Hans Petersen

Lovelace Respiratory Research Institute, Albuquerque, New Mexico, United States

Are you Hans Petersen?

Claim your profile

Publications (76)367.89 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is thought to result from an accelerated decline in forced expiratory volume in 1 second (FEV1) over time. Yet it is possible that a normal decline in FEV1 could also lead to COPD in persons whose maximally attained FEV1 is less than population norms. We stratified participants in three independent cohorts (the Framingham Offspring Cohort, the Copenhagen City Heart Study, and the Lovelace Smokers Cohort) according to lung function (FEV1 ≥80% or <80% of the predicted value) at cohort inception (mean age of patients, approximately 40 years) and the presence or absence of COPD at the last study visit. We then determined the rate of decline in FEV1 over time among the participants according to their FEV1 at cohort inception and COPD status at study end. Among 657 persons who had an FEV1 of less than 80% of the predicted value before 40 years of age, 174 (26%) had COPD after 22 years of observation, whereas among 2207 persons who had a baseline FEV1 of at least 80% of the predicted value before 40 years of age, 158 (7%) had COPD after 22 years of observation (P<0.001). Approximately half the 332 persons with COPD at the end of the observation period had had a normal FEV1 before 40 years of age and had a rapid decline in FEV1 thereafter, with a mean (±SD) decline of 53±21 ml per year. The remaining half had had a low FEV1 in early adulthood and a subsequent mean decline in FEV1 of 27±18 ml per year (P<0.001), despite similar smoking exposure. Our study suggests that low FEV1 in early adulthood is important in the genesis of COPD and that accelerated decline in FEV1 is not an obligate feature of COPD. (Funded by an unrestricted grant from GlaxoSmithKline and others.).
    No preview · Article · Jul 2015 · New England Journal of Medicine

  • No preview · Article · Jul 2015 · European Respiratory Journal
  • [Show abstract] [Hide abstract]
    ABSTRACT: Chronic obstructive pulmonary disease (COPD) includes the chronic bronchitis (CB) and emphysema phenotypes. While it is generally assumed that emphysema or chronic airway obstruction (CAO) is associated with worse quality of life than CB, this assumption has not been tested. The present study, analyses from the Lovelace Smokers' Cohort (LSC) were validated in the COPDGene Cohort. CB without CAO (CB only) was defined by self-reported cough productive of phlegm for at least 3 months/year for 2 consecutive years and postbronchodilator FEV1/FVC≥70%. CAO without CB (CAO only) was defined by a postbronchodilator FEV1/FVC<70% with no evidence of CB. Quality of life outcomes were obtained from the SGRQ and SF-36 questionnaires. A Priori Covariates included age, sex, pack-years of smoking, current smoking, and FEV1. Smokers with CB without CAO (LSC n=341; COPDGene=523) were younger, had a greater BMI, and less smoking exposure than those with CAO only (LSC n=302; COPDGene=2208). Compared to the latter group, quality of life scores were worse for those with CB only. Despite similar SGRQ Activity and SF-36 Role physical and physical functioning, SGRQ Symptoms and Impact scores and SF-36 Emotional and Social measures were worse in the CB only group, in both cohorts. After adjustment for covariates, CB only group remained a significant predictor for 'worse' symptoms, and emotional and social measures. This analysis is the first study to suggest that among subjects with COPD those with CB only present worse quality of life, symptoms and mental well-being than those with CAO only.
    No preview · Article · Mar 2015 · Chest
  • [Show abstract] [Hide abstract]
    ABSTRACT: Club cell secretory protein-16 (CC16) is the major secreted product of airway club cells, but its role in the pathogenesis of chronic obstructive pulmonary disease (COPD) is unclear. We measured CC16 airway expression in humans with and without COPD and CC16 function in a cigarette smoke (CS)-induced COPD murine model. Airway CC16 expression was measured in COPD patients, smokers without COPD and non-smokers. We exposed wild-type (WT) and CC16(-/-)mice to CS or air for up to 6 months, and measured airway CC16 expression, pulmonary inflammation, alveolar septal cell apoptosis, airspace enlargement, airway mucin 5AC (MUC5AC) expression, small airway remodelling and pulmonary function. Smokers and COPD patients had reduced airway CC16 immunostaining that decreased with increasing COPD severity. Exposing mice to CS reduced airway CC16 expression. CC16(-/-) mice had greater CS-induced emphysema, airway remodelling, pulmonary inflammation, alveolar cell apoptosis, airway MUC5AC expression, and more compliant lungs than WT mice. These changes were associated with increased nuclear factor-κB (NF-κB) activation in CC16(-/-) lungs. CS-induced acute pulmonary changes were reversed by adenoviral-mediated over-expression of CC16. CC16 protects lungs from CS-induced injury by reducing lung NF-κB activation. CS-induced airway CC16 deficiency increases CS-induced pulmonary inflammation and injury and likely contributes to the pathogenesis of COPD. Copyright ©ERS 2015.
    No preview · Article · Feb 2015 · European Respiratory Journal
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Genome-wide association studies (GWAS) of chronic obstructive pulmonary disease (COPD) have identified disease-susceptibility loci, mostly in subjects of European descent. We hypothesized that, by studying Hispanic populations, we would be able to identify unique loci that contribute to COPD pathogenesis in Hispanics but remain undetected in GWAS of non-Hispanic populations. Methods: We conducted a meta-analysis of two GWAS of COPD in independent cohorts of Hispanics in Costa Rica and the United States (MESA). We performed a replication study of the top SNPs in an independent Hispanic cohort in New Mexico (the Lovelace Smokers Cohort). We also attempted to replicate prior findings from GW-studies in non-Hispanic populations in Hispanic cohorts. Results: We found no genome-wide significant association with COPD in our meta-analysis of Costa Rica and MESA. After combining the top results from this meta-analysis with those from our replication study in the Lovelace Smokers Cohort, we identified two SNPs approaching genome-wide significance for an association with COPD. The first (rs858249, combined P value=6.1x10-8) is near the genes KLHL7 and NUPL2 on chromosome 7. The second (rs286499 combined P value 8.4x10-8) is located in an intron of DLG2. The two most significant SNPs in FAM13A from a previous GW-study in non-Hispanics were associated with COPD in Hispanics. Conclusions: We have identified two novel loci (in or near the genes KLHL7/NUPL2 and DLG2) that may play a role in COPD pathogenesis in Hispanic populations.
    No preview · Article · Jan 2015
  • [Show abstract] [Hide abstract]
    ABSTRACT: Rationale: Inhaled corticosteroids (ICS) are widely used in the management of asthma. Prior research suggests that access to ICS among patients with asthma may vary by ethnicity. Objectives: Study objectives were to determine if there is a difference in the proportion of Hispanic and non-Hispanic white patients with asthma in the receipt of an ICS prescription and to determine independent predictors for the receipt of an ICS prescription for asthma. Methods: The 2009 US Medical Expenditure Panel Survey data were utilized to compare the receipt of ICS prescription among patients with asthma with the following inclusion criteria: Hispanic and non-Hispanic white ethnicity, age over 4 years, diagnostic codes for asthma. Multiple logistic regression was used to determine the influence of race/ethnicity and other significant factors on the receipt of an ICS prescription. Results: There were 1,469 patients with asthma, corresponding to a weighted sample of 14,401,069 US patients with asthma who met the inclusion criteria, represented by 16.1% Hispanic, 59.5% female, and mean age of 39.9 years. Among non-Hispanic white patients with asthma, 39.7% (35% children and 41% adults) had a receipt of an ICS prescription compared to 22.2% of Hispanic patients (23.9% children and 21.2% adults), P<0.001. In the multiple regression model, Hispanic patients aged ≥18 years had 43% lower odds (OR, 0.6; 95% CI. 0.3 to 0.9) of having a receipt of an ICS prescription compared to non-Hispanic white patients, independent of other factors. There was no significant difference in receipt of an ICS prescription between Hispanic and non-Hispanic white children with asthma (ages 4 to 17 years). Conclusion: The disparity in the receipt of ICS prescription between Hispanic and non-Hispanic white adult patients with asthma could result in suboptimal asthma management, a higher rate of exacerbations, and higher healthcare costs in this growing minority population. The differences and potential disparities in the receipt of an ICS prescription between Hispanic and non-Hispanic white patients with asthma warrant further investigation to better understand the reasons for such disparities, along with their impact on the US healthcare burden, and interventions that can be undertaken to reduce these disparities.
    No preview · Article · Dec 2014
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Despite implications for carcinogenesis and other chronic diseases, basic mechanisms of p53 and its variants in suppressing Bcl-2 levels are poorly understood. Bcl-2 sustains mucous cell metaplasia, whereas p53(-/-) mice display chronically increased mucous cells. Here we show that p53 decreases bcl-2 mRNA half-life by interacting with the 5' untranslated region (UTR). The p53-bcl-2 mRNA interaction is modified by the substitution of proline by arginine within the p53 proline-rich domain (PRD). Accordingly, more mucous cells are present in primary human airway cultures with p53(Arg) compared with p53(Pro). Also, the p53(Arg) compared with p53(Pro) displays higher affinity to and activates the promoter region of SAM-pointed domain-containing Ets-like factor (SPDEF), a driver of mucous differentiation. On two genetic backgrounds, mice with targeted replacement of prolines in p53 PRD show enhanced expression of SPDEF and Bcl-2 and mucous cell metaplasia. Together, these studies define the PRD of p53 as a determinant for chronic mucous hypersecretion.
    Full-text · Article · Nov 2014 · Nature Communications
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Chronic obstructive pulmonary disease (COPD) has been the only leading cause of death associated with a continuously increasing trend in the US over the past 30 years. The aim of this research was to identify predictors for all-cause in-hospital mortality for COPD patients. We conducted a cross-sectional study of patients with the discharge diagnosis of COPD, utilizing the 2007 Premier Perspective database. Inpatients aged 40 years and above were selected if they had a discharge with a primary diagnosis of COPD between January 1, 2007 and December 31, 2007. All data analyses were based on individual level. If a patient had multiple discharges, only the last discharge was included for mortality analysis. Predictors for mortality were identified by multiple logistic regressions. Bonferroni correction for multiple logistic regression models was adapted to control for family-wise errors. The total of 57,224 patients was selected for data analysis in the study. All-cause in-hospital mortality for patients with COPD was 2.4%. Older age, insurance coverage, elective admission, intensive care unit admission, prolonged length of stay, increased Deyo-adapted Charlson Index (DCI) score and Elixhauser comorbidities of renal failure, metastatic cancer, solid tumor without metastasis, and weight loss were identified as independent predictors for all-cause in-hospital mortality. Antibiotics and β-blockers were predictors of lower all-cause in-hospital mortality risk after adjusting for other factors. The nationwide discharge database provides useful information to identify predictors for all-cause in-hospital mortality of patients with COPD.
    Full-text · Article · Jul 2014 · SpringerPlus
  • [Show abstract] [Hide abstract]
    ABSTRACT: Gene methylation is an epigenetic change that involves a heritable modification of chromatin structure that alters gene expression without a change in DNA sequence. It has previously been shown that methylation of the GATA-4 gene promoter region in sputum DNA is associated with low lung function and increased odds of chronic obstructive pulmonary disease (COPD) among smokers. Given these findings, we hypothesized that GATA-4 gene methylation in sputum DNA would be associated with low health status, as measured by the St. George's Respiratory Questionnaire (SGRQ), in subjects with COPD. Self-reported SGRQ, spirometry, and induced sputum samples were obtained from 168 COPD subjects from the Lovelace Smokers Cohort. GATA-4 gene methylation was evaluated in sputum DNA using nested methylation-specific polymerase chain reaction (PCR) assays. Using general linear model with Poisson regression, we found that GATA-4 gene methylation was significantly associated with overall lower SGRQ health status (parameter estimate = .296, p < .001). This finding remained significant even after controlling for age, lung function, and other covariates. In an additional analysis using logistic regression and comparing extreme tertiles of overall SGRQ score, we confirmed that GATA-4 gene methylation was associated with a 3-fold increase in risk of poor health status (OR 2.95 and p = .028). The unexplored links between epigenetic changes and psychosocial factors such as health status are critical gaps in the literature. This study is the first to suggest that airway GATA-4 gene methylation status may independently predict health status in individuals with COPD.
    No preview · Article · Jun 2014 · Biological Research for Nursing
  • Source
    Akshay Sood · Hans Petersen · Paula Meek · Yohannes Tesfaigzi

    Preview · Article · Apr 2014 · American Journal of Respiratory and Critical Care Medicine
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Chronic mucous hypersecretion (CMH) contributes to COPD exacerbations and increased risk for lung cancer. Because methylation of gene promoters in sputum has been shown to be associated with lung cancer risk, we tested whether such methylation was more common in persons with CMH. Eleven genes commonly silenced by promoter methylation in lung cancer and associated with cancer risk were selected. Methylation specific PCR (MSP) was used to profile the sputum of 900 individuals in the Lovelace Smokers Cohort (LSC). Replication was performed in 490 individuals from the Pittsburgh Lung Screening Study (PLuSS). CMH was significantly associated with an overall increased number of methylated genes, with SULF2 methylation demonstrating the most consistent association. The association between SULF2 methylation and CMH was significantly increased in males but not in females both in the LSC and PLuSS (OR = 2.72, 95 % CI = 1.51-4.91, p = 0.001 and OR = 2.97, 95 % CI = 1.48-5.95, p = 0.002, respectively). Further, the association between methylation and CMH was more pronounced among 139 male former smokers with persistent CMH compared to current smokers (SULF2; OR = 3.65, 95 % CI = 1.59-8.37, p = 0.002). These findings demonstrate that especially male former smokers with persistent CMH have markedly increased promoter methylation of lung cancer risk genes and potentially could be at increased risk for lung cancer.
    Preview · Article · Jan 2014 · Respiratory research
  • Source
    Akshay Sood · Hans Petersen · Paula Meek · Yohannes Tesfaigzi
    [Show abstract] [Hide abstract]
    ABSTRACT: Rationale: The literature on the effect of obesity and weight gain on respiratory outcomes in smokers is contradictory. Objective: To examine the cross-sectional effect of body mass index (BMI) and longitudinal effect of change in BMI upon spirometry and health status among smokers at risk for and with milder COPD. Methods and Measurements: Participants from the Lovelace Smokers' Cohort were followed for a median period of 6 years - 75% of whom were at risk and 25% had COPD at baseline examination. BMI and gain in BMI were examined as continuous independent variables, both overall and after stratification into three categories - normal-weight; overweight; and obese, based on baseline weight. Spirometry and health status (as assessed by St. George Respiratory Questionnaire total and subscale scores) were dependent variables. Covariates included age, sex, ethnicity, pack-years of smoking, and current smoking status. Cross-sectional analysis used linear and logistic regression while longitudinal analysis used mixed model approach. Main Results: In cross-sectional analyses, higher BMI was associated with worse health status among obese but better health status among normal-weight smokers. In longitudinal analyses, weight gain was associated with decrease in FEV1 and health status among obese smokers but an increase in these outcomes among normal-weight smokers. Conclusions: Weight gain affects respiratory outcomes differently between obese and normal-weight smokers. While FEV1 and health status decrease with weight gain among obese smokers, they improve among normal-weight smokers. The non-linear relationship between weight gain and respiratory outcomes suggests that this effect of excess weight is unlikely to be mechanical alone.
    Preview · Article · Nov 2013 · American Journal of Respiratory and Critical Care Medicine
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Adenovirus (HAdV) infections are associated with significant morbidity and mortality in pediatric hematopoietic stem cell transplant (HSCT) recipients. Serial HAdV polymerase chain reaction (PCR) testing is sometimes used to identify adenoviremia with a goal of early intervention. It is laborious and costly to serially test all HSCT recipients. We aimed to derive a prediction rule using data available at the time of HSCT to identify those who did and did not develop adenoviremia. An accurate prediction model could allow for more focused HAdV testing. Methods: We retrospectively identified 126 pediatric patients that: (1) received HSCT at The Children’s Hospital of Philadelphia between 2006 and 2012; and, (2) underwent surveillance HAdV PCR testing. Using stochastic gradient boosting (SGB) methodology we derived a prediction model to discriminate between those patients who did and did not develop adenoviremia in a 6-month post transplant period. To establish a balanced dataset, adenoviremic patients were compared to randomly selected controls. The model was repeated 100 times to achieve an average confusion matrix. Predictors included age, race, gender, previous HSCT, indication for HSCT, allogeneic vs. autologous HSCT, match status, stem cell source, T-cell depletion, receipt of conditioning, total body irradiation and presence of chronic comorbid conditions at time of HSCT. Results: Twenty-nine (23%) patients developed adenoviremia; median time to adenoviremia was 37 days (IQR: 20 to 69 days). No single baseline characteristic accurately discriminated those with and without adenoviremia. The best-fit SGB predictive model had a sensitivity of 75% (95% CI: 0.55 – 0.88) and specificity of 77% (95% CI: 0.57 – 0.90). The false positive and negative rates were 0.23 (95% CI: 0.10 – 0.43) and 0.25 (95% CI: 0.11 – 0.44), respectively with an average out of bag error of 0.21. Conclusion: PCR surveillance testing in pediatric HSCT recipients commonly identified adenoviremia. The derived model for predicting adenoviremia had reasonable sensitivity, specificity and out of bag error. Refining the model to include additional baseline variables such as specific conditioning medications and more adenoviremia events is necessary to reduce the false positive and false negative rates.
    No preview · Conference Paper · Oct 2013
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Cigarette smoking is the most important risk factor for chronic obstructive pulmonary disease (COPD) in the United States. Host factors that influence rapid rate of FEV1 decline in smokers and how decline rate influences risk for developing COPD are unknown. Characterize the rate of FEV1 decline in ever-smokers, compare the risk of incident COPD between rapid decliners and others, and determine the effect of selected drugs on rapid decline. A total of 1,170 eligible ever-smokers from the longitudinal Lovelace Smokers Cohort with repeat spirometry tests over a minimum follow-up period of 3 years (mean follow-up: 5.9 years) were examined, including 809 ever-smokers without baseline spirometric abnormality. Longitudinal absolute decline in postbronchodilator FEV1 obtained from the slope defined by the spirometric values over all examinations was annualized and classified as 'rapid' (≥30 ml/year), 'normal' (0 to -29.9 ml/year) or 'no' decline (>0 ml/year). Logistic regression and Kaplan-Meir survival curves were used for analysis. Approximately 32% of ever-smokers exhibited rapid decline. Among ever-smokers without baseline spirometric abnormality, rapid decline was associated with increased risk for incident COPD [OR 1.88; p = 0.003]. The use of angiotensin converting enzyme (ACE) inhibitor at baseline examination was protective against rapid decline, particularly among those with co-morbid cardiovascular disease, hypertension, or diabetes [OR 0.48; 0.48 and 0.12 respectively; p≤ 0.02 for all analyses]. Ever-smokers with rapid decline in FEV1 are at higher risk for developing COPD. Use of ACE inhibitors by smokers may protect against 'rapid' decline and progression to COPD.
    Full-text · Article · Sep 2013 · Chest
  • [Show abstract] [Hide abstract]
    ABSTRACT: The BODE index was developed as a prognostic mortality risk tool for persons with chronic obstructive pulmonary disease (COPD). It incorporates 4 measures: body mass index, lung obstruction, dyspnea, and exercise capacity. The intent of this study was to examine how well a BODE-like index constructed using a simpler lung function measure, peak expiratory flow, in combination with physical functioning and symptom information more readily found in survey data (a quasi-BODE index), performs in identifying persons at higher risk of mortality and whether it may be extended as an assessment of mortality risk to persons without diagnosed COPD. Using US national survey data from the Health Retirement Study for 2006-2010, each unit increase in the quasi-BODE index score was associated with a multiplicative 50% increase in mortality risk (odds ratio = 1.50, 95% confidence interval: 1.41, 1.59). The quasi-BODE index is a multidimensional health status instrument based on the BODE index, which is a good predictor of mortality. The quasi-BODE index was compiled using simple measures of physical and respiratory function. It is a potentially useful prognostic instrument for older adult populations with or without COPD, including those with severe physical limitations, particularly when combined with demographic factors and comorbid conditions. © 2013 © The Author 2013. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: [email protected] /* */
    No preview · Article · Aug 2013 · American journal of epidemiology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objectives: Asthma exacerbations have well-established clinical and economic impact, yet lack consensus on characterization of an episode's severity. Asthma treatment guidelines outline the concept of a moderate asthma exacerbation; however, a clear definition that can be operationalized has not been proposed, Methods: Adult asthma (ICD-9: 493.XX) patients, with at least 9 months of continuous enrolment in the Fallon Community Health Plan were included in the retrospective cohort study. Patients diagnosed with Chronic Obstructive Pulmonary Disease (COPD) or other lower respiratory tract conditions were excluded. The first reported asthma-related event following a 2-week symptom-free period was designated as the index event. Asthma-related events were categorized as (1) moderate exacerbations (symptom-based) or (2) severe exacerbations (claims-based). Timing between and temporal sequence of asthma-related events along with average costs were calculated, Results: Of 3126 eligible patients, 55% reported an asthma-related event followed by a recurrent event(s). Moderate exacerbations followed by recurrent moderate exacerbations were most frequent (20%) with the shortest interval between exacerbations (mean: 83 days [SD 87]). Moderate exacerbations followed by severe exacerbations occurred in 16% of patients with an average of 176.74 (SD 176.94) days between events, Conclusions: Patient report of asthma bothersome enough to initiate contact with a clinician, but not requiring oral corticosteroid (OCS), is a definition for a moderate exacerbation that can be operationalized for research purposes. Further work is needed to demonstrate whether identification of moderate exacerbations will allow interventions that impact the frequency and timing of future exacerbations.
    No preview · Article · Mar 2013 · Journal of Asthma
  • [Show abstract] [Hide abstract]
    ABSTRACT: Human adenovirus (HAdV) is one of the most feared infections among immunocompromised patients. In particular, in liver transplant patients, HAdV has been implicated in acute liver failure with resultant mortality. The development of current molecular techniques and surveillance testing protocols have provided tools for early detection of HAdV infection, prior to or at the early onset of HAdV disease. Although reduction in immune suppression is the mainstay of therapy, many researchers have also advocated for early administration of antiviral therapy. In multiple reports, cidofovir treatment has been associated with declines in HAdV viral loads or clinical improvement in solid organ and bone marrow transplant recipients. However, there have also been case reports that raise questions about the effectiveness of antiviral therapy in controlling systemic HAdV disease. We report a case of a 26-month-old male recipient of a liver transplantation for hepatoblastoma who developed adenoviremia with an associated hepatitis and gastroenteritis. He recovered with reduced immune suppression but without antiviral therapy, thus avoiding potential toxicities associated with cidofovir therapy. This case a contrast to previous reports, and it highlights the ambiguity regarding which patients should receive HAdV-specific antiviral therapy. Additional knowledge regarding specific pediatric host factors and HAdV factors that predict poor outcomes are needed. Such information would allow clinicians to better stratify patients by risk at the time of adenoviremia detection so that low-risk patients are not unnecessarily exposed to medications with potential toxicities.
    No preview · Article · Feb 2013
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective: To compare budesonide/formoterol (BFC) and fluticasone propionate/salmeterol (FSC) in their ability to reduce COPD exacerbations using a novel risk stratification approach. Design: Retrospective cohort study with propensity matching and stratification by short-acting beta2-agonist (SABA) use. Participants: 7704 COPD patients identified using 2 U.S. health claims databases (study period: 1/1/2004 to 4/30/2009). Measurements: Users of BFC and FSC were stratified by SABA fills in the 6 months prior to the start of therapy (index date). Exacerbation events before and after the index date were compared, and proportional hazard models used to examine exacerbation risk by baseline SABA use. Results: At baseline, 6% (6.2%, BFC; 5.8%, FSC) had a COPD-related hospitalization or emergency department (ED) visit. Post-index, this was reduced to 4.8% (P < 0.001) among all patients (4.9%, BFC, 4.7%, FSC). Change was greatest among high SABA users (9% pre-index to 4.9% post-index, P < 0.001). SABA use post-index was reduced in both groups, with slightly lower need for SABA refills seen among BFC users. SABA use was correlated with increased exacerbations during the baseline period and was predictive of exacerbations during the follow-up period. Conclusions: BFC and FSC had equivalent effectiveness in reduction in ED visits and hospitalizations for COPD exacerbations, but BFC users had lower subsequent need for SABA fills. Increased SABA use is a predictor of COPD exacerbation among COPD patients in the general population.
    Full-text · Article · Feb 2013 · Journal of clinical outcomes management: JCOM
  • [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND: National asthma treatment guidelines recommend either the use of inhaled corticosteroids (ICS) or ICS in combination with a long-acting bronchodilator for the treatment of moderate to severe asthma. Even though asthma is common among older adults, few studies have assessed the differences in effectiveness between these two recommended therapies in patients over 65 years of age. OBJECTIVE: The aim of this study was to assess the association of the fluticasone-salmeterol combination (FSC) or ICS initiation on asthma-related events in Medicare-eligible asthma patients. METHODS: This was a retrospective observational study using a large health claims database (July 1, 2001 to June 30, 2008). Subjects 65 to 79 years of age with 12-month preindex and 3- to 12-month postindex eligibility, an asthma diagnosis (ICD-493.xx), and with 1 or more FSC or ICS claims at index were included. Subjects with an FSC or ICS claim in the preindex and any claim for chronic obstructive pulmonary disease were excluded. Subjects were observed until they had an event (emergency department [ED] inpatient hospitalization [IP], combined IP/ED or oral corticosteroid [OCS] use) or were no longer eligible in the database, whichever came first. Cox proportional hazards regression was used to assess risk of an asthma-related event (IP, ED, or IP/ED). Baseline characteristics (age, sex, region, index season, comorbidities, preindex use of short-acting β-agonists, OCS, other asthma controllers, and asthma-related ED/IP visits) were independent covariates in the model. RESULTS: A total of 10,837 met the criteria (4843 ICS and 5994 FSC). Age (70.4 and 70.5 years, respectively) and the percentage of female subjects (65.5% and 64.8%, respectively) were similar. Asthma-related events were also similar at baseline. Postindex unadjusted rates occurring after >30 days were ED (1.8% vs 1.5%, P = 0.18), IP (2.7% vs 1.7%, P < 0.001), and ED/IP (4.1% vs 2.8%, P < 0.001) for ICS and FSC, respectively. Subjects who received FSC were associated with a 32% (adjusted HR = 0.68; 95% CI, 0.51-0.91) lower risk of experiencing an IP visit and a 22% (HR = 0.78; 95% CI, 0.62-0.98) lower risk of experiencing an ED/IP visit. No differences were observed for ED visits (HR = 0.94; 95% CI, 0.68-1.29). CONCLUSIONS: In Medicare-eligible asthma patients, FSC use was associated with lower rates of asthma-related serious exacerbations compared with ICS.
    No preview · Article · Oct 2012
  • Source

    Full-text · Article · Jun 2012 · Value in Health

Publication Stats

781 Citations
367.89 Total Impact Points

Institutions

  • 2000-2015
    • Lovelace Respiratory Research Institute
      • • Respiratory Immunology and Asthma Program
      • • Division of Clinical and Outcomes Research
      Albuquerque, New Mexico, United States