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BackgroundIn addition to lung involvement, several other diseases and syndromes coexist in patients with chronic obstructive pulmonary disease (COPD). Our purpose was to investigate the prevalence of idiopathic arterial hypertension (IAH), ischemic heart disease, heart failure, peripheral vascular disease (PVD), diabetes, osteoporosis, and anxious depressive syndrome in a clinical setting of COPD outpatients whose phenotypes (predominant airway disease and predominant emphysema) and severity (mild and severe diseases) were determined by clinical and functional parameters.MethodsA total of 412 outpatients with COPD were assigned either a predominant airway disease or a predominant emphysema phenotype of mild or severe degree according to predictive models based on pulmonary functions (forced expiratory volume in 1 second/vital capacity; total lung capacity %; functional residual capacity %; and diffusing capacity of lung for carbon monoxide %) and sputum characteristics. Comorbidities were assessed by objective medical records.ResultsEighty-four percent of patients suffered from at least one comorbidity and 75% from at least one cardiovascular comorbidity, with IAH and PVD being the most prevalent ones (62% and 28%, respectively). IAH prevailed significantly in predominant airway disease, osteoporosis prevailed significantly in predominant emphysema, and ischemic heart disease and PVD prevailed in mild COPD. All cardiovascular comorbidities prevailed significantly in predominant airway phenotype of COPD and mild COPD severity.ConclusionSpecific comorbidities prevail in different phenotypes of COPD; this fact may be relevant to identify patients at risk for specific, phenotype-related comorbidities. The highest prevalence of comorbidities in patients with mild disease indicates that these patients should be investigated for coexisting diseases or syndromes even in the less severe, pauci-symptomatic stages of COPD. The simple method employed to phenotype and score COPD allows these results to be translated easily into daily clinical practice.

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Patients treated for lung cancer may develop lung toxicity induced by chemotherapy (DILD), radiation or combined radiation recall pneumonitis. In the literature, some cases of immune-mediated pneumonitis have been reported associated with immunotherapy. The clinical and radiologic features of interstitial lung toxicity are unspecific, dyspnea and dry cough are the most common symptoms while the most frequent radiological pattern is the cryptogenic organizing pneumonia (COP). Why only some individuals treated with these drugs develop interstitial lung toxicity is unclear. Old age, ethnicity, doses, drug interactions, oxygen damage and radiation therapy are known risk factors, as well as pre-existing lung disease. There are no clear indicators of the risk of developing lung toxicity secondary to drugs or radiation for individual patients. In the last few years some studies have reported the utility of KL 6 for the evaluation of DILD. The treatment is based on high doses of systemic steroids or immune suppressor. In this study we report severe interstitial lung damage in patients treated with different anti-blastic, immune and radiation therapies. Treated with surgery, chemotherapy, immuno-and radiotherapy for lung cancer, they unfortunately died of severe DILD.

Abstract. Idiopathic pulmonary fibrosis (IPF) is a rare interstitial lung disease limited to the lung with an undefined etiopathogenesis and a very short life expectancy (less than 5 years). IPF susceptibility has been associated with several genetic and environmental risk factors and the prognosis isIdiopathic pulmonary fibrosis (IPF) is an interstitial lung disease with poor prognosis and an undefined etiopathogenesis. Several genetic and environmental risk factors for IPF have been identified including cigarette smoking, metal dust and other pollutant exposure, genetic mutations and polymorphisms (1-5). IPF prognosis is really poor (less than 5 years) and is conditioned by comorbidities negatively affecting patients' quality of life and survival (e.g. gastro-esophageal reflux, depression, venous thromboembolism, pulmonary hypertension and other cardiovascular disorders, and lung cancer) (6-10). The incidence of pulmonary neoplasm is much higher in IPF patients than in the general population (11). Ozawa et al. (12) for instance, reported 3.3%, 15.4% and 54.7% of lung cancer incidence in IPF patients after one, five and ten years of follow-up, respectively (12). Common mechanisms shared by the two diseases remain unknown. An aberrant expression of miRNAs regulating non-small cell lung cancer (NSCLC) and IPF has been suggested together with a crucial role of tyrosine kinase inhibitor directed against growth factors (plateletderived growth factor, vascular endothelial growth factor and fibroblast growth factor) (13,14).Lung cancer (LC) significantly reduces survival of IPF patients, including patients with combined pulmonary emphysema and pulmonary fibrosis (15). It generally occurs in the peripheral areas of the lower lobes, where fibrotic changes are predominant. In particular, LC develops from honeycomb areas or in the border between honeycombing and non fibrotic areas and the squamous cell carcinoma is the predominant histological type (16,17). Invasive diagnostic or therapeutic procedures for neoplasms promote the development of Acute exacerbations (AE) in 80% of IPF patients and the lung surgical treatment puts about 1/5 of them at high risk of death (17,18). A perioperative Pirfenidone treatment has recently been proposed to reduce the incidence of postoperative acute events (18)(19)(20). In this context, the therapeutic management of LC is a difficult task and is still questioned, especially in IPF patients with severe fibrotic involvement, whether the tumor should be treated or not (21,22). Although Lee et al. (15) reported that radiotherapy and surgical treatments of LC result in a reduced survival of IPF patients, according to Kumar et al. (19) lung resection in selected cases can improve their survival. Furthermore, Tomassetti and colleagues (21) have suggested that in mild IPF patients the sublobar resection in 773