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ABSTRACT: Chronic cough is the only symptom of cough variant asthma (CVA) and atopic cough (AC). Cysteinyl leukotriene receptor antagonists have been shown to be effective in CVA, but there are no reports on their effectiveness in AC. To evaluate the antitussive effect of montelukast, a leukotriene receptor antagonist, in CVA and AC.
Seventy-five patients with chronic cough received diagnostic bronchodilator therapy with oral clenbuterol hydrochloride for 6 days. Of the 75 patients, 48 and 27 met the simplified diagnostic criteria for CVA and AC, respectively. Patients with CVA were randomly divided into 3 groups: montelukast, clenbuterol, and montelukast plus clenbuterol. Patients with AC were randomly divided into 2 groups: montelukast and placebo. The efficacy of cough treatment was assessed with a subjective cough symptom scale (0 meant "no cough" and 10 denoted "cough as bad as at first visit"). The cough scale, pulmonary function test, and peak expiratory flow rate (PEF) were evaluated before and after 2 weeks of treatment.
In patients with CVA, 2-week treatment with montelukast, clenbuterol, and montelukast plus clenbuterol all significantly decreased cough scores and treatment with montelukast plus clenbuterol was superior to treatment with montelukast alone. In the montelukast plus clenbuterol group, PEF values in the morning and evening significantly increased after 2 weeks compared with values before treatment. In patients with AC, scores on the cough scale did not differ significantly between the montelukast group and the placebo group.
Montelukast was confirmed to suppress chronic non-productive cough in CVA, whereas it was not effective in non-productive cough in AC.
Allergology International 03/2010; 59(2):185-92.
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ABSTRACT: A 47-year-old man visited his family doctor because of chronic productive cough. Though there were no abnormal chest X-ray film findings, he was diagnosed as tuberculosis on the basis of a sputum examination. Therefore, he was introduced to our hospital and as tracheobronchial tuberculosis was diagnosed by the bronchofiberscopic findings, showing ulceration with a white nodules from the lower part of trachea to the left main bronchus. By treatment, the ulcer change was improved, but the left main bronchus narrowed to pinhole size. Furthermore, the flow-volume curve became worse, and stridor appeared. We inserted Dumon stent in the left main bronchus 4 months later. As a result, his symptoms and flow-volume curve were improved, and we removed the stent 4 years and 6 months later. In this valuable case, we could observe the progress of the post-tuberculosis bronchial stenosis respiratory physiologically.
Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society. 11/2008; 46(10):842-6.
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ABSTRACT: A 72 year-old man. He was diagnosed with rheumatoid arthritis in 2002. In January 2005 he noted productive cough and fever; he was diagnosed as eosinophilic pneumonia (EP). We discontinued administration of bucillamine and methotrexate and started to treat with oral prednisolone 30 mg daily. To rule out drug-induced EP, prednisolone was tapered by 10 mg per week. Consolidation occurred in the right lower lobe when prednisolone was decreased to 5 mg daily. After increasing the dose of prednisolone to 30 mg daily again, consolidation was promptly resolved. It was considered to be important to rule out drug-induced EP.
Internal Medicine 02/2008; 47(6):527-31. · 0.94 Impact Factor
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ABSTRACT: A 65-year-old asymptomatic man was admitted to our hospital because a chest abnormal shadow had been pointed out on a medical examination. Our investigation resulted that the consolidation in the left lung had been initially documented in 2002, and had been expanding every year. Bronchofiberscopy showed flare, swelling and stenosis of the left B8, B9 and B10. Because the biopsy specimen from the B9 showed a mass of bacteria and surrounding granulation tissue, pulmonary actinomycosis was diagnosed. Pulmonary actinomycosis should be considered in the differential diagnosis of abnormal chest shadows regardless of the absence of symptoms.
Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society. 07/2007; 45(6):494-8.
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ABSTRACT: Because the investigation of epidermal growth factor receptor gene (EGFR) status as a predictor of gefitinib efficacy in Japanese patients has shown promise, the authors evaluated EGFR mutations and gene amplification in biopsy specimens from Japanese patients with nonsmall cell lung cancer (NSCLC) who received treatment with gefitinib to analyze the correlation between EGFR gene status and clinical outcome.
Fifty-nine patients were enrolled in this study. EGFR gene amplification was evaluated by fluorescence in situ hybridization (FISH), and EGFR mutations in exons 18, 19, and 21 were analyzed by polymerase chain reaction and direct sequencing.
EGFR mutations were detected in 17 patients (28.8%). FISH-positive results were observed in 26 patients (48.1%). The response rate was significantly higher in the patients with EGFR mutations than in the patients without mutations (58.8% vs 14.3%; P=.0005). No significant difference in the response rate was observed between FISH-positive patients and FISH-negative patients (31.8% vs 21.4%; P=.4339). EGFR mutation was correlated with both a longer time to progression (TTP) (7.3 months vs 1.8 months; P=.0030) and longer overall survival (OS) (18.9 months vs 6.4 months; P=.0092). No significant differences in TTP or OS were observed between FISH-positive patients andFISH-negative patients. The results from a multivariate analysis indicated that EGFR mutations maintained a significant association with longer TTP and longer OS.
The results of this study suggested that EGFR mutations may serve as predictors of response and survival and that the role of EGFR gene amplification is not a predictor of gefitinib efficacy in Japanese patients with NSCLC.
Cancer 06/2007; 109(9):1836-44. · 4.77 Impact Factor
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ABSTRACT: We report a case of pulmonary proteinosis detected at an early stage and followed up on chest CT. A 49-year-old man underwent detailed examinations because of abnormal shadows on chest CT taken on a routine medical examination. The chest CT revealed almost symmetrical ground glass opacities (GGOs) in both lungs with thickened alveolar septa. We could not make a definitive diagnosis even with bronchoalveolar lavage and transbronchial lung biopsy, but after about half a year, the GGOs increased. VATS-biopsy demonstrated alveoli filled with PAS-positive granular materials, and we made a diagnosis of pulmonary alveolar proteinosis. This case was found at an early stage and we were then able to follow up the disease.
Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society. 04/2007; 45(3):277-81.
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ABSTRACT: A 71-year-old man was found to have right hydropneumothorax by chest X-ray film on a regular checkup. Thoracic drainage and bullectomy by thoracoscopy did not improve the pneumothorax, so pleurodesis with OK-432 was done. Pneumothorax recurred twice, requiring thoracic drainage and pleurodesis. Although pneumothorax was treated successfully, increased pleural effusion, pleural thickening and subcutaneal tumor at the thoracic drainage suture site developed. The concentration of hyaluronic acid in the pleural fluid was very high. The histological examination of the biopsied subcutaneous tumor showed mixed type malignant pleural mesothelioma. Chemotherapy with gemcitabine and vinorelbine could not control the progression.
Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society. 12/2006; 44(11):807-11.
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Hideharu Kimura,
Kazuo Kasahara,
Kazuhiko Shibata,
Takashi Sone,
Akihiro Yoshimoto,
Toshiyuki Kita,
Yukari Ichikawa,
Yuko Waseda,
Kazuyoshi Watanabe,
Hiroki Shiarasaki,
Yoshihisa Ishiura,
Masayuki Mizuguchi, Yasuto Nakatsumi,
Tatsuhiko Kashii,
Masashi Kobayashi,
Hideo Kunitoh,
Tomohide Tamura,
Kazuto Nishio,
Masaki Fujimura,
Shinji Nakao
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ABSTRACT: The authors evaluate the efficacy and safety of gefitinib monotherapy in chemotherapy-naive patients with advanced non-small-cell lung cancer (NSCLC). A secondary endpoint is to evaluate the relationship between clinical manifestations and epidermal growth factor receptor (EGFR) mutation status.
Japanese chemotherapy-naive NSCLC patients were enrolled. They had measurable lesions, Eastern Cooperative Oncology Group performance status of 0 to 2, and adequate organ and bone marrow function. Patients received 250 mg of oral gefitinib daily. EGFR mutations in exon 18, 19, and 21 of DNA extracted from tumor and serum were analyzed by genomic polymerase chain reaction and direct sequence.
All 30 patients were eligible for the assessment of efficacy and safety. An objective response and stable disease were observed in 10 patients (33.3%) and nine patients (30.0%), respectively. The median time to progression was 3.3 months and the median overall survival was 10.6 months. The 1-year survival rate was 43.3%. Grade 3 toxicities were observed in seven patients. EGFR mutation was observed in four of 13 (30.8%) tumors, and two of them achieved partial response. In serum samples, three of 10 patients with EGFR mutations in the serum before treatment had a response to gefitinib. EGFR mutation was observed in 10 of 27 and significantly more frequently observed in the posttreatment samples from patients with a partial response or stable disease than in those from patients with progressive disease (p = 0.006).
Gefitinib monotherapy in chemotherapy-naive NSCLC patients was active, with acceptable toxicities. These results warrant further evaluation of gefitinib monotherapy as a first-line therapy. The EGFR mutation in serum DNA may be a biomarker for monitoring the response to gefitinib during treatment.
Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 04/2006; 1(3):260-7. · 4.55 Impact Factor
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Hideharu Kimura,
Kazuo Kasahara,
Kazuhiko Shibata,
Takashi Sone,
Akihiro Yoshimoto,
Toshiyuki Kita,
Yukari Ichikawa,
Yuko Waseda,
Kazuyoshi Watanabe,
Hiroki Shiarasaki,
Yoshihisa Ishiura,
Masayuki Mizuguchi, Yasuto Nakatsumi,
Tatsuhiko Kashii,
Masashi Kobayashi,
Hideo Kunitoh,
Tomohide Tamura,
Kazuto Nishio,
Masaki Fujimura,
Shinji Nakao
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ABSTRACT: Background: The authors evaluate the efficacy and safety of gefitinib monotherapy in chemotherapy-naive patients with advanced non-small-cell lung cancer (NSCLC). A secondary endpoint is to evaluate the relationship between clinical manifestations and epidermal growth factor receptor (EGFR) mutation status.
Methods: Japanese chemotherapy-naive NSCLC patients were enrolled. They had measurable lesions, Eastern Cooperative Oncology Group performance status of 0 to 2, and adequate organ and bone marrow function. Patients received 250 mg of oral gefitinib daily. EGFR mutations in exon 18, 19, and 21 of DNA extracted from tumor and serum were analyzed by genomic polymerase chain reaction and direct sequence.
Results: All 30 patients were eligible for the assessment of efficacy and safety. An objective response and stable disease were observed in 10 patients (33.3%) and nine patients (30.0%), respectively. The median time to progression was 3.3 months and the median overall survival was 10.6 months. The 1-year survival rate was 43.3%. Grade 3 toxicities were observed in seven patients. EGFR mutation was observed in four of 13 (30.8%) tumors, and two of them achieved partial response. In serum samples, three of 10 patients with EGFR mutations in the serum before treatment had a response to gefitinib. EGFR mutation was observed in 10 of 27 and significantly more frequently observed in the posttreatment samples from patients with a partial response or stable disease than in those from patients with progressive disease (p = 0.006).
Conclusions: Gefitinib monotherapy in chemotherapy-naive NSCLC patients was active, with acceptable toxicities. These results warrant further evaluation of gefitinib monotherapy as a first-line therapy. The EGFR mutation in serum DNA may be a biomarker for monitoring the response to gefitinib during treatment.
Journal of Thoracic Oncology 02/2006; 1(3):260-267. · 3.66 Impact Factor
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ABSTRACT: A prospective multicentre study was conducted to elucidate the causes of chronic cough in Japan.
All consecutive and unselected patients complaining of cough lasting 8 weeks or more, who visited our clinics from 1 June to 31 December 2001, were registered. The causes of chronic cough were diagnosed based on the criteria for definite and probable causes of cough as recommended by the Japanese Cough Research Society.
Of the 248 patients enrolled, 72 patients (29.0%) were unavailable for follow up before their diagnostic assessment had been finalized. Among the 176 patients who were adequately assessed, a diagnosis was made in 165 patients (93.7%) either as single cause or as one of two causes: atopic cough in 48 (29.1%) and 11 patients (6.7%); cough variant asthma in 46 (27.9%) and nine patients (5.5%); cough predominant asthma in 14 (8.5%) and three patients (1.8%); and sinobronchial syndrome (SBS) in 28 (17.7%) and 14 patients (8.5%), respectively. A diagnosis of gastro-oesophageal reflux-associated cough was made in a total of four patients (2.4%).
Atopic cough, asthmatic cough consisting of cough variant asthma and cough predominant asthma, and SBS are major causes of chronic cough in Japan.
Respirology 04/2005; 10(2):201-7. · 2.42 Impact Factor
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ABSTRACT: We previously reported that a 6-month low-dose course of ofloxacin combined with long-term low-dose erythromycin therapy (EM therapy) was superior to EM therapy alone for sinobronchial syndrome (SBS), especially during the initial 2 months of treatment. However, there was no data as to whether discontinuation of low-dose ofloxacin after 2 months results in symptom relapse. This study was designed to clarify this issue.
Twenty-three patients with SBS received a 2-month course of levofloxacin (LVFX) therapy (100 mg once a day) concurrent with a 6-month course of EM therapy (200 mg three times a day) (group A). Eighteen other patients were given the EM therapy alone (group B). Clinical parameters, including quantity of morning sputum, were recorded in a daily symptom diary, and reviewed by each doctor in charge at 2-4 week intervals.
The quantity of morning sputum decreased more rapidly in group A than in group B. No relapse of symptoms was recognized after discontinuation of LVFX in group A.
A 2-month low-dose course of LVFX in conjunction with long-term EM therapy may be efficacious for the treatment of SBS, as evidenced by rapid improvement of expectoration without any relapse after LVFX discontinuation.
Respirology 01/2003; 7(4):317-24. · 2.42 Impact Factor
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ABSTRACT: Hereditary nonpolyposis colorectal cancer kindreds are frequently associated with cancers in various organs, including endometrium, stomach, and ovary. However, hematologic malignancy has rarely been reported in association with this cancer syndrome. We present here the case of a probable hereditary nonpolyposis colon cancer patient in whom non-Hodgkin's lymphoma developed after curative resection of colon cancer. Our experience with this rare case encouraged us to review the literature for reports indicating a possible relationship between these diseases.
A 52-year-old male whose family history was consistent with the criteria for hereditary nonpolyposis colon cancer underwent right hemicolectomy for ascending colon cancer. Histologically the tumor consisted of adenocarcinoma that was moderately differentiated with mucinous foci and that invaded beyond the muscularis propria. Neither metastasis nor lymphoma was found in paracolonic lymph nodes. Eight months after surgery, the patient developed non-Hodgkin's lymphoma of T-cell origin involving the ileum and lungs. Both colon cancer and lymphoma frequently showed microsatellite DNA instability, sharing alteration in a locus of chromosome 7 (D7S501).
A possible association of hematologic malignancy with hereditary nonpolyposis colon cancer reported in the literature, together with a report that MSH2-deficient mice are susceptible to malignant lymphoma, strongly supports the finding that this patient's lymphoma was related to hereditary nonpolyposis colon cancer. Overall, this case manifested a distinct clinical course similar to that observed in an animal model that is deficient in DNA mismatch repair machinery, thus providing scientific and clinical implications for understanding the molecular basis of these tumors and for critical management of hereditary nonpolyposis colorectal cancer patients, respectively.
Diseases of the Colon & Rectum 03/2002; 45(2):273-9. · 3.13 Impact Factor
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ABSTRACT: PURPOSE: Hereditary nonpolyposis colorectal cancer kindreds are frequently associated with cancers in various organs, including endometrium, stomach, and ovary. However, hematologic malignancy has rarely been reported in association with this cancer syndrome. We present here the case of a probable hereditary nonpolyposis colon cancer patient in whom non-Hodgkins lymphoma developed after curative resection of colon cancer. Our experience with this rare case encouraged us to review the literature for reports indicating a possible relationship between these diseases.
RESULTS: A 52-year-old male whose family history was consistent with the criteria for hereditary nonpolyposis colon cancer underwent right hemicolectomy for ascending colon cancer. Histologically the tumor consisted of adenocarcinoma that was moderately differentiated with mucinous foci and that invaded beyond the muscularis propria. Neither metastasis nor lymphoma was found in paracolonic lymph nodes. Eight months after surgery, the patient developed non-Hodgkins lymphoma of T-cell origin involving the ileum and lungs. Both colon cancer and lymphoma frequently showed microsatellite DNA instability, sharing alteration in a locus of chromosome 7 (D7S501).
CONCLUSION: A possible association of hematologic malignancy with hereditary nonpolyposis colon cancer reported in the literature, together with a report that MSH2-deficient mice are susceptible to malignant lymphoma, strongly supports the finding that this patients lymphoma was related to hereditary nonpolyposis colon cancer. Overall, this case manifested a distinct clinical course similar to that observed in an animal model that is deficient in DNA mismatch repair machinery, thus providing scientific and clinical implications for understanding the molecular basis of these tumors and for critical management of hereditary nonpolyposis colorectal cancer patients, respectively.
Diseases of the Colon & Rectum 01/2002; 45(2):273-279. · 3.13 Impact Factor
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ABSTRACT: It has been considered that thromboxane A2 (TXA2) is involved in the development of bronchial hyperresponsiveness (BHR), a characteristic feature of asthma. To ensure the involvement of TXA2 in BHR of asthma, effects of a 1-week treatment with two orally active TXA2 antagonists, BAY u 3405 and S-1452, on BHR were examined in 10 and 13 patients with stable asthma, respectively, in two consecutive double-blinded, randomized, placebo-controlled, two-phase crossover studies. Provocative concentration of methacholine causing a 20% fall in FEV, (PC20-FEV1) with BAY u 3405 (0.78 (GSEM, 1.50) mg/ml) was significantly greater than the value with placebo (0.65 (GSEM, 1.46) mg/ml) (ratio 1.23 times, 95% CI 1.01 to 1.46: P=0.0401). PC20-FEV1 was also significantly increased with S-1452 (0.43 (GSEM, 1.39) mg/ml) compared with placebo (0.29 (GSEM, 1.27) mg/ml) (ratio 1.75 times, 95% CI 1.05 to 2.45: P=0.0189). Baseline pulmonary function was not altered by these treatments. These results may ensure that TXA2 is significantly involved in the BHR of asthma while the degree of contribution may be small.
Pulmonary Pharmacology.
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Kazuo Kasahara,
Kazuhiro Shibata,
Hiromoto Shintani,
Kei-Ichi Iwasa,
Takashi Sone,
Hideharu Kimura,
Kouichi Nobata,
Tatsuki Hirose,
Yuzo Yoshimi,
Nobuyuki Katayama,
Yoshihisa Ishiura,
Toshiyuki Kita,
Koichi Nishi, Yasuto Nakatsumi,
Yoshiki Ryoma,
Masaki Fujimura,
Shinji Nakao
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ABSTRACT: To determine the optimum dose of OK-432 for intrathoracic administration, a multicenter randomized phase II trial was conducted in patients with malignant pleural effusion due to non-small cell lung cancer. Patients with histologically- or cytologically-proven malignant pleural effusions were randomized to arm A (10 Klinische Einheit (KE) of OK-432) or arm B (1 KE of OK-432). OK-432 was injected intrapleurally over 30 min on days 1 and 3 and the chest tube was clamped for 6 h. If control was inadequate on day 8, 10 KE was administered on days 8 and 10 in each treatment arm. Forty patients were enrolled and 38 patients were eligible (19 in arm A and 19 in arm B). The effusion control rate on day 8 was 79% in arm A and 53% in arm B, while control rates on day 28 were 74% and 84%, respectively. The median drainage time after administration was significantly shorter in arm A (4.0 +/- 1.2 days) than in arm B (7.0 +/- 1.7 days). The total drainage volume was also significantly less in arm A than in arm B. No grade 4 toxicities or treatment-related deaths were observed in either treatment arm. Intrathoracic injection of OK-432 is a feasible treatment for malignant pleural effusion. Although the malignant pleural effusion control rate was equivalent in each treatment arm, faster control and less drainage were achieved in arm A. A dose of OK-432 10 KE/body is, therefore, recommended for further trial.
Anticancer research 26(2B):1495-9. · 1.73 Impact Factor
