Bronchial Schwannoma Masquerading as Cause of Hemoptysis in a Patient with Pulmonary Embolism / General Medicine

A 78-year-old woman who had a history of left deep venous thrombosis was referred to our hospital with a sudden hemoptysis. Thoracic computed tomography showed a solitary pulmonary nodule in the right lower lobe. Based on her medical history of deep venous thrombosis, she was tentatively diagnosed as having pulmonary embolism and successfully treated by inserting an inferior vena cava filter and anticoagulant therapy with warfarin [Please confirm whether previous sentence is correct]. However, the lung nodule on thoracic computed tomography was still depicted four months later. With suspicion of a malignant tumor, including possible lung cancer, a right segmentectomy was performed. Pathological assessment of the resected specimen showed the tumor was derived from the right bronchial wall, but was not ruptured into the intratracheal lumen, as well as coexistence with intraalveolar hemorrhage near the tumor. The lung nodule was diagnosed as bronchial schwannoma. Thus, the origin of the hemoptysis was found to be pulmonary embolism due to deep vein thrombosis, and not by bronchial schwannoma, which was also present in the lung.

Pott's Disease and Cold Abscesses / General Medicine

Tuberculous spondylitis, or so-called Pott's disease, seems to be overlooked because of a lack of severe inflammation in the insidious generating process and tends to cause non-specific symptoms, such as back pain, fever, weakness, and weight loss. Diagnostic delay is common and the results can be disastrous. Discriminating between Pott's disease and other diseases, such as malignancy and pyogenic infection, is difficult. However, the inflammatory process in Pott's disease tends to spare the disk space, while that of pyogenic infection typically affects the area. Herein, we present a patient with Pott's disease who showed the characteristic clinical and radiological findings.

Impact of Air Pollution on Allergic Diseases

The incidence of allergic diseases in most industrialized countries has increased. Although the exact mechanisms behind this rapid increase in prevalence remain uncertain, a variety of air pollutants have been attracting attention as one causative factor. Epidemiological and toxicological research suggests a causative relationship between air pollution and the increased incidence of asthma, allergic rhinitis, and other allergic disorders. These include ozone, nitrogen dioxide and, especially particulate matter, produced by traffic-related and industrial activities. Strong epidemiological evidence supports a relationship between air pollution and the exacerbation of asthma and other respiratory diseases. Recent studies have suggested that air pollutants play a role in the development of asthma and allergies. Researchers have elucidated the mechanisms whereby these pollutants induce adverse effects; they appear to affect the balance between antioxidant pathways and airway inflammation. Gene polymorphisms involved in antioxidant pathways can modify responses to air pollution exposure. While the characterization and monitoring of pollutant components currently dictates pollution control policies, it will be necessary to identify susceptible subpopulations to target therapy/prevention of pollution-induced respiratory diseases.

Additive Effect of Diesel Exhaust Particulates and Ozone on Airway Hyperresponsiveness and Inflammation in a Mouse Model of Asthma

Allergic airway diseases are related to exposure to atmospheric pollutants, which have been suggested to be one factor in the increasing prevalence of asthma. Little is known about the effect of ozone and diesel exhaust particulates (DEP) on the development or aggravation of asthma. We have used a mouse asthma model to determine the effect of ozone and DEP on airway hyperresponsiveness and inflammation. Methacholine enhanced pause (P(enh)) was measured. Levels of IL-4 and IFN-gamma were quantified in bronchoalveolar lavage fluids by enzyme immunoassays. The OVA-sensitized-challenged and ozone and DEP exposure group had higher P(enh) than the OVA-sensitized-challenged group and the OVA-sensitized-challenged and DEP exposure group, and the OVA-sensitized-challenged and ozone exposure group. Levels of IFN-gamma were decreased in the OVA-sensitized-challenged and DEP exposure group and the OVA-sensitized-challenged and ozone and DEP exposure group compared to the OVA-sensitized-challenged and ozone exposure group. Levels of IL-4 were increased in the OVA-sensitized-challenged and ozone exposure group and the OVA-sensitized-challenged and DEP exposure group, and the OVA-sensitized-challenged and ozone and DEP exposure group compared to OVA-sensitized-challenged group. Co-exposure of ozone and DEP has additive effect on airway hyperresponsiveness by modulation of IL-4 and IFN-gamma suggesting that DEP amplify Th2 immune response.