Patient and Health Care Professional Perspectives: A Case Study of the Lung Cancer Integrated Care Pathway.

INTRODUCTION: The purpose of this study was to evaluate the perception of the quality of care, considering both patient experience and health care professionals' perceptions as well as patient outcome measures of an integrated lung cancer pathway. METHODS: A cross-sectional study was conducted in 2016 at Ferrara University Hospital, Italy. OPportunity for Treatment In ONcology (OPTION) questionnaires were administered to 77 patients, and the Care Process Self-Evaluation Tool (CPSET) questionnaires were given to 38 health care professionals. The effectiveness of the pathway was evaluated by analysing the tool's positive impact on lung cancer surgery volume and 30-day mortality. RESULTS: Seventy-seven patients were enrolled, and 38 health care professionals assessed the CPSET questionnaire. The highest scores were related to "respect" (100%), "satisfaction" (98.7%), and "trust" (97.4%) on the OPTION and to "patient-focused vision" (97.2%) and "patient engagement" (94.4%) on the CPSET. The lowest scores were related to "information" (26%) and "cooperation with general practitioner" (17.6%) on the OPTION and "cooperation between the hospital and primary care" (23.5%) for the CPSET. The outcomes analysis shows an increase in the volume of activity and a decrease in 30-day mortality after pathway implementation. DISCUSSION: The lung cancer pathway is a patient-centred intervention that enables care to be shaped for patient needs in order to improve the quality and efficiency of service and clinical outcome.

Phospho-p38 MAPK expression in COPD patients and asthmatics and in challenged bronchial epithelium.

BACKGROUND: The role of mitogen-activated protein kinases (MAPK) in regulating the inflammatory response in the airways of patients with chronic obstructive pulmonary disease (COPD) and asthmatic patients is unclear. OBJECTIVES: To investigate the expression of activated MAPK in lungs of COPD patients and in bronchial biopsies of asthmatic patients and to study MAPK expression in bronchial epithelial cells in response to oxidative and inflammatory stimuli. METHODS: Immunohistochemical expression of phospho (p)-p38 MAPK, p-JNK1 and p-ERK1/2 was measured in bronchial mucosa in patients with mild/moderate (n = 17), severe/very severe (n = 16) stable COPD, control smokers (n = 16), control non-smokers (n = 9), in mild asthma (n = 9) and in peripheral airways from COPD patients (n = 15) and control smokers (n = 15). Interleukin (IL)-8 and MAPK mRNA was measured in stimulated 16HBE cells. RESULTS: No significant differences in p-p38 MAPK, p-JNK or p-ERK1/2 expression were seen in bronchial biopsies and peripheral airways between COPD and control subjects. Asthmatics showed increased submucosal p-p38 MAPK expression compared to COPD patients (p < 0.003) and control non-smokers (p < 0.05). Hydrogen peroxide (H2O2), cytomix (tumour necrosis factor-α + IL-1ß + interferon-γ) and lipopolysaccharide (LPS) upregulated IL-8 mRNA at 1 or 2 h. p38 MAPKα mRNA was significantly increased after H2O2 and LPS treatment. JNK1 and ERK1 mRNA were unchanged after H2O2, cytomix or LPS treatments. CONCLUSION: p-p38 MAPK expression is similar in stable COPD and control subjects but increased in the bronchi of mild asthmatics compared to stable COPD patients. p38 MAPK mRNA is increased after bronchial epithelial challenges in vitro. These data together suggest a potential role for this MAPK in Th2 inflammation and possibly during COPD exacerbations.

Gastrointestinal bleeding in lung leiomyosarcoma history: report of a case.

The paper presents an unusual case of single small bowel metastasis from primary lung leiomyosarcoma (PLL) presenting with abdominal pain and gastrointestinal (GI) bleeding successfully treated by surgery with radical aim.

Primary Pulmonary Epithelioid Hemangioendothelioma: A Rare Cause of PET-Negative Pulmonary Nodules.

We report here a case of primary pulmonary epithelioid hemangioendothelioma diagnosed in a 67-year-old Caucasian man, presenting with exertion dyspnoea, dry cough, and multiple bilateral pulmonary nodules revealed by computed tomography. At the 18F-fluorodeoxyglucose positron emission tomography, these nodules were negative. The histopathological diagnosis was made on a pulmonary wedge resection (performed during video-thoracoscopic surgery).

Mechanisms involved in lung cancer development in COPD.

Lung cancer and chronic obstructive pulmonary disease (COPD) are leading causes of morbidity and mortality worldwide. They share a common environmental risk factor in cigarette smoke exposure and a genetic predisposition represented by the incidence of these diseases in only a fraction of smokers. COPD is also a major independent risk factor for lung carcinoma, among long-term smokers. Smokers with COPD also have a higher risk of developing a specific histological subtype of non-small cell lung cancer termed squamous cell carcinoma. For these reasons the focus of this review is on the potential pathogenic molecular links between tobacco smoking-related COPD and squamous cell carcinoma. We believe that we need to promote more studies on the molecular and cellular pathobiology of smokers with premalignant bronchial lesions of the squamous cell lung carcinoma compared with a control group of smokers with and without COPD to unravel the complex molecular interactions between COPD and early squamous cell lung carcinoma. These studies should also look at younger healthy smokers in combination with risk models of lung cancer and COPD. Overall these studies may allow the discovery of new molecular targets of the early carcinogenesis process that in the foreseeable future may render the early diagnosis and treatment, and may be even the prevention, of invasive squamous cell lung carcinoma a reality.