COPD Deaths Research Articles

S167 Expansion of the red cell distribution width and evolving iron deficiency as predictors of poor outcome in chronic obstructive pulmonary disease

BackgroundChronic obstructive pulmonary disease (COPD) is a multi-system disorder driven partly by diffuse inflammation, malnutrition and haematological aberrations. Because the red blood cell distribution width (RDW) is a surrogate of...

More Hospital COPD Deaths Seen in Rural Vets

More Hospital COPD Deaths Seen in Rural Vets

COPD AND GENDER AND OBESITY: IS THERE A LINK? A STUDY OF PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE AMONG INNER CITY NEW YORKERS

PURPOSE: In recent years, COPD has become an increasing problem among women. In the US, the absolute numbers of COPD cases, hospitalizations, and deaths among women have exceeded those among men. Many studies have suggested that COPD may be under-diagnosed among women. Obesity and smoking are independently associated with COPD, both of which have increased significantly in inner city areas. We conducted this study to better understand gender-based differences among patients with COPD at our institution that predominantly serves inner-city New-Yorkers.

Pathogenesis of Chronic “Cor pulmonale” in COPD

Although “cor pulmonale” represents a leading cause of death in advanced COPD, there is no clear consensus on its definition. Pulmonary hypertension has been traditionally considered the pathogenetic mechanism leading to right heart dysfunction in COPD, with peripheral oedema usually being attributed to the venous congestion secondary to the increase of right-ventricle filling pressure. The loss in pulmonary capillaries and the vascular remodelling, secondary to chronic hypoxia, cigarette-smoke exposition and systemic inflammation, are well known causes of endothelial dysfunction and pulmonary hypertension in COPD patients. Other mechanisms, such as hypoxic vasoconstriction and alveolar capillary compression in hyperinflated lungs can contribute to the rise of pulmonary arterial pressure during COPD exacerbations, exercise and sleep. In the last decades, however, the role of pulmonary pressure overload in the development of right heart failure has been debated mostly, because of the lack of a clear correlation between pulmonary artery pressure values and the presence of peripheral oedema and/or haemodynamic signs of right heart failure. In addition, the presence of distinct renal and hormonal alterations, suggests that oedema formation in advanced phases of COPD is mostly due to sodium and water retention induced by hypercapnic acidosis and aggravated by severe hypoxemia. Future studies are needed to clarify the possible role of “intermittent hypoxia”, elicited by exercise or sleep, on right heart function and also on sodium and water handling in COPD patients. Keywords: Pulmonary hypertension, vascular remodelling, lung hyperinflation, right heart dysfunction

Diurnal temperature range as a novel risk factor for COPD death

Although the relationship between day-to-day temperature changes and COPD mortality is well established, it is not known whether temperature variation within one day, that is diurnal temperature range (DTR), is a risk factor for acute COPD death, independent of the absolute temperature level. In a time-series study, the relationship between DTR and daily COPD mortality between 2001 and 2004 in Shanghai, China was assessed. A semi-parametric generalized additive model was used to allow for long-term and seasonable trends in COPD mortality, as well as variation in air pollution and weather. There was a significant association between DTR and daily COPD mortality. A 1 degrees C increase in the 4-day moving average for DTR corresponded to a 1.25% (95% confidence interval: 0.35-2.15) increase in COPD mortality. These findings suggest that DTR is a novel risk factor for acute COPD death.

A Major Cause of Death in COPD and Risk Factors for Lung Cancer—a Dilemma or a Mistake?

A Major Cause of Death in COPD and Risk Factors for Lung Cancer—a Dilemma or a Mistake?

A Major Cause of Death in COPD and Risk Factors for Lung Cancer—a Dilemma or a Mistake?

A Major Cause of Death in COPD and Risk Factors for Lung Cancer—a Dilemma or a Mistake?

Prevention of Death in COPD

Prevention of Death in COPD

Analysis of Deaths Caused by Obstructive Pulmonary Diseases in Pomerania Province in 2001–2004

Lung diseases, especially COPD, are one of the leading causes of death. The aim of the study was to assess mortality caused by COPD, asthma and cor pulmonale in the years 2001-2004 in the Pomerania province. Death certificates of patients who died of asthma, COPD or cor pulmonale registered in Regional Health Centre were analyzed. The mortality rate for COPD was 14.02/100 000, asthma 2.04/100 000 and cor pulmonale 2.4/100 000 inhabitants. Mortality rate from COPD increased from 12.5/100 000 found in 2001 to 15.6/100 000 found in 2004 (p = 0.005). The number of deaths was higher in the winter time. The peak mortality was found in patients 65 years old. 71% of COPD and cor pulmonale patients died in the hospital, whereas 75% of asthma deaths occurred at home (p = 0.0001). The mortality rates from chronic respiratory diseases in the analyzed population are comparable to data found in other studies. The alarming result is the increase in the number of COPD deaths and high percentage of asthma patients who die at home.

Influenza and COPD Mortality Protection as Pleiotropic, Dose-Dependent Effects of Statins

Published data on antiinflammatory and immunomodulatory effects of statins suggest they may reduce mortality risks associated with an unchecked immune response to selected infections, including influenza and COPD. We assessed whether statin users had reduced mortality risks from these conditions. We conducted a matched cohort study (n = 76,232) and two separate case-control studies (397 influenza and 207 COPD deaths) to evaluate whether statin therapy is associated with increased or decreased mortality risk and survival time using health-care encounter data for members of health maintenance organizations. For the cohort study, baseline illness risks from all causes prior to initiation of statin therapy were used to statistically adjust for the occurrence of outcomes after initiation of treatment. For moderate-dose (>/= 4 mg/d) statin users, this cohort study found statistically significant reduced odds ratios (ORs) of influenza/pneumonia death (OR, 0.60; 95% confidence interval [CI], 0.44 to 0.81) and COPD death (OR, 0.17; 95% CI, 0.07 to 0.42) and similarly reduced survival hazard ratios. Findings were confirmed with the case-control studies. Confounding factors not considered may explain some of the effects observed. This study found a dramatically reduced risk of COPD death and a significantly reduced risks of influenza death among moderate-dose statin users.

Characteristics of Adults Dying with COPD

To describe factors associated with COPD deaths in the United States. Cross-sectional survey. A total of 12,803 decedents in the National Mortality Followback Survey, a nationally representative sample of US deaths in 1993. We compared the characteristics of adults > or = 35 years of age who died with COPD (bronchitis, emphysema, chronic airway obstruction) with those dying without COPD listed on their death certificates. Of the estimated 225,400 adults who died with COPD in 1993, 16.7% had never smoked. People dying with COPD were more likely than those dying without COPD to be current smokers (odds ratio [OR], 6.5; 95% confidence interval [CI], 4.3 to 9.9) or former smokers (OR, 3.7; 95% CI, 2.5 to 5.3), have a history of asthma (OR, 5.0; 95% CI, 3.2 to 7.8), be underweight (OR, 4.5; 95% CI, 2.8 to 7.2), and be of the white race (OR, 3.1; 95% CI, 2.4 to 4.0), after controlling for age group and sex. A significant proportion of COPD-related deaths occurs in never-smokers. Factors such as a history of asthma and being underweight are associated with COPD mortality and may provide additional opportunities for intervention.

Histamine airway hyper-responsiveness and mortality from chronic obstructive pulmonary disease: a cohort study

Smoking and airway lability, which is expressed by histamine airway hyper-responsiveness, are known risk factors for development of respiratory symptoms. Smoking is also associated with increased mortality risks. We studied whether airway hyper-responsiveness is associated with increased mortality, and whether this risk was independent of smoking and reduced lung function. We followed up 2008 inhabitants of the communities of Vlagtwedde, Vlaardingen, and Meppel (Netherlands), who had histamine challenge test data, from 1964-72 for 30 years. Follow-up was 99% successful (29 patients lost to follow-up) with 1453 participants alive and 526 deaths (246 died from cardiovascular disease, 54 from lung cancer, and 21 from chronic obstructive pulmonary disease [COPD]). Mortality from COPD increased with more severe hyper-responsiveness; relative risks of 3.83 (95% CI 0.97-15.1), 4.40 (1.16-16.7), 4.78 (1.27-18.0), 6.69 (1.71-26.1), and 15.8 (3.72-67.1) were associated with histamine thresholds of 32 g/L, 16 g/L, 8 g/L, 4 g/L, and 1 g/L, respectively, compared with no hyper-responsiveness. These risks were adjusted for sex, age, smoking, lung function, body-mass index, positive skin tests, eosinophilia, asthma, and city of residence. Increased histamine airway hyper-responsiveness predicts mortality from COPD. Although this trend was more pronounced in smokers, an increasing proportion of COPD deaths with increasing hyper-responsiveness was also present among individuals who had never smoked.

Upregulation of Gelatinases A and B, Collagenases 1 and 2, and Increased Parenchymal Cell Death in COPD

A central feature in the pathogenesis of COPD is the inflammation coexisting with an abnormal protease/antiprotease balance. However, the possible role of different serine and metalloproteinases remains controversial. We examined the expression of gelatinases A and B (matrix metalloproteinase [MMP]-2 and MMP-9); collagenases 1, 2, and 3 (MMP-1, MMP-8, and MMP-13); as well as the presence of apoptosis in lung tissues of 10 COPD patients and 5 control subjects. In addition, gelatinase-A and gelatinase-B activities were assessed in BAL obtained from eight COPD patients, and from six healthy nonsmokers and six healthy smoker control subjects. Tertiary referral center and university laboratories of biochemistry, and lung cell kinetics. Immunohistochemical analysis of COPD lungs showed a markedly increased expression of collagenases 1 and 2, and gelatinases A and B, while collagenase 3 was not found. Neutrophils exhibited a positive signal for collagenase 2 and gelatinase B, whereas collagenase 1 and gelatinase A were revealed mainly in macrophages and epithelial cells. BAL gelatin zymography showed a moderate increase of progelatinase-A activity and intense bands corresponding to progelatinase B. In situ end labeling of fragmented DNA displayed foci of positive endothelial cells, although some alveolar epithelial, interstitial, and inflammatory cells also revealed intranuclear staining. These findings suggest that there is an upregulation of collagenase 1 and 2 and gelatinases A and B, and an increase in endothelial and epithelial cell death, which may contribute to the pathogenesis of COPD through the remodeling of airways and alveolar structures.

Trends in COPD morbidity and mortality in Tecumseh, Michigan.

Trends in COPD morbidity and mortality were investigated among the population of Tecumseh, Michigan, for the period 1959 to 1987. COPD was mentioned on the death certificates of 11% (102) of deceased men and 13% (24) of deceased women. Forty-one percent of these deaths was attributed to COPD as the underlying cause and the remainder to COPD as a contributory cause. Usage of diagnostic terms changed during the course of the study; emphysema was mentioned on 81% of certificates completed prior to 1968, whereas COPD was entered on 77% of the certificates written after 1978. Proportional mortality rates of COPD increased from 8% during 1959 to 1967 to 13.3% during 1979 to 1987 among men, and from 2.7% during the earlier years to 4.3% during the later years among women. Death rates for COPD and for all causes combined increased among men from the early 1960s to the late 1970s, then declined. Death rates for all causes combined were stable among women, but COPD death rates may have increased. Prevalence rates for chronic bronchitis were lower at the third examination than at the second in both sexes. Prevalence of obstructive airway disease was highest at the first and lower at the second and third examinations in men but not in women. Agreement between study diagnoses of COPD and entry of COPD on death certificates was poor. COPD was recorded on the death certificate for only 21% of men and only 6% of women who had COPD diagnosed at a study examination.(ABSTRACT TRUNCATED AT 250 WORDS)