Introduction Whether HIV influences pulmonary function remains controversial. We assessed dynamic pulmonary function in people living with HIV (PLWHIV) and uninfected controls.
Methods A total of 1098 PLWHIV from the Copenhagen Co-morbidity in HIV infection study and 12 161 age-matched and sex-matched controls from the Copenhagen General Population Study were included. Lung function was assessed using FEV1 and FVC, while airflow limitation was defined by the lower limit of normal (LLN) of FEV1/FVC and by FEV1/FVC<0.7 with FEV1predicted <80% (fixed). Logistic and linear regression models were used to determine the association between HIV and pulmonary function adjusting for potential confounders (including smoking and socioeconomic status).
Results In predominantly white men with mean (SD) age of 50.6 (11.1) the prevalence of airflow limitation (LLN) was 10.6% (95% CI 8.9% to 12.6%) in PLWHIV and 10.6% (95% CI 10.0 to 11.1) in uninfected controls. The multivariable adjusted OR for airflow limitation defined by LLN for HIV was 0.97 (0.77–1.21, P<0.78) and 1.71 (1.34–2.16, P<0.0001) when defined by the fixed criteria. We found no evidence of interaction between HIV and cumulative smoking in these models (P interaction: 0.25 and 0.17 for LLN and fixed criteria, respectively). HIV was independently associated with 197 mL (152–242, P<0.0001) lower FEV1 and 395 mL (344–447, P<0.0001) lower FVC, and 100 cells/mm3 lower CD4 nadir was associated with 30 mL (7–52, P<0.01) lower FEV1 and 51 mL (24–78, P<0.001) lower FVC.
Conclusion HIV is a risk factor for concurrently decreased FEV1 and FVC. This excess risk is not explained by smoking or socioeconomic status and may be mediated by prior immunodeficiency.
Trial registration number NCT02382822.
- COPD epidemiology
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Contributors AnR was responsible for concept, data collection, and statistical analysis, and drafted the manuscript. JL, TB, JG, BGN and JV were responsible for concept and have had content review and editing input. SA was partly responsible for statistical analysis and has had content review and editing input. AR and AM had content review and editing input, and provided statistical support. SDN was the project leader, was responsible for concept and data collection, and has had content review and editing input.
Funding This work was supported by Rigshospitalet Research Council, Region Hovedstaden, the Lundbeck Foundation, the Novo Nordisk Foundation, and the Danish National Research Foundation grant 126. The study was designed, conducted, analysed and written by the authors without involvement of any commercial party.
Competing interests AnR: Travelling grants from Gilead. TB: Personal fees from Bristol Myers Squibb (BMS) and from Gilead and non-financial support from BMS, and from Gilead. AsR: No conflicts of interests. AM: Honoraria, lecture fees and travel support from BMS, BI, Pfizer, Merck, ViiV and Wragge. JG: Honoraria for consulting and presenting paid to his institution from Gilead, Abbvie, ViiV, BMS, MSD, Janssen and Medivir. JV: Honoraria for consulting and presenting from AstraZeneca, Boehringer-Ingelheim, Chiesi, GlaskoSmithKline and Novartis. SDN: Unrestricted research grants from the Novo Nordisk Foundation, the Lundbeck Foundation and the Rigshospitalet Research Council; travelling grants from Gilead, MSD, BMS and GSK/ViiV; advisory board activity for Gilead and GSK/ViiV.
Ethics approval The study was approved by the Regional Ethics Committee of Copenhagen (COCOMO: H-15017350; CGPS: H-KF-01-144/01). Written informed consent was obtained from all participants.
Provenance and peer review Not commissioned; externally peer reviewed.
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