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Original Research: COPD |

Increased COPD Among HIV-Positive Compared to HIV-Negative Veterans* FREE TO VIEW

Kristina Crothers, MD; Adeel A. Butt, MD, MS; Cynthia L. Gibert, MD; Maria C. Rodriguez-Barradas, MD; Stephen Crystal, PhD; Amy C. Justice, MD, PhD; for the Veterans Aging Cohort 5 Project Team
Author and Funding Information

*From Pulmonary and Critical Care Medicine (Dr. Crothers), Department of Internal Medicine, Yale University School of Medicine, New Haven, CT; Infectious Diseases (Dr. Butt), Department of Internal Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA; the Department of Medicine (Dr. Gibert), George Washington University, Washington DC; Medical Service (Dr. Rodriguez-Barradas), Infectious Diseases, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX; Center on Pharmacotherapy (Dr. Crystal), Chronic Disease Management, and Outcomes, Rutgers University, New Brunswick, NJ; and General Internal Medicine (Dr. Justice), Department of Internal Medicine, Veterans Affairs Connecticut Healthcare System, West Haven, CT.

Correspondence to: Amy C. Justice, MD, PhD, VA Connecticut Healthcare System, 950 Campbell Ave, Mailstop 11-ACSLG, West Haven, CT 06516; e-mail: amy.justice2@va.gov



Chest. 2006;130(5):1326-1333. doi:10.1378/chest.130.5.1326
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Background: Limited data prior to highly active antiretroviral therapy (HAART) suggested the possibility of an increased risk of COPD among those persons with HIV infection. We sought to determine whether HIV infection is associated with increased prevalence of COPD in the era of HAART.

Methods: Prospective observational study of 1,014 HIV-positive and 713 HIV-negative men who were enrolled in the Veterans Aging Cohort 5 Site Study. COPD was determined by patient self-report and International Classification of Diseases, ninth revision (ICD-9), diagnostic codes. Cigarette smoking and injection drug use (IDU) were determined by self-report, and alcohol abuse was determined by ICD-9 diagnostic codes. Laboratory and pharmacy data were obtained from electronic medical records.

Results: The prevalence of COPD as determined by ICD-9 codes was 10% in HIV-positive subjects and 9% in HIV-negative subjects (p = 0.4), and as determined by patient self-report was 15% and 12%, respectively (p = 0.04). After adjusting for age, race/ethnicity, pack-years of smoking, IDU, and alcohol abuse, HIV infection was an independent risk factor for COPD. HIV-infected subjects were approximately 50 to 60% more likely to have COPD than HIV-negative subjects (by ICD-9 codes: odds ratio [OR], 1.47; 95% confidence interval [CI], 1.01 to 2.13; p = 0.04 ; by patient self-report: OR, 1.58; 95% CI, 1.14 to 2.18; p = 0.005).

Conclusions: HIV infection was an independent risk factor for COPD, when determined either by ICD-9 codes or patient self-report. Health-care providers should be aware of the increased likelihood of COPD among their HIV-positive patients. The possibility that HIV infection increases susceptibility to and/or accelerates COPD deserves further investigation and has implications regarding the pathogenesis of COPD.

Figures in this Article

COPD, consisting of pulmonary emphysema and chronic bronchitis, is the fourth leading cause of death worldwide, and is projected to increase further as a cause of morbidity and mortality.12 Yet, COPD continues to be underdiagnosed, and our understanding of risk factors that contribute to COPD is incomplete.23 Although cigarette smoking is the major risk factor, COPD does not develop in all smokers, suggesting that other factors are involved.45

HIV-positive patients may represent a population with increased susceptibility to COPD. Studies67 conducted prior to the widespread availability of highly active antiretroviral therapy (HAART) suggested that HIV infection is associated with pulmonary emphysema. In a study by Diaz and colleagues,6 15% of 114 HIV-positive subjects had radiographic emphysema compared to only 2% of 44 HIV-negative subjects (p = 0.025). Other studies8also conducted prior to HAART indicated that HIV infection may be associated with increased airway hyperresponsiveness. In a study by Poirier and colleagues,930% of HIV-positive smokers had increased bronchial hyperresponsiveness in response to methacholine challenge compared to 13% of HIV-negative smokers (p < 0.05). As bronchial hyperresponsiveness is a risk factor for progressive COPD in smokers,10 these data suggest that an interaction between smoking and HIV infection could accelerate the development of COPD.

Studies have not compared the prevalence of COPD among HIV-positive and HIV-negative patients in the era of HAART. On the one hand, HAART could be protective against COPD in HIV-positive persons, possibly through decreased viral replication and fewer opportunistic infections. On the other hand, the risk of COPD may now be further increased among HIV-positive persons, as patients are living longer while receiving HAART and the prevalence of cigarette smoking is high among HIV-positive populations.11

Thus, we sought to determine whether HIV infection is associated with an increased risk for COPD in the era of HAART. We studied subjects who were enrolled in the Veterans Aging Cohort 5 Site Study (VACS 5), which is a prospective study designed to examine, among other goals, the impact of comorbid conditions on the outcomes of HIV-positive patients. In this analysis, we compared the prevalence and risk factors for COPD in HIV-positive and HIV-negative subjects. Some of these results have been presented previously at the American College of Chest Physicians annual meeting.12

VACS 5 is an observational study of 1,031 HIV-positive and 740 HIV-negative subjects matched for age, race, and site who were enrolled from 2001 to 2002 from the outpatient infectious disease and general medicine clinics at five US Veterans Affairs (VA) medical centers. The institutional review boards approved the study at all locations, and participants provided written informed consent. All consecutive HIV-positive patients were eligible to participate, and the 1,031 HIV-positive subjects enrolled represent 49% of all HIV-positive patients who were seen at the five VA medical centers. HIV-negative subjects were block-matched by age and race categories to the HIV-positive subjects. At study entry, all subjects completed a self-administered questionnaire (available at www.vacohort.org). Additional data sources included electronic medical and pharmacy records, and International Classification of Diseases, ninth revision (ICD-9), diagnostic codes from the national administrative VA database. Because the study included < 3% women, we excluded female subjects from our analysis.

We used two sources to define COPD (ICD-9 diagnostic codes and patient self-report) and conducted parallel analyses using these two independent measures. We determined the prevalence of COPD using ICD-9 codes in the 5 years prior to study enrollment. Used previously in other studies to define COPD,13these codes include diagnoses for bronchitis (490), chronic bronchitis (491), emphysema (492), and chronic airway obstruction not otherwise specified (496). Asthma-related codes (493) were not included in this definition of COPD. Inpatient codes had to occur at least once and outpatient codes at least twice, as this improves the accuracy of ICD-9 codes when compared to other sources of clinical data.14However, while highly specific (94%), we have found that ICD-9 codes for the diagnosis of chronic obstructive lung disease (ie, COPD and asthma) are not very sensitive (52%) when compared to the diagnosis of chronic obstructive lung disease documented in health-care provider progress notes, which were obtained by standardized chart review.15

Thus, because we suspected that many providers of health care for patients with HIV may be unaware of their patients’ COPD, we also determined the prevalence of COPD using patient self-report. From the baseline questionnaire, we analyzed subject responses to the question of whether a doctor had ever told them they had “chronic lung disease (emphysema, asthma, chronic bronchitis, or chronic obstructive lung disease).” This item was used previously in the VA 1999 Large Health Survey of Veteran Enrollees.16

Smoking status was based on self-report.17Current smokers were those who reported the current or any use of cigarettes within the last 4 weeks, and former smokers were those who had quit > 4 weeks ago. Subjects were asked how many cigarettes they had smoked per day and for how many years. The number of cigarettes smoked per day was truncated at four or more packs, and the number of years of smoking was truncated such that individuals were ≥ 10 years old when starting to smoke. In addition, subjects were asked about “cough or trouble catching your breath” as part of a validated symptom index, which was scored on a 4-point Likert scale.18 If the symptom was present, bothersome cough/dyspnea corresponded to a score of ≥ 3 on the Likert scale.

From the questionnaire, subjects were classified as injection drug users if they had ever used injection drugs or if their HIV risk factor was injection drug use (IDU). Using ICD-9 codes, we determined a history of alcohol abuse, bacterial pneumonia, Pneumocystis jirovecii pneumonia (PCP), and tuberculosis. Laboratory data at study enrollment were obtained through the electronic medical record. The use of HAART was determined from electronic pharmacy records.

Parallel analyses were conducted using either ICD-9 codes or patient self-report of COPD as our primary outcome. We used standard parametric and nonparametric methods to conduct descriptive analyses. We used logistic regression to determine the impact of HIV status on the risk of COPD. Multivariate models were adjusted for age, race/ethnicity, alcohol abuse, IDU, and number of pack-years of smoking. Age and pack-years were expressed per 10 years. We imputed the values for the number of pack-years of smoking in HIV-positive and HIV-negative current and former smokers for whom these data were missing (n = 74 or 6% of smokers), using the mean number of pack-years of smoking for each group. Results were unchanged when subjects with imputed values were included.

We also generated a logistic regression model exploring the factors associated with COPD in HIV-positive subjects alone. In addition to adjusting for age, race/ethnicity, alcohol abuse, IDU, and number of pack-years of smoking as described above, we also adjusted for a history of bacterial pneumonia and CD4+ T-cell counts, as these varied in HIV-positive subjects with and without COPD. We included HAART use in the model as an important predictor of interest, although neither HAART use nor HIV viral load had significant univariate associations with COPD. The square root of the CD4+ T-cell count was used to approximate a normal distribution, and the change in CD4+ T-cell count was expressed per 50 cells.

All analyses were performed using a statistical software package (Stata, version 9.1; StataCorp; College Station, TX). A p value of ≤ 0.05 was considered to be statistically significant.

We excluded female subjects (n = 42) and those subjects without a known smoking status (n = 2). Thus, 1,727 of 1,771 subjects (98%) who were enrolled in VACS 5 were included in the analytic sample.

HIV-Positive and HIV-Negative Subjects Enrolled in VACS 5

Compared to the HIV-negative subjects, HIV-positive subjects were significantly younger and more likely to be black (Table 1 ). The prevalence of cigarette smoking was equally high in both groups; however, HIV-positive subjects were significantly more likely to be current smokers than HIV-negative subjects (HIV-positive subjects, 46%; HIV-negative subjects, 36%; p < 0.001). HIV-positive smokers had significantly fewer pack-years of smoking than their HIV-negative counterparts. A history of IDU was more common in HIV-positive subjects than in HIV-negative subjects (31% vs 12%, respectively; p < 0.001). HIV-positive subjects were also more likely to have a history of alcohol abuse (24% vs 18%, respectively; p = 0.001).

The prevalence of COPD by ICD-9 codes was 10% in HIV-positive subjects and 9% in HIV-negative subjects (p = 0.4 [by univariate analysis]). The prevalence of COPD by patient self-report was slightly higher (HIV-positive subjects, 15%; HIV-negative subjects, 12%; p = 0.04). The prevalence of COPD by either measure increased significantly for both HIV-positive and HIV-negative subjects when stratified according to increasing pack-years of smoking and age (Fig 1 ).

HIV-Positive Subjects With and Without COPD

Next, we compared the characteristics of HIV-positive subjects with and without COPD. Regardless of the method used to identify COPD, HIV-positive subjects with COPD were significantly older, had smoked more, and were more likely to have IDU and a history of bacterial pneumonia than their HIV-positive counterparts without COPD (Table 2 ). HIV-positive subjects with COPD, as determined by ICD-9 codes, were more likely to have received a diagnosis of alcohol abuse (p = 0.005), but this association was not significant when comparing HIV-positive subjects with and without self-reported COPD.

We determined whether the degree of immunodeficiency and level of the HIV suppression differed in HIV-positive subjects with and without COPD. In those subjects with COPD diagnosed by ICD-9 codes, the median CD4 count was significantly lower compared to subjects without COPD (269 vs 376 cells/μL, respectively; p = 0.002). However, there was no significant difference in CD4 counts when comparing them in HIV-positive subjects with and without COPD by self-report (335 vs 372 cells/μL, respectively; p = 0.1). There were no differences in HIV viral load or use of HAART between groups using either measure of COPD.

Predictors of COPD among HIV-Positive and HIV-Negative Subjects

HIV infection was an independent risk factor for COPD after adjusting for age, race/ethnicity, pack-years of smoking, IDU, and alcohol abuse (Table 3 ). Using multivariate logistic regression, HIV-positive subjects were nearly 50% more likely to have received a diagnosis of COPD by ICD-9 codes compared to HIV-negative subjects (odds ratio [OR], 1.47; 95% confidence interval [CI], 1.01 to 2.13; p = 0.04). They were approximately 60% more likely to have a diagnosis of COPD by patient self-report (OR, 1.58; 95% CI, 1.14 to 2.19; p = 0.005).

ORs for other predictors of COPD were increased or decreased in a consistent direction when comparing the two models (Table 3). The number of pack-years of smoking and alcohol abuse were strongly associated with the occurrence of COPD in both models (p ≤ 0.01). Increasing age was also significantly associated with COPD determined by ICD-9 codes (p ≤ 0.001) and tended to be associated with COPD by patient self-report (p = 0.06). Black subjects were less likely to have COPD determined by patient self-report only (p = 0.005). IDU was significantly associated with COPD by patient self-report (p = 0.008) and also tended to be associated with COPD by ICD-9 codes (p = 0.06).

Predictors of COPD Among HIV-Positive Subjects

In addition, we generated a logistic regression model to examine the predictors of COPD among HIV-positive subjects only, adjusting for age, race/ethnicity, pack-years of smoking, IDU, and alcohol abuse, as well as history of bacterial pneumonia, CD4+ T-cell count, and the use of HAART (Table 4 ). Pack-years of smoking, IDU, and bacterial pneumonia were all significantly associated with COPD using either method of COPD diagnosis (all p < 0.05). Age was significantly associated with COPD determined by ICD-9 codes only (p = 0.02). In terms of HIV-associated variables, COPD determined by ICD-9 codes was less likely with higher CD4+ T-cell counts (p = 0.047). However, while the OR was also decreased, this association was not significant for COPD determined by patient self-report. The use of HAART was not associated with COPD in either model.

In this study, we found that HIV infection was an independent risk factor for COPD in the present HAART era. Although the prevalence of COPD was not significantly different in HIV-positive and HIV-negative subjects by univariate analysis, the HIV-positive subjects were significantly younger and had smoked fewer pack-years of cigarettes than the HIV-negative subjects. Both of these factors would be expected to decrease the likelihood of COPD in the HIV-positive group. However, after we adjusted for known risk factors of COPD and measured differences between HIV-positive and HIV-negative subjects, namely, age, race/ethnicity, pack-years of smoking, IDU, and alcohol abuse, we found that HIV-positive subjects were actually 50 to 60% more likely to have COPD compared to HIV-negative subjects. This increased risk among HIV-positive subjects was consistent across the two different COPD models, using two independent measures for the diagnosis of COPD.

In both HIV-positive and HIV-negative subjects, the risk for COPD increased according to age and the number of pack-years of cigarettes smoked. Additional factors associated with COPD in one or both multivariate models were a history of alcohol abuse and IDU, whereas black subjects appeared to be less likely to have COPD. These findings are consistent with those of previous studies,1920 although earlier reports2122 of the interaction of alcohol with COPD have been conflicting. Our data suggest that HIV-positive patients may be more susceptible to COPD, given the increased likelihood of COPD in HIV-infected subjects after adjusting for other known risk factors.

Among HIV-positive subjects, predictors significantly associated with COPD by either method of diagnosis were number of pack-years of smoking, IDU, and a history of bacterial pneumonia. Whether the association of COPD with bacterial pneumonia is related in part to the development of airway obstruction following pneumonia, as has been previously described,23 or to the fact that subjects with preexisting COPD are at increased risk for bacterial pneumonia is not clear from this analysis, as we cannot be certain when COPD first developed. In terms of other findings, increasing age was significantly associated with COPD only by ICD-9 codes. The association of alcohol abuse with COPD was not significant among HIV-positive individuals after CD4+ T-cell counts and HAART were entered into the model (data not otherwise shown). Interestingly, subjects with higher CD4+ T-cell counts were significantly less likely to have COPD by ICD-9 codes, although this finding was not significant for determination of COPD by patient self-report. The reasons for this finding are not entirely clear, but raise questions about the role of immune system incompetence in the development and/or progression of COPD and require further study.

The mechanisms by which HIV infection may increase the risk of COPD are unknown. HIV infection can result in the intense infiltration into the lung of CD8+ T cells,24which have been shown to secrete large amounts of interferon (IFN)-γ.25While it is unclear whether this lymphocytic alveolitis and expression of IFN-γ play any role in the development of COPD in HIV-positive persons, the overexpression of IFN-γ has been shown to cause emphysema in animal models.26 It is also uncertain whether the degree of HIV-related immunodeficiency and the use of HAART impact the development of COPD.

Additionally, episodes of clinical pneumonia or colonization with respiratory organisms may contribute to airway obstruction,23,2728 which may be of particular relevance to the pathogenesis of COPD in immunosuppressed persons with HIV disease. For example, a history of bacterial pneumonia or PCP has been associated with significant expiratory airflow limitation in subjects with HIV infection.23 In addition, colonization with Pneumocystis jirovecii, the organism that is responsible for human PCP, has been associated with the presence and severity of COPD in HIV-negative patients.,29P jirovecii has also been identified in the sputum of asymptomatic HIV-negative patients with chronic bronchitis30and has been detected with higher frequency in HIV-positive smokers compared to nonsmokers in the absence of active PCP.31Further, chronic viral infections such as those with adenovirus are thought to be involved in the pathogenesis of COPD.32 Although we observed that HIV-positive subjects with COPD were more likely to have had bacterial pneumonia and did not observe an association with PCP, no conclusions regarding causality can be drawn from this study.

Our study has certain limitations. Our study consisted of male veterans, and the results may not be applicable to all populations, despite an equally high prevalence of smoking in other studies of HIV-infected nonveterans.11,33 Similar to other epidemiologic studies, our definition of COPD was based on patient self-report or ICD-9 codes and was not based on spirometry. In order to address this limitation, we used two independent methods to diagnose COPD. The consistency of our findings using these two independent measures for determining COPD strengthens the validity of our results. Further, data from other epidemiologic studies3,20,3438 support that we are more likely to underestimate than to overestimate the prevalence of COPD by either of these measures. For example, in the Third National Health and Nutrition Examination Survey,34 12% of white participants who were > 45 years of age had undiagnosed airway obstruction detected on spirometry, whereas only 3.1% self-reported COPD and 2.7% self-reported asthma. Other studies3638 have likewise shown that the diagnosis of COPD is underestimated when using administrative data compared to chart extraction. We have also found that the diagnosis of chronic obstructive lung disease (ie, COPD and asthma) by ICD-9 codes is accurate but underestimates cases when compared to standardized chart extraction documenting the diagnosis of chronic obstructive lung disease according to provider progress notes in our review of HIV-positive subjects enrolled in the Veterans Aging Cohort Study 3 Site Study (specificity 94%, sensitivity 52%).,15

The associations identified in this observational study do not prove a causal relationship between HIV infection and COPD. Although a number of statistical controls were utilized, and we adjusted for factors known to be associated with COPD and for measured differences between HIV-positive and HIV-negative subjects, we cannot exclude the possibility that the differential risk is the result of unmeasured differences in the two populations rather than being a direct causal effect of HIV infection. For example, we did not identify occupational or environmental exposures that may contribute to COPD. As all subjects were veterans, however, it is unlikely that HIV-positive veterans were preferentially exposed to substances that might contribute to COPD compared to HIV-negative veterans. Furthermore, we had insufficient data to determine the association of the smoking of nontobacco products such as marijuana with COPD. As marijuana smoking has been associated with symptoms of chronic bronchitis,39 further investigation in this area is required. Finally, we cannot conclude whether HIV infection is associated with a particular subtype of COPD or completely rule out an association with asthma.

Nonetheless, our results suggest the importance of a closer examination of the relationship between HIV infection and COPD, and the role of additional risk factors and mediating variables in this relationship. HIV-positive patients are experiencing increased noninfectious complications and comorbid illnesses as survival has improved among those receiving HAART.40Cigarette smoking is associated with a substantially increased risk of COPD among HIV-positive patients, and current smoking is associated with significantly increased mortality and decreased quality of life.41 Given the high prevalence of cigarette smoking among HIV-positive persons in our study and in others,11 combined with these data demonstrating an apparent increased risk for COPD conferred by HIV infection, COPD is likely to contribute substantially to the morbidity and mortality of HIV-positive patients in the era of HAART.

Our findings suggest that increased awareness of COPD among providers of HIV-positive patients is warranted and that HIV-infected persons may be a high-risk group that might benefit from screening spirometry. While the National Lung Health Program calls for spirometry in smokers over the age of 45 years and in any patients with respiratory symptoms,42 further studies are required to identify high-risk populations.2,4243 Earlier identification of COPD is important, as undiagnosed airway obstruction is associated with impaired health and functional status,34 and the appropriate management of COPD is associated with health benefits, such as decreased symptoms and COPD exacerbations, and with improved smoking cessation, exercise capacity, and quality of life.42,4447

In conclusion, we found that HIV infection is an independent risk factor for COPD, when determined by either ICD-9 codes or by patient self-report, after adjusting for age, race/ethnicity, number of pack-years of smoking, IDU, and alcohol abuse in a cohort of male veterans in the HAART era. Providers should be aware of the likelihood of increased COPD among their HIV-positive patients. The possibility that HIV infection increases susceptibility to and/or accelerates COPD deserves further investigation, and has implications regarding the pathogenesis of COPD in HIV-positive as well as HIV-negative persons.

Abbreviations: CI = confidence interval; HAART = highly active antiretroviral therapy; ICD-9 = International Classification of Diseases, ninth revision; IDU = injection drug use; IFN = interferon; OR = odds ratio; PCP = Pneumocystis jirovecii pneumonia; VA = Veterans Affairs; VACS 5 = Veterans Aging Cohort 5 Site Study

Data for this study were collected from subjects enrolled in VACS 5 at five Veterans Affairs Medical Centers in the United States (Atlanta, the Bronx, Houston, Los Angeles, and Manhattan). Data were analyzed at the coordinating center at the West Haven Veterans Affairs Medical Center, West Haven, CT.

This research was supported by National Institutes of Health/National Center for Research Resources grant K12 RR0117594-01 (to K.C.), National Institute on Alcohol Abuse and Alcoholism grant 3U01 AA 13566, National Institute on Aging (NIA) grant K23 AG00826, a Robert Wood Johnson Generalist Faculty Scholar Award, and an Interagency Agreement among NIA, National Institute of Mental Health, and Veterans Health Affairs (to A.C.J.).

The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Table Graphic Jump Location
Table 1. Characteristics of HIV-Positive and HIV-Negative Subjects in VACS 5
* 

Values are given as the median (interquartile range).

Figure Jump LinkFigure 1. Prevalence of COPD among HIV-positive and HIV-negative subjects stratified by number of pack-years of smoking or age. Left top and bottom, A: the prevalence of COPD as diagnosed by ICD-9 codes. Right top and bottom, B: the prevalence of COPD as diagnosed by patient self-report. The p values are given for the likelihood of COPD in HIV-positive subjects vs HIV-negative subjects adjusted for either age or smoking group. HIV+ = HIV-positive; HIV− = HIV-negative.Grahic Jump Location
Table Graphic Jump Location
Table 2. Characteristics of HIV-Positive Subjects With and Without COPD
* 

Values are given as the median (interquartile range).

Table Graphic Jump Location
Table 3. Predictors of COPD in HIV-Positive and HIV-Negative Subjects*
* 

Values are given as the OR (95% CI).

 

Significant at p ≤ 0.05.

Table Graphic Jump Location
Table 4. Predictors of COPD in HIV-Positive Subjects*
* 

Values are given as the OR (95% CI).

 

Significant at p ≤ 0.05.

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Kieszak, SM, Flanders, WD, Kosinski, AS, et al A comparison of the Charlson comorbidity index derived from medical record data and administrative billing data.J Clin Epidemiol1999;52,137-142. [CrossRef] [PubMed]
 
Quan, H, Parsons, GA, Ghali, WA Validity of information on comorbidity derived from ICD-9-CCM administrative data.Med Care2002;40,675-685. [CrossRef] [PubMed]
 
Wilchesky, M, Tamblyn, RM, Huang, A Validation of diagnostic codes within medical services claims.J Clin Epidemiol2004;57,131-141. [CrossRef] [PubMed]
 
Moore, BA, Augustson, EM, Moser, RP, et al Respiratory effects of marijuana and tobacco use in a U.S. sample.J Gen Intern Med2005;20,33-37. [CrossRef] [PubMed]
 
Justice, AC, Landefeld, CS, Asch, SM, et al Justification for a new cohort study of people aging with and without HIV infection.J Clin Epidemiol2001;54(suppl),S3-S8
 
Crothers, K, Griffith, TA, McGinnis, KA, et al The impact of cigarette smoking on mortality, quality of life, and comorbid illness among HIV-positive veterans.J Gen Intern Med2005;20,1142-1145. [CrossRef] [PubMed]
 
Ferguson, GT, Enright, PL, Buist, AS, et al Office spirometry for lung health assessment in adults: a consensus statement from the National Lung Health Education Program.Chest2000;117,1146-1161. [CrossRef] [PubMed]
 
Petty, TL, Weinmann, GG Building a national strategy for the prevention and management of and research in chronic obstructive pulmonary disease: national Heart, Lung, and Blood Institute Workshop Summary. Bethesda, Maryland, August 29–31, 1995.JAMA1997;277,246-253. [CrossRef] [PubMed]
 
Gorecka, D, Bednarek, M, Nowinski, A, et al Diagnosis of airflow limitation combined with smoking cessation advice increases stop-smoking rate.Chest2003;123,1916-1923. [CrossRef] [PubMed]
 
Rennard, SI Treatment of stable chronic obstructive pulmonary disease.Lancet2004;364,791-802. [CrossRef] [PubMed]
 
Sin, DD, McAlister, FA, Man, SF, et al Contemporary management of chronic obstructive pulmonary disease: scientific review.JAMA2003;290,2301-2312. [CrossRef] [PubMed]
 
Tomas, LH, Varkey, B Improving health-related quality of life in chronic obstructive pulmonary disease.Curr Opin Pulm Med2004;10,120-127. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1. Prevalence of COPD among HIV-positive and HIV-negative subjects stratified by number of pack-years of smoking or age. Left top and bottom, A: the prevalence of COPD as diagnosed by ICD-9 codes. Right top and bottom, B: the prevalence of COPD as diagnosed by patient self-report. The p values are given for the likelihood of COPD in HIV-positive subjects vs HIV-negative subjects adjusted for either age or smoking group. HIV+ = HIV-positive; HIV− = HIV-negative.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1. Characteristics of HIV-Positive and HIV-Negative Subjects in VACS 5
* 

Values are given as the median (interquartile range).

Table Graphic Jump Location
Table 2. Characteristics of HIV-Positive Subjects With and Without COPD
* 

Values are given as the median (interquartile range).

Table Graphic Jump Location
Table 3. Predictors of COPD in HIV-Positive and HIV-Negative Subjects*
* 

Values are given as the OR (95% CI).

 

Significant at p ≤ 0.05.

Table Graphic Jump Location
Table 4. Predictors of COPD in HIV-Positive Subjects*
* 

Values are given as the OR (95% CI).

 

Significant at p ≤ 0.05.

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Quan, H, Parsons, GA, Ghali, WA Validity of information on comorbidity derived from ICD-9-CCM administrative data.Med Care2002;40,675-685. [CrossRef] [PubMed]
 
Wilchesky, M, Tamblyn, RM, Huang, A Validation of diagnostic codes within medical services claims.J Clin Epidemiol2004;57,131-141. [CrossRef] [PubMed]
 
Moore, BA, Augustson, EM, Moser, RP, et al Respiratory effects of marijuana and tobacco use in a U.S. sample.J Gen Intern Med2005;20,33-37. [CrossRef] [PubMed]
 
Justice, AC, Landefeld, CS, Asch, SM, et al Justification for a new cohort study of people aging with and without HIV infection.J Clin Epidemiol2001;54(suppl),S3-S8
 
Crothers, K, Griffith, TA, McGinnis, KA, et al The impact of cigarette smoking on mortality, quality of life, and comorbid illness among HIV-positive veterans.J Gen Intern Med2005;20,1142-1145. [CrossRef] [PubMed]
 
Ferguson, GT, Enright, PL, Buist, AS, et al Office spirometry for lung health assessment in adults: a consensus statement from the National Lung Health Education Program.Chest2000;117,1146-1161. [CrossRef] [PubMed]
 
Petty, TL, Weinmann, GG Building a national strategy for the prevention and management of and research in chronic obstructive pulmonary disease: national Heart, Lung, and Blood Institute Workshop Summary. Bethesda, Maryland, August 29–31, 1995.JAMA1997;277,246-253. [CrossRef] [PubMed]
 
Gorecka, D, Bednarek, M, Nowinski, A, et al Diagnosis of airflow limitation combined with smoking cessation advice increases stop-smoking rate.Chest2003;123,1916-1923. [CrossRef] [PubMed]
 
Rennard, SI Treatment of stable chronic obstructive pulmonary disease.Lancet2004;364,791-802. [CrossRef] [PubMed]
 
Sin, DD, McAlister, FA, Man, SF, et al Contemporary management of chronic obstructive pulmonary disease: scientific review.JAMA2003;290,2301-2312. [CrossRef] [PubMed]
 
Tomas, LH, Varkey, B Improving health-related quality of life in chronic obstructive pulmonary disease.Curr Opin Pulm Med2004;10,120-127. [CrossRef] [PubMed]
 
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