Smoking Cessation by Phone Counselling in a Lung Cancer Screening Program: A Retrospective Comparative Cohort Study.

Introduction: Smoking cessation integration within lung cancer screening programs is challenging. Currently, phone counselling is available across Canada for individuals referred by healthcare workers and by self-referral. We compared quit rates after phone counselling interventions between participants who self-refer, those referred by healthcare workers, and those referred by a lung cancer screening program. Methods: This is a retrospective cohort study of participants referred to provincial smoking cessation quit line in contemporaneous cohorts: self-referred participants, healthcare worker referred, and those referred by a lung cancer screening program if they were still actively smoking at the time of first contact. Baseline, covariates (sociodemographic information, smoking history, and history of mental health disorder) and quit intentions (stage of change, readiness for change, previous use of quit programs, and previous quit attempts) were compared among the three cohorts. Our primary outcome was defined as self-reported 30-day abstinence rates at 6 months. Multivariable logistic regression was used to identify whether group assignment was associated with higher quit rates. Results: Participants referred by a lung cancer screening program had low quit rates (12%, 95% CI: 5-19) at six months despite the use of phone counselling. Compared to patients who were self-referred to the smoking cessation phone helpline, individuals referred by a lung cancer screening program were much less likely to quit (adjusted OR 0.37; 95% CI: 0.17-0.8), whereas those referred by healthcare workers were twice as likely to quit (adjusted OR 2.16 (1.3-3.58)) even after adjustment for differences in smoking intensity and quit intentions. Conclusions: Phone counselling alone has very limited benefit in a lung cancer screening program. Participants differ significantly from those who are otherwise referred by healthcare workers. This study underlines the importance of a dedicated and personalized tobacco treatment program within every lung cancer screening program. The program should incorporate best practices and encourage treatment regardless of readiness to quit.

Surgical Prehabilitation in Patients with Cancer: State-of-the-Science and Recommendations for Future Research from a Panel of Subject Matter Experts.

This review by a 10-member panel of experts in surgical prehabilitation addresses processes that may improve oncologic care. Surgical prehabilitation is the process on the continuum of care that occurs between the time of cancer diagnosis and the beginning of surgical treatment. The panel focused on the current state-of-the-science and recommended future research that would help to identify the elements that enhance preoperative physical, nutritional, and psychological health in anticipation of surgery, mitigate the burden of disease, facilitate the return of patient health status to baseline values, decrease postoperative morbidity, and reduce health care costs.

Using laboratory models to test treatment: morphine reduces dyspnea and hypercapnic ventilatory response.

RATIONALE: Opioids are commonly used to relieve dyspnea, but clinical data are mixed and practice varies widely. OBJECTIVES: Evaluate the effect of morphine on dyspnea and ventilatory drive under well-controlled laboratory conditions. METHODS: Six healthy volunteers received morphine (0.07 mg/kg) and placebo intravenously on separate days (randomized, blinded). We measured two responses to a CO(2) stimulus: (1) perceptual response (breathing discomfort; described by subjects as "air hunger") induced by increasing partial pressure of end-tidal carbon dioxide (Pet(CO2)) during restricted ventilation, measured with a visual analog scale (range, "neutral" to "intolerable"); and (2) ventilatory response, measured in separate trials during unrestricted breathing. MEASUREMENTS AND MAIN RESULTS: We determined the Pet(CO2) that produced a 60% breathing discomfort rating in each subject before morphine (median, 8.5 mm Hg above resting Pet(CO2)). At the same Pet(CO2) after morphine administration, median breathing discomfort was reduced by 65% of its pretreatment value; P < 0.001. Ventilation fell 28% at the same Pet(CO2); P < 0.01. The effect of morphine on breathing discomfort was not significantly correlated with the effect on ventilatory response. Placebo had no effect. CONCLUSIONS: (1) A moderate morphine dose produced substantial relief of laboratory dyspnea, with a smaller reduction of ventilation. (2) In contrast to an earlier laboratory model of breathing effort, this laboratory model of air hunger established a highly significant treatment effect consistent in magnitude with clinical studies of opioids. Laboratory studies require fewer subjects and enable physiological measurements that are difficult to make in a clinical setting. Within-subject comparison of the response to carefully controlled laboratory stimuli can be an efficient means to optimize treatments before clinical trials.

Physiologic changes and clinical correlates of advanced dyspnea.

PURPOSE OF REVIEW: To discuss the pathophysiology of dyspnea as it relates to patients suffering with chronic respiratory illness or end-stage disease. RECENT FINDINGS: There are several publications highlighting important new concepts in this field including a new multidimensional model of dyspnea, similar to that developed for pain, that sheds new insight into the pathophysiology. Research in pulmonary rehabilitation, exercise testing and distractive auditory stimulation has also contributed to our understanding. Finally, there are new data on the emotional response of laboratory-induced dyspnea. SUMMARY: Dyspnea is a complex symptom widely prevalent in advanced disease that involves multiple causes and pathophysiologies. The sensation of dyspnea is subjective and often evokes discomfort, fear, and anxiety. We recommend that this symptom be evaluated whenever vital signs are taken.

Obstructive sleep apnea and erectile dysfunction: still a neglected risk factor?

INTRODUCTION: Erectile dysfunction (ED) is a well-known entity with determined risk factors, which generally has a negative impact on quality of life. Obstructive sleep-disordered breathing (SDB), often referred to as obstructive sleep apnea, stands among the possible risk factors for ED. DISCUSSION: Literature review suggests that SDB induces a spectrum of abnormalities in neural, hormonal, and vascular regulation that may contribute to the development of ED. While more studies are required to imply SDB as a risk factor for ED, several case series and expert opinion have contributed evidence for a causal relationship. CONCLUSION: In clinical practice, men presenting with symptoms of sexual dysfunction often have concomitant sleep disorders requiring treatment. There is now evidence to suggest that treating SDB may be an effective treatment for ED. It is the authors' opinion that patients with erectile dysfunction would benefit from a sleep evaluation.

Airway epithelial gene expression in the diagnostic evaluation of smokers with suspect lung cancer.

Lung cancer is the leading cause of death from cancer in the US and the world. The high mortality rate (80-85% within 5 years) results, in part, from a lack of effective tools to diagnose the disease at an early stage. Given that cigarette smoke creates a field of injury throughout the airway, we sought to determine if gene expression in histologically normal large-airway epithelial cells obtained at bronchoscopy from smokers with suspicion of lung cancer could be used as a lung cancer biomarker. Using a training set (n = 77) and gene-expression profiles from Affymetrix HG-U133A microarrays, we identified an 80-gene biomarker that distinguishes smokers with and without lung cancer. We tested the biomarker on an independent test set (n = 52), with an accuracy of 83% (80% sensitive, 84% specific), and on an additional validation set independently obtained from five medical centers (n = 35). Our biomarker had approximately 90% sensitivity for stage 1 cancer across all subjects. Combining cytopathology of lower airway cells obtained at bronchoscopy with the biomarker yielded 95% sensitivity and a 95% negative predictive value. These findings indicate that gene expression in cytologically normal large-airway epithelial cells can serve as a lung cancer biomarker, potentially owing to a cancer-specific airway-wide response to cigarette smoke.