BackgroundRed cell distribution width (RDW), one of many routinely examined parameters, shows the heterogeneity in erythrocyte size. We investigated the association of RDW levels with clinical parameters and prognosis of lung cancer patients.MethodsClinical and laboratory data from 332 patients with lung cancer in a single institution were retrospectively studied by univariate analysis. Kaplan-Meier survival analysis and Cox proportional hazard models were used to examine the effect of RDW on survival.ResultsThe RDW levels were divided into two groups: high RDW (>=15%), n=73 vs. low RDW, n=259 (<15%). Univariate analysis showed that there were significant associations of high RDW values with cancer stage, performance status, presence of other disease, white blood cell count, hemoglobin, mean corpuscular volume, platelet count, albumin level, C-reactive protein level, and cytokeratin 19 fragment level. Kruskal-Wallis tests revealed an association of RDW values with cancer stage in patients irrespective of comorbidity (patient with/without comorbidity: p<0.0001, patient without comorbidity: p<0.0001). Stages I-IV lung cancer patients with higher RDW values had poorer prognoses than those with lower RDW values (Wilcoxon test: p=0.002). In particular, the survival rates of stage I and II patients (n=141) were lower in the high RDW group (n=19) than in the low RDW group (n=122) (Wilcoxon test: p<0.001). Moreover, multivariate analysis showed higher RDW is a significant prognostic factor (p=0.040).ConclusionRDW is associated with several factors that reflect inflammation and malnutrition in lung cancer patients. Moreover, high levels of RDW are associated with poor survival. RDW might be used as a new and convenient marker to determine a patient’s general condition and to predict the mortality risk of lung cancer patients.

Half of patients with empyema were HCAE patients, who had comorbidities, bacteriological profile and outcome different from CAE patients. The patient with HCAE should be differentiated from CAE patient, and the stratification of patients based on risk factors may be useful for treatment strategy.

An 84-year-old woman being treated for miliary tuberculosis (TB) with rifampicin (RFP), isoniazid (INH), ethambutol (EB) and corticosteroids suffered from a persistent fever for five months. While tapering the dose of prednisolone, chest computed tomography (CT) revealed diffuse ground glass opacities (GGO) and bronchoalveolar lavage fluid (BALF) showed an increase in lymphocytes. After the anti-TB drugs were discontinued and the dose of the corticosteroids was increased, the CT findings and fever improved considerably. However, readministration of RFP provoked an inflammatory reaction, leading to a diagnosis of RFP-induced pneumonitis. This condition is very rare. This is the first report of RFP-induced pneumonitis occurring during adjunct steroid therapy.

It is possible that asthma tends to involve autoimmunity associated with antinuclear antibody more frequently than COPD because asthma is the more robust factor for antinuclear antibody positivity. Antinuclear antibody and rheumatoid factor are associated with eosinophilic responses, but they do not work as biomarkers for disease severity.

Gefitinib and erlotinib, epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), are widely used anticancer drugs for patients with non-small cell lung cancer (NSCLC), especially for those with EGFR-activating mutations. Both agents are considered to be less toxic compared with cytotoxic drugs; however, serious adverse events including interstitial lung disease (ILD) which can be fatal occur rarely. After such an event, physicians avoid to use another TKI. In such cases, patients and physicians are forced to make difficult decisions or reluctantly choose TKI when there is no other option. Here we report a case of a patient with lung adenocarcinoma who showed good recovery from gefitinib-induced ILD by high-dose corticosteroid therapy. The patient was then administrated erlotinib as second-line chemotherapy and showed tumor shrinkage without ILD after 6 months of treatment. We discuss the common features of the cases in the previous documentations and ours which were successfully retreated with erlotinib after gefitinib-induced ILD had previously developed.