• Tuberculosis and Respiratory Diseases
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• v.49 no.4
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• pp.441-452
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• 2000

Background : It is well known that the prevalence of lung cancer is higher in idiopathic pulmonary fibrosis (IPF) patients than in the general population. This high prevalence is explained by the concept of 'scar carcinoma'. There have been several reports on the prevalence of histologic typo of lung cancer in IPF with conflicting results. Despite of the high smoker rate in almost all previous reports, none considered the smoking history of patients. Therefore we performed a separate studies on fibrosis associated lung cancer and smoking associated lung cancer. The purpose of this study is to investigate the proportion of lung cancer in IPF that is fibrosis associated and to determine the most common histologic type in fibrosis associated lung cancer in IPF. Method : A retrospective review of medical records and radiologic studies was performed for cases of lung cancer with IPF. We investigated smoking history, sequence of diagnosis of lung cancer and IPF, histologic type of lung cancer and the cancer location, especially whether the location is associated with fibrosis. To evaluate the proportion of fibrous associated lung cancer, the lung cancer in IPF were categorized according to the presence of fibrosis at cancer location. Results : Fifty seven patients were subjects for this analysis. Six (11%) cases were diagnosed as lung cancer during follow-up for IPF, and both diseases were diagnosed simultaneously in the others. Ninety four percent of patients were smokers and the average smoking amount was 47.1$\pm$21.9 pack-year. Among the patients with IPF and lung cancer, 42(80.8%) cases were considered as "fibrosis associated". The remainder was "not fibrosis associated" and probably was due to smoking etc. Although the most frequent histologic type was squamous cell carcinoma as a whole, adenocarcinoma was the prominent histologic type in "fibrosis associated lung cancer." Conclusion : Considering the proportion of "fibrosis not associated lung cancer" in the patients with IPF and lung cancer, significant proportion of lung cancer in IPF may not be fibrosis induced. This may influence the distribution of histologic type of lung cancer in IPF.

• Tuberculosis and Respiratory Diseases
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• v.63 no.1
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• pp.83-87
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• 2007

Idiopathic pulmonary fibrosis (IPF) is strongly associated with lung cancer compared with the general population. However, other types of idiopathic interstitial pneumonia (IIP) are rarely associated with lung cancer. We describe a case of a primary lung cancer associated with IIP other than IPF, which was considered to be nonspecific interstitial pneumonia (NSIP), and NSIP disappeared spontaneously after treating the primary lung cancer.

• Tuberculosis and Respiratory Diseases
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• v.85 no.2
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• pp.122-136
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• 2022

Although chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD) have distinct clinical features, both diseases may coexist in a patient because they share similar risk factors such as smoking, male sex, and old age. Patients with both emphysema in upper lung fields and diffuse ILD are diagnosed with combined pulmonary fibrosis and emphysema (CPFE), which causes substantial clinical deterioration. Patients with CPFE have higher mortality compared with patients who have COPD alone, but results have been inconclusive compared with patients who have idiopathic pulmonary fibrosis (IPF). Poor prognostic factors for CPFE include exacerbation, lung cancer, and pulmonary hypertension. The presence of interstitial lung abnormalities, which may be an early or mild form of ILD, is notable among patients with COPD, and is associated with poor prognosis. Various theories have been proposed regarding the pathophysiology of CPFE. Biomarker analyses have implied that this pathophysiology may be more closely associated with IPF development, rather than COPD or emphysema. Patients with CPFE should be advised to quit smoking and undergo routine lung function tests, and pulmonary rehabilitation may be helpful. Various pharmacologic agents and surgical approaches may be beneficial in patients with CPFE, but further studies are needed.

• IMMUNE NETWORK
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• v.15 no.3
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• pp.142-149
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• 2015

Lung fibrosis is a life-threatening disease caused by overt or insidious inflammatory responses. However, the mechanism of tissue injury-induced inflammation and subsequent fibrogenesis remains unclear. Recently, we and other groups reported that Th17 responses play a role in amplification of the inflammatory phase in a murine model induced by bleomycin (BLM). Osteopontin (OPN) is a cytokine and extracellular-matrix-associated signaling molecule. However, whether tissue injury causes inflammation and consequent fibrosis through OPN should be determined. In this study, we observed that BLM-induced lung inflammation and subsequent fibrosis was ameliorated in OPNdeficient mice. OPN was expressed ubiquitously in the lung parenchymal and bone-marrow-derived components and OPN from both components contributed to pathogenesis following BLM intratracheal instillation. Th17 differentiation of $CD4^+$ ${\alpha}{\beta}$ T cells and IL-17-producing ${\gamma}{\delta}$ T cells was significantly reduced in OPN-deficient mice compared to WT mice. In addition, Th1 differentiation of $CD4^+$ ${\alpha}{\beta}$ T cells and the percentage of IFN-$\gamma$-producing ${\gamma}{\delta}$ T cells increased. T helper cell differentiation in vitro revealed that OPN was preferentially upregulated in $CD4^+$ T cells under Th17 differentiation conditions. OPN expressed in both parenchymal and bone marrow cell components and contributed to BLM-induced lung inflammation and fibrosis by affecting the ratio of pathogenic IL-17/protective IFN-$\gamma$ T cells.

• Journal of Chest Surgery
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• v.37 no.12
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• pp.1032-1035
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• 2004

The specific diagnosis in diffuse interstitial lung disease may be obtained through open lung biopsy. Diffuse interstitial lung disease is often associated with lung cancer. We report one case of lung adenocarcinoma with idiopathic pulmonary fibrosis in whom previous open lung biopsy had been performed. We need general concepts about sites of open lung biopsy in these patients. Therefore, we report this case and document other references.

• Tuberculosis and Respiratory Diseases
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• v.85 no.4
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• pp.313-319
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• 2022

Environmental exposure to air pollution is known to have adverse effects on various organs. Air pollution has greater effects on the pulmonary system as the lungs are directly exposed to contaminants in the air. Here, we review the associations of air pollution with the development, morbidity, and mortality of pulmonary diseases. Short-and long-term exposure to air pollution have been shown to increase mortality risk even at concentrations below the current national guidelines. Ambient air pollution has been shown to be associated with lung cancer. Particularly long-term exposure to particulate matter with a diameter <2.5 ㎛ (PM_2.5) has been reported to be associated with lung cancer even at low concentrations. In addition, exposure to air pollution has been shown to increase the incidence risk of chronic obstructive pulmonary disease (COPD) and has been correlated with exacerbation and mortality of COPD. Air pollution has also been linked to exacerbation, mortality, and development of asthma. Exposure to nitrogen dioxide (NO₂) has been demonstrated to be related to increased mortality in patients with idiopathic pulmonary fibrosis. Additionally, air pollution increases the incidence of infectious diseases, such as pneumonia, bronchitis, and tuberculosis. Furthermore, emerging evidence supports a link between air pollution and coronavirus disease 2019 transmission, susceptibility, severity and mortality. In conclusion, the stringency of air quality guidelines should be increased and further therapeutic trials are required in patients at high risk of adverse health effects of air pollution.

• Journal of the Korean Society of Radiology
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• v.81 no.3
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• pp.688-700
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• 2020

Purpose To compare the incidence, survival rate, and CT findings of acute exacerbation (AE) of idiopathic pulmonary fibrosis (IPF) between patients with and without lung cancer. Materials and Methods From June 2004 to July 2018, 89 consecutive patients diagnosed with IPF were included. Among them, 26 patients had IPF with lung cancer (IPF-LCA), and 63 patients had IPF alone. The clinical characteristics and CT findings associated with IPF, lung cancer, and AE were reviewed. Surgery and chemotherapy were performed for 6 and 23 cases of lung cancer, respectively, as the first- or second-line anticancer treatment. The overall survival, CT findings, disease-free period before AE, and duration from the onset of AE to death were compared. Results The incidence of AE was 61.5% in the IPF-LCA group and 58.7% in the IPF group (p = 0.806). The mean overall survival in the IPF-LCA and IPF groups were 16.8 and 83.0 months, respectively (p < 0.001). The mean durations from the start of the lung cancer treatment to the onset of AE were 16.0 and 4.6 months in cases of surgical treatment and chemotherapy, respectively. In comparison of death from AE, the survival rate was significantly lower in the IPF-LCA group than in the IPF group (p = 0.008). In the CT findings associated with AE, the IPF-LCA group tended to have a peribronchial (p < 0.001) or asymmetric distribution (p = 0.016). Conclusion In patients with IPF who develop lung cancer, the rate of death from AE is higher than that in patients with IPF alone. They tend to have unusual CT patterns associated with AE, such as a peribronchial or asymmetric distribution.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.2
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• pp.637-642
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• 2014

The pathogenesis of hepatocellular carcinoma (HCC) related to habitual betel quid (BQ) chewing is unclear. Risk of HCCis increased with adverse hepatic fibrosis. This study aimed to assess the impact of chronic viral hepatitis on adverse hepatic fibrosis in HCC related to BQ chewing. This hospital-based case-control study enrolled 200 pairs of age- and gender-matched patients with HCC and unrelated healthy controls. Serologic hepatitis B surface antigen (HBsAg), antibodies to hepatitis C virus (anti-HCV), ${\alpha}$-fetoprotein (AFP), and surrogate markers for significant hepatic fibrosis were measured. Information on substance-use habits was obtained with a questionnaire. By analysis of surrogate markers for hepatic fibrosis, the prevalence of significant hepatic fibrosis in patients chewing BQ was between 45.8% and 91.7%, whereas that for patients without BQ chewing was between 18.4% and 57.9%. The difference was significant (P <0.05 for each surrogate marker). Multivariate analysis indicated that cirrhosis with Child-Pugh C (odds ratio (OR) = 3.28; 95% confidence interval (CI), 1.29-8.37), thrombocytopenia (OR = 3.92, 95% CI, 1.77-8.68), AFP >400 mg/L (OR = 2.21, 95% CI, 1.05-4.66) and male gender (OR = 4.06, 95% CI, 1.29-12.77) were independent factors associated with habitual BQ chewing. In conclusion, adverse hepatic fibrosis and severe liver damage play important roles in the pathogenesis of BQ-related HCC, which could be aggravated by chronic hepatitis B and hepatitis C. BQ-cessation programs and prevention of chronic HBV/HCV infection are needed to prevent HCC related to BQ chewing.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.7
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• pp.3405-3409
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• 2016

Malignant pleural mesothelioma (MPM), an aggressive malignant tumor of mesothelial origin associated with asbestos exposure, shows a limited response to conventional chemotherapy and radiotherapy. Therefore, the overall survival of MPM patients remains very poor. Progress in the development of therapeutic strategies for MPM has been limited. We recently reported that the calpain inhibitor, calpeptin exerted inhibitory effects on pulmonary fibrosis by inhibiting the proliferation of lung fibroblasts. In the present study, we examined the preventive effects of calpeptin on the cell growth of MPM, the origin of which is mesenchymal cells, similar to lung fibroblasts. Calpeptin inhibited the proliferation of MPM cells, but not mesothelial cells. It also prevented 1) the expression of angiopoietin (Ang)-1 and Tie-2 mRNA in MPM cells, but not mesothelial cells and 2) the Ang-1-induced proliferation of MPM cells through an NF-kB dependent pathway, which may be the mechanism underlying the preventive effects of calpeptin on the growth of MPM cells. These results suggest potential clinical use of calpeptin for the treatment of MPM.

• Tuberculosis and Respiratory Diseases
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• v.44 no.3
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• pp.661-668
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• 1997

The majority of lung cancers associated with hyperamylasemia are adenocarcinomas. Here we report an unusual case of a 54-year-old male patient who complained of dyspnea, anterior chest wall discomfort and facial edema for one month, presenting with a huge mediastinal mass and hyperamylasemia complicated by pericardial effusion. Histological evaluation of mediastinal mass revealed small cell carcinoma and pericardium showed nonspecific inflammation with fibrosis. The serum amylase had an electrophoretic mobility similar to that of salivary gland enzyme. There were no evidence of a salivary or pancreatic causes of hyperamylasemia. After chemotherapy, parenchymal lung lesions improved and hyperamylasemia disappeared. For the management of pericardial effusion, a pericardial window was formed. We concluded that the striking increase in serum amylase was due to the ectopic production of this enzyme by the tumor.