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Biomedical subjects

H Matsuse

Publications and source records attributed to H Matsuse.

43 records · Page 3Linked to original sources

Investigation of the mechanism of alcohol-induced bronchial asthma.

BACKGROUND: Many Japanese patients with asthma experience episodes or exacerbation of asthma after alcohol consumption. This phenomenon is not seen in Caucasians and is specific to Asians. This has been thought to be attributable to a difference in alcohol metabolism, in particular the metabolism of acetaldehyde, between Asians and Caucasians. METHODS: An oral ethanol challenge test, a leukocyte histamine release test, and an ELISA for detection of IgE specific to acetaldehyde-human serum albumin conjugate were carried out in 42 adults with bronchial asthma and nine healthy adults. RESULTS: Fifty-five percent of the patients with asthma responded to the ethanol challenge and showed a 20% or greater reduction in forced expiratory volume in 1 second. Blood acetaldehyde and plasma histamine levels were significantly higher in responders than in nonresponders. The leukocyte histamine release test revealed no ethanol-induced histamine release. Acetaldehyde, on the other hand, was found to induce histamine release in a volume-dependent manner. The histamine release was significantly higher in the asthma group (both responders and nonresponders) than in the healthy control group. ELISA did not detect any IgE specific to acetaldehyde-human serum albumin conjugate. CONCLUSION: Alcohol-induced bronchial asthma seems to develop as follows. Alcohol elevates blood acetaldehyde levels, which leads to degranulation of mast cells (or basophils). The resultant release of chemical mediators, such as histamine, induces asthma.

Acetaldehyde↗

Inhibitory effect of thromboxane A2 synthetase inhibitor, DP-1904, on antigen-induced contraction of human lung parenchyma.

BACKGROUND: Several mediators are released from mast cells during allergic reactions. These substances cause contraction of airway smooth muscles, increase the permeability of blood vessels, and enhance mucous secretion. Among these mediators, thromboxane A2 (TXA2) has a particularly strong bronchoconstrictive effect. OBJECTIVES: We examined antigen-induced contraction of excised human lungs and the suppressive effects of TXA2 synthetase inhibitor on TXA2 release. METHODS: Human lung parenchymal strips were subjected to passive sensitization with sera of 5+ RAST titer to the mite. They were suspended in magnus baths, to which buffer and 10(-4) to 10(-8) M of DP-1904, an inhibitor of TXA2 synthetase, were added. Following the measurement of TXB2 and leukotriene (LT) concentrations in each bath, parenchymal contraction was induced by the addition of a mite antigen. The concentration of TXB2 and LT was measured after contraction. RESULTS: Antigen-induced release of TXB2 was significantly suppressed by DP-1904 in a concentration-dependent manner. DP-1904 did not inhibit parenchymal contraction and the release of LT. CONCLUSIONS: Antigen-induced parenchymal contraction was not suppressed by inhibition of TXA2 release, suggesting that DP-1904 may not be effective in asthma.

Aged↗

A clinical study of mortality due to asthma.

BACKGROUND: Despite identification of the pathophysiologic mechanisms of asthma and improvement in therapy, asthma mortality has not decreased in recent years. OBJECTIVE: The pathophysiology and asthma-related death preventive measures were investigated with a physician-based questionnaire survey. METHODS: Questionnaires were sent to physicians primarily involved in treating asthma in Nagasaki Prefecture, Japan. The clinical characteristics of 32 patients who died of asthma (fatal cases) from 1984 to 1992 were compared with those of 17 patients with severe asthma who survived as a result of treatment by mechanical ventilation (nearly fatal cases). RESULTS: The number of deaths due to asthma increased in the last 2 years. Fatal cases and nearly fatal cases included patients with severe asthma as well as patients with mild asthma. Analysis of the clinical histories of patients judged to have died suddenly revealed the presence of persistent wheezing in these patients for a few days prior to the fatal episode. Airway obstruction was more marked and bronchial hyperresponsiveness was greater in fatal cases compared with those of a group of 70 patients without a history of nearly fatal acute asthma. CONCLUSIONS: The following measures may help prevent asthma deaths. Both patients and physicians should realize that even mild episodes can lead to severe, even fatal acute asthma. The severity of asthma should be evaluated not only by symptoms and peak expiratory flow rates but also bronchial hyperresponsiveness. Treatment should include reduction of bronchial hyperresponsiveness using oral or inhaled corticosteroids.

Adult↗

[Six cases of allergic bronchopulmonary aspergillosis].

Six cases of allergic bronchopulmonary aspergillosis (ABPA) were evaluated. In four cases, diagnosis and steroid therapy were delayed, which resulted in irreversible pulmonary dysfunction. The important points for early diagnosis were: (1) Differentiation from pulmonary tuberculosis, (2) the presence of bronchial asthma was not essential for diagnosis, and (3) fungi other than Aspergillus fumigatus might cause this syndrome.

Adult↗

[A dementia occurred during therapy for multi-drug resistant pulmonary tuberculosis].

A 47-year-old woman was thirdly admitted to our hospital for therapy to multi-drug resistant tuberculosis of the lung in June 88. Although she was treated with TH, PAS and EVM, M. tuberculosis were positive constantly in her sputum. She complained of sleep disturbance, irritability, headache on September 89, she was diagnosed reactive depression. But her symptoms were progressive, low level of intelligence test in November, apatic in December and became spastic paralysis and vegetable state at next year. She was died of pneumonia in November 90. Her autopsy findings showed no brain atrophy nor meningitis. Microscopically, central chromatolysis were showed in Betz cells and anterior horn cells, these findings sometimes suspected for Peragulla, but we could not obtained definite pathological diagnosis, because we could not have been obtained findings indicating for Peragulla. Finally, we reported the clinical course and autopsy findings of dementia occurred during therapy for multi-drug resistant pulmonary tuberculosis.

Dementia↗

Diagnostic problems in chronic eosinophilic pneumonia.

To identify the problems involved in the diagnosis of chronic eosinophilic pneumonia (CEP), clinical findings were analysed for 43 patients diagnosed clinically or pathologically with CEP during the past 10 years. About 28% of patients showed peripheral blood eosinophilia and a typical pattern of pulmonary oedema on chest X-ray at initial examination. Eosinophilia was demonstrated in peripheral blood in 86% of patients, in bronchoalveolar lavage (BAL) in 100%, and in transbronchial lung biopsy (TBLB) specimens in 64% of patients. Peripheral blood tests, BAL, and TBLB were all positive for eosinophilia in 60% of patients. BAL was the single test most likely to be positive among the diagnostic tests used in the present study. When CEP is suspected clinically, an understanding of which site is examined by each of the diagnostic tests and of the likelihood of a positive result in each test will facilitate the selection of the most appropriate tests for individual patients.

Adult↗