scholarly journals CD4+T Cell Kinetics and Activation in Human Immunodeficiency Virus–Infected Patients Who Remain Viremic Despite Long‐Term Treatment with Protease Inhibitor–Based Therapy

2002 ◽  
Vol 185 (3) ◽  
pp. 315-323 ◽  
Author(s):  
Steven G. Deeks ◽  
Rebecca Hoh ◽  
Robert M. Grant ◽  
Terri Wrin ◽  
Jason D. Barbour ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Protease Inhibitor ◽  
Cell Kinetics ◽  
Term Treatment ◽  
Cd4 T Cell ◽  
Long Term Treatment ◽  
Immunodeficiency Virus

scholarly journals Gradually increased dyslipidemia  in human immunodeficiency virus infected male patients with tenofovir plus lamivudine plus efavirenz primary treatment: a 3-year follow-up study

2020 ◽  
Author(s):  
dafeng liu ◽  
Bennan Zhao ◽  
Xinyi Zhang ◽  
Fengjiao Gao ◽  
Jun Kang ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Cd4 T Cell ◽  
Infected Male ◽  
Significant Difference ◽  
Immunodeficiency Virus ◽  
Male Patients ◽  
Cd4 T Cell Count

Abstract IntroductionSince the start of highly active antiretroviral therapy (HAART) with TDF plus 3TC plus EFV, the long-term dynamic characteristics of lipid and purine metabolism in patients infected with human immunodeficiency virus (HIV) was unclear and worth studying.MethodsA prospective follow-up cohort study was the way. Sixty-one treatment-naive HIV infected male patients were divided into three groups based on the baseline CD4 + T cell count (26, 12, 23cases in < 200, from 200 to 350, > 350 three groups, respectively). Lipid and purine metabolism parameters of those patients within 144 weeks were analyzed.ResultTG, TC, LDL-c and HDL-c level all gradually increased within 144 weeks, but statistical significances of TC level and HDL-c level were only found (F = 4.214, 5.518, P = 0.001, 0.000 ,respectively). Moreover the percentage of hypercholesterolemia, hyper LDL cholesterolemia and hypertriglyceridemia all gradually increased, low HDL cholesterolemia gradually decreased, but there was only obvious difference of the latter (χ2 = 16.105, P = 0.0007).Furthermore the lower the baseline CD4 + T lymphocyte counts, the higher TG level, the lower TC level, LDL-c level and HDL-c level, but only significant difference of LDL-c level between three groups at baseline was found (F = 3.256,P = 0.0457).Although UA level and the percentages of hyperuricemia gradually increased within 144 weeks, but there was no significant difference between different follow-up time points groups and between three CD4 + T cell count groups (all P༞0.05).ConclusionsThese findings provide a reference for clinicians to monitor lipid metabolism parameters closely during long-term HAART with TDF plus 3TC plus EFV regimen.

Anti-Human Immunodeficiency Virus Drug Combination Strategies

1998 ◽  
Vol 9 (3) ◽  
pp. 187-203 ◽  
Author(s):  
A-M Vandamme ◽  
K Van Vaerenbergh ◽  
E De Clercq
Keyword(s):  
Human Immunodeficiency Virus ◽  
Drug Resistance ◽  
Salvage Therapy ◽  
Highly Active Antiretroviral Therapy ◽  
Term Treatment ◽  
New Drugs ◽  
Resistance Testing ◽  
Long Term Treatment ◽  
Immunodeficiency Virus

It is now generally accepted that mono- and bitherapy for human immunodeficiency virus type 1 (HIV-1) infection are only transiently efficient mainly due to virus drug resistance. To obtain a sustained benefit from antiviral therapy, current guidelines recommend at least triple-drug combinations, or the so-called highly active antiretroviral therapy (HAART). In some patients, HAART can be problematic, either because it is difficult to remain compliant or because previous suboptimum therapies have limited the choice of drugs. For compliant drug-naive patients, HAART should be able to offer long-term virus suppression, when changing from first- to second- to third-line HAART at drug failure. Long-term treatment might ultimately result in multi-drug resistant virus leaving few options for salvage therapy. HIV drug resistance testing to guide this salvage therapy and the development of new drugs to allow new options will therefore remain priorities in anti-HIV drug research.

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