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Yutaka Usui

Publications and source records attributed to Yutaka Usui.

9 recordsLinked to original sources
PubMed2006

A clinical study of hypersensitivity pneumonitis presumably caused by feather duvets.

BACKGROUND: Bird fancier's lung (BFL) is a type of hypersensitivity pneumonitis induced by the inhalation of bird-related antigens. The BFL induced by feathers is difficult to diagnose because feathers are generally unrecognized as a causative antigen. OBJECTIVE: To determine the clinical features of BFL presumably induced by feather duvets (feather duvet lung) to provide clues for diagnosis. METHODS: We performed a retrospective review of the medical records of patients with feather duvet lung evaluated between April 1, 2000, and June 30, 2003, at the Tokyo Medical and Dental University Hospital in Japan. RESULTS: Seven patients with feather duvet lung were included in this study; 4 patients had acute disease and 3 had chronic BFL. Duration of contact with feather duvets was 1 month to 10 years. Serum KL-6 and surfactant protein D levels were elevated in all the patients. Specific antibodies against avian antigens were positive in acute BFL but negative in chronic BFL. Antigen-induced lymphocyte proliferation in peripheral blood or bronchoalveolar lavage cells was positive in all the patients. The diagnosis was confirmed by an environmental or inhalation provocation test. CONCLUSIONS: Feather duvets can induce acute and chronic BFL. Physicians should be aware of feather duvets as a cause of BFL because feather duvets are becoming more prevalent.

Adult↗
PubMed2006

Proinflammatory and anti-inflammatory cytokine gene polymorphisms in hypersensitivity pneumonitis.

Hypersensitivity pneumonitis (HP) is an immunologically-mediated lung disease caused by repeated inhalation of dispersed antigen. Various cytokines have been reported to be involved in the immunopathogenesis of HP Recently, some reports suggested an association between the genetic control of cytokine production and disease susceptibility. To evaluate whether cytokine gene polymorphisms are associated with HP, we performed a case-control association study involving 61 patients with HP, consisting of summer-type HP (SHP) and bird fancier's lung (BFL, also named bird fancier's disease), as well as 101 healthy controls. Polymorphisms of the genes for tumor necrosis factor (TNF)-alpha (-308G/A, -857C/T, -863C/A, -1031T/C), interleukin (IL)-10 (-592C/A, -819C/T, -1082G/A), transforming growth factor (TGF)-beta1 (-509C/T, +869T/C), and IL-6 (-634C/G) were examined by restriction fragment length polymorphism analysis. There were no significant differences in allele frequency and genotype distribution among control, SHP, and BFL group. When HP group was divided into acute or chronic, no significant differences were detected between any groups. LPS-stimulated IL-6 secretion by whole blood cells was similar between subjects with GG genotype and non-GG genotype in IL-6 -634C/G polymorphism. In conclusion, the association between HP susceptibility and cytokine polymorphisms studied was not demonstrated.

Alveolitis, Extrinsic Allergic↗
PubMed2004

Chronic bird fancier's lung presenting with acute exacerbation due to use of a feather duvet.

A 67-year-old man was admitted due to fever and exertional dyspnea. He used to raise budgerigars and hill mynahs from 1980 to 1988. He was diagnosed as having chronic bird fancier's lung (BFL) based on a positive peripheral lymphocyte proliferation to pigeon serum in 1994. His disease was stable until 2000. Three months before admission he became a daily user of a feather duvet. A chest CT showed newly-developed peribronchial ground-glass opacities and preexisting honeycombing. Inhalation provocation test was positive. Administration of steroids improved his condition. He has been well after refraining from the use of the feather duvet.

Aged↗
PubMed2004

[Chronic summer-type hypersensitivity pneumonitis presenting with acute exacerbation].

A 77-year-old man was admitted to our hospital. He had first noticed a cough, sputum production, and low-grade fever during the summer of 1988. He was diagnosed as having summer-type hypersensitivity pneumonitis (HP) in 1989 on the basis of positive findings of anti-Trichosporon antibodies in the serum and bronchoalveolar lavage (BAL) fluid and and in environmental provocation tests. Thereafter, he presented with re-exacerbation of his disease in summer every year. In 1995, he retired from his work at a moldy hotel and moved to another house to avoid the causative antigen completely. There was no recurrence for the following 5 years. He suffered from cough, sputum production, and dyspnea 4 months after returning to his previous moldy house in October, 2000. A chest CT scan showed peribronchial and subpleural honeycombing, ground glass opacities, and traction bronchiectasis. BAL demonstrated that the lymphocyte count had changed from 78.9% to 42.9% and the CD4/CD8 ratio from 0.39 to 4.07 in 12 years. Antigen avoidance and steroid therapy have improved his condition. However, he stayed repeatedly in his moldy house, and finally died from acute exacerbation in March, 2002. Postmortem examination demonstrated diffuse alveolar damage (DAD) superimposed on honeycombing in the lungs.

Aged↗
PubMed2004

[Pneumoconiosis diagnosed in a dentist].

A 74-year-old man was admitted to our hospital because of exertional dyspnea in January 2003. He had first noticed slight exertional dypnea in 1997, which had since gradually progressed. He has been a dentist since the age of 23. Chest radiography demonstrated bilateral reticular shadows, infiltrates, and thickened pleural adhesion, which had progressed for one year and five months. Chest CT scans disclosed irregular peribronchial opacities, centrilobular nodules, and interlobular septal lines. Bronchoalveolar lavage fluid showed an increase in total cells and lymphocytosis with an increased CD 4/CD 8 ratio. Transbronchial lung biopsy demonstrated fibrosis around bronchioles, involving adjacent alveolar structures and scattered birefringent particles under polarized light. Energy-dispersive X-ray analysis (EDXA) of the small particles around the bronchioles using electron microscopy showed high peaks for silicon (Si) and aluminium (Al). Pneumoconiosis, possibly induced by some of the mechanical and technical procedures of dentistry, was diagnosed.

Aged↗
PubMed2003

[A case of acute bird fancier's lung caused by feather duvet].

A 57-year-old woman was admitted to our hospital because of cough and low-grade fever for 2 months and shortness of breath for 2 weeks. She had raised two budgerigars for the last 15 years and had been using a feather duvet for one year. A chest radiograph showed diffuse ground-glass opacities in both lung fields, and a chest CT scan showed centrilobular micronodules and ground-glass opacities. Bronchoalveolar lavage (BAL) revealed a marked increase in lymphocytes, and a transbronchial lung biopsy (TBLB) specimen showed alveolitis due to the infiltration of mononuclear cells. Since she had specific antibodies against pigeon and budgerigar dropping extracts and her peripheral blood lymphocytes proliferated on addition of pigeon serum, she was diagnosed as having bird fancier's lung (BFL). She was treated with steroids, which brought about a marked improvement. After she visited her husband who had been hospitalized where a feather duvet was provided for each patient, both subjective and objective findings deteriorated. This deterioration was preventable when she wore a protective mask for micro-dust while visiting her husband. The feather duvets seemed to induce acute BFL in this case, though raising budgerigars may well be related to her sensitization with bird-related antigens.

Acute Disease↗
PubMed2002

TA-19, a novel protein antigen of Trichosporon asahii, in summer-type hypersensitivity pneumonitis.

The most common form of hypersensitivity pneumonitis in Japan is summer-type hypersensitivity pneumonitis (SHP), which is caused by the inhalation of Trichosporon asahii or Trichosporon mucoides. To seek protein antigens relevant to the immunopathogenesis of SHP, we constructed a cDNA expression library of T. asahii, a major causative yeast species of SHP. Using the immunoscreening method, we identified and cloned a novel gene encoding a 19-kD protein, named TA-19, which proved to be specifically recognized in the bronchoalveolar lavage (BAL) fluids and sera of patients with SHP. IgG, IgA, and IgM antibodies to the recombinant TA-19 protein were significantly elevated in the sera as well as in the BAL fluids from SHP patients compared with those from non-SHP groups. This protein also induced SHP-specific proliferation of the mononuclear cells from both the peripheral blood and BAL. These results reveal that TA-19 derived from T. asahii may play a relevant role in specific cellular and humoral immune responses in patients with SHP.

Administration, Inhalation↗
PubMedDate not supplied

The characterization of gefitinib sensitivity and adverse events in patients with non-small cell lung cancer.

BACKGROUND: Factors predicting gefitinib sensitivity and adverse events in non-small cell lung cancer (NSCLC) remain controversial. PATIENTS AND METHODS: Correlations among clinicopathological characteristics, gefitinib sensitivity and adverse events were studied in 154 patients with NSCLC, whereas epidermal growth factor receptor (EGFR) mutations were analyzed in 44 patients. RESULTS: Female, non-smoker, adenocarcinoma of stage I-II, and gefitinib effectiveness correlated with longer time to progression (TTP) and overall survival (OS), while the rate of interstitial lung disease in patients undergoing thoracic radiotherapy and stomatitis in females or those who never smoked were significantly higher. EGFR mutations were identified in 18 cases, and among 34 gefitinib-treated patients, 16 patients harboring mutations tended to do better, both in terms of TTP and OS. The results of the mutation analysis from surgical and non-surgical specimens were identical. CONCLUSION: Certain clinicopathological characteristics and EGFR mutations can be either predictive of gefitinib sensitivity or adverse events.

Aged↗