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HIV Infection Is Associated With Increased Risk for Acute Exacerbation of COPD.

ABSTRACT: BACKGROUND:Poorly controlled HIV infection is associated with increased risk for chronic obstructive pulmonary disease (COPD). Acute exacerbations of COPD (AECOPD) are major contributors to morbidity and mortality. Little is known about the association between HIV infection and AECOPD. METHODS:We identified 167 individuals with spirometry-confirmed COPD from a longitudinal study of current or former injection drug users at risk or with HIV infection. AECOPD, defined as self-report of worsening breathing requiring treatment with antibiotics or steroids, was assessed at 6-month study visits. Multivariable logistic regression identified factors associated with AECOPD. RESULTS:Of 167 participants, the mean age was 52 years; 89% were black, 30% female, and 32% HIV infected (median CD4 count: 312 cells per milliliter, 46% with detectable HIV RNA). After adjusting for age, gender, smoking history, comorbidity treatment, and airflow obstruction severity, HIV was independently associated with a 2.47 increased odds of AECOPD [95% confidence interval (CI): 1.22 to 5.00]. Compared with HIV-uninfected persons, HIV-infected persons with undetectable (<50 copies/mL) HIV RNA levels and those with a CD4 count ?350 cells per cubic millimeter demonstrated increased AECOPD (odds ratio, 2.91; 95% CI: 1.26 to 6.71; odds ratio, 4.16; 95% CI: 1.87 to 9.27, respectively). Higher AECOPD risk was observed with higher CD4 counts irrespective of treatment for comorbid diseases. CONCLUSIONS:HIV infection is independently associated with increased odds of AECOPD, potentially due to differences in treatment access and to variable disease manifestation by immune status. Providers should be aware that HIV infection may increase risk for AECOPD and that symptom may be more discernible with intact immune function.

SUBMITTER: Lambert AA

PROVIDER: S-EPMC4422097 | biostudies-literature | 2015 May

REPOSITORIES: biostudies-literature

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HIV Infection Is Associated With Increased Risk for Acute Exacerbation of COPD.

Lambert Allison A AA Kirk Gregory D GD Astemborski Jacquie J Mehta Shruti H SH Wise Robert A RA Drummond M Bradley MB

Journal of acquired immune deficiency syndromes (1999) 20150501 1

<h4>Background</h4>Poorly controlled HIV infection is associated with increased risk for chronic obstructive pulmonary disease (COPD). Acute exacerbations of COPD (AECOPD) are major contributors to morbidity and mortality. Little is known about the association between HIV infection and AECOPD.<h4>Methods</h4>We identified 167 individuals with spirometry-confirmed COPD from a longitudinal study of current or former injection drug users at risk or with HIV infection. AECOPD, defined as self-report ...[more]

PMID: 25942460

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Project description:Background: Decreased but measurable serum IgA levels (?70 mg/dL) have been associated with risk for infections in some populations, but are unstudied in COPD. This study tested the hypothesis that subnormal serum IgA levels would be associated with exacerbation risk in COPD.Methods: Data were analyzed from 1,049 COPD participants from the observational cohort study SPIROMICS (535 (51%) women; mean age 66.1 (SD 7.8), 338 (32%) current smokers) who had baseline serum IgA measured using the Myriad RBM biomarker discovery platform. Exacerbation data was collected prospectively (mean 944.3 (SD 281.3) days), and adjusted linear, logistic and zero-inflated negative binomial regressions were performed.Results: Mean IgA was 269.1 mg/dL (SD 150.9). One individual had deficient levels of serum IgA (<7 mg/dL) and 25 (2.4%) had IgA level ?70 mg/dL. Participants with IgA ?70 mg/dL were younger (62 vs. 66 years, p = 0.01) but otherwise similar to those with higher IgA. In adjusted models, IgA ?70 mg/dL was associated with higher exacerbation incidence rates (IRR 1.71, 95% CI 1.01-2.87, p = 0.044) and greater risk for any severe exacerbation (OR 2.99, 95% CI 1.30-6.94, p = 0.010). In adjusted models among those in the lowest decile (<120 mg/dL), each 10 mg/dL decrement in IgA (analyzed continuously) was associated with more exacerbations during follow-up (? 0.24, 95% CI 0.017-0.46, p = 0.035).Conclusions: Subnormal serum IgA levels were associated with increased risk for acute exacerbations, supporting mildly impaired IgA levels as a contributing factor in COPD morbidity. Additionally, a dose-response relationship between lower serum IgA and number of exacerbations was found among individuals with serum IgA in the lowest decile, further supporting the link between serum IgA and exacerbation risk. Future COPD studies should more comprehensively characterize immune status to define the clinical relevance of these findings and their potential for therapeutic correction.

Project description:Cardiac autonomic modulation (CAM) is impaired in patients with stable COPD. Exacerbation aggravates the patients' health status and functional capacity. While the clinical and functional effects of exacerbation are known, no studies investigated CAM during exacerbation and whether there is a relationship between CAM and functional capacity and dyspnea.Thirty-two patients with moderate to severe COPD were enrolled into two groups: stable COPD (GSta, n=16) and acute exacerbation of COPD (GAE, n=16). The GAE patients were evaluated 24-48 hours after starting standard therapy for COPD exacerbation during hospitalization; the GSta patients were evaluated in an outpatient clinic and included in the study if no decompensation episodes had occurred during the previous month. The heart rate (HR) and R-wave peak detection intervals in ms (RRi) were registered using a heart rate monitor (Polar® system) at rest in seated position during 10 minutes. CAM was assessed by heart rate variability (HRV) linear and non-linear analysis. Functional capacity was evaluated by handgrip strength test, performed by Jamar® dynamometer, and dyspnea was scored using the modified scale of the Medical Research Council.GAE presented higher parasympathetic CAM values compared with GSta for square root of the mean squared differences of successive RRi (RMSSD; 17.8±5.6 ms vs 11.7±9.5 ms); high frequency (HF; 111.3±74.9 ms2 vs 45.6±80.7 ms2) and standard deviation measuring the dispersion of points in the plot perpendicular to the line of identity (SD1; 12.7±3.9 ms vs 8.3±6.7 ms) and higher CAM values for standard deviation of the mean of all of RRi (STD RRi; 19.3±6.5 ms vs 14.3±12.5 ms); RRi tri (5.2±1.7 ms vs 4.0±3.0 ms); triangular interpolation of NN interval histogram (TINN; 88.7±26.9 ms vs 70.6±62.2 ms); low frequency (LF; 203±210.7 ms2 vs 101.8±169.7 ms2) and standard deviation measuring the dispersion of points along the line of identity (SD2; 30.4±14.8 ms vs 16.2±12.54 ms). Lower values were observed for the complexity indices: approximate entropy (ApEn; 0.9±0.07 vs 1.06±0.06) and sample entropy (SampEn; 1.4±0.3 vs 1.7±0.3). Significant and moderate associations were observed between HF (nu) and handgrip strength (r=-0.58; P=0.01) and between LF (ms2) and subjective perception of dyspnea (r=-0.53; P=0.03).COPD exacerbated patients have higher parasympathetic CAM than stable patients. This should be interpreted with caution since vagal influence on the airways determines a narrowing and not a better clinical condition. Additionally, functional capacity was negatively associated with parasympathetic CAM in COPD exacerbation.

Project description:Study objectivesSleep is an important dimension in the care of chronic obstructive pulmonary disease (COPD), but its relevance to exacerbations is unclear. We wanted to assess whether sleep quality as measured by the Pittsburgh Sleep Quality Index (PSQI) is associated with an increased risk of COPD exacerbations and does this differ by socio-environmental exposures.MethodsWe included 1647 current and former smokers with spirometrically confirmed COPD from the SPIROMICS cohort. We assessed incidence rate ratios for exacerbation using zero-inflated negative binomial regression adjusting for demographics, medical comorbidities, and multiple metrics of disease severity, including respiratory medications, airflow obstruction, and symptom burden. Our final model adjusted for socio-environmental exposures using the Area Deprivation Index, a composite measure of contemporary neighborhood quality, and Adversity-Opportunity Index, a composite measure of individual-level historic and current socioeconomic indicators. We used a pre-determined threshold of 20% missingness to undertake multiple imputation by chained equations. As sensitivity analyses, we repeated models in those with complete data and after controlling for prior exacerbations. As an exploratory analysis, we considered an interaction between socio-environmental condition and sleep quality.ResultsAfter adjustment for all co-variates, increasing PSQI scores (range 0-21) were associated with a 5% increased risk for exacerbation per point (p = .001) in the imputed dataset. Sensitivity analyses using complete cases and after controlling for prior exacerbation history were similar. Exploratory analysis suggested less effect among those who lived in poor-quality neighborhoods (p-for-interaction = .035).ConclusionsPoor sleep quality may contribute to future exacerbations among patients with COPD. This represents one target for improving disease control.Clinical trial registrationSubpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS). ClinicalTrials.gov Identifier# NCT01969344. Registry URL: https://clinicaltrials.gov/ct2/show/.

Project description:Matrix metalloprotease 9 (MMP-9) is associated with inflammation and lung remodeling in chronic obstructive pulmonary disease (COPD). We hypothesized that elevated circulating MMP-9 represents a potentially novel biomarker that identifies a subset of individuals with COPD with an inflammatory phenotype who are at increased risk for acute exacerbation (AECOPD). We analyzed Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS) and Genetic Epidemiology of COPD (COPDGene) cohorts for which baseline and prospective data were available. Elevated MMP-9 was defined based on >95th percentile plasma values from control (non-COPD) sample in SPIROMICS. COPD subjects were classified as having elevated or nonelevated MMP-9. Logistic, Poisson, and Kaplan-Meier analyses were used to identify associations with prospective AECOPD in both cohorts. Elevated MMP-9 was present in 95/1,053 (9%) of SPIROMICS and 41/140 (29%) of COPDGene participants with COPD. COPD subjects with elevated MMP-9 had a 13%-16% increased absolute risk for AECOPD and a higher median (interquartile range; IQR) annual AECOPD rate (0.33 [0-0.74] versus 0 [0-0.80] events/year and 0.9 [0.5-2] versus 0.5 [0-1.4] events/year for SPIROMICS and COPDGene, respectively). In adjusted models within each cohort, elevated MMP-9 was associated with increased odds (odds ratio [OR], 1.71; 95%CI, 1.00-2.90; and OR, 3.03; 95%CI, 1.02-9.01), frequency (incidence rate ratio [IRR], 1.45; 95%CI, 1.23-1.7; and IRR, 1.24; 95%CI, 1.03-1.49), and shorter time-to-first AECOPD (21.7 versus 31.7 months and 14 versus 21 months) in SPIROMICS and COPDGene, respectively. Elevated MMP-9 was independently associated with AECOPD risk in 2 well-characterized COPD cohorts. These findings provide evidence for MMP-9 as a prognostic biomarker and potential therapeutic target in COPD. ClinicalTrials.gov: NCT01969344 (SPIROMICS) and NCT00608764 (COPDGene). This work was funded by K08 HL123940 to JMW; R01HL124233 to PJC; Merit Review I01 CX000911 to JLC; R01 (R01HL102371, R01HL126596) and VA Merit (I01BX001756) to AG. SPIROMICS (Subpopulations and Intermediate Outcomes in COPD Study) is funded by contracts from the NHLBI (HHSN268200900013C, HHSN268200900014C,HHSN268200900015C HHSN268200900016C, HHSN268200900017C, HHSN268200900018C, HHSN268200900019C, and HHSN268200900020C) and a grant from the NIH/NHLBI (U01 HL137880), and supplemented by contributions made through the Foundation for the NIH and the COPD Foundation from AstraZeneca/MedImmune; Bayer; Bellerophon Therapeutics; Boehringer-Ingelheim Pharmaceuticals Inc.; Chiesi Farmaceutici; Forest Research Institute Inc.; GlaxoSmithKline; Grifols Therapeutics Inc.; Ikaria Inc.; Novartis Pharmaceuticals Corporation; Nycomed GmbH; ProterixBio; Regeneron Pharmaceuticals Inc.; Sanofi; Sunovion; Takeda Pharmaceutical Company; and Theravance Biopharma and Mylan. COPDGene is funded by the NHLBI (R01 HL089897 and R01 HL089856) and by the COPD Foundation through contributions made to an Industry Advisory Board composed of AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Novartis, Pfizer, Siemens, and Sunovion.

Dataset Information

HIV Infection Is Associated With Increased Risk for Acute Exacerbation of COPD.

Publications

HIV Infection Is Associated With Increased Risk for Acute Exacerbation of COPD.

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