Biomedical subjects

H Matsuse

Publications and source records attributed to H Matsuse.

At least 37 records · Page 2Linked to original sources

PubMed2000

Genetic susceptibility to renal ischemia reperfusion injury revealed in a murine model.

BACKGROUND: The development of genetically engineered mice has led to increased use of mouse models to study renal ischemic reperfusion injury (IRI). We hypothesized that susceptibility to IRI could result from strain differences due to genetic factors. METHODS: Our study compared recovery subsequent to renal IRI in NIH Swiss, C57BL/6, and BALB/c mice. Serum creatinine (SCr) and blood urea nitrogen (BUN) levels were evaluated postischemia. We also conducted reverse transcriptase-polymerase chain reaction (RT-PCR) analyses of renal cytokines and adhesion molecules postischemia. RESULTS: At 48 hr postischemia, renal dysfunction in NIH Swiss mice was significantly reduced, compared with other groups (P<0.01). BUN measurements confirmed renal protection at 48 hr in the NIH Swiss group. RT-PCR analysis of mRNA postischemia demonstrated that, between strains, there was little difference in mRNA expression for renal cytokines and adhesion molecules. CONCLUSIONS: NIH Swiss mice appear to be resistant in susceptibility to renal IRI. Early expression of pro-inflammatory genes was not associated with resistance to IRI, thus genetic factors could be important in outcome after renal IRI.

Animals↗

PubMed2000

Effects of sodium cromoglycate on cytokine production following antigen stimulation of a passively sensitized human lung model.

BACKGROUND: Interleukin-5 (IL-5) and tumor necrosis factor-alpha (TNF-alpha) play key roles in bronchial asthma. Sodium cromoglycate (DSCG) and dexamethasone (Dex) are used in the treatment of asthma as anti-inflammatory agents. OBJECTIVE: We investigated whether DSCG inhibited the expression of IL-5 and TNF-alpha mRNA and proteins from isolated human lungs, and compared these findings with those of Dex. METHODS: Human lung specimens were passively sensitized with sera from atopic patients, then preincubated in the presence of DSCG (10(-3), 10(-4), 10(-5) M) or Dex (10(-6) M) for 2 hours. The specimens were stimulated with Dermatophagoides antigen, then cultured for 48 hours. The supernatant was collected 1, 2, 4, 8, 24, and 48 hours to measure IL-5 and TNF-alpha by enzyme-linked immunosorbent assay. mRNA expression was examined by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: Tumor necrosis factor-alpha protein reached a peak level at 4 hours (156.57 +/- 18.29 pg/mL). Dex decreased TNF-alpha protein to 31.86 +/- 4.67 pg/mL (P < .001). There was also a decrease of TNF-alpha protein to 107.43 +/- 14.25 pg/mL by 10(-4) MD SCG (P < .001). Antigenic stimulation also increased the release of IL-5 protein at 4 hours and the peak level was observed at 24 hours (150.29 +/- 19.12 pg/mL). Dex decreased IL-5 protein to 28.57 +/- 5.27 pg/mL (P < .0001), 10(-4) M DSCG also decreased to 111.57 +/- 15.28 pg/mL (P < .05). RT-PCR analysis showed persistence of IL-5 and TNF-alpha mRNA expression from 1 to 24 hour after antigen stimulation. Dex but not DSCG inhibited IL-5 and TNF-alpha mRNA levels. CONCLUSION: Our results showed that DSCG significantly inhibited IL-5 and TNF-alpha production by human lung specimens, suggesting that it acts as an anti-inflammatory agent.

Aged↗

PubMed2000

Differential cytokine mRNA expression in Dermatophagoides farinae allergen-sensitized and respiratory syncytial virus-infected mice.

The interaction between mite allergen sensitization and respiratory syncytial virus (RSV) infection at the level of cytokine mRNA expression was examined in a murine model in the present study. Primary RSV infection enhances expression of inflammatory cytokines such as IL-6, IFN-gamma, and eotaxin in the lung and upregulates the expression of Th2-like cytokines IL-10 and IL-13 in the spleen in BALB/c mice. Mite antigen-sensitized and RSV-infected (ASRSV) mice show enhanced (P < 0.05) total serum IgE compared to antigen-sensitized mice. However, the levels of viral mRNA in the lung tissues are comparable between RSV-infected and ASRSV mice. It is concluded that compartmentalization of cytokine expression following RSV infection plays a role in the augmentation of Th2-like and IgE antibody response to RSV.

Allergens↗

PubMed2000

Two patients with occupational asthma who returned to work with dust respirators.

OBJECTIVES: To assess the efficacy of dust respirators in preventing asthma attacks in patients with occupational asthma (asthma induced by buckwheat flour or wheat flour). METHODS: The effect of the work environment was examined in two patients with occupational asthma with and without the use of a commercially available mask or a dust respirator. Pulmonary function tests were performed immediately before and after work and at 1 hourly intervals for 14 hours after returning to the hospital. RESULTS: In patient 1, environmental exposure resulted in no symptoms during and immediately after work, but coughing, wheezing, and dyspnoea developed after 6 hours. Peak expiratory flow rate (PEFR) decreased by 44% 7 hours after leaving the work environment, showing only a positive late asthmatic reaction (LAR). In patient 2, environmental exposure resulted in coughing and wheezing 10 minutes after initiation during bread making, and PEFR decreased by 39%. After 7 hours, PEFR decreased by 34%. The environmental provocation tests in both patients were repeated after wearing a commercial respiratory. This resulted in a complete suppression of LAR in patient 1 and of immediate asthmatic reaction (IAR) and LAR in patient 2. CONCLUSIONS: Two patients with asthma induced by buckwheat flour or wheat flour in whom asthmatic attacks could be prevented with a dust respirator are reported. Dust respirators are effective in preventing asthma attacks induced by buckwheat flour and wheat flour.

Adult↗

PubMed2000

Hexamethylene diisocyanate causes contraction of canine tracheal smooth muscles through activation of muscarinic receptors.

BACKGROUND: Asthma caused by occupational exposure to hexamethylene diisocyanate (HDI) is well known; however, the exact pathogenic mechanisms remain unclear. METHODS: Experiments were performed using a standard canine tracheal smooth muscle (CTSM) strip preparation in an isolated bath to determine the effect of HDI on tracheal smooth muscle contraction. HDI concentration-response curves were constructed and the effects of different receptor antagonists on HDI-induced smooth muscle contraction were determined. To determine whether HDI and acetylcholine (ACh) bind to a common muscarinic receptor, ACh concentration-response curves in the absence or presence of HDI and concentration-response curves for HDI and ACh in the presence or absence of atropine were plotted. RESULTS: HDI caused contraction of CTSM, with a threshold concentration of 10(-7) M. The EC(50) (HDI concentration that produced 50% of the maximal response) was 6.2+/-0.7 x10(-7) M and the maximal contractile response (174+/-55 g/g of tissue) occurred at a concentration of 5.0+/-0.8 x 10(-6) M. Atropine, a muscarinic blocker, significantly inhibited HDI-induced contractile responses. HDI shifted the ACh concentration-response curve to the right. The mean pA(2) for atropine against ACh (8.93+/-0.27) was not significantly different from that against HDI (8.03+/-0.12). CONCLUSIONS: Our results indicated that HDI causes contraction of CTSM through the activation of muscarinic receptors. Direct stimulation of muscarinic receptors by HDI may play an important role in HDI-induced asthma.

Acetylcholine↗

PubMed1999

Intranasal IFN-gamma gene transfer protects BALB/c mice against respiratory syncytial virus infection.

Respiratory syncytial virus (RSV) is a major respiratory pathogen in infants, young children and the elderly and causes severe bronchiolitis and asthma. In an effort to develop a preventive IFN-gamma therapy against RSV infection, an intranasal gene transfer strategy was utilized. Intranasal administration of a plasmid expressing the IFN-gamma cDNA (pIFN-gamma) resulted in the expression of IFN-gamma in murine lungs and decreased RSV replication. The mice administered with pIFN-gamma and then infected with RSV exhibited a significant decrease in broncho-alveolar lavage lymphocyte and neutrophil counts. A significant reduction in epithelial cell damage, infiltration of mononuclear cells in the peribronchiolar and perivascular regions, and thickening of the septa was observed in the lungs of mice treated with pIFN-gamma when compared to controls. These results suggest that intranasal IFN-gamma gene transfer results in decreased RSV replication and pulmonary inflammation and may be useful against RSV infection.

Administration, Intranasal↗

PubMed1999

In vitro responses to antigen stimulation: comparison between human lung parenchyma resected from asthmatic patients and non-asthmatic patients.

BACKGROUND: The airway of asthmatic patients is hyperresponsive to various stimuli in vivo. There are, however, only a few reports that compared the in vivo responsiveness of asthmatic patients and non-asthmatic subjects to those of lung parenchyma in vitro. OBJECTIVES: To compare the contractile response, release of various chemical mediators, and responsiveness to drugs in samples of lung parenchyma excised from asthma patients with those of non-asthmatic subjects. METHODS: Human lung parenchymal strips were subjected to passive sensitization with sera of 5+ RAST titer to mites. The strip was suspended in a magnus bath containing a buffer solution. Parenchymal contraction was induced by PGF2 alpha. After washing, the baseline concentrations of thromboxane B2 (TXB2), leukotriene (LT), and histamine were measured in each bath and then contraction was induced by the addition of a mite antigen. The concentrations of TXB2, LT, and histamine were measured after contraction. The inhibitory effects of TXA2 synthetase inhibitor (DP-1904) and TXA2 receptor antagonist (AA-2414) were also evaluated in both tissue samples. RESULTS: There were no significant differences between lung parenchymal tissues of asthmatic and non-asthmatic patients with regard to PGF2 alpha-induced contraction, antigen-induced contraction, release of chemical mediators, and the response to drugs. CONCLUSION: Unlike the response in vivo, there are no differences in the response to stimuli in vitro between lung parenchymal tissues of asthmatic and non-asthmatic patients.

Aged↗

PubMed1999

Sensitivity to the house dust mite and airway hyperresponsiveness in a young adult population.

BACKGROUND: The pathogenic mechanisms of airway hyperresponsiveness (AHR) in asthma are unknown and only a few studies have examined the importance of sensitivity to antigens in AHR in young adults. OBJECTIVE: We investigated the correlation between AHR and sensitivity to specific antigens, atopy, history of childhood asthma and spirometry in a young adult population. METHODS: Based on the results of interviews with 447 students at our university, 308 non-smoker students were classified into six groups. Group 1 comprised subjects with intermittent mild bronchial asthma; group 2, subjects with history of childhood asthma; group 3, subjects with atopic disease, and a RAST score for Dermatophagoides farinae (Def) of > or = 2; group 4, normal subjects with a RAST score for Def of > or = 2; group 5, subjects with cedar pollinosis; and group 6, normal subjects. We measured AHR to methacholine (MCh), spirometry, immunoglobulin E-radioimmunosorbent test (IgE-RIST), IgE-radioallergosorbent test to six common antigens, eosinophil cationic protein (ECP), and eosinophil count in peripheral blood in each subject. RESULTS: Airway hyperresponsiveness to MCh did not correlate with IgE-RIST, eosinophil count, or ECP. The highest AHR to MCh was present in groups 1 and 2 and lowest in groups 5 and 6. Multiple regression analysis showed that sensitivity to Def was the only factor that significantly influenced AHR to MCh. Airway hyperresponsiveness to MCh of groups with a RAST score for Def of 0/1 was lower than groups with a RAST score of 2 to 6. Airway hyperresponsiveness to MCh did not correlate with the degree of positivity to Def antigen among positive sensitized groups (RAST score 2 to 6). CONCLUSIONS: Sensitivity to mite antigen may be important in the pathogenesis of AHR and Def is a major contributing antigen in young adults in Japan. Once asthma occurs, AHR remains positive for a long time even after the disappearance of asthma-related symptoms.

Adult↗

PubMed1999

Corticosteroid resistance in mild asthma: markers of persistent inflammation.

BACKGROUND: Bronchial hyperresponsiveness (BHR) is an important feature of asthma. Glucocorticosteroids (GCS) reduce BHR, probably by suppressing allergic inflammation. There are, however, two groups of asthmatics with either GCS-responsive or non-responsive BHR to methacholine. We investigated the mechanism of non-GCS-responsive BHR in mild asthma. METHODS: Non-GCS-responsive BHR asthma was defined as failure of reduction of BHR to methacholine after a 2-week course of oral prednisolone (30 mg/day). The expression of interleukin (IL)-4, IL-5, IFN-gamma mRNA in peripheral blood mononuclear cells, eosinophil count, serum cortisol, eosinophilic cationic protein (ECP), and spirometry were measured in five non-GCS-responsive BHR asthmatics and six patients with GCS-responsive BHR asthma before and after prednisolone therapy. RESULTS: With the exception of serum ECP and expression of IL-5 mRNA, no significant differences were observed between GCS-responsive BHR and non-GCS-responsive BHR asthma. The mean ECP level was significantly higher in non-GCS-responsive BHR than in GCS-responsive BHR asthma before and after prednisolone therapy. Interleukin-5 mRNA was detected in all asthmatics before prednisolone therapy; however, after prednisolone therapy, IL-5 mRNA was only detected in non-GCS-responsive BHR asthmatics. CONCLUSIONS: Our findings suggest that activation of eosinophils appears to persist in some asthmatics with non-GCS-responsive BHR due to continuous IL-5 production by lymphocytes.

Administration, Oral↗

PubMed1999

Sodium cromoglycate inhibits antigen-induced cytokine production by peripheral blood mononuclear cells from atopic asthmatics in vitro.

BACKGROUND: Several anti-allergic anti-inflammatory drugs are used for the treatment of asthma including glucocorticosteroids (GCS), sodium cromoglycate (SCG), leukotriene (LT) inhibitors, and LT receptor antagonists. The major mechanism of the anti-inflammatory action of GCS is inhibition of cytokine production by T-lymphocytes: however, the mechanisms of anti-inflammatory effects of SCG are still unclear. OBJECTIVE: We elucidated the anti-inflammatory effects of SCG by investigating its effects on cytokine production by peripheral blood mononuclear cells (PBMCs) obtained from atopic asthmatics. METHODS: Peripheral blood mononuclear cells were obtained from seven atopic asthmatics and sensitized with Dermatophagoides farinae (DJ) or concanavalin A (ConA). We compared the effects of SCG on interleukin (IL)-5 and interferon (IFN)-gamma production by sensitized PBMCs with that of dexamethasone (Dex). Based on their clinical concentrations, we compared the effects of 10(-6) to 10(-4) M of SCG to those of 10(-6) M Dex. RESULTS: Stimulation with ConA increased the production of IL-5 and IFN-gamma. Dex significantly inhibited the production of both cytokines but SCG showed no inhibitory effects. On the other hand, Df stimulation increased IL-5 production only. Dermatophagoides farinae-induced overproduction of IL-5 was inhibited by SCG and Dex. CONCLUSIONS: Our results suggested that SCG has antigen-specific anti-allergic inflammatory effects.

Adult↗

PubMed1999

Inhibitory effects of azelastine hydrochloride in alcohol-induced asthma.

BACKGROUND: Alcohol-induced bronchoconstriction is due to high blood concentrations of acetaldehyde, a metabolic product of ethanol, which lead to the release of histamine from basophils and mast cells. OBJECTIVE: We examined the inhibitory effects of azelastine hydrochloride, which inhibits histamine release and blocks H1 receptors, in alcohol-induced asthma. METHODS: Subjects were 13 Japanese asthmatic patients. We measured the change in FEV1 after ingestion of 30 g of pure ethanol. Blood ethanol, acetaldehyde, histamine, leukotriene C4 (LTC4), and thromboxane B2 (TXB2) concentrations were also measured. Alcohol challenge test was repeated in responders after administration of azelastine for 1 week at 4 mg/day. RESULTS: Of 13 asthmatic patients, five (38.5%) tested positive during an ethanol challenge test, represented by a fall more than 20% in FEV1. The responders had a high blood ethanol, and showed a rise in blood acetaldehyde and histamine concentrations, but not in LTC4 or TXB2. After azelastine treatment, there was no significant fall in FEV1 among responders. Neither the rise in blood ethanol nor blood acetaldehyde levels were blunted by treatment with azelastine, but the rise in blood histamine was blunted by this treatment. CONCLUSION: Our results suggest that antihistamine agents may be effective against alcohol-induced asthma by both blocking H1 receptors and inhibiting histamine release.

Acetaldehyde↗

PubMed1999

A recombinant BCG vaccine generates a Th1-like response and inhibits IgE synthesis in BALB/c mice.

The tubercle vaccine, bacille Calmette-Guérin (BCG), is a strong inducer of T-helper type 1 (Th1) responsiveness, and it has been suggested that recombinant BCG (rBCG), which produces and secretes antigens, may be used to prevent allergic diseases. The effects of rBCG vaccination on allergic responses in a murine model were examined in this study. A BCG-Escherichia coli shuttle vector was developed with the promoter and signal sequence of the alpha-antigen of Mycobacterium bovis, and the vector was tested using E. coli beta-galactosidase as the model antigen and allergen. This vector enabled the expression of the E. coli beta-galactosidase gene in BCG, which was detected in its protein extract by immunoblotting analysis. Vaccination of mice with a single dose of 106 recombinant BCG generated a beta-galactosidase-specific antibody response. The splenocytes of vaccinated mice compared with controls produced significantly higher amounts of interferon-gamma (IFN-gamma) (P<0. 01) and interleukin-2 (IL-2) (P<0.05) and lower amounts of IL-5 (P<0. 01). Mice vaccinated with rBCG had significantly less (P<0.01) serum IgE compared with controls. These results together demonstrate that rBCG secreting antigens or allergens may be utilized for the induction of a Th1-like response and the down-regulation of IgE antibody response.

Animals↗

PubMed1999

A case of menstruation-associated asthma: treatment with oral contraceptives.

A menstrual rhythm has been documented for exacerbations of asthma, which may have important clinical relevance to the patient with severe asthma. We report the case of a 26-year-old patient with menstruation-associated asthma who showed a dramatic response to oral contraceptives. It was noted that falls in peak respiratory flow rate coincided with ovulation. We concluded that oral contraceptive therapy is useful in this particular group of asthmatic patients.

Adult↗

PubMed1998

Respiratory syncytial virus induces the expression of 5-lipoxygenase and endothelin-1 in bronchial epithelial cells.

Respiratory syncytial virus (RSV) infection causes and exacerbates asthma, yet the mechanism by which RSV triggers asthma is poorly understood. Herein, an in vitro model of RSV infection was established using HEp-2 and BEAS-2B bronchial epithelial cell lines, and the expression of 5-lipoxygenase (5-LO), and endothelin-1 (ET-1) was examined. RSV infection increased the expression of 5-LO mRNA and protein in both cell lines, as detected by RT-PCR and western blot analysis, respectively. The levels of leukotrienes also increased in the supernatants of RSV infected cells. Furthermore, RSV infection increased the expression of ET-1 mRNA and protein following RSV infection in a time-dependent manner. It is concluded that RSV infection upregulates the expression of ET-1 and 5-LO in the epithelial cells leading to the production of leukotrienes, which may mediate the consequent exacerbation of asthma.

Arachidonate 5-Lipoxygenase↗

PubMed1998

Effect of synthetase inhibitors and receptor antagonists in antigen-induced contraction of human lung parenchyma.

BACKGROUND: Chemical mediators induce bronchoconstriction, enhance vascular permeability, and promote inflammation. The use of synthetase inhibitors and receptor antagonists of these mediators may be useful in the treatment of asthma. OBJECTIVES: We evaluated the role of chemical mediators in mite antigen-induced contraction in resected human lung parenchyma using synthetase inhibitors and receptor antagonists for these mediators. METHODS: Resected human lung parenchymal specimens were passively sensitized with serum obtained from patients with asthma showing an IgE RAST score for mites > or = 5. The specimens were suspended in Magnus bath filled with buffer. After confirmation of contraction using PGF2 alpha, buffer or synthetase inhibitors or receptor antagonists of various chemical mediators were added. Contraction of parenchyma was induced by the addition of mite antigen, and the concentration of thromboxaneB2 (TXB2), leukotriene (LT), and histamine was measured before and after contraction. RESULTS: Thromboxane A2 (TXA2) synthetase inhibitors significantly inhibited TXB2 release but not contraction. Leukotriene synthetase inhibitors significantly inhibited both LT release and contraction. The magnitude of the inhibitory effect was in the order of LT receptor antagonist > 5-lipoxygenase inhibitor > TXA2 receptor antagonist > PAF antagonist, TXA2 synthetase inhibitor, antihistamine > cyclooxygenase inhibitor. CONCLUSION: Among chemical mediators, LT appears to be the most closely involved in the immediate antigen-induced contractile response in resected human lung parenchyma. Receptor antagonists produced a more marked inhibition of antigen-induced contraction than synthetase inhibitors.

Aged↗

PubMed1998

Comparison of three treatment regimens of inhaled sodium cromoglycate in the management of adult patients with severe, steroid-dependent asthma.

BACKGROUND: Asthmatic patients whose asthma remains poorly controlled despite treatment with high doses of inhaled corticosteroids and co-administration of oral corticosteroids are a difficult problem in therapeutics. OBJECTIVE: To investigate the relative efficacy of three treatment regimens of inhaled sodium cromoglycate in the treatment of adult, severe, corticosteroid-dependent patients as determined by the reduction in the dose of oral corticosteroids and change in lung function. METHODS: Open, randomized, group comparative trial of 12 weeks duration in asthmatic patients attending a hospital outpatient department. Patients whose asthma is (1) severe according to the classification of the Japanese Society of Allergology, (2) stable, and (3) needing treatment with at least 1600 microg of inhaled beclomethasone dipropionate and 5 mg or greater of oral prednisolone per day. The three treatment regimens of inhaled sodium cromoglycate were group A received sodium cromoglycate powder at a dose of 16 mg/day administered by a metered dose inhaler. Group N received sodium cromoglycate aqueous solution at a dose of 80 mg/day administered by a nebulizer. Group C received sodium cromoglycate aqueous solution (80 mg/day) combined with salbutamol (3 mg/day) administered by a nebulizer. The main outcome measures were a change in the daily dose of oral corticosteroids and in lung function with twice daily measurements of peak expiratory flow (PEF) recorded in the morning (PEF AM) and in the evening (PEF PM). RESULTS: Mean reduction in oral corticosteroid dose/day was group A, 3.68 mg (95% CI 1.35,5.95); group N, 3.59 mg (95% CI 0.73,6.45); and group C, 3.97 mg (95% CI 1.81,6.13). The dosage reductions are all significant but with no differences between the groups. The mean increase in PEF over the last 4 weeks of treatment compared with baseline values was significant in all groups. The increases in group C are significantly greater than those in the other groups. These changes are all significant and the increases in group C are significantly greater than those in the other groups. CONCLUSIONS: Inhaled sodium cromoglycate may be a useful additional treatment in the management of adult patients with severe, oral steroid-dependent asthma. Of the three methods of administration compared in this trial the most useful immediate results were obtained when the drug was administered as an aqueous solution mixed with salbutamol and delivered by a powered nebulizer.

Administration, Inhalation↗

PubMed1998

Effects of cysteinyl-leukotriene receptor antagonist, thromboxane A2 receptor antagonist, and thromboxane A2 synthetase inhibitor on antigen-induced bronchoconstriction in patients with asthma.

BACKGROUND: Leukotriene (LT) and thromboxane A2 (TXA2) receptor antagonists have been used in the treatment of asthma. OBJECTIVES: We examined the effects of an LT receptor antagonist, TXA2 receptor antagonist, and TXA2 synthetase inhibitor on bronchoprovocation test (BPT) in patients with mild-to-moderate atopic asthma. METHODS: BPT was performed four times in each of six asthmatics. Development of the immediate asthmatic reaction (IAR) and late asthmatic reaction (LAR) was confirmed on the first BPT (BPT1). After a 7-day washout period, an LT receptor antagonist (pranlukast, 450 mg/d), TXA2 receptor antagonist (seratrodast, 80 mg/d), or TXA2 synthetase inhibitor (ozagrel, 800 mg/d) was administered orally over 7 days at random using a cross-over method (BPT2-4). Blood levels of LTB4, LTC4, LTD4, 11-dehydrothromboxane B2, eosinophil cationic protein, and histamine were measured at reaction phases of pre-BPT, IAR, and LAR. RESULTS: Administration of pranlukast suppressed IAR by 80.5% (p < 0.0001) and LAR by 54.6% (p = 0.0391). Ozagrel significantly suppressed IAR by 39.5% (p = 0.0413), but the fall in FEV1 was >20% (21.56+/-4.173%). Seratrodast did not suppress IAR or LAR. Blood levels of chemical mediators did not correlate with the suppressive effects of the tested drugs. CONCLUSIONS: The LT receptor antagonist was considered to be the most effective. LT might play a more important role in the pathogenesis of asthma than TXA2. Our data showed that measurement of blood levels of chemical mediators is not useful in identifying the pathogenic mechanisms of asthma.

Administration, Oral↗

PubMed1997

Aspirin-induced asthma as a risk factor for asthma mortality.

We have recently reported severe airway obstruction and bronchial hyperresponsiveness (BHR) in fatal asthma compared with patients without a history of near-fatal asthma. Based on these findings, we evaluated whether aspirin-induced asthma (AIA) is a risk factor for asthma mortality by analyzing pulmonary function and BHR. FEV1.0% and methacholine inhalation threshold were significantly lower in the fatal asthma group compared with the AIA and non-AIA groups. However, there were no significant differences between the AIA and non-AIA groups. Our results suggested that AIA is not a risk factor for asthma mortality if avoidance of aspirin and aspirin-like drugs is assured.

Adult↗