Tavitiya Sudjaritruk1, Linda Aurpibul2, Penh Sun Ly3, Thoa Phan Kim Le4, Torsak Bunupuradah5, Rawiwan Hansudewechakul6, Pagakrong Lumbiganon7, Kulkanya Chokephaibulkit8, Nik Khairulddin Nik Yusoff9, Lam Van Nguyen10, Kamarul Azahar Mohd Razali11, Moy Siew Fong12, Revathy A Nallusamy13, Nia Kurniati14, Viet Chau Do15, David C Boettiger16, Annette H Sohn17, Azar Kariminia16. 1. Department of Pediatrics, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand; Research Institute for Health Sciences, Chiang Mai University, Chiang Mai, Thailand. Electronic address: tavitiya.s@cmu.ac.th. 2. Research Institute for Health Sciences, Chiang Mai University, Chiang Mai, Thailand. 3. National Centre for HIV/AIDS, Dermatology and STDs, Phnom Penh, Cambodia. 4. Infectious Disease Department, Children's Hospital 1, Ho Chi Minh City, Vietnam. 5. HIV-NAT, The Thai Red Cross AIDS Research Centre, Bangkok, Thailand. 6. Department of Pediatrics, Chiangrai Prachanukroh Hospital, Chiang Rai, Thailand. 7. Department of Pediatrics, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand. 8. Department of Pediatrics, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand. 9. Department of Pediatrics, Hospital Raja Perempuan Zainab II, Kota Bharu, Kelantan, Malaysia. 10. Infectious Disease Department, National Hospital of Pediatrics, Hanoi, Vietnam. 11. Department of Pediatrics, Pediatric Institute, Hospital Kuala Lumpur, Kuala Lumpur, Malaysia. 12. Department of Pediatrics, Hospital Likas, Kota Kinabalu, Malaysia. 13. Department of Pediatrics, Penang Hospital, Georgetown, Penang, Malaysia. 14. Department of Child Health, Cipto Mangunkusumo - Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia. 15. Infectious Disease Department, Children's Hospital 2, Ho Chi Minh City, Vietnam. 16. Faculty of Medicine, The Kirby Institute, UNSW Australia, Sydney, Australia. 17. TREAT Asia/amfAR-The Foundation for AIDS Research, Bangkok, Thailand.
Abstract
PURPOSE: To assess the incidence and predictors of postsuppression virologic rebound (VR) among adolescents on stable combination antiretroviral therapy in Asia. METHODS: Perinatally HIV-infected Asian adolescents (10-19 years) with documented virologic suppression (two consecutive viral loads [VLs] <400 copies/mL ≥6 months apart) were included. Baseline was the date of the first VL <400 copies/mL at age ≥10 years or the 10th birthday for those with prior suppression. Cox proportional hazards models were used to identify predictors of postsuppression VR (VL >1,000 copies/mL). RESULTS: Of 1,379 eligible adolescents, 47% were males. At baseline, 22% were receiving protease inhibitor-containing regimens; median CD4 cell count (interquartile range [IQR]) was 685 (448-937) cells/mm3; 2% had preadolescent virologic failure (VF) before subsequent suppression. During adolescence, 180 individuals (13%) experienced postsuppression VR at a rate of 3.4 (95% confidence interval: 2.9-3.9) per 100 person-years, which was consistent over time. Median time to VR during adolescence (IQR) was 3.3 (2.1-4.8) years. Wasting (weight-for-age z-score <-2.5), being raised by grandparents, receiving second-line protease inhibitor-based regimens, starting combination antiretroviral therapy after 2005, and having preadolescent VF were independent predictors of adolescent VR. At VR, median age, CD4 cell count, and VL (IQR) were 14.8 (13.2-16.4) years, 507 (325-723) cells/mm3, and 4.1 (3.5-4.7) log10 copies/mL, respectively. CONCLUSIONS: A modest and consistent incidence of postsuppression VR was documented during adolescence in our cohort. Having poor weight, receiving second-line regimens, and prior VF were associated with an increased VR rate. Adolescents at higher risk of VR may benefit from more intensive VL monitoring to enhance adherence management.
PURPOSE: To assess the incidence and predictors of postsuppression virologic rebound (VR) among adolescents on stable combination antiretroviral therapy in Asia. METHODS: Perinatally HIV-infected Asian adolescents (10-19 years) with documented virologic suppression (two consecutive viral loads [VLs] <400 copies/mL ≥6 months apart) were included. Baseline was the date of the first VL <400 copies/mL at age ≥10 years or the 10th birthday for those with prior suppression. Cox proportional hazards models were used to identify predictors of postsuppression VR (VL >1,000 copies/mL). RESULTS: Of 1,379 eligible adolescents, 47% were males. At baseline, 22% were receiving protease inhibitor-containing regimens; median CD4 cell count (interquartile range [IQR]) was 685 (448-937) cells/mm3; 2% had preadolescent virologic failure (VF) before subsequent suppression. During adolescence, 180 individuals (13%) experienced postsuppression VR at a rate of 3.4 (95% confidence interval: 2.9-3.9) per 100 person-years, which was consistent over time. Median time to VR during adolescence (IQR) was 3.3 (2.1-4.8) years. Wasting (weight-for-age z-score <-2.5), being raised by grandparents, receiving second-line protease inhibitor-based regimens, starting combination antiretroviral therapy after 2005, and having preadolescent VF were independent predictors of adolescent VR. At VR, median age, CD4 cell count, and VL (IQR) were 14.8 (13.2-16.4) years, 507 (325-723) cells/mm3, and 4.1 (3.5-4.7) log10 copies/mL, respectively. CONCLUSIONS: A modest and consistent incidence of postsuppression VR was documented during adolescence in our cohort. Having poor weight, receiving second-line regimens, and prior VF were associated with an increased VR rate. Adolescents at higher risk of VR may benefit from more intensive VL monitoring to enhance adherence management.
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