소아 호흡기 질환에서의 Fominoben의 진해효과에 관한 임상적 연구

고영률 최신의학사 1988 最新醫學 Vol.31 No.9

특별연제 : 알레르기 반응에서의 호중구의 역할

고영률 대한천식알레르기학회 1992 천식 및 알레르기 Vol.12 No.2

논평: 기관지천식에서 기관지확장제에 대한 반응

고영률 대한천식알레르기학회 1993 천식 및 알레르기 Vol.13 No.3

유착분자

고영률 대한천식알레르기학회 1993 천식 및 알레르기 Vol.13 No.4

논평: 항원 흡입 유발 검사에서 기도반응을 결정하는 요인

고영률 대한천식알레르기학회 1994 천식 및 알레르기 Vol.14 No.1

운동과 항원에 의해 유발된 천식에서의 호증구의 활성화 상태에 관한 비교 연구

고영률,윤경애,김희주,최중환,김현 대한천식알레르기학회 1994 천식 및 알레르기 Vol.14 No.4

Asthma is considered today t,o be an inflam- matory disease. The chronic asthmatic disease characterized by a bronchial hyperreactivity is assumed to be the resu 1t of an ongoing inflam- matory process. The mechanism responsible for the inflammatory events are not entirely under- stood, but recent investigations point to a cru- cial role for the granulocytes such as neutro- phils or eosinophils. Some studies suggest that circulating neutrophils from asthmatic subjects are activated after challenge with allergen. Exercise is one of the most ubiquitous trig- gers of acute bouts of asthma. LARs have been described following strenuous exercise in sever- al studies, although the prevalence is low. How- ever, most authors reported that airway respon- siveness is not increased after exercise, even in the subjects with LAR to exercise. We have fre- quently seen asthmatic children whose com- plaint is that symptoms are exacerbated at night after strenuous daytime exercise. There- fore, it is crucial to know whether exercise can induce airway inflammation, as in allergen in- duced asthma. However, it is very difficult to pursue this, especially in children, because bronchoalveolar lavage or endotracheal biopsy is not feasible both technically and ethically. Therefore, as an indirect measure to investigate whether exercise can induce airway inflammation, as in allergen induced asthma, we measured the activation status of neutrophil granulocyte in the early and late phase of allergenor exercise induced asthma. Eight subjects who showed EAR and LAR (group 1), or EAR only (group 2) to allergen( Dermatophagoides pteronyssinus) challenge were selected. Similarly eight subjects who showed EAR and LAR (group 3), or EAR only (group 4) to exercise challenge were selected. Neutrophil granulocytes were separated from the venous blood at baseline, the early phase, the late phase, and 24 hours after each stimuli. Complement receptors(CR1 and CR3) were enumerated with monoclonal antibodies against the receptors and flow cytometry. Then migratory responses of neutrophils to LTB,(10 'M/L) were measured, and superoxide anion generations stimulated by PMA(10 M/L) were also measured. In the dual responders(Group 1 and 3), there was a significantly increased expression of CR1 and CR3, at EAR and LAR after allergen or exercise challenge. In the single responders (Group 2 and 4), CR1 expression was increased at EAR and late phase after allergen or exercise challenge, but CR3 expression was increased only at EAR. Neutrophil chemotaxis to LTB, did not show a significant change in the time course after allergen or exercise challenge in any group. Superoxide anion generation stimulated by PMA did not show any change, either. These results indicate that not only allergen but also exercise can activate neutrophils in accordance with the airway response t,o the stimuli. The present findings suggest that exercise can also have the potential to induce airway inflammation. Therefore exercise should be understood not only as a triggering factor of bronchoconstriction but also as one that incites or deter- iorates airway inflammation.

루우프 이뇨제 흡입이 항원유발후의 천식반응에 미치는 영향

고영률,윤경애,김희주 대한천식알레르기학회 1991 천식 및 알레르기 Vol.11 No.5

Inhaled furosemide, a loop diuretic that can interfere with ion and water transport across airway epithelium, prevents the immediate bronchoconstriction induced by exercise or allergen challenges in patients with asthma. To evaluate the effect of inhaled furosemide on both the immediate and late phases of the asthmatic response to the specific allergen challenge in patients with allergic asthma, and the role of inhibition of the Na /Cl cotransporter in the mechanisms of the protective properties of inhaled furosemide on asthmatic airways, seventeen asthma patients with dual responses to house dust mite(Dermatophagoides pteronyssinus) after normal saline were subjected to bronchial provocation with the same allergen after furosemide(n=10) or bumetanide(n=8) inhalation. Pulmonary function(FVC, FEV2, PEFR, MMEF) was monitored every one hour for 10 hours after allergen challenge, and 24 hours later methacholine sensitivity was measured. The data were compared between after furosemide or bumetanide inhalation and after normal saline inhalation. Treatment with furosemide profoundly inhibited both the early and late asthmatic reaction induced by a specific allergen challenge. Significant differences were seen in the postallergen bronchoconstrictor response to inhaled methacholine between after furosemide and after saline administration. Bumetanide, another loop diuretic, fails to inhibit both the early and late asthmatic reaction provoked by allergen, and to affect postallergen nonspecific bronchial hyperreactivity. Although further investigation as to clinical asthma is needed, results suggest that inhaled furosemide has clinical benefit in the treatment of allergic asthma. As the airway effects of furosemide were demonstrated apart from bumetanide, the protective effect of furosemide may be independent of its shared properties with bumetanide, Na/Cl transport inhibition.

호흡기질환의 진단적 접근 방법과 실제 호흡기 질환의 기능적 평가 방법

고영률 대한소아알레르기호흡기학회 1999 Supplement Vol.9 No.1

N/A

소아알레르기심포지엄 ( 87 ~ 90 ) : 일반연제 : 소아 기관지천식에서의 폐기능의 변화

고영률 대한소아알레르기호흡기학회 1991 Allergy Asthma & Respiratory Disease Vol.1 No.1

N/A

소아 기관지천식에서의 Ketotifen의 예방효과

고영률,최중환,이병구 대한천식알레르기학회 1988 천식 및 알레르기 Vol.8 No.3

Ketotifen is a new, orally acitive drug of the benzocycloheptathiophene class, which has shown to possess strong antianaphylactic as well as antihistaminic properties in pharmacological tests. Previously controlled clinical trials with this agent have established that ketotifen has significant prophylactic properties in the prevention of bronchial reactivity by various stimuli. The purpose of this study is to evaluate the prophylactic effect of ketotifen in childhood asthma. A double blind placebo controlled study was carried out in 30 atopic asthrnatic children, Patients were randomly allocated into two groups, one active ingradient (ketotifen)(20patients) and the other placebo (10 patients).After a 4-w'eeks' baseline assessment period, ketotifen was given at a dosage of 0.03mg/kg ' twice daily over a period of 12 weeks, whereas placebo group was given inactive powder or syrup identical in appearance to ketotifen over the same period, Throughout the study, parents were asked to keep a daily diary of symptom severity and intake of concomitant asthmatic medications, while PEFR was measured at the OPD visit every one week. Those patients receiving ketotifen had fewer asthmatic symptoms and distinct improvement in nor- mal activity and well being, whereas those on placebo had essentially no changes of above parameters in spite of the fact that concomitant medication was increased more often. The necessity of using ,stimulants and theophyllin was considerably decreased in patients under prophylactic treatrnent with ketotifen. An analysis of PEFR reading demonstrated that ketot.ifen showed superiority over placebo and progressive increase over the whole course of treatment in the ketotifen group. Three of the ketotifen patients showed adverse reactions, whereas none of the placebo patients exhibited any side effects. They hardly, however, caused any clinical problems and disappeared despite of con- tinuance therapy. Global assessment at the end of the study rated the treatment with ketotifen as very effective or effective in 12 of 20(60%), whereas the same rating was given to only of 2 of 10 treated with the corresponding placebo. In conclusion, ketotifen appears well tolerated and sufficiently effective to provide benefit in the prophylactic treatment in most children with extrinsic asthma.