Search

Your search keyword '"Ende, M.E. van der"' showing total 21 results
Start Over Author "Ende, M.E. van der"
21 results on '"Ende, M.E. van der"'

1. Progression of liver fibrosis following acute hepatitis C virus infection in HIV-positive MSM

Author

Newsum, A.M., Kooij, K.W., Boyd, A., Smit, C., Wit, F.W.N.M., Meer, J.T.M. van der, Prins, M., Reiss, P., Valk, M. van der, Eden, H. van, Molenkamp, R., Pijnappel, F., Reesink, H.W., Schinkel, J., Steba, G.S., Berk, G.E.L. van den, Brinkman, K., Hooijenga, I., Kwa, D., Meche, N. van der, Toonen, A., Vos, D., Broekhuizen, M. van, Lauw, E.N., Mulder, J.W., Arend, J.E., Kessel, A. van, Silvius, B., Versloot, M., Boonstra, A., Rijnders, B.J.A., Brokking, W., Eeden, A. van, Elsenburg, L., Nobel, H.E., Laar, T.J.W. van de, Veldt, W. van der, Geerlings, S.E., Goorhuis, A., Hovius, J.W., Lempkes, B., Nellen, F.J.B., Poll, T. van der, Prins, J.M., Vugt, M. van, Wiersinga, W.J., Duinen, M. van, Eden, J. van, Hazenberg, A., Hes, A.M.H. van, Pijnappel, F.J.J., Smalhout, S.Y., Weijsenfeld, A.M., Jurriaans, S., Back, N.K.T., Zaaijer, H.L., Berkhout, B., Cornelissen, M.T.E., Schinkel, C.J., Wolthers, K.C., Peters, E.J.G., Agtmael, M.A. van, Bomers, M., Sigaloff, K.C.E., Heitmuller, M., Laan, L.M., Ang, C.W., Houdt, R. van, Jonges, M., Pettersson, A.M., Prehn, J. van, Berge, M. van den, Stegeman, A., Baas, S., Looff, L.H. de, Wintermans, B., Veenemans, J., Pronk, M.J.H., Ammerloan, H.S.M., Munnik, E.S. de, Jansz, A.R., Tjhie, J., Wegdam, M.C.A., Deiman, B., Scharnhorst, V., Elsenburg, L.J.M., Nobel, H., Damen, M., Kasteren, M.E.E. van, Berrevoets, M.A.H., Brouwer, A.E., Adams, A., Kruijf-van de Wiel, B.A.E. de, Keelan-Pfaf, S., Ven, B. van de, Ven, B. van der, Buiting, A.G.M., Murck, J.L., Versteeg, D., Ende, M.E. van der, Box, H.I., Gorp, E.C.M. van, Nouwen, J.L., Schurink, C.A.M., Verbon, A., Vries-Sluijs, T.E.M.S. de, Jong-Peltenburg, N.C. de, Bassant, N., Beek, J.E.A. van, Vriesde, M., Zonneveld, L.M. van, Berg-Cameron, H.J. van den, Groot, J. de, Boucher, C.A.B., Koopmans, M.P.G., Kampen, J.J.A. van, Branger, J., Douma, R.A., Duijf-van de Ven, C.J.H.M., Schippers, E.F., Nieuwkoop, C. van, IJperen, J.M. van, Geilings, J., Hut, G. van der, Burgel, N.D. van, Leyten, E.M.S., Gelinck, L.B.S., Mollema, F., Davids-Veldhuis, S., Hartingsveld, A.Y. van, Wildenbeest, G.S., Heikens, E., Groeneveld, P.H.P., Bouwhuis, J.W., Lammers, A.J.J., Kraan, S., Hulzen, A.G.W. van, Kruiper, M.S.M., Bliek, G.L. van der, Bor, P.C.J., Bloembergen, P., Wolthagen, M.H.M., Ruijs, G.J.H.M., Kroon, E., Boer, M.G.J. de, Scheper, H., Jolink, H., Dorama, W., Holten, N. van, Claas, E.C.J., Wessels, E., Hollander, J.G. den, Pogany, K., Roukens, A., Douma, R., Kastelijns, M., Smit, J.V., Smit, E., Struik-Kalkman, D., Tearno, C., Niekerk, T. van, Pontesilli, O., Lowe, S.H., Lashof, A.M.L.O., Posthouwer, D., Ackens, R.P., Burgers, K., Schippers, J., Enberg-Maes, B.W., Loo, I.H.M. van, Havenith, T.R.A., Vrouenraets, S.M.E., Broekhuizen, M.C. van, Vlasblom, D.J., Kroeze, M., Smits, P.H.M., Weijer, S., Moussaoui, R. el, Bosma, A.S., Vonderen, M.G.A. van, Kampschreur, L.M., Faber, S., Steeman-Bouma, R., Wed, J., Kootstra, G.J., Delsing, C.E., Burg-van de Plas, M. van der, Heins, H., Kortmann, W., Twillert, G. van, Renckens, R., Ruiter-Pronk, D., Truijen-Oud, E.A. van, Stuart, J.W.T.C., Jansen, E.R., Hoogewerf, M., Rozemeijer, W., Reijden, W.A. van der, Sinnige, J.C., Blok, W.L., Frissen, P.H.J., Lettinga, K.D., Schouten, W.E.M., Veenstra, J., Brouwer, C.J., Geerders, G.E., Hoeksema, K., Kleene, M.J., Knapen, M., Meche, I.B. van der, Mulder-Seeleman, E., Toonen, A.J.M., Wijnands, S., Crevel, R. van, Dofferhoff, A.S.M., Hofstede, H.J.M. ter, Hoogerwerf, J., Keuter, M., Richel, O., Albers, M., Grintjes-Huisman, K.J.T., Haan, M. de, Marneef, M., Strik-Albers, R., Rahamat-Langendoen, J., Stelma, E.E., Burger, D., Gisolf, E.H., Hassing, R.J., Claassen, M., Beest, G. ter, Bentum, P.H.M. van, Langebeek, N., Tiemessen, R., Swanink, C.M.A., Lelyveld, S.F.L. van, Soetekouw, R., Prijt, L.M.M. van der, Swaluw, J. van der, Bermon, N., Jansen, R., Herpers, B.L., Veenendaal, D., Verhagen, D.W.M., Wijk, M. van, Bierman, W.F.W., Bakker, M., Kleinnij, APH - Global Health, AII - Infectious diseases, Graduate School, Infectious diseases, APH - Aging & Later Life, Global Health, APH - Methodology, APH - Digital Health, APH - Personalized Medicine, Gastroenterology & Hepatology, Internal Medicine, Virology, Medical Microbiology & Infectious Diseases, Med Microbiol, Infect Dis & Infect Prev, MUMC+: DA MMI Staf (9), RS: CAPHRI - R4 - Health Inequities and Societal Participation, MUMC+: TPZ Verpleegkundig Team Infectieziekten (9), MUMC+: DA MMI Infectieserologie (9), MUMC+: DA MMI AIOS (9), MUMC+: DA KFT Medische Staf (9), Anatomy and neurosciences, Amsterdam Movement Sciences - Rehabilitation & Development, Internal medicine, and Microbes in Health and Disease (MHD)

Subjects
Liver Cirrhosis, Male, 0301 basic medicine, HIV Infections, Disease, DISEASE, 0302 clinical medicine, ANTIRETROVIRAL THERAPY, STAGE, Interquartile range, HEPATOCELLULAR-CARCINOMA, Immunology and Allergy, 030212 general & internal medicine, Immunodeficiency, Netherlands, liver fibrosis, RISK, education.field_of_study, IMMUNODEFICIENCY, Coinfection, HIV/hepatitis C virus coinfection, MEN, Hepatitis C, Markov Chains, Infectious Diseases, Hepatocellular carcinoma, Disease Progression, SEX, Adult, medicine.medical_specialty, Population, Immunology, acute hepatitis C virus infection, 03 medical and health sciences, SDG 3 - Good Health and Well-being, Internal medicine, medicine, Humans, MSM, Homosexuality, Male, education, Retrospective Studies, Hepatitis, business.industry, fibrosis-4, Retrospective cohort study, NONINVASIVE INDEX, medicine.disease, Confidence interval, INDIVIDUALS, 030104 developmental biology, business
Abstract

Background: Whether continued, accelerated liver fibrosis progression occurs following acute hepatitis C virus infection (AHCVI) in HIV-positive MSM is unknown.Design and methods: HIV-positive MSM from the AIDS Therapy Evaluation in the Netherlands and MSM Observational Study for Acute Infection with Hepatitis C-cohorts with primary AHCVI and at least one fibrosis-4 (FIB-4) measurement less than 2 years before and 1 year after estimated AHCVI were included. Mixed-effect linear models were used to evaluate (time-updated) determinants of FIB-4 levels over time. Determinants of transitioning to and from FIB-4 1.45 were examined using multistate Markov models.Results: Of 313 MSM, median FIB-4 measurements per individual was 12 (interquartile range = 8-18) and median follow-up following AHCVI was 3.5 years (interquartile range = 1.9-5.6). FIB-4 measurements averaged at 1.00 [95% confidence interval (CI) = 0.95-1.05] before AHCVI, 1.31 (95% CI = 1.25-1.38) during the first year of AHCVI and 1.10 (95% CI = 1.05-1.15) more than 1 year after AHCVI. Mean FIB-4 more than 1 year after AHCVI was higher for chronically infected patients compared with those successfully treated (P = 0.007). Overall FIB-4 scores were significantly higher with older age, lower CD4(+) cell count, longer duration from HIV-diagnosis or AHCVI, and nonresponse to HCV-treatment. At the end of follow-up, 60 (19.2%) and eight MSM (2.6%) had FIB-4 between 1.45-3.25 and >= 3.25, respectively. Older age, lower CD4(+) cell count and detectable HIV-RNA were significantly associated with higher rates of progression to FIB-4 > 1.45, whereas older age, longer duration from HIV-diagnosis and nonresponse to HCV-treatment were significantly associated with lower rates of regression to FIB-4Conclusion: In this population of HIV-positive MSM, FIB-4 scores were higher during the first year of AHCVI, but FIB-4 >= 3.25 was uncommon by the end of follow-up. Well controlled HIV-infection appears to attenuate FIB-4 progression. Copyright (C) 2019 Wolters Kluwer Health, Inc. All rights reserved.

Published
2019

2. Predictive Performance of Cardiovascular Disease Risk Prediction Algorithms in People Living With HIV

Author

Zoest, R.A. van, Law, M., Sabin, C.A., Vaartjes, I., Valk, M. van der, Arends, J.E., Reiss, P., Wit, F.W., Geerlings, S.E., Godfried, M.H., Goorhuis, A., Hovius, J.W., Kuijpers, T.W., Nellen, F.J.B., Poll, D.T. van der, Prins, J.M., Vugt, H.J.M. van, Wiersinga, W.J., Wit, F.W.M.N., Duinen, M. van, Eden, J. van, Hes, A.M.H. van, Pijnappel, F.J.J., Weijsenfeld, A.M., Jurriaans, S., Back, N.K.T., Zaaijer, H.L., Berkhout, B., Cornelissen, M.T.E., Schinkel, C.J., Wolthers, K.C., Peters, E.J.G., Agtmael, M.A. van, Bomers, M., Heitmuller, M., Laan, L.M., Ang, C.W., Houdt, R. van, Pettersson, A.M., Vandenbroucke-Grauls, C.M.J.E., Berge, M. van den, Stegeman, A., Baas, S., Looff, L.H. de, Wintermans, B., Veenemans, J., Pronk, M.J.H., Ammerlaan, H.S.M., Munnik, E.S. de, Jansz, A.R., Tjhie, J., Wegdam, M.C.A., Deiman, B., Scharnhorst, V., Eeden, A. van, Brokking, W., Groot, M., Elsenburg, L.J.M., Damen, M., Kwa, I.S., Kasteren, M.E.E. van, Brouwer, A.E., Erve, R. van, Kruijf-van de Wiel, B.A.F.M. de, Ven, B. van de, Buiting, A.G.M., Kabel, P.J., Versteeg, D., Ende, M.E. van der, Bax, H.I., Gorp, E.C.M. van, Nouwen, J.L., Rijnders, B.J.A., Schurink, C.A.M., Verbon, A., Vries-Sluijs, T.E.M.S. de, Jong-Peltenburg, N.C. de, Bassant, N., Beek, J.E.A. van, Vriesde, M., Zonneveld, L.M. van, Berg-Cameron, H.J. van den, Groot, J. de, Zeeuw-de Man, M. de, Boucher, C.A.B., Koopmans, M.P.G., Kampen, J.J.A. van, Pas, S.D., Branger, J., Douma, R.A., Duijf-van de Ven, C.J.H.M., Schippers, E.F., Nieuwkoop, C. van, IJperen, J.M. van, Geilings, J., Hut, G. van der, Burgel, N.D. van, Leyten, E.M.S., Gelinck, L.B.S., Davids-Veldhuis, S., Hartingsveld, A.Y. van, Meerkerk, C., Wildenbeest, G.S., Heikens, E., Groeneveld, P.H.P., Bouwhuis, J.W., Lammers, A.J.J., Kraan, S., Hulzen, A.G.W. van, Kruiper, M.S.M., Bliek, G.L. van der, Bor, P.C.J., Bloembergen, P., Wolfhagen, M.J.H.M., Ruijs, G.J.H.M., Kroon, F.P., Boer, M.G.J. de, Scheper, H., Jolink, H., Dorama, W., Holten, N. van, Claas, E.C.J., Wessels, E., Hollander, J.G. den, Pogany, K., Roukens, A., Kastelijns, M., Smit, J.V., Smit, E., Struik-Kalkman, D., Tearno, C., Niekerk, T. van, Pontesilli, O., Lowe, S.H., Lashof, A.M.L.O., Posthouwer, D., Ackens, R.P., Burgers, K., Schippers, J., Weijenberg-Maes, B., Loo, I.H.M. van, Havenith, T.R.A., Mulder, J.W., Vrouenraets, S.M.E., Lauw, F.N., Broekhuizen, M.C. van, Vlasblom, D.J., Smits, P.H.M., Weijer, S., Moussaoui, R. el, Bosma, A.S., Vonderen, M.G.A. van, Kampschreur, L.M., Dijkstra, K., Faber, S., Weel, J., Kootstra, G.J., Delsing, C.E., Burg-van de Plas, M. van der, Heins, H., Kortmann, W., Twillert, G. van, Renckens, R., Ruiter-Pronk, D., Truijen-Oud, F.A. van, Stuart, J.W.T.C., IJzerman, E.P., Jansen, R., Reijden, W.A. van der, Brinkman, K., Berk, G.E.L. van den, Blok, W.L., Frissen, P.H.J., Lettinga, K.D., Schouten, W.E.M., Veenstra, J., Brouwer, C.J., Geerders, G.F., Hoeksema, K., Kleene, M.J., Meche, I.B. van der, Spelbrink, M., Toonen, A.J.M., Wijnands, S., Kwa, D., Regez, R., Crevel, R. van, Keuter, M., Ven, A.J.A.M. van der, Hofstede, H.J.M. ter, Dofferhoff, A.S.M., Hoogerwerf, J., Grintjes-Huisman, K.J.T., Haan, M. de, Marneef, M., Rahamat-Langendoen, J., Stelma, F.F., Burger, D., Gisolf, E.H., Hassing, R.J., Claassen, M., Beest, G. ter, Bentum, P.H.M. van, Langebeek, N., Tiemessen, R., Swanink, C.M.A., Lelyveld, S.F.L. van, Soetekouw, R., Prijt, L.M.M. van der, Swaluw, J. van der, Bermon, N., Herpers, B.L., Veenendaal, D., Verhagen, D.W.M., Wijk, M. van, Bierman, W.F.W., Bakker, M., Kleinnijenhuis, J., Kloeze, E., Stienstra, Y., Wilting, K.R., Wouthuyzen-Bakker, M., Boonstra, A., Meulen, P.A. van der, Weerd, D.A. de, Niesters, H.G.M., Leer-Buter, C.C. van, Knoester, M., Hoepelman, A.I.M., Barth, R.E., Bruns, A.H.W., Ellerbroek, P.M., Mudrikova, T., Oosterheert, J.J., Schadd, E.M., Wassenberg, M.W.M., Zoelen, M.A.D. van, Aarsman, K., Elst-Laurijssen, D.H., Rozemeijer, Graduate School, AII - Infectious diseases, APH - Aging & Later Life, Infectious diseases, Global Health, APH - Digital Health, APH - Personalized Medicine, APH - Global Health, Microbes in Health and Disease (MHD), Neurochirurgie, RS: MHeNs - R3 - Neuroscience, Med Microbiol, Infect Dis & Infect Prev, MUMC+: DA MMI Staf (9), RS: CAPHRI - R4 - Health Inequities and Societal Participation, Internal medicine, Pediatric surgery, Amsterdam Movement Sciences - Rehabilitation & Development, ACS - Diabetes & metabolism, AGEM - Digestive immunity, Medical Microbiology and Infection Prevention, Amsterdam Reproduction & Development (AR&D), Internal Medicine, Virology, and Medical Microbiology & Infectious Diseases

Subjects
Male, Heart disease, Human immunodeficiency virus (HIV), risk prediction algorithms, Blood Pressure, HIV Infections, Disease, 030312 virology, medicine.disease_cause, SUBCLINICAL ATHEROSCLEROSIS, Risk Factors, cardiovascular disease, FRAMINGHAM, Pharmacology (medical), Netherlands, 0303 health sciences, INFECTED PATIENTS, Framingham Risk Score, Middle Aged, Prediction algorithms, Cholesterol, Infectious Diseases, Anti-Retroviral Agents, Cardiovascular Diseases, HUMAN-IMMUNODEFICIENCY-VIRUS, Female, Risk assessment, Algorithms, Adult, Anti-HIV Agents, CARDIOLOGY/AMERICAN HEART ASSOCIATION, HEART-DISEASE, AMERICAN-COLLEGE, DATA-COLLECTION, Risk Assessment, EVENTS, 03 medical and health sciences, SDG 3 - Good Health and Well-being, INFLAMMATION, Environmental health, SCORE, medicine, Humans, Propensity Score, business.industry, HIV, medicine.disease, CD4 Lymphocyte Count, MYOCARDIAL-INFARCTION, Propensity score matching, Disease risk, business
Abstract

Background: People living with HIV (PLWH) experience a higher cardiovascular disease (CVD) risk. Yet, traditional algorithms are often used to estimate CVD risk. We evaluated the performance of 4 commonly used algorithms.Setting: The Netherlands.Methods: We used data from 16,070 PLWH aged > 18 years, who were in care between 2000 and 2016, had no pre-existing CVD, had initiated first combination antiretroviral therapy >1 year ago, and had available data on CD4 count, smoking status, cholesterol, and blood pressure. Predictive performance of 4 algorithms [Data Collection on Adverse Effects of Anti-HIV Drugs Study (D: A: D); Systematic COronary Risk Evaluation adjusted for national data (SCORE-NL); Framingham CVD Risk Score (FRS); and American College of Cardiology and American Heart Association Pooled Cohort Equations (PCE)] was evaluated using a Kaplan-Meier approach. Model discrimination was assessed using Harrell's C-statistic. Calibration was assessed using observed-versusexpected ratios, calibration plots, and Greenwood-Nam-D'Agostino goodness-of-fit tests.Results: All algorithms showed acceptable discrimination (Harrell's C-statistic 0.73-0.79). On a population level, D: A: D, SCORE-NL, and PCE slightly underestimated, whereas FRS slightly overestimated CVD risk (observed-versus-expected ratios 1.35, 1.38, 1.14, and 0.92, respectively). D: A: D, FRS, and PCE best fitted our data but still yielded a statistically significant lack of fit (Greenwood-Nam-D'Agostino chi(2) ranged from 24.57 to 34.22, P Conclusions: All algorithms perform reasonably well in PLWH, with SCORE-NL performing poorest. Prediction algorithms are useful for clinical practice, but clinicians should be aware of their limitations (ie, lack of fit and slight underestimation of CVD risk in low-risk groups).

Published
2019

3. Raltegravir in HIV-1-Infected Pregnant Women: Pharmacokinetics, Safety, and Efficacy

Author

Blonk, M.I., Colbers, A.P., Hidalgo-Tenorio, C., Kabeya, K., Weizsacker, K., Haberl, A.E., Molto, J., Hawkins, D.A., Ende, M.E. van der, Gingelmaier, A., Taylor, G.P., Ivanovic, J., Giaquinto, C., Burger, D.M., Ven, A.J. van der, Pharmacy, and Internal Medicine

Subjects
Adult, Microbiology (medical), medicine.medical_specialty, Anti-HIV Agents, HIV Infections, Pharmacology, Pharmacokinetics, SDG 3 - Good Health and Well-being, Interquartile range, HIV, MTCT, Pregnancy, Raltegravir, Infectious Diseases, Internal medicine, Raltegravir Potassium, medicine, Humans, Pregnancy Complications, Infectious, business.industry, Infant, Newborn, medicine.disease, Confidence interval, Clinical trial, lnfectious Diseases and Global Health Radboud Institute for Health Sciences [Radboudumc 4], Area Under Curve, Female, business, Viral load, Postpartum period, medicine.drug
Abstract

Contains fulltext : 153803.pdf (Publisher’s version ) (Closed access) BACKGROUND: The use of raltegravir in human immunodeficiency virus (HIV)-infected pregnant women is important in the prevention of mother-to-child HIV transmission, especially in circumstances when a rapid decline of HIV RNA load is warranted or when preferred antiretroviral agents cannot be used. Physiological changes during pregnancy can reduce antiretroviral drug exposure. We studied the effect of pregnancy on the pharmacokinetics of raltegravir and its safety and efficacy in HIV-infected pregnant women. METHODS: An open-label, multicenter, phase 4 study in HIV-infected pregnant women receiving raltegravir 400 mg twice daily was performed (Pharmacokinetics of Newly Developed Antiretroviral Agents in HIV-Infected Pregnant Women Network). Steady-state pharmacokinetic profiles were obtained in the third trimester and postpartum along with cord and maternal delivery concentrations. Safety and virologic efficacy were evaluated. RESULTS: Twenty-two patients were included, of which 68% started raltegravir during pregnancy. Approaching delivery, 86% of the patients had an undetectable viral load (

Published
2015

4. Factors associated with presenting late or with advanced HIV disease in the Netherlands, 1996-2014: results from a national observational cohort

Author

Coul, E.L. Op de, Sighem, A. van, Brinkman, K., Benthem, B.H. van, Ende, M.E. van der, Geerlings, S., Reiss, P., Koopmans †, P.P., Keuter, M., Ven, A.J.A.M. van der, Hofstede, H.J.M. ter, Dofferhoff, A.S.M., Crevel, R. van, Burger, D.M., et al., Coul, E.L. Op de, Sighem, A. van, Brinkman, K., Benthem, B.H. van, Ende, M.E. van der, Geerlings, S., Reiss, P., Koopmans †, P.P., Keuter, M., Ven, A.J.A.M. van der, Hofstede, H.J.M. ter, Dofferhoff, A.S.M., Crevel, R. van, Burger, D.M., and et al.

Abstract

Contains fulltext : 172538.pdf (publisher's version ) (Open Access), OBJECTIVES: Early testing for HIV and entry into care are crucial to optimise treatment outcomes of HIV-infected patients and to prevent spread of HIV. We examined risk factors for presentation with late or advanced disease in HIV-infected patients in the Netherlands. METHODS: HIV-infected patients registered in care between January 1996 and June 2014 were selected from the ATHENA national observational HIV cohort. Risk factors for late presentation and advanced disease were analysed by multivariable logistic regression. Furthermore, geographical differences and time trends were examined. RESULTS: Of 20 965 patients, 53% presented with late-stage HIV infection, and 35% had advanced disease. Late presentation decreased from 62% (1996) to 42% (2013), while advanced disease decreased from 46% to 26%. Late presentation only declined significantly among men having sex with men (MSM; p <0.001), but not among heterosexual males (p=0.08) and females (p=0.73). Factors associated with late presentation were: heterosexual male (adjusted OR (aOR), 1.59; 95% CI 1.44 to 1.75 vs MSM), injecting drug use (2.00; CI 1.69 to 2.38), age >/=50 years (1.46; CI 1.33 to 1.60 vs 30-49 years), region of origin (South-East Asia 2.14; 1.80 to 2.54, sub-Saharan Africa 2.11; 1.88 to 2.36, Surinam 1.59; 1.37 to 1.84, Caribbean 1.31; 1.13 to 1.53, Latin America 1.23; 1.04 to 1.46 vs the Netherlands), and location of HIV diagnosis (hospital 3.27; 2.94 to 3.63, general practitioner 1.66; 1.50 to 1.83, antenatal screening 1.76; 1.38 to 2.34 vs sexually transmitted infection clinic). No association was found for socioeconomic status or level of urbanisation. Compared with Amsterdam, 2 regions had higher adjusted odds and 2 regions had lower odds of late presentation. Results were highly similar for advanced disease. CONCLUSIONS: Although the overall rate of late presentation is declining in the Netherlands, targeted programmes to reduce late HIV diagnoses remain needed for all risk groups, but should

Published
2016

5. A once-daily HAART regimen containing indinavir + ritonavir plus one or two nucleoside reverse transcriptase inhibitors (PIPO study)

Author

Burger, D.M., Aarnoutse, R.E., Dieleman, J.P., Gyssens, I.C.J., Nouwen, J., Marie, S. de, Koopmans †, P.P., Stek Jr, M., and Ende, M.E. van der

Subjects
Effective Primary Care and Public Health [EBP 3], Microbial pathogenesis and host defense [UMCN 4.1]
Abstract

Item does not contain fulltext INTRODUCTION: There is an increased interest in developing once-daily regimens for the treatment of HIV-infected patients. A Phase II study was conducted to investigate the pharmacokinetics, and short-term safety and efficacy of an indinavir/ritonavir combination as part of a once-daily regimen. METHODS: HIV-infected patients with either proven poor compliance to HAART regimens in the past or an anticipated poor compliance to such a regimen in the future were eligible for this study. They received a once-daily regimen consisting of indinavir 1200 mg, ritonavir 400 mg, and one or two nucleoside reverse transcriptase inhibitors (NRTIs), also administered once daily with food. A 24 h pharmacokinetic profile was constructed in a subset of patients. Short-term safety and efficacy were evaluated at 4, 12 and 24 weeks after initiation of treatment. RESULTS: A total of 64 patients were included in this study, of whom 27 (42.2%) were treatment-naive. The geometric mean (+95% CI) of indinavir AUC0-24h, Cmax and Cmin as determined in an unselected group of 16 patients were 84.9 (69.7-103.5) mg/l x h, 12.0 (10.2-14.1) mg/l and 0.15 (0.09-0.26) mg/l, respectively. A large interpatient variability was observed, with five out of the 16 subjects having a Cmin value below the minimum effective concentration of 0.10 mg/l. During the 24 weeks of follow-up nine patients (14.1%) discontinued study medication, two due to medication-related toxicity. Gastrointestinal adverse events were reported most frequently (50.0%), followed by skin effects (45.3%), joint pain (9.4%) and urological complaints (7.8%). No patient developed nephrolithiasis. The median (+interquartile range) serum creatinine level in the 64 patients increased slightly from 74 (63-88) micromol/l to 79 (66-92) micromol/l during the 24 weeks of follow-up. One new patient reached a grade 1 elevation in serum creatinine, which normalized during the follow-up; five other patients with elevated serum creatinine at baseline remained stable. During the 24 weeks of follow-up, the proportion of patients with a viral load

Published
2003

6. von Willebrand Factor is elevated in HIV patients with a history of thrombosis

Author

Dries, L.W. van den, Gruters, R.A., Hövels-van der Borden, S.B.C., Kruip, M.J., Maat, M.P. de, Gorp, E.C. van, Ende, M.E. van der, Dries, L.W. van den, Gruters, R.A., Hövels-van der Borden, S.B.C., Kruip, M.J., Maat, M.P. de, Gorp, E.C. van, and Ende, M.E. van der

Abstract

Contains fulltext : 151953.pdf (publisher's version ) (Open Access), BACKGROUND: Arterial and venous thrombotic events are more prevalent in HIV infected individuals compared to the general population, even in the era of combination antiretroviral therapy. Although the mechanism is not fully understood, recent evidence suggests a role for chronic immune activation. METHODS: We reviewed the Dutch National HIV registry database for HIV infected patients in Rotterdam with a history of arterial or venous thrombosis and calculated the incidence. We collected samples from patients with and without thrombosis and compared plasma levels of lipopolysaccharide (LPS), LPS binding protein (LBP), soluble CD14 (sCD14), and von Willebrand Factor antigen level (vWF). RESULTS: During a 10-year period, a total of 60 documented events in 14,026 person years of observation (PYO) occurred, resulting in an incidence rate of 2.50, 2.21, and 4.28 for arterial, venous and combined thrombotic events per 1000 PYO, respectively. The vWF was elevated in the majority of study subjects (mean 2.36 SD +/- 0.88 IU/ml); we found a significant difference when comparing venous cases to controls (mean 2.68 SD +/- 0.82 IU/ml vs. 2.20 SD +/- 0.77 IU/ml; p = 0.024). This difference remained significant for recurrent events (mean 2.78 SD +/- 0.75; p = 0.043). sCD14 was positively correlated with LPS (r = 0.255; p = 0.003). CONCLUSION: The incidence of venous thrombosis was two-fold higher in HIV infected patients compared to age-adjusted data from general population cohort studies. We couldn't find a clear association between immune activation markers to either arterial or venous thrombotic events. We observed a marked increase in vWF levels as well as a correlation of vWF to first and recurrent venous thrombo-embolic events. These findings suggest that HIV infection is an independent risk factor for coagulation abnormalities and could contribute to the observed high incidence in venous thrombosis. This could be a reason to prolong anti-thrombotic treatment in HIV patients w

Published
2015

7. No Treatment versus 24 or 60 Weeks of Antiretroviral Treatment during Primary HIV Infection: The Randomized Primo-SHM Trial

Author

Grijsen, M.L., Steingrover, R., Wit, F.W.N.M., Jurriaans, S., Verbon, A., Brinkman, K., Ende, M.E. van der, Soetekouw, R., Wolf, F. de, Lange, J.M.A., Schuitemaker, H., Prins, J.M., Primo-SHM Study Grp, Dermatology, Other departments, AII - Amsterdam institute for Infection and Immunity, Global Health, Medical Microbiology and Infection Prevention, Experimental Immunology, Infectious diseases, Graduate School, Oral and Maxillofacial Surgery, and Internal Medicine

Subjects
Cart, Adult, Male, medicine.medical_specialty, Viral Diseases, Randomization, Human immunodeficiency virus (HIV), HIV Infections, medicine.disease_cause, Primary HIV infection, Drug Administration Schedule, SDG 3 - Good Health and Well-being, Internal medicine, medicine, Humans, business.industry, Hazard ratio, virus diseases, HIV, General Medicine, Middle Aged, Viral Load, Antiretroviral therapy, Surgery, Log-rank test, Infectious Diseases, Anti-Retroviral Agents, Medicine, Female, business, Viral load, Research Article
Abstract

In a three-arm randomized trial conducted among adult patients in HIV treatment centers in The Netherlands, Marlous Grijsen and colleagues examine the effects of temporary combination antiretroviral therapy during primary HIV infection., Background The objective of this study was to assess the benefit of temporary combination antiretroviral therapy (cART) during primary HIV infection (PHI). Methods and Findings Adult patients with laboratory evidence of PHI were recruited in 13 HIV treatment centers in the Netherlands and randomly assigned to receive no treatment or 24 or 60 wk of cART (allocation in a 1∶1∶1 ratio); if therapy was clinically indicated, participants were randomized over the two treatment arms (allocation in a 1∶1 ratio). Primary end points were (1) viral set point, defined as the plasma viral load 36 wk after randomization in the no treatment arm and 36 wk after treatment interruption in the treatment arms, and (2) the total time that patients were off therapy, defined as the time between randomization and start of cART in the no treatment arm, and the time between treatment interruption and restart of cART in the treatment arms. cART was (re)started in case of confirmed CD4 cell count, Editors' Summary Background Every year, nearly three million people become infected with HIV, the virus that causes AIDS. The first stage of HIV infection—primary HIV infection—lasts a few weeks and often goes undetected, although most individuals develop a short, flu-like illness. During this stage of infection, the immune system begins to make antibodies to HIV. The second stage of HIV infection, which lasts many years, also has no major symptoms but, during this stage, HIV slowly destroys immune system cells, including CD4 cells, a type of lymphocyte. Eventually, the immune system is unable to fight off other infections and patients enter the third phase of HIV infection—symptomatic HIV infection. The final stage—AIDS—is characterized by the occurrence of one or more AIDS-defining conditions, which include severe but unusual infections and several types of cancer. Early in the AIDS epidemic, most HIV-positive people died within ten years of infection. Nowadays, although there is still no cure for HIV infection, HIV has become a chronic disease because of the availability of combination antiretroviral therapy (cART; cocktails of several powerful drugs). This means that many HIV-positive people have a near-normal life span. Why Was This Study Done? It is currently recommended that people start cART when their CD4 count falls below 350 CD4 cells per cubic milliliter (cells/mm3) of blood, when they develop severe constitutional symptoms such as fever lasting longer than a month, or when they develop an AIDS-defining condition. But could a short course of cART during primary HIV infection be clinically beneficial? Some, but not all, nonrandomized studies have shown that such treatment reduces the viral set point (the stabilized viral load that is reached after the immune system begins to make antibodies to HIV; the viral load is the amount of virus in the blood) and slows the decline of CD4 cell count in patients. In this randomized trial (the Primo-SHM trial), the researchers assess the clinical benefit of temporary cART initiated during primary HIV infection by measuring its effects on the viral set point and on when patients have to restart cART during chronic HIV infection. In a randomized controlled trial, patients are assigned by the play of chance to receive different treatments and then followed to compare the effects of these treatments. What Did the Researchers Do and Find? The researchers assigned 168 patients with primary HIV infection to receive no treatment, 24 weeks of cART, or 60 weeks of cART. They measured the viral set point (the viral load in the blood 36 weeks after randomization in the no treatment arm and 36 weeks after cART interruption in the treatment arms) and determined the time off therapy (the time between randomization and the start of cART in the no treatment arm, and the time between treatment interruption and restart of cART in the treatment arms) for each patient. cART was (re)started following two consecutive CD4 counts below 350 cells/mm3 or when symptomatic HIV disease developed. The average viral set point was lower in the patients who received early cART than in those who had no treatment. Moreover, on average, the patients in the no treatment arm started cART 0.7 years after randomization whereas those in the 24- and 60-week treatment arms restarted cART after 3.0 and 1.8 years, respectively. There was no statistically significant difference between the 24-week and 60-week treatment arms in time off therapy. What Do These Findings Mean? These findings suggest that temporary cART during primary HIV infection can transiently lower the viral set point and can delay the need to restart cART during chromic HIV infection. They also suggest that 24 weeks of cART during primary HIV is as effective as 60 weeks of treatment. These findings need to be confirmed in other settings, and follow-up studies are needed to evaluate the long-term benefits of early temporary cART, but given the short time between cART interruption and treatment restart, the researchers suggest that not interrupting early cART, but instead continuing it for life, should be considered. However, they add, because patients are often physically and emotionally distressed at this stage of HIV infection, adherence to cART during primary HIV infection may be suboptimal, and so patients with primary HIV infection should be advised to start cART only when they feel ready to start treatment. Additional Information Please access these web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001196. Information is available from the US National Institute of Allergy and infectious diseases on HIV infection and AIDS, including information on the clinical progression of HIV infection NAM/aidsmap provides information about HIV/AIDS, including a factsheet on primary infection Information is available from Avert, an international AIDS charity on many aspects of HIV/AIDS, including detailed information on HIV treatment and care and on the stages of HIV infection (in English and Spanish) The World Health Organization's 2010 antiretroviral therapy guidelines provide recommendations on when to initiate cART Information about Primo-SHM is available Patient stories about living with HIV/AIDS are available through Avert and through the charity website Healthtalkonline

Published
2012

9. Associations between ABCB1, CYP2A6, CYP2B6, CYP2D6, and CYP3A5 alleles in relation to efavirenz and nevirapine pharmacokinetics in HIV-infected individuals.

Author

Heil, S.G., Ende, M.E. van der, Schenk, P.W., Heiden, I. van der, Lindemans, J., Burger, D.M., Schaik, R.H. van, Heil, S.G., Ende, M.E. van der, Schenk, P.W., Heiden, I. van der, Lindemans, J., Burger, D.M., and Schaik, R.H. van

Abstract

1 april 2012, Item does not contain fulltext, BACKGROUND: Human immunodeficiency virus (HIV)-infected individuals show large interindividual variation in response to antiretroviral therapy. Efavirenz (EFV) and nevirapine (NVP) are nonnucleoside reverse transcriptase inhibitors, which are prescribed in combination with other antiretroviral therapy in so-called highly active antiretroviral therapy. Recent studies provide evidence for the role of cytochrome P450 (CYP) genes, in particular CYP2B6, in relation to EFV and NVP pharmacokinetics. In this study, the authors investigated whether common ABCB1, CYP2A6, CYP2B6, CYP2D6, and CYP3A5 alleles are associated with plasma concentrations of EFV and NVP in HIV-infected individuals. METHODS: Plasma drug concentrations were quantified by high-performance liquid chromatography in 143 HIV-infected individuals receiving either EFV or NVP. Genotyping for common alleles was performed by restriction fragment length polymorphism and Taqman assays. Individuals were genotyped for 11 single-nucleotide polymorphisms in 5 genes. CYP2B6 haplotypes were reconstructed by PHASE. RESULTS: Plasma EFV concentrations were positively associated with CYP2B6 c.516G>T, c.785A>G, and c.983A>G single-nucleotide polymorphisms in HIV-infected individuals. Increased plasma concentrations of EFV and NVP were present in individuals with the CYP2B6*6/*6 or *6/*18 haplotype compared with CYP2B6*1/*1 [increase of 62% (95% confidence interval, 44.0-80.1) and 24% (95% confidence interval, 7.0-40.0), respectively, P < 0.01]. No significant association with other genes in relation to EFV or NVP concentrations was found. CONCLUSIONS: In this study, a strong association of CYP2B6*6 and CYP2B6*18 alleles in relation to EFV and NVP plasma concentrations was found, which confirmed previous studies.

Published
2012

10. Lower atovaquone/proguanil concentrations in patients taking efavirenz, lopinavir/ritonavir or atazanavir/ritonavir.

Author

Luin, M. van, Ende, M.E. van der, Richter, C., Visser, M. de, Faraj, D., Ven, A.J.A.M. van der, Gelinck, L., Kroon, F., Wit, F.W., Schaik, R.H. van, Kuks, P.F.M., Burger, D.M., Luin, M. van, Ende, M.E. van der, Richter, C., Visser, M. de, Faraj, D., Ven, A.J.A.M. van der, Gelinck, L., Kroon, F., Wit, F.W., Schaik, R.H. van, Kuks, P.F.M., and Burger, D.M.

Abstract

Contains fulltext : 87324.pdf (publisher's version ) (Closed access), HIV-infected travellers frequently use atovaquone/proguanil as malaria prophylaxis. We compared atovaquone/proguanil pharmacokinetics between healthy volunteers and HIV-infected patients taking efavirenz, lopinavir/ritonavir or atazanavir/ritonavir. The geometric mean ratio (95% confidence interval) area under the curve (AUC)0-->t for atovaquone relative to the healthy volunteers was 0.25 (0.16-0.38), 0.26 (0.17-0.41) and 0.54 (0.35-0.83) for patients on efavirenz, lopinavir/ritonavir and atazanavir/ritonavir, respectively. Proguanil plasma concentrations were also significantly lower (38-43%). Physicians should be alert for atovaquone/proguanil prophylaxis failures in patients taking efavirenz, lopinavir/ritonavir or atazanavir/ritonavir.

Published
2010

12. Steady-state nevirapine plasma concentrations are influenced by pregnancy.

Author

Nellen, J.F., Damming, M., Godfried, M.H., Boer, K., Ende, M.E. van der, Burger, D.M., Wolf, F. de, Wit, F.W., Prins, J.M., Nellen, J.F., Damming, M., Godfried, M.H., Boer, K., Ende, M.E. van der, Burger, D.M., Wolf, F. de, Wit, F.W., and Prins, J.M.

Abstract

Contains fulltext : 70941.pdf (publisher's version ) (Closed access), OBJECTIVES: Optimal plasma concentrations of antiretroviral drugs are required during pregnancy to treat maternal HIV infection and prevent mother-to-child transmission. We investigated the effect of pregnancy on nevirapine (NVP) plasma concentrations. METHODS: We included all HIV-1-infected women for whom NVP plasma concentrations were available as part of routine patient care at two university hospitals. Plasma NVP concentrations were compared for pregnant (n=45) and non-pregnant (n=152) women. Univariate and multivariate linear regression analyses were used to identify and adjust for other confounding factors associated with NVP plasma concentrations. For pregnant women who had a plasma NVP concentration available both during and outside pregnancy, a paired analysis was performed. RESULTS: Steady-state NVP plasma concentrations were lower in pregnant women: 5.2 mg/L (interquartile range 3.9-6.8) vs. 5.8 mg/L (4.3-7.7) (P=0.08). After adjusting for confounders, both pregnancy (regression coefficient=-0.90 mg/L, P=0.046) and African descent (regression coefficient=+1.13 mg/L, P=0.005) influenced NVP concentrations significantly. The paired analysis showed mean concentrations of 4.8 mg/L during pregnancy and 5.8 mg/L outside pregnancy (paired t-test, P=0.073). CONCLUSIONS: Pregnancy has a moderate but significant lowering effect on NVP plasma concentrations. Being of African descent compensates for the lowering effect of pregnancy on NVP concentrations.

Published
2008

13. Therapeutic drug monitoring of the HIV protease inhibitor atazanavir in clinical practice.

Author

Cleijsen, R.M., Ende, M.E. van der, Kroon, F.P., Lunel, F.V., Koopmans †, P.P., Gras, L., Wolf, F. de, Burger, D.M., Cleijsen, R.M., Ende, M.E. van der, Kroon, F.P., Lunel, F.V., Koopmans †, P.P., Gras, L., Wolf, F. de, and Burger, D.M.

Abstract

Contains fulltext : 52795.pdf (publisher's version ) (Closed access), BACKGROUND: Therapeutic drug monitoring (TDM) is being applied for a number of antiretroviral agents. Little is known about the use of TDM for atazanavir. METHODS: This is a retrospective cohort analysis on the use of TDM of atazanavir at three clinical sites in The Netherlands. Patients were divided into three groups: (i) all patients with evaluable data of plasma atazanavir concentrations and its relationship with hyperbilirubinaemia; (ii) patients who started atazanavir without documented evidence of protease inhibitor (PI) mutations; (iii) patients who started atazanavir with documented evidence of PI mutations. The genotypic inhibitory quotient (GIQ) was calculated by dividing the mean atazanavir plasma trough concentration by the number of PI mutations. RESULTS: A total of 108 patients were included; 70 (65.8%) were using atazanavir/ritonavir (300/100 mg once daily). No significant relationship was observed between atazanavir plasma trough concentration and antiviral response in patients starting atazanavir without PI mutations (group 2; n = 82). In contrast, a significant relationship was observed between atazanavir GIQ and treatment response in patients starting atazanavir while having PI mutations (group 3; n = 26). The cut-off value for GIQ most predictive of virological failure was 0.23 mg/L/mutation: patients (n = 8) with a GIQ equal to or below this value had 50% virological failure whereas patients (n = 18) with a GIQ above 0.23 mg/L/mutation had only 11% virological failure (chi(2): P = 0.030). Atazanavir plasma trough concentrations were significantly related with the occurrence of increased total bilirubin concentrations. CONCLUSIONS: TDM of atazanavir might be beneficial for patients with documented PI resistance or patients with hyperbilirubinaemia.

Published
2007

14. Pharmacokinetics of once-daily lopinavir/ritonavir and the influence of dose modifications.

Author

Porte, C.J.L. la, Schippers, E.F., Ende, M.E. van der, Koopmans †, P.P., Blok, W.L., Kauffmann, R.H., Kroon, F.P., Burger, D.M., Porte, C.J.L. la, Schippers, E.F., Ende, M.E. van der, Koopmans †, P.P., Blok, W.L., Kauffmann, R.H., Kroon, F.P., and Burger, D.M.

Abstract

Contains fulltext : 49125.pdf (publisher's version ) (Closed access), We studied the pharmacokinetics of lopinavir/ritonavir dosed at 800/200 mg a day in 20 HIV-1-infected patients, and evaluated the effect of dose modifications in the case of trough concentration (Ctrough) levels less than 1.0 mg/l. Ctrough levels after the daily administration of lopinavir/ritonavir were lower than with twice daily administration. Dose modifications in four patients with Ctrough levels less than 1.0 mg/l succeeded in only one patient. Therapeutic drug monitoring can identify patients with lower-than-expected lopinavir exposure in a larger study.

Published
2005

16. Clinical, immunological and virological response to different antiretroviral regimens in a cohort of HIV-2-infected patients.

Author

Ende, M.E. van der, Prins, J.M., Brinkman, K., Keuter, M., Veenstra, J., Danner, S.A., Niesters, H.G.M., Osterhaus, A.D., Schutten, M., Ende, M.E. van der, Prins, J.M., Brinkman, K., Keuter, M., Veenstra, J., Danner, S.A., Niesters, H.G.M., Osterhaus, A.D., and Schutten, M.

Abstract

Contains fulltext : 186259.pdf (publisher's version ) (Closed access), OBJECTIVE: To assess the clinical, immunological and virological response and the emergence of resistance towards antiretroviral therapy (ART) in a cohort of HIV-2-infected patients. DESIGN: Observational study. PATIENTS: HIV-2-infected patients residing in the Netherlands. RESULTS: From 1995 to 2001 seven patients failed various ART regimens. The resistance mutations were analysed retrospectively. Development of mutations proved to be similar to that observed in HIV-1-infected patients, with the exception of a higher occurrence of the Q151M mutation within the reverse transcriptase gene. In a prospective study, comprising 13 consecutive naive HIV-2-infected patients, all patients achieved plasma HIV-2-RNA suppression below the detection limit (500 copies/ml). The antiretroviral regimen consisted of two nucleoside reverse transcriptase inhibitors (NRTIs) and indinavir, with a boosting dose of ritonavir; the median follow-up was 91 weeks. Two patients experienced a temporary virological rebound, while at the same time therapeutic drug monitoring showed sub-therapeutic plasma levels of indinavir. CONCLUSION: Sustained viral suppression in HIV-2-infected patients can be achieved using an antiretroviral regimen of two NRTIs and boosted indinavir or lopinavir.

Published
2003

17. Treatment failure of nelfinavir-containing triple therapy can largely be explained by low nelfinavir plasma concentrations.

Author

Burger, D.M., Hugen, P.W.H., Aarnoutse, R.E., Hoetelmans, R.M., Jambroes, M., Nieuwkerk, P.T., Schreij, G., Schneider, M., Ende, M.E. van der, Lange, J.M.A., Burger, D.M., Hugen, P.W.H., Aarnoutse, R.E., Hoetelmans, R.M., Jambroes, M., Nieuwkerk, P.T., Schreij, G., Schneider, M., Ende, M.E. van der, and Lange, J.M.A.

Abstract

Contains fulltext : 119497.pdf (publisher's version ) (Closed access), The relationship between plasma concentrations of nelfinavir and virologic treatment failure was investigated to determine the minimum effective concentration of nelfinavir. Plasma samples were prospectively collected from treatment-naive patients who began taking nelfinavir, 1,250 mg BID + two nucleoside reverse transcription inhibitors (NRTIs). Nelfinavir concentration ratios were calculated by dividing each individual nelfinavir level by the time-adjusted population value. Virologic failure was defined as either no response (a detectable viral load after 6 months) or a relapse (detectable viral load after being undetectable, or an increase in viral load >1 log above nadir). Forty-eight patients were included with a median follow-up period of 8 months. The median concentration ratio of nelfinavir was 0.98 (interquartile range, 0.76-1.47). Virologic failure was observed in 29% of the patients. In a univariate analysis, the nelfinavir concentration ratio appeared to be the single determinant that was related to virologic failure (P = 0.039). Patients with a median ratio <0.90 had a relative risk of 3.0 (95% CI, 1.2-7.6) for virologic failure. Using this threshold, virologic failures were detected with 64% sensitivity and 74% specificity (P = 0.014). Virologic failure of nelfinavir-containing triple therapy can be explained, to a large extent, by low plasma levels of nelfinavir.

Published
2003

18. Limited patient adherence to highly active antiretroviral therapy for HIV-1 infection in an observational cohort study.

Author

Nieuwkerk, P.T., Sprangers, M.A.G., Burger, D.M., Hoetelmans, R.M., Hugen, P.W.H., Danner, S.A., Ende, M.E. van der, Schneider, M., Schrey, G., Meenhorst, P.L., Sprenger, H., Kauffmann, R.H., Jambroes, M., Chesney, M.A., Wolf, F. de, Lange, J.M.A., Nieuwkerk, P.T., Sprangers, M.A.G., Burger, D.M., Hoetelmans, R.M., Hugen, P.W.H., Danner, S.A., Ende, M.E. van der, Schneider, M., Schrey, G., Meenhorst, P.L., Sprenger, H., Kauffmann, R.H., Jambroes, M., Chesney, M.A., Wolf, F. de, and Lange, J.M.A.

Abstract

Contains fulltext : 185695.pdf (publisher's version ) (Closed access), BACKGROUND: Adherence to highly active antiretroviral therapy (HAART) for human immunodeficiency syndrome type 1 (HIV-1) infection is essential to sustain viral suppression and prevent drug resistance. We investigated adherence to HAART among patients in a clinical cohort study. METHODS: Patients receiving HAART had their plasma concentrations of protease inhibitors or nevirapine measured and completed a questionnaire on adherence. We determined the percentage of patients who reported taking all antiretroviral medication on time and according to dietary instructions in the past week. Drug exposure was compared between patients reporting deviation from their regimen and fully adherent patients. Among patients who received HAART for at least 24 weeks, we assessed the association between adherence and virologic outcome. RESULTS: A total of 224 of 261 eligible patients completed a questionnaire. Forty-seven percent reported taking all antiretroviral medication on time and according to dietary instructions. Patients who reported deviation from their regimen showed lower drug exposure compared with fully adherent patients (median concentration ratio, 0.81 vs 1.07; P =.001). Among those receiving HAART for at least 24 weeks, patients reporting deviation from their regimen were less likely to have plasma HIV-1 RNA levels below 500 copies/mL (adjusted odds ratio, 4.0; 95% confidence interval, 1.4-11.6) compared with fully adherent patients. CONCLUSIONS: Only half of the patients took all antiretroviral medication in accordance with time and dietary instructions in the preceding week. Deviation from the antiretroviral regimen was associated with decreased drug exposure and a decreased likelihood of having suppressed plasma HIV-1 RNA loads. Patient adherence should remain a prime concern in the management of HIV-1 infection.

Published
2001

19. Once-daily indinavir plus ritonavir:preliminary results of the PIPO study

Author

Burger, D.M., Hugen, P.W.H., Ende, M.E. van der, Wijngaarden, P. van, Aarnoutse, R.E., Reiss, P., Lange, J.M.A., Burger, D.M., Hugen, P.W.H., Ende, M.E. van der, Wijngaarden, P. van, Aarnoutse, R.E., Reiss, P., and Lange, J.M.A.

Abstract

Item does not contain fulltext

Published
2000

20. Immune restoration does not invariably occur following long term HIV-1 suppression during antiretroviral therapy.

Author

Pakker, N.G., Kroon, E.D., Roos, M.T.L., Otto, S.J., Hall, D., Wit, F.W., Hamann, D., Ende, M.E. van der, Claessen, F.A., Kauffmann, R.H., Koopmans †, P.P., Kroon, F.P., Napel, C.H.H. ten, Sprenger, H., Weigel, H.M., Montaner, J., Lange, J.M.A., Reiss, P., Schellekens, P.T.A., Miedema, F., Pakker, N.G., Kroon, E.D., Roos, M.T.L., Otto, S.J., Hall, D., Wit, F.W., Hamann, D., Ende, M.E. van der, Claessen, F.A., Kauffmann, R.H., Koopmans †, P.P., Kroon, F.P., Napel, C.H.H. ten, Sprenger, H., Weigel, H.M., Montaner, J., Lange, J.M.A., Reiss, P., Schellekens, P.T.A., and Miedema, F.

Abstract

Item does not contain fulltext

Published
1999

Catalog

Books, media, physical & digital resources
See catalog results