Vidya Mave1, Kristine M Erlandson2, Nikhil Gupte1, Ashwin Balagopal3, David M Asmuth4, Thomas B Campbell2, Laura Smeaton5, Nagalingeswaran Kumarasamy6, James Hakim7, Breno Santos8, Cynthia Riviere9, Mina C Hosseinipour10, Patcharaphan Sugandhavesa11, Rosa Infante12, Sandy Pillay13, Sandra W Cardoso14, Srikanth Tripathy15, Noluthando Mwelase16, Sima Berendes17, Bruno B Andrade18, David L Thomas3, Robert C Bollinger3, Amita Gupta1. 1. Johns Hopkins University-BJ Medical College Clinical Research Site, Pune, India Division of Infectious Diseases, Johns Hopkins University, Baltimore, Maryland. 2. Department of Medicine, University of Colorado Denver, Aurora. 3. Division of Infectious Diseases, Johns Hopkins University, Baltimore, Maryland. 4. Department of Medicine, University California Davis, Sacramento. 5. Harvard T. H. Chan School of Public Health, Boston, Massachusetts. 6. Y. R. Gaitonde Center for AIDS Research and Education, Chennai, India. 7. University of Zimbabwe, Harare. 8. Hospital Nossa Senhora de Conceição, Porto Alegre, Brazil. 9. Les Centres GHESKIO, Port-Au-Prince, Haiti. 10. University of North Carolina Project, Lilongwe, Malawi. 11. Research Institute for Health Sciences, Chiang Mai, Thailand. 12. IMPACTA Peru, San Miguel. 13. Durban International Clinical Research Site, Durban University of Technology, South Africa. 14. STD/AIDS Clinical Research Laboratory, Instituto de Pesquisa Clinica Evandro Chagas, Fundacao Oswaldo Cruz, Rio de Janeiro, Brazil. 15. National AIDS Research Institute, Pune, India. 16. Department of Medicine, University of Witwatersrand, Johannesburg, South Africa. 17. Malawi College of Medicine-Johns Hopkins University Research Project, Blantyre Liverpool School of Tropical Medicine, United Kingdom. 18. Unidade de Medicina Investigativa, Laboratório Integrado de Microbiologia e Imunorregulação, Centro de Pesquisas Gonçalo Moniz, Fundação Oswaldo Cruz, and Instituto Brasileiro para a Investigação da Tuberculose, Fundação José Silveira, Salvador, Brazil.
Abstract
BACKGROUND: Both wasting and obesity are associated with inflammation, but the extent to which body weight changes influence inflammation during human immunodeficiency virus infection is unknown. METHODS: Among a random virologically suppressed participants of the Prospective Evaluation of Antiretrovirals in Resource-Limited Settings trial, inflammatory markers were measured at weeks 0, 24, and 48 after antiretroviral therapy (ART) initiation. Associations between both baseline and change in body mass index (BMI; calculated as the weight in kilograms divided by the height in meters squared) and changes in inflammation markers were assessed using random effects models. RESULTS:Of 246 participants, 27% were overweight/obese (BMI, ≥ 25), and 8% were underweight (BMI < 18.5) at baseline. After 48 weeks, 37% were overweight/obese, and 3% were underweight. While level of many inflammatory markers decreased 48 weeks after ART initiation in the overall group, the decrease in C-reactive protein (CRP) level was smaller in overweight/obese participants (P = .01), and the decreases in both CRP (P = .01) and interleukin 18 (P = .02) levels were smaller in underweight participants. Each 1-unit gain in BMI among overweight/obese participants was associated with a 0.02-log10 increase in soluble CD14 level (P = .05), while each 1-unit BMI gain among underweight participants was associated with a 9.32-mg/L decrease in CRP level (P = .001). CONCLUSIONS: Being either overweight or underweight at ART initiation was associated with heightened systemic inflammation. While weight gain among overweight/obese persons predicted increased inflammation, weight gain among underweight persons predicted reduced inflammation.
RCT Entities:
BACKGROUND: Both wasting and obesity are associated with inflammation, but the extent to which body weight changes influence inflammation during human immunodeficiency virus infection is unknown. METHODS: Among a random virologically suppressed participants of the Prospective Evaluation of Antiretrovirals in Resource-Limited Settings trial, inflammatory markers were measured at weeks 0, 24, and 48 after antiretroviral therapy (ART) initiation. Associations between both baseline and change in body mass index (BMI; calculated as the weight in kilograms divided by the height in meters squared) and changes in inflammation markers were assessed using random effects models. RESULTS: Of 246 participants, 27% were overweight/obese (BMI, ≥ 25), and 8% were underweight (BMI < 18.5) at baseline. After 48 weeks, 37% were overweight/obese, and 3% were underweight. While level of many inflammatory markers decreased 48 weeks after ART initiation in the overall group, the decrease in C-reactive protein (CRP) level was smaller in overweight/obeseparticipants (P = .01), and the decreases in both CRP (P = .01) and interleukin 18 (P = .02) levels were smaller in underweight participants. Each 1-unit gain in BMI among overweight/obeseparticipants was associated with a 0.02-log10 increase in soluble CD14 level (P = .05), while each 1-unit BMI gain among underweight participants was associated with a 9.32-mg/L decrease in CRP level (P = .001). CONCLUSIONS: Being either overweight or underweight at ART initiation was associated with heightened systemic inflammation. While weight gain among overweight/obesepersons predicted increased inflammation, weight gain among underweight persons predicted reduced inflammation.
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