Sex Differences in Survival of Oxygen-dependent Patients with Chronic Obstructive Pulmonary Disease

Machado, Maria Christina Lombardi Oliveira; Krishnan, Jerry A.; Buist, Sonia; Bilderback, Andrew; Fazolo, Guilherme P.; Santarosa, Michelle G.; Queiroga, Fernando Ramos; Vollmer, William M.

doi:10.1164/rccm.200507-1057oc

Cited by 99 publications

(57 citation statements)

References 56 publications

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“…Oxygen prescriptions (duration and flow) should be based on arterial blood gas measurements and 6 minute walk tests results [80] . Longer term exposure to oxygen therapy (> 15 hr/day) over a number of years significantly improves survival [81,82] . Although oxygen therapy prescription during exercise is not well supported by evidence, in current practice, oxygen during exercise is being prescribed for individuals with severe COPD who become hypoxemic only when exercising.…”

Section: Oxygen Therapymentioning

confidence: 99%

Best practice in nursing care of dyspnea: The 6th vital sign in individuals with COPD

Bailey

Boyles

Cloutier

et al. 2013

JNEP

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Aim: The aim of this paper is to highlight evidence and key nursing practice, education, organization and policy recommendations from the original and revised Registered Nurses' Association of Ontario Best Practice Guideline, Nursing Care of Dyspnea: The 6th Vital Sign in Individuals with Chronic Obstructive Pulmonary Disease (COPD). This paper introduces the notion of dyspnea as the sixth vital sign and presents evidence from the RNAO Best Practice Guideline and other relevant literature to support and enhance nursing care of dyspnea in clients with COPD.Background: COPD is an increasingly serious health issue. Nurses have significant opportunity to positively influence client outcomes and quality of life by assessing dyspnea, identifying problems, and applying appropriate evidence-based interventions. Best practice guidelines developed by the RNAO provide a framework to enhance nursing practice and client care.Design: A panel of nurses was assembled for the initial development of the guideline and more recently, the revision to the original guideline.Method: A structured evidence review based on the scope of the original guideline and supported by three clinical questions was conducted to capture the relevant literature and guidelines published since the original publication.Results: As a result of this work recommendations for nursing practice and education are discussed. Organizational and policy recommendations are also outlined. Conclusions:Nurses have opportunity to positively influence client outcomes and quality of life by assessing dyspnea, identifying problems, and applying appropriate evidence-based interventions.Relevance to Clinical Practice: Recommendations made in the best practice guideline will enhance nursing care of dyspnea in clients with COPD and dyspnea should be recognized as the sixth vital sign in individuals with COPD.

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Section: Oxygen Therapymentioning

confidence: 99%

Best practice in nursing care of dyspnea: The 6th vital sign in individuals with COPD

Bailey

Boyles

Cloutier

et al. 2013

JNEP

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“…Gender differences: These differences for COPD survival prognosis have been reported repeatedly but remain controversial 8,[31][32][33] . Some have reported that women have better survival 8,31,32 , but others describe contradictory findings 33 .…”

Section: Components Of Copd Prognostic Scorementioning

confidence: 99%

“…Some have reported that women have better survival 8,31,32 , but others describe contradictory findings 33 . We hypothesize that it is difficult to adjust all coverable parameters in multiple-variable analysis when comparing both sexes because the two sexes have different FEV 1 predicting formulas and different reference values for exercise tolerance tests.…”

Section: Components Of Copd Prognostic Scorementioning

confidence: 99%

Chronic obstructive pulmonary disease prognostic score: A new index

Horita¹,

Koblížek²,

Plutinsky³

et al. 2016

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. The evaluation of chronic obstructive pulmonary disease (COPD) has been shifting from spirometry to focus on the patients' overall health. Despite the existence of many COPD prognostic scales, there remains a large gap for improvement, in particular a scale that incorporates the current focus on overall health. Methods. We proposed a new prognostic scale (the COPD Prognostic Score) through discussion among the authors based on published studies. Validation was retrospective, using data from the National Emphysema Treatment Trial. Results. The scores ranged from 0-16, where 16 indicated the poorest prognosis. We assigned 4 points each for forced expiratory volume in one second (%predicted), the modified Medical Research Council dyspnea scale, and age; 2 points for the hemoglobin level; and one point each for decreased activity and respiratory emergency admission in the last two years. The validation cohort included 607 patients and consisted of 388 men (73.9%) and 219 women (36.1%), mean age 67 ± 6 years and an average forced expiratory volume in one second (% predicted) of 27 ± 7%. A one-point increase in the score was associated with increased all-cause death, with a hazard ratio of 1.28 (95%CI: 1.21-1.36. P < 0.001). The areas under the receiver operating characteristic curves for two-year and five-year all-cause death for the new scale were 0.72 and 0.66, respectively. These values were higher than those given by the body mass index, airflow obstruction, dyspnea, and exercise capacity (BODE) index and age, dyspnea, airway obstruction (ADO) index. Conclusion. The preliminary validation for a new COPD prognostic scale: the COPD Prognostic Score was developed with promising results thus far. Above mentioned 16-point score accurately predicted 2-year and 5-year all-cause mortality among subjects who suffered from severe and very severe COPD.

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“…In this study, we report the role of the nmMLCK2 splice variant in vascular barrier regulation, and we describe the consequences of overexpressing this isoform specifically in murine endothelium. Furthermore, as several acute and chronic inflammatory pulmonary disorders, which include ALI and acute respiratory distress syndrome (ARDS), are influenced by gender, [ 13 ], [ 14 ], [ 15 ], [ 16 ], [ 17 ], [ 18 ], [ 19 ], [ 20 ], [ 21 ] and [ 22 ] age, [ 23 ], [ 24 ], [ 25 ], [ 26 ] and [ 27 ] or gender-age interactions, [ 28 ], [ 29 ] and [ 30 ] we designed our study to evaluate the influence of these comodifiers on postulated nmMLCK2-mediated increases in vascular paracellular transport. This is supported by findings in mice, which like humans, have varying respiratory properties that differ between sexes [ 31 ], [ 32 ] and [ 33 ] and with age, [ 34 ] and [ 35 ] information often neglected when describing a pulmonary phenotype.…”

Section: Translational Significancementioning

confidence: 99%

A transgenic mouse with vascular endothelial over-expression of the non-muscle myosin light chain kinase-2 isoform is susceptible to inflammatory lung injury: role of sexual dimorphism and age

Moitra

Evenoski

Sammani

et al. 2008

Translational Research

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We have generated genetically engineered mice that are uniquely susceptible to lipopolysaccharide (LPS)-induced and mechanical ventilation-induced lung injury in a sex-specific and age-specific manner. These mice express a nonmuscle isoform of the myosin light chain kinase gene (nmMLCK2) targeted to the endothelium. Homozygous mice have significantly reduced fecundity and litter survival until weaning, and they are initially growth delayed but eventually exceed the size of wildtype littermates. Mice at all ages show increased protein transport across the lung barrier; however, the phenotype is most discernible in 8-12-week-old male mice. When subjected to a clinically relevant LPS-induced lung injury model, 8-12-week-old young females and 30-36-week-old males seem to be the most significantly injured group. In contrast, 30-36-week-old males remain the most significantly injured group when mechanically ventilated at high tidal volumes, which is a clinically relevant model of mechanical stress lung injury. These data reveal that nmMLCK2 overexpression in the endothelium exacerbates lung injury in vivo in a sexually dimorphic and age-dependent manner.Actin microfilaments generate force by virtue of their ability to contract away from their site of attachment to the plasma membrane, and they do so via traction of the myosin light chain head groups attached to actin filaments by cross-bridges. The cross-bridge pulling action of myosin involves a conformational change in the molecule initiated by energetic phosphorylation of Ser19 on the myosin light chains. 1 The key enzyme involved in this phosphorylation event is myosin light chain kinase (MLCK), which exists in different tissues, and it may be characterized broadly as skeletal/cardiac, smooth muscle, and nonmuscle myosin light chain kinase (nmMLCK) isoforms. Although biochemical evidence for the existence of a Ca 2+ /calmodulin-dependent nonmuscle isoform in cultured endothelial cell (EC) was suggested earlier, [ 2 ] and [ 3 ] the controversy as to whether this enzymatic activity is identical to the 110-kDa protein found abundantly in smooth muscle preparations was resolved when we provided conclusive proof of a larger MLCK protein isoform (210 kDa) by cloning the gene (MYLK) from a human EC-derived cDNA library. 4 The gene was subsequently mapped to chromosome 3q21. 5

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Sex Differences in Survival of Oxygen-dependent Patients with Chronic Obstructive Pulmonary Disease

Abstract: Among patients with COPD on LTOT, women were more likely to die than men.

Cited by 99 publications

References 56 publications

Best practice in nursing care of dyspnea: The 6th vital sign in individuals with COPD

Best practice in nursing care of dyspnea: The 6th vital sign in individuals with COPD

Chronic obstructive pulmonary disease prognostic score: A new index

A transgenic mouse with vascular endothelial over-expression of the non-muscle myosin light chain kinase-2 isoform is susceptible to inflammatory lung injury: role of sexual dimorphism and age

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