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Original Research: COPD |

The Association of Weight With the Detection of Airflow Obstruction and Inhaled Treatment Among Patients With a Clinical Diagnosis of COPDBMI, Airflow Obstruction, Inhaled Therapy in COPD FREE TO VIEW

Bridget F. Collins, MD; David Ramenofsky, MD; David H. Au, MD; Jun Ma, MD, PhD; Jane E. Uman, MPH; Laura C. Feemster, MD
Author and Funding Information

From Health Services Research and Development (Drs Collins, Au, and Feemster and Ms Uman), Department of Veterans Affairs, Seattle, WA; Division of Pulmonary and Critical Care (Drs Collins, Ramenofsky, Au, and Feemster), Department of Medicine, University of Washington, Seattle, WA; and Department of Health Services Research (Dr Ma), Palo Alto Medical Foundation Research Institute, and Stanford Prevention Research Center (Dr Ma), Stanford University School of Medicine, Palo Alto, CA.

CORRESPONDENCE TO: Bridget F. Collins, MD, Health Services Research and Development, Department of Veterans Affairs, Puget Sound Health Care System, 1100 Olive Way, Ste 1400, Seattle, WA 98101; e-mail: bfc3@uw.edu


FOR EDITORIAL COMMENT SEE PAGE 1426

Part of this article has been presented in thematic poster form at the American Thoracic Society International Conference, May 17-20, 2013, Philadelphia, PA.

FUNDING/SUPPORT: This study was funded by an American Lung Association Career Investigator Award [CI-51755N]. Dr Collins is supported by the National Institutes of Health (NIH) [Training Grant T32-HL-007287]. Dr Au is supported by the Department of Veterans Affairs, Health Services Research and Development. Dr Ma is supported through internal funding from the Palo Alto Medical Foundation Research Institute. Dr Feemster was previously supported by the Department of Veterans Affairs, Health Services Research and Development, and is currently funded by an NIH National Heart, Lung, and Blood Institute K23 Mentored Career Development Award.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;146(6):1513-1520. doi:10.1378/chest.13-2759
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BACKGROUND:  Most patients with a clinical diagnosis of COPD have not had spirometry to confirm airflow obstruction (AFO). Overweight and obese patients report more dyspnea than normal weight patients, which may be falsely attributed to AFO. We sought to determine whether overweight and obese patients who received a clinical diagnosis of COPD were more likely to receive a misdiagnosis (ie, lack of AFO on spirometry) and be subsequently treated with inhaled medications.

METHODS:  The cohort comprised US veterans with COPD (International Classification of Diseases, 9th Revision, code; inhaled medication use; or both) and spirometry measurements from one of three Pacific Northwest Veterans Administration Medical Centers. The measured exposures were overweight and obesity (defined by BMI categories). Outcomes were (1) AFO on spirometry and (2) escalation or deescalation of inhaled therapies from 3 months before spirometry to 9 to 12 months after spirometry. We used multivariable logistic regression with calculation of adjusted proportions for all analyses.

RESULTS:  Fifty-two percent of 5,493 veterans who had received a clinical diagnosis of COPD had AFO. The adjusted proportion of patients with AFO decreased as BMI increased (P < .01 for trend). Among patients without AFO, those who were overweight and obese were less likely to remain off medications or to have therapy deescalated (adjusted proportions: normal weight, 0.69 [95% CI, 0.64-0.73]; overweight, 0.62 [95% CI, 0.58-0.65; P = .014]; obese, 0.60 [95% CI, 0.57-0.63; P = .001]).

CONCLUSIONS:  Overweight and obese patients are more likely to be given a misdiagnosis of COPD and not have their inhaled medications deescalated after spirometry demonstrated no AFO. Providers may be missing potential opportunities to recognize and treat other causes of dyspnea in these patients.

Figures in this Article

COPD and obesity are common and frequently coexisting conditions of increasing prevalence.1,2 Obese patients with COPD have greater symptom burden and receive more inhaled medications for any severity of airflow limitation.3 In general, obese patients are more likely than patients who are normal weight to report dyspnea, highlighting the difficulty in attributing symptoms of dyspnea to airflow obstruction (AFO) or to obesity and deconditioning.4 Despite this challenge, primary care clinicians report feeling comfortable diagnosing and treating patients with COPD based on history and examination alone, in the absence of confirmatory spirometry.5,6 Spirometry is recognized as the gold standard in the diagnosis of COPD,68 yet only one-third of patients with COPD have had spirometry in the 2 years prior to and within 6 months after diagnosis.8,9 Diagnosis of COPD without spirometry may increase the possibility of misclassification and mistreatment, particularly among patients who have more than one etiology for dyspnea.

Our goal was to assess whether in patients with clinically diagnosed COPD obesity is associated with a misdiagnosis defined as an absence of AFO on spirometry. Among such patients without AFO, we assessed whether obese patients were more likely than patients who are normal weight to receive potential inappropriate treatment defined as inhaled medications prescribed in the absence of AFO.

Study Design, Setting, and Subjects

This study was a secondary analysis of data collected from a cohort of US veterans from three Pacific Northwest Veterans Administration (VA) medical centers who received a clinical diagnosis of COPD and who had subsequent spirometry performed between January 2003 and December 2007. The index date was defined as the date of first spirometry within the study time period, and patients were subsequently followed for 2 years; the censoring date was January 1, 2009. Clinical diagnosis of COPD was defined by meeting at least one of the four criteria shown in Figure 1 and in e-Appendix 1. Exclusion criteria are also shown in Figure 1 and included in e-Appendix 1. Importantly, we excluded veterans with clinically diagnosed asthma (International Classification of Diseases, 9th Revision, codes 493.0, 493.1, 493.8, 493.9) to avoid potential misclassification. The institutional review board of the VA Puget Sound Healthcare System approved all protocols as well as a waiver of patient consent for this study (IRB project approval number 01386).

Figure Jump LinkFigure 1 –  Cohort formation. ICD.9 = International Classification of Diseases, 9th Revision.Grahic Jump Location
Data Collection

Data were collected from the VISN (Veterans Integrated Service Networks) 20 data warehouse, a relational database that includes data (clinical and nonclinical) for all patients receiving care at VA facilities throughout the Pacific Northwest. Spirometric measurements were obtained from the data warehouse or directly from the spirometer.

Exposures

BMI categories were as defined by the World Health Organization: (1) normal weight, 18.5 ≤ BMI < 25.0 kg/m2; (2) overweight, 25.0 ≤ BMI < 30.0 kg/m2; (3) class I obesity, 30.0 ≤ BMI < 35.0 kg/m2; (4) class II obesity, 35.0 ≤ BMI < 40.0 kg/m2; or (5) class III obesity, BMI ≥ 40.0 kg/m2.10 For analyses of medication changes following spirometry, classes I to III obesity were collapsed into a single category of BMI ≥ 30.0 kg/m2.

Outcomes

AFO was defined as a postbronchodilator value of FEV1/FVC below the lower limit of normal (LLN).11 Additional details are provided in e-Appendix 1. All analyses were done using the GOLD (Global Initiative for Chronic Obstructive Lung Disease) definition of AFO (FEV1/FVC < 70%).7

Among patients with COPD but no AFO, we examined whether inhaled medications were escalated or deescalated in the 9 to 12 months after the index date compared with the 3 months prior to the index date. Medication dispensation data were available for inhaled corticosteroids, long-acting β-agonists, ipratropium bromide, and short-acting β-agonists. Data on tiotropium use data were not collected because of the limited use of this medication within the VA during the study period.

Medication data were examined in 3-month blocks. Initial medication dispensation was in the 3 months prior to the index date. Therapeutic escalation or deescalation at 9 to 12 months after the index date was defined as stepping up or down by any degree within four levels defined as no medication, short-acting medication only, one long-acting medication, or two long-acting medications.

Statistical Analysis

We used multivariable logistic regression and calculated adjusted proportions using mean values for all covariates. Potential confounding covariates were added to models en bloc (e-Appendix 1) and were retained in the final models if P ≤ .10. We performed additional sensitivity analyses that excluded 494 patients who entered the cohort based only on inhaled medication use to address the possibility that some of these patients may have been empirically treated for asthma not COPD. Finally, because postbronchodilator spirometry is needed to demonstrate incompletely reversible AFO among patients with COPD, we performed a sensitivity analysis restricting the cohort to patients who had a postbronchodilator FEV1/FVC ratio available (n = 4,634).

Description of the Cohort

A total of 14,541 veterans had spirometry at one of three Pacific Northwest VA hospitals during the study period. Of those, 3,967 met exclusion criteria. Of the remaining 10,574 patients, 5,493 met inclusion criteria and made up the final cohort (Fig 1).

Patients were mostly older white men (Table 1). Of the 5,493 patients in the cohort, approximately 25% were normal weight, 35% were overweight, 23% had class I obesity, 10% had class II obesity, and 7% had class III obesity. Patients with a higher BMI were younger and less likely to have smoked in the year prior to the index date. The prevalence of comorbidities, such as sleep apnea, hypertension, and diabetes, was greater among patients with higher BMIs (Table 1).

Table Graphic Jump Location
TABLE 1 ]  Baseline Characteristics

Data are presented as mean ± SD or %. Normal weight, 18.5 ≤ BMI < 25 kg/m2; overweight, 25 ≤ BMI < 30 kg/m2; class I obesity, 30 ≤ BMI < 35 kg/m2; class II obesity, 35 ≤ BMI < 40 kg/m2; and class III obesity, BMI ≥ 40 kg/m2. ACS = acute coronary syndrome; AFO = airflow obstruction; CHF = congestive heart failure; HTN = hypertension; LLN = lower limit of normal.

Proportion of Veterans With a Clinical Diagnosis of COPD and AFO by BMI Class

The adjusted proportion of patients with AFO (defined by LLN criteria) detected by spirometry decreased with each level of obesity (P < .01 for trend) (Table 2). These results were robust when adjusted for age, smoking status in the prior year, white race, comorbidities, oral steroid use in the prior year, and site of care. The adjusted proportion of patients with AFO who were normal weight was 0.64 (0.61-0.66) compared with 0.53 (0.50-0.55, P ≤ .001) among overweight patients, 0.44 (0.41-0.47, P ≤ .001) among patients with class I obesity, 0.41 (0.37-0.46, P ≤ .001) among patients with class II obesity, and 0.37 (0.32-0.43, P ≤ .001) among patients with class III obesity (Table 2). Using the GOLD definition of airflow limitation produced similar results (data not shown).

Table Graphic Jump Location
TABLE 2 ]  Adjusted Proportion of Veterans With COPD With AFO (Defined by LLN) on Subsequent Spirometry

See Table 1 legend for expansion of abbreviations.

a 

Normal weight (18.5 ≤ BMI < 25 kg/m2), overweight (25 ≤ BMI < 30 kg/m2), class I obesity (30 ≤ BMI < 35 kg/m2), class II obesity (35 ≤ BMI < 40 kg/m2), class III obesity (BMI ≥ 40 kg/m2).

b 

Adjusted for mean values of age, smoking status in prior year, white race, comorbidities in the prior year (CHF, hypertension, depression, diabetes, sleep apnea), use of oral steroids in the prior year, and site of care.

c 

P < .001 for trend.

Medication Escalation and Deescalation After Spirometry Showed No AFO

Of the 2,680 patients who did not have evidence of AFO by spirometry (LLN), 53% were prescribed one or more inhaled medications during the 3-months prior to spirometry (Table 3). As seen in Table 3, overweight and obese patients were more likely than normal weight patients to be on an inhaled medication prior to spirometry. Similarly, 9 to 12 months after spirometry, 41% of patients without AFO were on an inhaled medication, with more frequent prescription in overweight and obese patients.

Table Graphic Jump Location
TABLE 3 ]  Percentage of Patients Without AFO on Inhaled Medications Before and After the Index Date

Data are presented as %. Normal weight, 18.5 ≤ BMI < 25 kg/m2; overweight, 25 ≤ BMI < 30 kg/m2; obese, BMI ≥ 30 kg/m2. See Table 1 legend for expansion of abbreviation.

We assessed deescalation of inhaled medication therapy and whether patients who did not have AFO remained off these medications. Overweight and obese patients were significantly less likely to experience deescalation of therapy or remain off therapy than were normal weight patients (P < .01 for trend) (Tables 4, 5). At the same time, overweight and obese patients were more likely to remain on maximal therapy or have intensification of treatment than were normal weight patients (P = .09 for trend) (Tables 4, 5). e-Figure 1 shows escalation and deescalation patterns for specific medication categories among all patients without AFO.

Table Graphic Jump Location
TABLE 4 ]  Adjusted Proportion of Misdiagnosed Veterans (by BMI Class) Who Had Changes in Medication Regimen Between 3 Mo Prior to and 9 to 12 Mo After Spirometry: Model 1

Model 1 had deescalation in therapy or remained off therapy.

a 

Normal weight (18.5 ≤ BMI < 25 kg/m2), overweight (25 ≤ BMI < 30 kg/m2), and obese (BMI ≥ 30 kg/m2).

b 

Adjusted for mean values of white race, acute coronary syndrome in the prior year, oral steroid use in the prior year, and site of care. P = .003 for trend.

Table Graphic Jump Location
TABLE 5 ]  Adjusted Proportion of Misdiagnosed Veterans (by BMI Class) Who Had Changes in Medication Regimen Between 3 Mo Prior to and 9 to 12 Mo After Spirometry: Model 2

Model 2 had escalation in therapy or stayed on maximal therapy.

a 

Normal weight (18.5 ≤ BMI < 25 kg/m2), overweight (25 ≤ BMI < 30 kg/m2), and obese (BMI ≥ 30 kg/m2).

b 

Adjusted for mean values of oral steroid use in the prior year and site of care. P = .09 for trend.

Sensitivity Analyses

We repeated the analyses in a subset of 4,999 patients who entered the cohort based on an International Classification of Diseases, 9th Revision, COPD codes (inclusion criteria 1-3 [e-Appendix 1]). Results were similar to those described previously (e-Appendix 1, e-Tables 1, 2). Excluding the 859 patients who did not have postbronchodilator spirometry values, we found similar results (e-Tables 3, 4), with overweight and obese patients less likely to have AFO on subsequent spirometry and less likely to deescalate or remain off therapy in its absence. Overweight patients remained more likely to escalate or stay on maximal therapy despite a lack of AFO, although the association between obese patients and escalation of therapy no longer persisted.

We demonstrate that overweight and obese patients were more likely than normal weight patients to receive a misdiagnosis of COPD and more likely to be inappropriately treated with inhaled medications. This study is the first, to our knowledge, to show a dose-response relationship between BMI and COPD misdiagnosis. COPD and obesity are already associated with substantial economic costs, which will increase as the incidence of COPD and obesity continue to rise.12,13 Treating individuals who do not truly have COPD with costly medications that may be ineffective or potentially harmful could result in lower quality of care for this patient population at an increased expense. As the prevalence of both obesity and COPD increase, substantial financial resources expended for such care have negative implications for patients and health-care payers.

Accurate diagnosis of COPD is crucial to the delivery of efficient, cost-effective, and high-quality medical care. Although spirometry is considered the gold standard for COPD diagnosis and is a National Quality Forum-endorsed measure of care quality, many patients with COPD continue to be treated for COPD despite never having had spirometry.8,9,14 In addition, misdiagnosis is common; many patients given a clinical diagnosis of COPD do not have AFO on spirometry.15,16

We found that as BMI class increased, the proportion of patients with AFO on spirometry decreased, supporting an association between weight and misclassification of COPD consistent with prior studies. Walters et al15 found that among primary care patients with COPD, BMI ≥ 25 kg/m2 was associated with a higher likelihood of COPD misdiagnosis when confirmatory spirometry was performed. In a study of adults undergoing confirmatory spirometry prior to discharge after hospitalization for COPD exacerbation, Prieto Centurion et al16 found that obese patients were four times as likely as normal weight patients to lack AFO. These findings have important implications because obese patients are at greater risk of diabetes, hypertension, coronary heart disease, and mortality compared with normal weight patients.1719 Among obese patients misdiagnosed with COPD, missing the chance to diagnose and treat other conditions associated with dyspnea, particularly cardiovascular disease, may put them at even greater risk of poor health outcomes.

Many primary care providers, often the only providers managing patients with mild to moderate COPD, do not follow established guidelines in the management of COPD, particularly regarding inhaled medication use.20,21 Salinas et al21 showed that only one of four primary care physicians adhered > 90% of the time to guideline recommendations regarding spirometry or long-acting bronchodilator use. Although spirometry is not frequently used in COPD diagnosis, (appropriate) prescription of inhaled medications increases after spirometry is used in the diagnosis of COPD in the primary care setting.5,22 Fewer data are available about cessation of inhaled medications if spirometry shows no evidence of AFO. The present results are concerning because inhaled medications used to treat COPD are not benign.2325 Inhaled corticosteroids have been demonstrated to increase the risk of pneumonia, and older patients initiating a long-acting β-agonist or a long-acting anticholinergic have been shown to be at increased risk of acute coronary syndrome and heart failure.23,26,27

In the present cohort, overweight and obese patients were less likely to experience deescalation or to stay off inhaled medications and were more likely to experience escalation of therapy or remain on maximal therapy after negative spirometry results compared with normal weight patients. This finding has implications for safety, cost, and quality of care. Patient overuse of inhaled medications is not uncommon in COPD; patients without COPD who receive and overuse inhaled medications may be at greater risk of dose-dependent adverse effects without the benefit of symptom relief.2830 Furthermore, studies have shown that as the number of medications increases, medication adherence often decreases; thus, the addition of medications that are not indicated may affect patient adherence with other necessary medications, further compromising health.31 Overweight and obese patients could be especially vulnerable to such effects because they have more comorbidities, greater use of prescription medications, and higher pharmacy costs than normal weight patients.12,17,32

It is possible that patients who did not have AFO did have emphysema or simple chronic bronchitis. Although there has been intensive study surrounding the clinical meaning of emphysema found on CT scans, in particular, there is no evidence that treating either of these conditions with inhaled medications in the absence of AFO is beneficial, and such treatment is not recommended by current guidelines.7,3335

The relationship between obesity and pulmonary function is complex. During cardiopulmonary exercise testing, obese patients with COPD do not report greater intensity of dyspnea or experience more exercise limitation than normal weight patients with similar AFO, perhaps because obesity can reduce functional residual capacity.36 However, we have demonstrated that obese patients with COPD report more activity-related dyspnea (by modified Medical Research Council score) and worse health-related quality of life than do normal weight patients with the same severity of AFO.3 Severity of dyspnea may be related to degree of hyperinflation, which is affected by obesity as well as by COPD severity.36 We did not have lung volume data, making it difficult to further speculate on how such relationships may have contributed to the results. It is also possible that inhaled bronchodilators may have differential effects on airways of obese patients who have higher small airway resistance at baseline due to lower lung volumes.37 We also did not have data on waist-hip circumference; body fat distribution may influence respiratory dynamics and, therefore, symptoms.37

Limitations

The present cohort comprising US veterans yielded a study population of largely white older men, which could limit generalizability. Additionally, the results apply only to those patients who had spirometry. Because pulmonologists are more likely to use spirometry in COPD diagnosis and management of inhaled medications, it is possible that the study underestimates the magnitude of the associations between obesity and COPD misdiagnosis and between obesity and management of inhaled medications after spirometry.14,20 Additional limitations include those involved with the use of administrative data. However, use of the VA system allowed access to complete, integrated health-care records, including information on medication dispensation. Although we enrolled patients through 2007 and followed up through 2009, GOLD and other guidelines have recommended spirometry for a COPD diagnosis since 2001, and prior to that, this was included in American Thoracic Society treatment practice guidelines. More current articles continue to suggest that the majority of patients receive COPD diagnoses without spirometry, suggesting that practice patterns in this area have been relatively stable over the past several years.6,38,39

We do not know whether veterans had additional spirometry after study entrance or at non-VA facilities. It is also possible that the providers adjusting patient medications were not aware of spirometry results, although the VA has an integrated system where notes and test results are centralized in a common electronic medical record. Some veterans without AFO at the index date may have gone on to have repeat spirometry that did show AFO that may have subsequently guided medication decisions, although we expect that repeat spirometry was uncommon. To address the possibility that asthma may have been misclassified as COPD, we performed a sensitivity analysis excluding the 494 patients who entered the cohort only by inhaled medication use, and the results were unchanged.

Despite these limitations, the study has several strengths, including a large sample size that allowed us to examine the effects of BMI on misdiagnosis across five BMI classes and across three different centers, decreasing the likelihood that the results were influenced by local practice patterns. We also used both the LLN and the GOLD definitions of AFO, achieving similar results for both despite the limitations of each method.18 Regardless of the AFO criteria used, we found that as BMI increased, so did the likelihood of COPD misdiagnosis.

Overweight and obese patients are more likely than normal weight patients to be given a misdiagnosis of COPD and are more likely to be treated with inhaled medications even after spirometry shows no AFO. Missing the correct etiology of dyspnea or other symptoms indicative of COPD suggests that providers may be missing potential opportunities to recognize and treat other causes of dyspnea in overweight and obese patients, thereby missing opportunities to improve quality of care, reduce costs, and decrease medication use.

Author contributions: B. F. C. and L. C. F. had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. The authors assume full responsibility for the accuracy and completeness of the findings presented. B. F. C., D. H. A., J. E. U., and L. C. F. contributed to study design and data analysis and interpretation; D. H. A., J. E. U., and L. C. F. contributed to data collection and management; B. F. C., D. R., D. H. A., J. E. U., and L. C. F. contributed to preparation, review, and approval of the manuscript; and J. M. contributed to review and approval of the manuscript.

Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Au is a coinvestigator on a grant from Gilead for work that is unrelated to this manuscript. Drs Collins, Ramenofsky, Ma, and Feemster and Ms Uman have reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Role of sponsors: The funding bodies played no role in the study design, analysis and interpretation of the findings, or drafting the manuscript and did not review or approve the manuscript prior to submission.

Other contributions: The views are those of the authors and do not necessarily reflect the position or policy of the Department of Veterans Affairs or the National Institutes of Health.

Additional information: The e-Appendix, e-Figures, and e-Tables can be found in the Supplemental Materials section of the online article.

AFO

airflow obstruction

GOLD

Global Initiative for Chronic Obstructive Lung Disease

LLN

lower limit of normal

VA

Veterans Administration

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Martinez CH, Kim V, Chen Y, et al; COPDGene Investigators. The clinical impact of non-obstructive chronic bronchitis in current and former smokers. Respir Med. 2014;108(3):491-499. [CrossRef] [PubMed]
 
Qaseem A, Wilt TJ, Weinberger SE, et al; American College of Physicians; American College of Chest Physicians; American Thoracic Society; European Respiratory Society. Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline update from the American College of Physicians, American College of Chest Physicians, American Thoracic Society, and European Respiratory Society. Ann Intern Med. 2011;155(3):179-191. [CrossRef] [PubMed]
 
Fujimoto K, Kitaguchi Y, Kubo K, Honda T. Clinical analysis of chronic obstructive pulmonary disease phenotypes classified using high-resolution computed tomography. Respirology. 2006;11(6):731-740. [CrossRef] [PubMed]
 
Ora J, Laveneziana P, Ofir D, Deesomchok A, Webb KA, O’Donnell DE. Combined effects of obesity and chronic obstructive pulmonary disease on dyspnea and exercise tolerance. Am J Respir Crit Care Med. 2009;180(10):964-971. [CrossRef] [PubMed]
 
Salome CM, King GG, Berend N. Physiology of obesity and effects on lung function. J Appl Physiol (1985). 2010;108(1):206-211. [CrossRef] [PubMed]
 
Joo MJ, Sharp LK, Au DH, Lee TA, Fitzgibbon ML. Use of spirometry in the diagnosis of COPD: a qualitative study in primary care. COPD. 2013;10(4):444-449. [CrossRef] [PubMed]
 
Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease, NHLBI/WHO workshop report. Global Initiative for Chronic Obstructive Lung Disease website. http://www.goldcopd.org/uploads/users/files/GOLDWkshp2001.pdf. Published 2001. Accessed September 17, 2013.
 

Figures

Figure Jump LinkFigure 1 –  Cohort formation. ICD.9 = International Classification of Diseases, 9th Revision.Grahic Jump Location

Tables

Table Graphic Jump Location
TABLE 1 ]  Baseline Characteristics

Data are presented as mean ± SD or %. Normal weight, 18.5 ≤ BMI < 25 kg/m2; overweight, 25 ≤ BMI < 30 kg/m2; class I obesity, 30 ≤ BMI < 35 kg/m2; class II obesity, 35 ≤ BMI < 40 kg/m2; and class III obesity, BMI ≥ 40 kg/m2. ACS = acute coronary syndrome; AFO = airflow obstruction; CHF = congestive heart failure; HTN = hypertension; LLN = lower limit of normal.

Table Graphic Jump Location
TABLE 2 ]  Adjusted Proportion of Veterans With COPD With AFO (Defined by LLN) on Subsequent Spirometry

See Table 1 legend for expansion of abbreviations.

a 

Normal weight (18.5 ≤ BMI < 25 kg/m2), overweight (25 ≤ BMI < 30 kg/m2), class I obesity (30 ≤ BMI < 35 kg/m2), class II obesity (35 ≤ BMI < 40 kg/m2), class III obesity (BMI ≥ 40 kg/m2).

b 

Adjusted for mean values of age, smoking status in prior year, white race, comorbidities in the prior year (CHF, hypertension, depression, diabetes, sleep apnea), use of oral steroids in the prior year, and site of care.

c 

P < .001 for trend.

Table Graphic Jump Location
TABLE 3 ]  Percentage of Patients Without AFO on Inhaled Medications Before and After the Index Date

Data are presented as %. Normal weight, 18.5 ≤ BMI < 25 kg/m2; overweight, 25 ≤ BMI < 30 kg/m2; obese, BMI ≥ 30 kg/m2. See Table 1 legend for expansion of abbreviation.

Table Graphic Jump Location
TABLE 4 ]  Adjusted Proportion of Misdiagnosed Veterans (by BMI Class) Who Had Changes in Medication Regimen Between 3 Mo Prior to and 9 to 12 Mo After Spirometry: Model 1

Model 1 had deescalation in therapy or remained off therapy.

a 

Normal weight (18.5 ≤ BMI < 25 kg/m2), overweight (25 ≤ BMI < 30 kg/m2), and obese (BMI ≥ 30 kg/m2).

b 

Adjusted for mean values of white race, acute coronary syndrome in the prior year, oral steroid use in the prior year, and site of care. P = .003 for trend.

Table Graphic Jump Location
TABLE 5 ]  Adjusted Proportion of Misdiagnosed Veterans (by BMI Class) Who Had Changes in Medication Regimen Between 3 Mo Prior to and 9 to 12 Mo After Spirometry: Model 2

Model 2 had escalation in therapy or stayed on maximal therapy.

a 

Normal weight (18.5 ≤ BMI < 25 kg/m2), overweight (25 ≤ BMI < 30 kg/m2), and obese (BMI ≥ 30 kg/m2).

b 

Adjusted for mean values of oral steroid use in the prior year and site of care. P = .09 for trend.

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Qaseem A, Wilt TJ, Weinberger SE, et al; American College of Physicians; American College of Chest Physicians; American Thoracic Society; European Respiratory Society. Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline update from the American College of Physicians, American College of Chest Physicians, American Thoracic Society, and European Respiratory Society. Ann Intern Med. 2011;155(3):179-191. [CrossRef] [PubMed]
 
Fujimoto K, Kitaguchi Y, Kubo K, Honda T. Clinical analysis of chronic obstructive pulmonary disease phenotypes classified using high-resolution computed tomography. Respirology. 2006;11(6):731-740. [CrossRef] [PubMed]
 
Ora J, Laveneziana P, Ofir D, Deesomchok A, Webb KA, O’Donnell DE. Combined effects of obesity and chronic obstructive pulmonary disease on dyspnea and exercise tolerance. Am J Respir Crit Care Med. 2009;180(10):964-971. [CrossRef] [PubMed]
 
Salome CM, King GG, Berend N. Physiology of obesity and effects on lung function. J Appl Physiol (1985). 2010;108(1):206-211. [CrossRef] [PubMed]
 
Joo MJ, Sharp LK, Au DH, Lee TA, Fitzgibbon ML. Use of spirometry in the diagnosis of COPD: a qualitative study in primary care. COPD. 2013;10(4):444-449. [CrossRef] [PubMed]
 
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