian, Mallory T., Emily L. Heil, Hyunuk Sueng y Neha Sheth Pandit. "Virologic suppression in patients with a documented M184V/I mutation based on the number of active agents in the antiretroviral regimen". SAGE Open Medicine 8 (enero de 2020): 205031212096057. http://dx.doi.org/10.1177/2050312120960570.

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Objectives: The optimal antiretroviral therapy for patients with the M184V/I mutation is not known. The primary objective of this study was to determine the efficacy of various antiretroviral therapies in patients with HIV and the M184V/I mutation based on the number of active antiretroviral agents. Methods: A retrospective chart review was conducted of 100 treatment-experienced patients harboring the M184V/I mutation seen at an urban HIV clinic. Efficacy was classified as percentage of patients with viral suppression defined as HIV RNA viral load <200 copies/mL at last measurement on current antiretroviral therapy, stratified by the number of active antiretroviral agents. Results: The primary outcome of viral suppression occurred in 70.6% (12/17) of patients on <2 active agents, 77.2% (44/57) on 2–2.5 active agents, and 69.2% (18/26) on 3 active agents. No significant difference was found between viral suppression and patients on <2 and 2–2.5 antiretroviral agents (odds ratio = 0.71, 95% confidence interval = (0.21, 2.39), p = 0.8) or between patients on 3 and 2–2.5 active agents (odds ratio = 0.66, 95% confidence interval = (0.23, 1.88), p = 0.7). The most commonly prescribed regimen consisted of a boosted protease inhibitor with an integrase strand transfer inhibitor and two nucleoside reverse transcriptase inhibitors, one of which being lamivudine or emtricitabine. Conclusion: Similar rates of viral suppression were observed in patients regardless of the number of active antiretroviral agents prescribed. Regimens containing less than 3 active agents may maintain virologic suppression in patients with the M184V/I mutation. Further studies are needed to determine optimal antiretroviral therapy for patients with the M184V/I mutation.

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21

Permanyer, Marc, Ester Ballana, Alba Ruiz, Roger Badia, Eva Riveira-Munoz, Encarna Gonzalo, Bonaventura Clotet y José A. Esté. "Antiretroviral Agents Effectively Block HIV Replication after Cell-to-Cell Transfer". Journal of Virology 86, n.º 16 (13 de junio de 2012): 8773–80. http://dx.doi.org/10.1128/jvi.01044-12.

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Cell-to-cell transmission of HIV has been proposed as a mechanism contributing to virus escape to the action of antiretrovirals and a mode of HIV persistence during antiretroviral therapy. Here, cocultures of infected HIV-1 cells with primary CD4+T cells or lymphoid cells were used to evaluate virus transmission and the effect of known antiretrovirals. Transfer of HIV antigen from infected to uninfected cells was resistant to the reverse transcriptase inhibitors (RTIs) zidovudine (AZT) and tenofovir, but was blocked by the attachment inhibitor IgGb12. However, quantitative measurement of viral DNA production demonstrated that all anti-HIV agents blocked virus replication with similar potency to cell-free virus infections. Cell-free and cell-associated infections were equally sensitive to inhibition of viral replication when HIV-1 long terminal repeat (LTR)-driven green fluorescent protein (GFP) expression in target cells was measured. However, detection of GFP by flow cytometry may incorrectly estimate the efficacy of antiretrovirals in cell-associated virus transmission, due to replication-independent Tat-mediated LTR transactivation as a consequence of cell-to-cell events that did not occur in short-term (48-h) cell-free virus infections. In conclusion, common markers of virus replication may not accurately correlate and measure infectivity or drug efficacy in cell-to-cell virus transmission. When accurately quantified, active drugs blocked proviral DNA and virus replication in cell-to-cell transmission, recapitulating the efficacy of antiretrovirals in cell-free virus infections andin vivo.

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Buss, Neil y Nick Cammack. "Measuring the Effectiveness of Antiretroviral Agents". Antiviral Therapy 6, n.º 1 (enero de 2001): 1–7. http://dx.doi.org/10.1177/135965350100600101.

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Considerable progress has been made recently in developing effective antiretroviral combination therapy that can suppress viral replication and delay disease progression in individuals infected with HIV. A range of up to 15 approved antiretroviral agents is now available, which target two different viral enzymes, while several agents are in clinical development. The rapid development and approval of antiretroviral agents, driven by the urgency of clinical need as well as the complexity of possible combinations, has precluded the extensive comparative clinical testing of regimens, which is necessary to establish the relative efficacy of various different agents. The lack of an appropriate animal model for HIV disease also increases reliance on in vitro measures. Several different in vitro and in vivo parameters have been defined in an attempt to quantify the effectiveness of antiretroviral agents, most importantly the 50% inhibitory and effective concentrations (IC50 and EC50). However, the clinical relevance of these measures is uncertain. Additionally, considerable variation exists in the usage of the terms ‘IC50’ and ‘EC50’ in recent publications in the literature. These issues pose interpretation problems to clinicians seeking information on the relative clinical efficacy of the agents. In this brief review, we attempt to clarify the different measures available and their potential utility for clinical decision-making, focusing particularly on the example of HIV protease inhibitors. There are many different quantifiable parameters that give information regarding the effectiveness of an antiviral drug. These include: inhibition of the viral target enzyme (inhibition constant, Ki); selectivity for viral versus host enzymes; inhibition of viral replication in cell culture (IC50); ratio of efficacy to cytotoxicity in vitro (therapeutic index); inhibition of viral replication or symptoms in an appropriate animal model of the disease (EC50); and the effect on surrogate markers, such as viral load or CD4 cell count, after administration to humans ( in vivo EC50). Each of these different parameters gives valid information about the properties of an antiretroviral agent, which can help to build up a picture of its potential clinical utility relative to other drugs. However, to gain meaningful results, it is important to apply this information intelligently, understanding the limitations of each parameter.

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23

Boffito, Marta, David Back y José M. Gatell. "Twenty years of boosting antiretroviral agents". AIDS 29, n.º 17 (noviembre de 2015): 2229–33. http://dx.doi.org/10.1097/qad.0000000000000800.

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Dudley, M. N. "Clinical Pharmacokinetics Of Nucleoside Antiretroviral Agents". Journal of Infectious Diseases 171, Supplement 2 (1 de marzo de 1995): S99—S112. http://dx.doi.org/10.1093/infdis/171.supplement_2.s99.

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25

Flexner, Charles. "New antiretroviral agents in clinical development". Current Opinion in Infectious Diseases 5, n.º 6 (diciembre de 1992): 798–805. http://dx.doi.org/10.1097/00001432-199212000-00009.

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Stanic, Anela y Tulip K. Schneider. "Overview of Antiretroviral Agents in 2005". Journal of Pharmacy Practice 18, n.º 4 (agosto de 2005): 228–46. http://dx.doi.org/10.1177/0897190005278612.

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To date, 25 antiretroviral agents (including fixed-dose combinations) have gained approval by the Food and Drug Administration and are currently available on the market for the treatment of HIV-1 infection. New protease inhibitors, atazanavir sulfate (Reyataz) and fosamprenavir (Lexiva), were licensed, in addition to the nucleoside analogue reverse transcriptase inhibitor (NRTI) emtricitabine (Emtriva) and 2 fixed-dose NRTI combinations, emtricitabine/tenofovir disoproxil fumarate (Truvada) and lamivudine/abacavir (Epzicom). These newly licensed antiretroviral agents allow for lower pill burden and dosing schedule simplification, and some agents such as atazanavir sulfate are associated with improved lipid profile in comparison to other currently marketed protease inhibitors. In addition, a new class of anti-retroviral agents, entry inhibitors, of which a subclass exists called fusion inhibitors with its representative member, enfuvirtide (Fuzeon), which is currently the only available drug in its class, was marketed almost 2 years ago. Despite a remarkable progress in the treatment of HIV infection noted during the past decade, significant challenges to therapy such as tolerability issues and emergence of drug-resistant strains remain. Therefore, new antiretroviral drug development has focused on a design of drugs that work against the resistant strains of HIV and/or have a novel mechanism of action.

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Myers, M. W. "New Antiretroviral Agents in the Clinic". Clinical Infectious Diseases 12, n.º 5 (1 de septiembre de 1990): 944–50. http://dx.doi.org/10.1093/clinids/12.5.944.

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MAHONEY, DIANA. "Antiretroviral Agents Prevent HIV-1 Infection". Family Practice News 42, n.º 13 (agosto de 2012): 24. http://dx.doi.org/10.1016/s0300-7073(12)70542-x.

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29

Reed, Caitlin y Eric S. Daar. "Novel antiretroviral agents in HIV therapy". Current Infectious Disease Reports 8, n.º 6 (noviembre de 2006): 489–96. http://dx.doi.org/10.1007/s11908-006-0024-6.

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Hughes, Christine A., Michelle Foisy y Alice Tseng. "Interactions between antifungal and antiretroviral agents". Expert Opinion on Drug Safety 9, n.º 5 (29 de marzo de 2010): 723–42. http://dx.doi.org/10.1517/14740331003752694.

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Morris, Jennifer L. y Donna M. Kraus. "New Antiretroviral Therapies for Pediatric HIV Infection". Journal of Pediatric Pharmacology and Therapeutics 10, n.º 4 (1 de octubre de 2005): 215–47. http://dx.doi.org/10.5863/1551-6776-10.4.215.

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Human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome affect millions of children worldwide. The development of antiretroviral therapy has significantly improved the morbidity and mortality of pediatric patients infected with HIV. Currently, 4 classes of antiretroviral agents exist: nucleoside / nucleotide reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, protease inhibitors, and entry inhibitors. A total of 21 single-entity antiretroviral agents and 4 co-formulated antiretroviral products hold Food and Drug Administration (FDA) approval for treatment of HIV-1 infection. However, not all of these agents are indicated for use in patients less than 18 years of age. Since the year 2000, 7 new antiretroviral agents (atazanavir, emtricitabine, enfuvirtide, fosamprenavir, lopinavir/ritonavir, tenofovir, and tipranavir) have been approved by the FDA for use in adult patients as part of combination therapy for the treatment of HIV-1 infection. Although only 3 of these newer agents (emtricitabine, enfuvirtide, and lopinavir/ritonavir) are currently FDA approved for use in pediatric patients, pediatric clinical studies of the other 4 new agents are currently underway. The purpose of this article is to review these 7 new antiretroviral agents and describe their roles in the treatment of pediatric HIV infection. For each drug, the following information will be addressed: FDA-approved indication and age groups, clinical efficacy, pharmacokinetics, adverse drug reactions, clinically relevant drug interactions, pediatric and adult dosing, dosage forms, administration, and place in the treatment of pediatric HIV infection.

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Thenin-Houssier, Suzie y Susana T. Valente. "HIV-1 Capsid Inhibitors as Antiretroviral Agents". Current HIV Research 14, n.º 3 (4 de marzo de 2016): 270–82. http://dx.doi.org/10.2174/1570162x14999160224103555.

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Lange, Joep MA y Jintanat Ananworanich. "The discovery and development of antiretroviral agents". Antiviral Therapy 19, Suppl 3 (2014): 5–14. http://dx.doi.org/10.3851/imp2896.

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Nikolopoulos, Georgios, Stefanos Bonovas, Argirios Tsantes y Nikolaos Sitaras. "HIV/AIDS: Recent Advances in Antiretroviral Agents". Mini-Reviews in Medicinal Chemistry 9, n.º 8 (1 de julio de 2009): 900–910. http://dx.doi.org/10.2174/138955709788681609.

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Fridland, Arnold, Michele C. Connelly y Brian L. Robbins. "Cellular Factors for Resistance against Antiretroviral Agents". Antiviral Therapy 5, n.º 3 (1 de abril de 1999): 181–85. http://dx.doi.org/10.1177/135965350000500301.

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Substantial advancements have been made in our understanding of the complex replication cycle of, and immunopathology associated with HIV infection as well as the drugs used to treat the disease. The nucleoside reverse transcriptase inhibitors remain the cornerstones of current antiviral treatment modalities. Unfortunately, their long-term use often leads to adverse reactions and the emergence of virus mutants with decreased susceptibility to therapeutic agents. In addition to viral resistance, prolonged antiviral treatment may affect metabolic changes in the host cells that can diminish the efficacy of the treatment. Thus, both viral and cellular resistance mechanisms must be considered in the context of failing antiviral chemotherapy. This review article concerns the intracellular pharmacology of antiviral nucleoside analogues in human lymphoid cells and the possible impact of a newly identified nucleotide transporter on drug resistance.

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Husstedt, IW, D. Reichelt, U. Oelker-Grueneberg y S. Evers. "Neurotoxic effect of antiretroviral agents on CNS". Journal of the International AIDS Society 11, Suppl 1 (2008): P163. http://dx.doi.org/10.1186/1758-2652-11-s1-p163.

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Antoniou, Tony y Alice Lin-In Tseng. "Interactions between Recreational Drugs and Antiretroviral Agents". Annals of Pharmacotherapy 36, n.º 10 (octubre de 2002): 1598–613. http://dx.doi.org/10.1345/aph.1a447.

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OBJECTIVE: To summarize existing data regarding potential interactions between recreational drugs and drugs commonly used in the management of HIV-positive patients. DATA SOURCES: Information was obtained via a MEDLINE search (1966–August 2002) using the MeSH headings human immunodeficiency virus, drug interactions, cytochrome P450, medication names commonly prescribed for the management of HIV and related opportunistic infections, and names of commonly used recreational drugs. Abstracts of national and international conferences, review articles, textbooks, and references of all articles were also reviewed. STUDY SELECTION AND DATA EXTRACTION: Literature on pharmacokinetic interactions was considered for inclusion. Pertinent information was selected and summarized for discussion. In the absence of specific data, prediction of potential clinically significant interactions was based on pharmacokinetic and pharmacodynamic properties. RESULTS: All protease inhibitors (PIs) and nonnucleoside reverse transcriptase inhibitors are substrates and potent inhibitors or inducers of the cytochrome P450 system. Many classes of recreational drugs, including benzodiazepines, amphetamines, and opioids, are also metabolized by the liver and can potentially interact with antiretrovirals. Controlled interaction studies are often not available, but clinically significant interactions have been observed in a number of case reports. Overdoses secondary to interactions between the “rave” drugs methylenedioxymethamphetamine (MDMA) or γ-hydroxybutyrate (GHB) and PIs have been reported. PIs, particularly ritonavir, may also inhibit metabolism of amphetamines, ketamine, lysergic acid diethylmide (LSD), and phencyclidine (PCP). Case series and pharmacokinetic studies suggest that nevirapine and efavirenz induce methadone metabolism, which may lead to symptoms of opiate withdrawal. A similar interaction may exist between methadone and the PIs ritonavir and nelfinavir, although the data are less consistent. Opiate metabolism can be inhibited or induced by concomitant PIs, and patients should be monitored for signs of toxicity and/or loss of analgesia. PIs should not be coadministered with midazolam and triazolam, since prolonged sedation may occur. CONCLUSIONS: Interactions between agents commonly prescribed for patients with HIV and recreational drugs can occur, and may be associated with serious clinical consequences. Clinicians should encourage open dialog with their patients on this topic, to avoid compromising antiretroviral efficacy and increasing the risk of drug toxicity.

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Treisman, Glenn J. y Adam I. Kaplin. "Neurologic and psychiatric complications of antiretroviral agents". AIDS 16, n.º 9 (junio de 2002): 1201–15. http://dx.doi.org/10.1097/00002030-200206140-00002.

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39

Burger, David, Erik Stroes y Peter Reiss. "Drug interactions between statins and antiretroviral agents". Current Opinion in HIV and AIDS 3, n.º 3 (mayo de 2008): 247–51. http://dx.doi.org/10.1097/coh.0b013e3282fbaa54.

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40

Savatier, Nathalie, Didier Rocancourt, Claire Bonnerot y Jean-François Nicolas. "A novel system for screening antiretroviral agents". Journal of Virological Methods 26, n.º 2 (noviembre de 1989): 229–35. http://dx.doi.org/10.1016/0166-0934(89)90153-5.

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41

McNicholl, Ian y Joan McNicholl. "On the Horizon: Promising Investigational Antiretroviral Agents". Current Pharmaceutical Design 12, n.º 9 (1 de marzo de 2006): 1091–103. http://dx.doi.org/10.2174/138161206776055804.

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42

Johnson, R. Paul y Robert T. Schooley. "Update on antiretroviral agents other than zidovudine". Aids 3, Supplement (enero de 1989): S145–152. http://dx.doi.org/10.1097/00002030-198901001-00022.

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43

Raines, Charles, Olivia Radcliffe y Glenn J. Treisman. "Neurologic and Psychiatric Complications of Antiretroviral Agents". Journal of the Association of Nurses in AIDS Care 16, n.º 5 (septiembre de 2005): 35–48. http://dx.doi.org/10.1016/j.jana.2005.07.004.

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44

Otto, Ashley O., Christina G. Rivera, John D. Zeuli y Zelalem Temesgen. "Hepatotoxicity of Contemporary Antiretroviral Drugs: A Review and Evaluation of Published Clinical Data". Cells 10, n.º 5 (20 de mayo de 2021): 1263. http://dx.doi.org/10.3390/cells10051263.

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Contemporary antiretroviral agents afford enhanced potency and safety for patients living with HIV. Newer antiretroviral drugs are often better tolerated than those initially approved in the early stages of the HIV epidemic. While the safety profile has improved, adverse drug reactions still occur. We have segregated the antiretroviral agents used in contemporary practice into class groupings based on their mechanism of antiviral activity (non-nucleoside reverse transcriptase inhibitors, nucleoside reverse transcriptase inhibitors, integrase inhibitors, protease inhibitors, and entry inhibitors) while providing a review and discussion of the hepatoxicity seen in the most relevant clinical literature published to date. Clinical literature for individual agents is discussed and agent comparisons afforded within each group in tabular format. Our review will provide a summative overview of the incidence and medications associated with hepatic adverse reactions linked to the use of contemporary antiretroviral drugs.

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45

Atta, Mohamed G., Sophie De Seigneux y Gregory M. Lucas. "Clinical Pharmacology in HIV Therapy". Clinical Journal of the American Society of Nephrology 14, n.º 3 (29 de mayo de 2018): 435–44. http://dx.doi.org/10.2215/cjn.02240218.

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The success of combination antiretroviral therapy in the treatment of HIV-1–positive individuals has shifted clinical attention toward combination antiretroviral drug regimens that optimize tolerability, long-term safety, and durable efficacy. Wherever patients have access to treatment, morbidity and mortality are increasingly driven by non–HIV-associated comorbidities, which may be observed earlier than in age-matched controls and despite the best available combination antiretroviral therapy. Similarly, HIV-1–positive individuals are now diagnosed and treated earlier with anticipated lifelong therapy. The contribution of specific antiretroviral agents to long-term morbidity and mortality is dependent on the pharmacologic characteristics of these agents, and it is increasingly important in this context.

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46

Harrigan, P. Richard y Brendan A. Larder. "Extent of Cross-Resistance between Agents Used To Treat Human Immunodeficiency Virus Type 1 Infection in Clinically Derived Isolates". Antimicrobial Agents and Chemotherapy 46, n.º 3 (marzo de 2002): 909–12. http://dx.doi.org/10.1128/aac.46.3.909-912.2002.

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ABSTRACT The phenomenon of cross-resistance to antiretroviral agents used to treat human immunodeficiency virus type 1 infection is well known but so far has been only qualitatively described. Here, we quantitate the degree of cross-resistance among all commonly prescribed antiretroviral agents in almost 5,000 clinically derived recombinant isolates collected in the United States since January 2000.

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47

Onukak, E. E., A. E. Onukak, E. C. Akwiwu y J. O. Akpotuzor. "Impact of Antiretroviral Agents on Blood Cell Parameters". Sokoto Journal of Medical Laboratory Science 8, n.º 1 (27 de mayo de 2023): 44–55. http://dx.doi.org/10.4314/sokjmls.v8i1.6.

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Human immunodeficiency virus infection continues to be a major public health challenge in under-developed regions due to poverty, war and illiteracy. In developed countries, where much success has been achieved in fighting the menace, access to improved therapy is largely responsible. Nevertheless, studies have linked HIV and antiretroviral therapy with increased risk of cytopenia of all major blood cell lines and associated morbidities such as anaemia and platelet-driven cardiovascular events. Some antiretroviral agents such as zidovudine are associated with bone marrow suppression and an increased risk of developing anaemia Stavudine, azidothymidine and lamivudine have been linked with macrocytic anaemia in patients taking them. Lamivudine in combination with zidovudine causes neutropenia, anaemia and thrombocytopenia. Nevirapine causes eosinophilia, granulopenia and increased enzyme activities. Abacavir sulphate has been linked with increased risk of platelet-driven cardiovascular complications. The advocacy for combined therapy has helped to curb the effects of these agents when taken individually. Prolonged use of highly active antiretroviral therapy has been shown to correct some of these cytopenias and their associated morbidities. In managing HIV-infected patients however regular monitoring of their blood cell parameters and CD4+ count is required to ascertain the efficacy of the regimen being used in treatment.

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Hoetdmans, Richard MW. "Pharmacology of Antiretroviral Drugs". Antiviral Therapy 4, n.º 3_suppl (1 de abril de 1998): 29–41. http://dx.doi.org/10.1177/135965359900403s01.

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In this paper, an overview of the pharmacokinetics of currently available antiretroviral drugs is provided. Included in this article are the agents zidovudine, stavudine, zalcitabine, lamivudine, didanosine, abacavir, nevirapine, delavirdine, efavirenz, saquinavir, indinavir, ritonavir and nelfinavir. Key pharmacokinetic parameters, drug penetration in body compartments and drug interactions are discussed for each agent.

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Doran, Cynthia M. "New Approaches to Using Antiretroviral Therapy for the Management of Hiv Infection". Annals of Pharmacotherapy 31, n.º 2 (febrero de 1997): 228–36. http://dx.doi.org/10.1177/106002809703100215.

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Objective To review the changes that have occurred in the past 2 years in the management of HIV infection with antiretroviral agents by contrasting the 1994 with the 1996 Guidelines. Data Sources Conference proceedings, clinical experience of the author and her colleagues, and English-language articles from the body of scientific literature identified via MEDLINE, AIDSLINE, and Current Contents served as data sources. Data Synthesis Current antiretroviral management strategies include movement away from using zidovudine monotherapy, institution of combination antiretroviral therapy earlier in HIV disease, the use of newer agents such as lamivudine, protease inhibitors (i.e., saquinavir, ritonavir, indinavir), and nonnucleoside reverse transcriptase inhibitors (i.e., nevirapine, delavirdine), prevention of vertical transmission with zidovudine, and use of HIV-1 RNA determinations (viral load) to guide the initiation and alteration of antiretroviral therapy. These strategies represent a dramatic change from the 1994 Guideline, which recommended zidovudine monotherapy in nonpregnant and pregnant individuals whose CD4 cell counts were less than 500 cells/mm3, when many of the newer agents were not available and the assays to determine viral load were strictly investigational. Conclusions The difference between the 1994 and 1996 Guidelines is substantial. It is likely that within a year's time, newer information on pathogenesis and antiretroviral agents in development will be known and further management strategies will need to be disseminated. Until then, the International AIDS Society — USA Guidelines for 1996 should be followed as the standard of care.

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Marino-Merlo, Francesca, Emanuela Balestrieri, Claudia Matteucci, Antonio Mastino, Sandro Grelli y Beatrice Macchi. "Antiretroviral Therapy in HTLV-1 Infection: An Updated Overview". Pathogens 9, n.º 5 (1 de mayo de 2020): 342. http://dx.doi.org/10.3390/pathogens9050342.

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The human T cell leukemic/lymphotropic virus type 1 (HTLV-1), discovered several years ago, is the causative agent for a rapid progressive haematological malignancy, adult T cell leukemia (ATL), for debilitating neurological diseases and for a number of inflammatory based diseases. Although the heterogeneous features of the diseases caused by HTLV-1, a common topic concerning related therapeutic treatments relies on the use of antiretrovirals. This review will compare the different approaches and opinions in this matter, giving a concise overview of preclinical as well as clinical studies covering all the aspects of antiretrovirals in HTLV-1 infection. Studies will be grouped on the basis of the class of antiretroviral, putting together both pre-clinical and clinical results and generally following a chronological order. Analysis of the existing literature highlights that a number of preclinical studies clearly demonstrate that different classes of antiretrovirals, already utilized as anti-HIV agents, are actually capable to efficiently contrast HTLV-1 infection. Nevertheless, the results of most of the clinical studies are generally discouraging on the same point. In conclusion, the design of new antiretrovirals more specifically focused on HTLV-1 targets, and/or the establishment of early treatments with antiretrovirals could hopefully change the perspectives of diseases caused by HTLV-1.

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