Malignant pleural mesothelioma (MPM) is an aggressive, treatment-resistant, and generally fatal disease. A 68-year-old male who was diagnosed with MPM at another hospital came to our hospital with dyspnea. We advised him to take combination chemotherapy but he refused to take the treatment. That was because he had already received chemotherapy with supportive care at another hospital but his condition worsened. Thus, we recommended photodynamic therapy (PDT) to deal with the dyspnea and MPM. After PDT, the dyspnea improved and the patient then decided to take the combination chemotherapy. Our patient received chemotherapy using pemetrexed/cisplatin. Afterwards, he received a single PDT treatment and then later took chemotherapy using gemcitabine/cisplatin. The patient showed a survival time of 27 months, which is longer than median survival time in advanced MPM patients. Further research and clinical trials are needed to demonstrate any synergistic effect between the combination chemotherapy and PDT.
Aged ; Drug Therapy* ; Drug Therapy, Combination ; Dyspnea ; Humans ; Male ; Mesothelioma* ; Photochemotherapy* ; Pleura

BACKGROUND: Few reports have documented the clinical characteristics and treatment outcomes of adult patients with Elizabethkingia meningoseptica infection. METHODS: Medical records of patients over 18 years of age and suspected of having an E. meningoseptica infection from March 1, 2006 to February 28, 2013 were reviewed retrospectively. Their clinical characteristics, antimicrobial susceptibility results, and treatment outcomes were analyzed. RESULTS: E. meningoseptica was isolated from 30 patients. Median age was 68.5 years, and infections were more frequent in males (17, 56.7%). The most common isolation source was sputum (23, 76.7%), and pneumonia was the most common condition (21, 70%) after excluding two cases of colonization. This bacterium was most susceptible to minocycline (27, 90%) and fluoroquinolones, including levofloxacin (20, 66.7%) and ciprofloxacin (18, 60%). The mortality rate due directly to E. meningoseptica infection was 20% (6/30), and uncontrolled pneumonia was the only cause of death. After isolating E. meningoseptica, the numbers of patients with pneumonia (9/9, 100% vs. 12/21, 57.1%), history of hemodialysis (5/9, 55.6% vs. 3/21, 14.3%), tracheostomy (8/9, 88.9 vs. 10/21, 47.6%), and median Charlson comorbidity index score (6 [range, 3-9] vs. 4 [range, 0-9]) were significantly higher in non-survivors than those in survivors (p < 0.05, for each). However, only 12 (40%) patients received appropriate antibiotics. CONCLUSIONS: E. meningoseptica infection most commonly presented as pneumonia in adults with severe underlying diseases. Despite the high mortality rate, the rate of appropriate antibiotic use was notably low.
Adult* ; Anti-Bacterial Agents ; Cause of Death ; Chryseobacterium ; Ciprofloxacin ; Colon ; Comorbidity ; Cross Infection ; Fluoroquinolones ; Humans ; Levofloxacin ; Male ; Medical Records ; Minocycline ; Mortality ; Pneumonia ; Renal Dialysis ; Retrospective Studies ; Sputum ; Survivors ; Tertiary Care Centers* ; Tracheostomy

BACKGROUND: Recent studies have suggested an association between chronic cough and gastroesophageal reflux. Our study aimed to assess the utility of a proton-pump inhibitor in unexplained chronic cough patients. METHODS: Patients with chronic cough of unknown etiology were evaluated using a chest x-ray, methacholine challenge test, and an empirical trial of postnasal drip therapy. After excluding other potential causes of the cough, forty patients were included in the study and treated for 8 weeks with a proton-pump inhibitor. RESULTS: Eleven and three patients in the first and second 4 weeks were lost to follow-up, leaving twenty-six patients finally included in the study. Of these patients, two were unimproved, eight partially responded to the proton-pump inhibitor and sixteen responded completely after the 8 week treatment. CONCLUSION: We suggest that empirical treatment with a proton pump inhibitor in all patients with persistent cough, which is not secondary to asthma or postnasal drip syndrome, represents a practical and simple approach to this ailment.
Asthma ; Cough* ; Gastroesophageal Reflux ; Humans ; Lost to Follow-Up ; Methacholine Chloride ; Proton Pumps ; Thorax

Anomalous systemic arterial supply to the lung is a rare congenital anomaly. The lung supplied by the anomalus systemic artery has a normal bronchial tree, which is usually in the basal segment of the lung, especially in the left lung. Most of patients are asymptomatic, but the main clinical symptoms of this disease are hemoptysis and exertional dyspnea. CT is useful for the diagnosis and showed a retrocardiac nodular shadow connected to the descending aorta branching into the basal segments of the relatively normal lower lobe. Surgery is indicated for all patients. Here we report a case of anomalous systemic arterial supply to normal basal segments of left lower lobe in a patient with hemoptysis with a review of the relevant literature.
Aorta, Thoracic ; Arteries ; Diagnosis ; Dyspnea ; Hemoptysis ; Humans ; Lung

BACKGROUND: IFN-gamma is the main effector mediator of the host immune response against Mycobacterium tuberculosis. Evaluating the IFN-gamma gene expression in response to M. tuberculosis antigens may help in elucidating the host defense mechanism against M. tuberculosis and in the development of a vaccine. METHODS: The IFN-gamma mRNA expression in the lymphocytes obtained from pleural effusions from tuberculous pleurisy patients (TB-PLC) after in vitro stimulation with whole cell M. tuberculosis(H37Rv), purified protein derivatives(PPD), man-lipoarabinamman (man-LAM), ara-LAM and Antigen 85B(Ag85B) were evaluated. The degree of IFN-gamma mRNA expression was determined by a semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) method. RESULTS: M. tuberculosis induced the expression of IFN-gamma mRNA in the TB-PLC in time and dose dependent manners. The PPD and Ag85B induced high levels of IFN-gamma mRNA expression in the TB-PLC. However, man-LAM inhibited IFN-gamma mRNA expression in the TB-PLC, while ara-LAM did not. CONCLUSION: IFN-gamma mRNA expression in TB-PLC is stimulated by PPD and Ag85B, but inhibited by man-LAM.
Gene Expression ; Humans ; Interferon-gamma ; Lymphocytes* ; Mycobacterium tuberculosis ; Pleural Effusion ; RNA, Messenger ; Tuberculosis* ; Tuberculosis, Pleural

BACKGROUND: Nitric Oxide (NO) is a multi-faceted molecule with dichotomous regulatory roles in many areas of biology. NO can promote apoptosis in some cells, whereas it inhibits apoptosis in other cell types. This study was performed to characterize NO-induced cell death in lung epithelial cells and to investigate the roles of cell death regulators including iron, bcl-2 and p53. METHODS: A549 cells were used for lung epithelial cells. SNP (sodium nitroprusside) and SNAP (S-nitroso-N-acetyl-penicillamine) were used for NO donor. Cytoxicity assay was done by MTT assay and crystal violet assay. Apoptotic assay was done by fluorescent microscopy after double staining with propidium iodide and hoecst 33342. Iron inhibition study was done with RBCs and FeSO4. For bcl-2 study, bcl-2 overexpressing cells (A549-bcl-2) were used and for p53 study, Western blot analysis and p53 functionally knock-out cells (A549-E6) were used. RESULTS: SNP and SNAP induced dose-dependent cell death in A549 cells and fluorescent microscopy revealed that SNAP induced apoptosis in low doses but necrosis in high doses while SNP induced exclusively necrotic cell death. Iron inhibition study using RBCs and FeSO4 significantly blocked SNAP-induced cell death. And also SNAP-induced cell death was blocked by bcl-2 overexpression. Finally, we found that SNAP activate p53 by Western blot analysis and that SNAP-induced cell death was decreased in the abscence of p53. CONCLUSION: In lung epithelial cells, NO can induce cell death, more precisely apoptosis in low doses and necrosis in high doses. And iron, bcl-2, and p53 play important roles in NO-induced cell death.
Apoptosis ; Biology ; Blotting, Western ; Cell Death* ; Epithelial Cells* ; Gentian Violet ; Humans ; Iron ; Lung* ; Microscopy ; Necrosis ; Nitric Oxide* ; Propidium ; Tissue Donors

PURPOSE: High frequency of p53 mutations in lung cancer is a major obstacle to chemotherapy-induced apoptosis because p53 is known to play an important role as a final translator for cancer apoptosis. Members of the TNF family have potential as anti-tumor agents because they induce apoptosis regardless of the p53 phenotype. Despite these advantages, the clinical utility of both TNF-alpha and FasL has been hampered by toxic side effects including NF-kappaB activation leading to septic shock and lethal hepatocyte apoptosis respectively. TRAIL (TNF-related apoptosis-inducing ligand), or Apo2L (Apo2 ligand) is a newly identified member of the family which appears to be tumor-selective and less toxic to the normal cells owing to distinct decoy receptor expression. Recently, it was described that TRAIL also can activate NF-kappaB which is a well-known anti-apoptotic transcriptional factor. MATERIALS AND METHODS: We found that TRAIL activates NF-kappaB in A549 (wt p53) and NCI-H1299 (null p53) lung cancer cells by luciferase reporter gene assay and electromobility shift assay. We set out to identify an agent that would sensitize lung cancer cells to TRAIL-induced apoptosis through inhibition of NF-kappaB activation. RESULTS: We found that triptolide, an oxygenated diterpene extracted and purified from the Chinese herb Tripterygium wilfordii sensitized A549 and NCI-H1299 cells to TRAIL-induced apoptosis through inhibition of NF-kappaB activation. Pretreatment with MG132 which is a well-known NF-kappaB inhibitor by blocking degradation of IkappaBalpha also greatly sensitized lung cancer cells to TRAIL-induced apoptosis. Triptolide did not block DNA binding of NF-kappaB activated by TRAIL as in the case of TNF-alpha. It has been already proven that triptolide blocks transactivation of p65 which plays a key role in NF-kappaB activation. CONCLUSION: These observations suggest that triptolide may be a potentially useful drug to enhance TRAIL-induced tumor killing in lung cancer.
Apoptosis ; Asian Continental Ancestry Group ; Cell Death* ; DNA ; Genes, Reporter ; Hepatocytes ; Homicide ; Humans ; Luciferases ; Lung Neoplasms* ; Lung* ; NF-kappa B* ; Oxygen ; Phenotype ; Shock, Septic ; Transcriptional Activation ; Tripterygium ; Tumor Necrosis Factor-alpha

BACKGROUND: Photodynamic therapy (PDT) is a new therapeutic method aimed at the selective destruction of cancer cells. The outcome is death of cancer cells through apoptosis or necrosis. The aim of this study was to investigate the characterization of PDT induced cell death in A549 lung cancer cells. MATERIALS AND METHODS: A549 cells were used as the lung cancer cell. 5 aminolevulinic acid (ALA) was used as the photosensitizer and a 632nm diode laser (Biolitec, Germany) as the light source. Cells were incubated with various concentrations of ALA. The 632nm diode laser was then administered for various laser irradiation times. The treated cells were incubated with 24, 48 and 72 hours. The cell viabilities were measured using the crystal violet assay and light microscopy. To observe the cell death mechanism after PDT, cells were observed under fluorescence microscopy after double staining with Hoechst 33342 and propium iodide after PDT. RESULTS: In the crystal violet assay at 24 hours after PDT with a 3.2 J/cm2 laser irradiation power, the cell viabilities were 89.56 +/- 4.11, 87.67 +/- 5.48, and 69.37 +/- 8.84 with ALA concentrations of 10, 100, and 1 mg/ml, respectively. In crystal violet assay at 24 hours after PDT with 1mg/ml of ALA, the cell viabilities were 74 +/- 19.85, 55 +/- 6.1, and 49.06 +/- 16.64% with 1.6, 3.2 and 6.4 J/cm2 laser irradiation powers, respectively. However, increasing the interval time after PDT did not change the cell viabilities. In the apoptosis assay, photodynamic therapy was inducing the apoptotic cell death. CONCLUSIONS: This study shows the apoptotic anticancer effect of photodynamic therapy in A549 lung cancer cells. However, further evaluations with other cancer cells and photosensitizers are necessary.
Aminolevulinic Acid ; Apoptosis ; Cell Death* ; Cell Survival ; Gentian Violet ; Lasers, Semiconductor* ; Lung Neoplasms* ; Lung* ; Microscopy ; Microscopy, Fluorescence ; Necrosis ; Photochemotherapy* ; Photosensitizing Agents

PURPOSE: We have examined that dexamethasone inhibits apoptotic cell death of A549 lung epithelial cells through TRAIL and anti-cancer drugs. The purpose of the study is to determine the roles of GR, cIAP and NF- kappaB in this mechanism. MATERIALS AND METHODS: In the A549 lung epithelial cell line, TRAIL, taxol, doxorubicine & gemcitabine were used to investigate cell toxicity. Cells were pretreated 12 hours in advance with dexamethasone. RU486 was pretreated 30 minutes before dexamethasone. Crystal violet assay was used for cell toxicity tests. Apoptosis assay was performed by taking morphologic surveys with fluorescent microscopy after double staining with Hoechst 33342 & propium iodide. RT-PCR was used to investigate the gene expression of cIAP1 & cIAP2 by dexamethasone. Ad-IkappaBalpha-SR transduction study was used for the role of NF-kappaB. RESULTS: TRAIL and anti-cancer drug-induced apoptosis was partially suppressed in A549 cells pretreated with dexamethasone. The inhibitory effect on cell death disappeared in A549 cells pretreated with RU486. Using RT-PCR, changes of cIAP1 and cIAP2 genes manifestation in A549 cells subsequent to pretreatment with dexamethasone were examined. The results showed an increase in cIAP2 expression during a course of time which was suppressed by RU486 pretreatment. Induction of cIAP2 expression changes by dexamethasone was uniquely observed despite the blockade of NF-kappa by Ad-IkappaB alpha-SR transduction. CONCLUSIONS: These results suggest that dexametha sone inhibits TRAIL- and anti-cancer drug-induced apoptosis in A549 cells by inducing cIAP2 gene expression through a GR-mediated, NF-kappa-independent pathway.
Apoptosis ; Cell Death* ; Dexamethasone* ; Doxorubicin ; Epithelial Cells ; Gene Expression ; Gentian Violet ; Lung ; Microscopy ; Mifepristone ; NF-kappa B ; Paclitaxel ; Prednisone ; Toxicity Tests

BACKGROUND: Steroid therapy has been shown to improve the clinical outcome in acute respiratory distress syndrome (ARDS) patients wit histological evidence of fibroproliferation in the lung tissue and no identifiab le soure of infection. Because the histopathological features of acute interstitial pneumonia (AIP) are identical with that of ARDS, early steroid therapy was used in AIP patients who had histological evidence of fibroproliferation in the lung tissue and no identifiable source of infection. We analyzed seven years of our experience to evaluate the efficacy of early steroid therapy in AIP. METHODS: A retrospective review was performed on AIP patients who received steroid therapy within 7 days of mechanical ventilatory support in Dankook University Hospital between May 1995 and May 2002. AIP was diagnosed clinically by ARDS without a known cause of the etiology and pathologically by a lung biopsy showing a fibroproliferative stage of diffuse alveolar damage. The clinical response and physiologic parameters were evaluated during steroid therapy. RESULTS: Five AIP patients received intravenous methylprednisolone (1-2mg/kg every 6 hours) after 0.6+/-1.7 days of mechanial ventilatory support. Lung biopsies were performed after 1.8+/-0.4 days of mechanical ventilatory support. Four patients(80%) survived and were extubated after 2.8+/-0.4 days of steroid therapy with improvement in the PaO2 ration (127.4+/-10.1 at day 0 to 223.8+/-37.6 at day 7) by steroid therappy. However, one patient(20%) died of respiratory failure after 15 days of steroid therapy. CONCLUSION: Early steroid therapy sppears to be beneficial in AIP patients without evidence of infection. However, as our study group was too small, futher large scale studies to define the effectiveness of steroids are required.
Biopsy ; Humans ; Lung ; Lung Diseases, Interstitial* ; Methylprednisolone ; Respiratory Distress Syndrome, Adult ; Respiratory Insufficiency ; Retrospective Studies ; Steroids