Incidence of brain metastasis in lung adenocarcinoma at initial diagnosis on the basis of stage and genetic alterations.

OBJECTIVE: Patients with lung adenocarcinoma (ADC) are at higher risk of the development of brain metastasis (BM), and genetic alterations are associated with BM. PATIENTS AND METHODS: A total of 598 patients with lung ADC in our institution between January 2014 and December 2014 were reviewed retrospectively. We evaluated the incidence of BM by stage and genetic alterations. RESULTS: Of the 598 patients, 97 (16.2%) had BM, which occurred across all stages. The incidence of BM showed a tendency to increase as the stage increased (p < 0.001, trend test). Although patients with EGFR mutations had BM across all stages, those with ALK or K- mutations had BM only in stage III and IV diseases. Regardless of types of mutations, the incidence of BM showed a tendency to increase as the T or N staging increased (p < 0.001 for each of EGFR, ALK, and K-RAS mutations, trend test). Whereas BM incidence showed a tendency to increase as the M staging increased in patients with EGFR-mutant lung ADC (p < 0.001, trend test), there was no linear trend between M staging and ALK (p = 0.469, trend test) or K-RAS mutations (p = 0.066, trend test). After adjusting covariables, EGFR mutations were associated with BM in never-smokers (adjusted OR = 2.07, 95% CI = 1.02-4.34) and K-RAS mutations were risk factors for BM in males (adjusted OR = 3.86, 95% CI = 1.01-14.43). CONCLUSIONS: BM occurred in approximately 16% of lung ADC patients, including 3% with stage I diseases. Whereas EGFR-mutant lung ADC had BM across all stages, ALK- or K-RAS-mutant lung ADC had BM only in advanced stages. EGFR mutations were risk factors for BM among never-smokers and K-RAS mutations were risk factors among males.

Lung function, coronary artery calcification, and metabolic syndrome in 4905 Korean males.

BACKGROUND: Impaired lung function is an independent predictor of cardiovascular mortality. We assessed the relationships of lung function with insulin resistance (IR), metabolic syndrome (MetS), systemic inflammation and coronary artery calcification score (CACS) measured by computed tomography (CT) scan an indicator of coronary atherosclerosis. METHODS: We identified 4905 adult male patients of the Health Promotion Center in Samsung Medical Center between March 2005 and February 2008 and retrospectively reviewed the following data for these patients: pulmonary function, CT-measured CACS, anthropometric measurement, fasting glucose, insulin, lipid profiles, serum C-reactive protein (CRP) and homeostatic model assessment (HOMA-IR). MetS was defined according to the AHA/NHLBI criteria. RESULTS: When the subjects were divided into four groups according to quartiles of FVC or FEV(1) (% pred), serum CRP level, HOMA-IR, prevalence of MetS and CACS significantly increased as the FVC or FEV(1) (% pred) decreased. The odds ratios (ORs) for MetS in the lowest quartiles of FVC and FEV(1) (% pred) were 1.85 (95% CI, 1.49-2.30; p<0.001) and 1.47 (95% CI, 1.20-1.81; p<0.001) respectively. The ORs for the presence of coronary artery calcification in the lowest quartiles of FVC and FEV(1) (% pred) were 1.31 (95% CI, 1.09-1.58; p=0.004) and 1.22 (95% CI, 1.02-1.46; p=0.029) respectively. Obesity, CRP, HOMA-IR, and the presence of coronary artery calcium were independent risk predictors for impaired lung function. CONCLUSION: Metabolic syndrome, insulin resistance, coronary atherosclerosis, and systemic inflammation are closely related to the impaired lung function.

High virulent clinical isolates of Mycobacterium abscessus from patients with the upper lobe fibrocavitary form of pulmonary disease.

Pulmonary disease caused by nontuberculous mycobacteria (NTM), including Mycobacterium abscessus, can be classified into two distinct types of clinical disease; the upper lobe fibrocavitary (UC) form and nodular bronchiectatic (NB) form. However, the relationship between mycobacterial strain virulence and disease type in the pulmonary M. abscessus diseases has not been reported. To determine the differential virulence between strains causing two forms of disease, we obtained clinical isolates from patients with the UC and NB form of pulmonary disease caused by M. abscessus. In present study, we investigated the intracellular growth of clinical isolates in macrophages and their pathogenicity in C57BL/6 mice. For the isolates from the UC form, intracellular macrophage growth was faster and higher levels of cytokines were induced in macrophages than for those from NB form. Moreover, severe lung inflammation was only observed in mice intranasally infected with the isolate from the UC form with the increase of bacterial load. These findings suggest that M. abscessus isolates from the UC form of pulmonary disease are more virulent than those from NB form. This differential virulence of clinical strains may be one of the important factors involved in the determination of the disease form of pulmonary M. abscessus disease.

Tracheal stenosis depends on the extent of cartilaginous injury in experimental canine model.

To test the hypothesis that the development of tracheal stenosis would depend on the extent of tracheal cartilaginous injury, either 90 degrees (n=6) or 180 degrees (n=6) of anterior wall of 4 tracheal rings were cauterized in 12 mongrel dogs using Nd-YAG laser. Beginning at 3 weeks after cauterization, 180 degrees tracheal injury resulted in life-threatening tracheal stenosis whereas 90 degrees injury did not. Gross and microscopic examinations showed that after 180 degrees injury, tracheal stenosis was accompanied by the loss of tracheal cartilage and dense fibrosis. These results indicate that tracheal stenosis depends on the extent of tracheal injury in experimental canine model.