[A case of interstitial pneumonia with smoldering adult T-cell leukemia].

A 66-year-old woman was admitted because of dry cough and dyspnea. Computed tomography showed ground-glass opacities and traction bronchiectasis in both lung fields. Then, ATL cells appeared in her peripheral blood, and the number of lymphocytes in BALF increased. Inverse PCR for HTLV-1 clonality of the peripheral blood revealed a polyclonal pattern, and she was given a diagnosis of smoldering adult T-cell leukemia. Using BALF flow cytometry, both CD4- and CD25-positive cells accounted for only 0.8%. Secondary interstitial pneumonia was diagnosed and we started therapy with prednisolone and cyclophosphamide. BALF flow cytometry may be useful in the differential diagnosis of ATL lung lesions.

A case of immunoglobulin G4-related respiratory disease with multiple lung cysts: A case report.

A 48-year-old man was admitted for evaluation of abnormal shadows on chest radiograph. Chest computed tomography (CT) showed cysts, nodules, and cervical and axillary lymphadenopathies. Elevated serum levels of IgG4 and interleukin (IL)-6 suggested IgG4-related disease (IgG4-RD) or multicentric Castleman's disease (MCD). Histologic findings of the cervical lymph node and right lung S6 biopsies revealed numerous IgG4-positive plasma cells. Although CT findings of the lungs were atypical for IgG4-RD, consistent histologic findings, clinical symptoms, and laboratory data made us conclude IgG4-RD. Because histologic findings of IgG4-RD and MCD have similarities, differentiating between the two diseases should consider the clinical presentation.

Biological interaction of cigarette smoking on the association between genetic polymorphisms involved in inflammation and the risk of lung cancer: A case-control study in Japan.

Chronic inflammation serves an important role in lung carcinogenesis, thus genetic polymorphisms involved in this pathway may affect the risk of lung cancer. The present case-control study focused on the association between lung cancer risk and genetic polymorphisms involved in inflammatory pathways. The study comprised 462 lung cancer cases and 379 controls from Japan. The roles of interleukin 8 (IL8) rs4073, nuclear factor kappa B (NFκB) rs28362491, cytochrome b-245, alpha polypeptide (CYBA) rs4673, NAD(P) H dehydrogenase, quinone 1 (NQO1) rs1800566, nitric oxide synthase 2 and inducible (NOS2) rs2297518 polymorphisms in lung carcinogenesis were investigated. An unconditional logistic model was used to estimate the odds ratio (OR) and 95% confidence interval (CI) for the association between the genetic polymorphisms and lung cancer risk. The multiplicative and additive [relative excess risk due to interaction, attributable proportion due to interaction (AP) and synergy index (SI)] interactions with cigarette smoking were also determined. A significant association was revealed between the TT genotype of NQO1 rs1800566 and an increased risk of lung cancer (OR=1.78; 95% CI=1.14-2.79). The additive interaction evaluations between CYBA rs4673 (AP=0.50, 95% CI=0.15-0.85; SI=2.66, 95% CI=1.01-6.99) and smoking were also statistically significant. NQO1 rs1800566 was significantly associated with lung cancer risk and smoking may influence the association between CYBA rs4673 and the risk of lung cancer. Additional studies with larger control and case populations are warranted in order to confirm the CYBA rs4673-smoking association suggested by the present study.

Probucol attenuates hyperoxia-induced lung injury in mice.

Hyperoxic lung injury is pathologically characterized by alveolar edema, interlobular septal edema, hyaline membrane disease, lung inflammation, and alveolar hemorrhage. Although the precise mechanism by which hyperoxia causes lung injury is not well defined, oxidative stress, epithelial cell death, and proinflammatory cytokines are thought to be involved. Probucol-a commercially available drug for treating hypercholesterolemia-has been suggested to have antioxidant and antiapoptotic effects. This study aimed to assess whether probucol could attenuate hyperoxic lung injury in mice. Mice were exposed to 95% O2 for 72 h, with or without pre-treatment with 130 µg/kg probucol intratracheally. Probucol treatment significantly decreased both the number of inflammatory cells in the bronchoalveolar lavage fluid and the degree of lung injury in hyperoxia-exposed mice. Probucol treatment reduced the number of cells positive for 8-hydroxyl-2'-deoxyguanosine or terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and suppressed NF-κB activation, Bax expression, and caspase-9 activation in lung tissues from hyperoxia-exposed mice. These results suggest that probucol can reduce oxidative DNA damage, apoptotic cell death, and inflammation in lung tissues. Intratracheal administration of probucol may be a novel treatment for lung diseases induced by oxidative stress, such as hyperoxic lung injury and acute respiratory distress syndrome.