Allergic bronchopulmonary aspergillosis(ABPA) is a syndrome seen in patients with asthma and cystic fibrosis. It is characterized by chronic cololinization of the airways with a ubiquitous fungus, Aspergillus fumigatus. Clinically, it is a syndrome characterized by recurrent episodes of wheezing, mucus production, pulmonary infiltrates, and elevated levels of serum IgE. ABPA patients are also accompanied with bronchiectasis in 89% and observed in 10% of cystic fibrosis that show the features of end-stage lung pattern. There are few reports of ABPA associated with bullae. We will report here a case of ABPA developing in an old cicartrical and bullous lesion of a lung.
Aspergillosis, Allergic Bronchopulmonary* ; Aspergillus fumigatus ; Asthma ; Blister ; Bronchiectasis ; Cystic Fibrosis ; Fungi ; Humans ; Immunoglobulin E ; Lung* ; Mucus ; Respiratory Sounds

Allergic asthma is associated with persistent functional and structural changes in the airways and involves many different cell types. Many proteins involved in allergic asthma have been identified individually, but complete protein profiles (proteome) have not yet been reported. Here we have used a differential proteome mapping strategy to identify tissue proteins that are differentially expressed in mice with allergic asthma and in normal mice. Mouse lung tissue proteins were separated using two-dimensional gel electrophoresis over a pH range between 4 and 7, digested, and then analyzed by matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MS). The proteins were identified using automated MS data acquisition. The resulting data were searched against a protein database using an internal Mascot search routine. This approach identified 15 proteins that were differentially expressed in the lungs of mice with allergic asthma and normal mice. All 15 proteins were identified by MS, and 9 could be linked to asthma-related symptoms, oxidation, or tissue remodeling. Our data suggest that these proteins may prove useful as surrogate biomarkers for quantitatively monitoring disease state progression or response to therapy.
Animals ; Asthma/genetics/immunology/*metabolism ; Comparative Study ; Disease Models, Animal ; Electrophoresis, Gel, Two-Dimensional ; Gene Expression/immunology ; Gene Expression Profiling ; Lung/immunology/metabolism/pathology ; Male ; Mice ; Mice, Inbred BALB C ; Ovalbumin/immunology ; Proteome/*analysis/genetics/immunology ; Proteomics/methods ; RNA, Messenger/genetics/metabolism ; Research Support, Non-U.S. Gov't ; Reverse Transcriptase Polymerase Chain Reaction ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

PURPOSE: We prospectively conducted a multi-center, open-label, randomized phase II trial to compare the efficacy and safety of docetaxel plus cisplatin (DC) and etoposide plus cisplatin (EC) for treating advanced stage non-small cell lung cancer (NSCLC). MATERIALS AND METHODS: Seventy-eight previously untreated patients with locally advanced, recurrent or metastatic NSCLC were enrolled in this study. The patients received cisplatin 75 mg/m2 on day 1 and either docetaxel 75 mg/m2 on day 1 or etoposide 100 mg/m2 on days 1 to 3 in the DC or EC arm, respectively, every 3 weeks. RESULTS: The objective response rate was 39.4% (15/38) and 18.4% (7/38) (p=0.023) in the DC and EC arms, respectively. The median time to progression (TTP) was 5.9 and 2.7 months (p=0.119), and the overall survival was 12.1 and 8.7 months (p=0.168) in the DC and EC arms, respectively. The prognostic factors for longer survival were an earlier disease stage (stage III, p=0.0095), the responders to DC (p=0.0174) and the adenocarcinoma histology (p=0.0454). The grades 3 and 4 toxicities were similar in both arms, with more febrile neutropenia (7.9% vs. 0%) and fatigue (7.9% vs. 0%) being noted in the DC arm. CONCLUSION: DC offered a superior overall response rate than does EC, along with tolerable toxicity profiles, although the DC drug combination did not show significantly improved survival and TTP.
Adenocarcinoma ; Arm ; Carcinoma, Non-Small-Cell Lung* ; Cisplatin* ; Etoposide* ; Fatigue ; Febrile Neutropenia ; Humans ; Prospective Studies