Objectives: To evaluate the inhibitory effect of corticosteroids including hydrocortisone, methyl- prednisolone, dexamethasone on the survival of eosinophils. Method: Eosinophils were purified from allergic patients with peripheral eosinophilia. Survival rate of eosinophils in the presence of IL  5 were measured by using flowcytometer. The inhibitory effect of corticosteroids were compared to spontaneous and IL  5 induced survival of eosinophils rates. Results: 1) Spontaneous survival rates of eosinophils rapidly decreased below 10k at the 3rd day of culture in the absence of IL  5, 2) IL  5 prolonged the survival of eosino- phils dose dependently. 3) Corticosteroids including hydrocortisone, methylprednisolone, dexamethasone did not have any inhibitory effect on the spontaneous survival of eosinophils.  4) Hydrocortisone significantly decreased IL  5  induced prolongation of eosinophil survival dose dependently. The blocking effect became apparent after the 4th day of culture. 5) Biologically equivalent dosages of hyd- rocortisone, methylprednisolone, dexamethasone had the inhibitory potency on the survival of eosinophils in descending order. Conclusion.' Corticosteroids had different effects on survival of eosinophils induced by IL  5 even when used at the concentration of biologically eqivalent dosages. The effect of corticosteroid was not immediate, but delayed upto 4 days or more.

Skin prick test(SPT) is an economic and sensitive test to detect a specific IgE. Theophylline, oral beta2-agonist. Oral corticosteroids, and antihistamines are the commomly prescribed drugs in patients with allergic diseases but there are many situations that SPT are performed while taking those durgs. It has been suggested that theophylline, oral beta2- agonist, and corticosteroid inhibit the release of mediators from mast cells in vitro. To evaluate the effects of theophylline, oral Salbutamol,  and Prednisolone on the results of SPT, we measured skin resgonse to histamine codeine, and allergens before and after the mediestions of therapeutic dosage for 7 days in 10 healthy subjects. The results were as follows. L. In SPT with histamines(lmg/ml), the mean wheal sizes(mm +SE) before and after medications of theophylline, beta2-agonist, corticosteroid, and antihistmaine were 4.37+ 0.23 and 4.27+0.20, 4.17 + 0.28 and 3.87 + 0. 28, 4.49 + 0.29 and 3.98 + 0.36, and 4.82 + 0.40 and 1.82+0.35, respectively. Theophylline, bata2-agonist and corticosteroid had no significant effect on the result of SPT with histamine. 2. In SPT with codeine(10mg/ml), the mean wheal sizes(mm+-SE) before and after medications of theophylline, beta2-agonist, corticosteroid, snd antihistamines were 4.00 + 0.37 a,nd 4.05+0.26, 4.51+0.28 and 4.28+0.36 4.31+0.37 and 4.41+0.29, and 4.39+0.30 and 2.05+0.28 respectively. Theophy'Rine, beta2-agonist and corticosteroid had no significant effect on the result of SPT with codeine. 3. In SPT with allergens, the mean wheal sizes(mm +SE) before and after medications of theophylline, beta2-agonist, corticosteroid, and antihistamines were 5.86 + 0.65 and 4.95 +0.97, 6.00+0.79 and 5.58+1.17, 5.12+0.70 and 4.09 + 0.60, and 5.72 + 0.67 and 3.05 + 0. 37, respectively. Theophylline, beta2-agonist and corticosteroid had no significant effect on the result of SPT with allergens. In conclusion, it is suggested that theophyl- line, oral Salbutamol, and Prdnisolone have no significant effect on the result of skin prick  test with histamine, codeine and allergens.

Backgroued: The relationship between allergic rhinitis and bronchial asthma is controversial although it is well known that one is often accompanied by the other. Some considers these two as pathophysiologically the same, differing only in target organs. Bronchial hyperreactivity of asthma patients has been well documented, but whether they also have nasal hyperreactivity is unknown. Therefore we performed this study to evaluate the nasal reactivity of the patients with  allergic bronchial asthma. Method: 8 patients with allergic bronchial asthma who had no nasal symptoms were tested. 7 patients with allergic rhinitis and 5 healthy normal volunteers were also tested as positive and negative control respectively. To evaluate nasal reactivity, we challenged nasal mucosa with histamine and specific allergen. Before and during challenge, we recorded symptom score and nasal airway resistance by anterior rhinomanometric measurement. Results '. 1. 7 out of 8 asthmatic subjects had negative response and one weakly positive response. None of normal volunteers and all rhinitic patients showed positive response. 2. Mean logarithmic concentration of PCSS4  Histamine(concentration of hista- mine that provokes symptom scores of 4 out of total 6 points) of asthmatic, rhinitic, and normal subjects were 1.89+-0.22, 1.88+-0.16, and 0.75 +- 0.40mg/dl, respectively(Mean +- SE). There was no difference in nasal reactivity between asthmatics and normal subjects although patients with allergic rhinitis showed markedly increased reactivity compared to the other groups. 3. In specific allergen challenge test, all asthmatics showed negative responses. Conclusions . There was no difference in nasal reactivity between normal subjects and the patients with allergic bronchial asthma who had no nasal symptoms.

Cough, one of the most common respiratory symptoms, is the sole clinical manifestation in cough variant asthma. But the reason why cough develops in cough-variant asthma without showing dyspnea or wheezing is still unknown. Therefore capsaicin, tachykinin related reproducible tussive agent, was used to measure the cough sensitivity in the cough variant asthmatics, t,he classic asthmatics, and the normal control group. Cough sensitivity to capsaicin in the cough variant asthmatics increased significantly as compared to the control group and the classic asthmatics, but there were no differences between the control group and the classic asthmatics. Cough sensitivity to capsaicin showed no signif icant correlation with nonspecific airway hyperresponsiveness measured by methacholine. And correlation between cough sensitivity to capsaicin and base- line PFT was not significant. These results suggest that the cough in cough-variant asthma is related to the increased cough sensitivity to capsaicin and the mechanism of the capsaicin-induced cough is different from that of the nonspecific airway responsiveness t,o methacholine. There may be a role of tachykinin, such as substance P or neurokinin A, to cause cough in cough variant ast.hma.

Sinusitis is a common problem in children with bronchial asthma. The sinusitis may exacerbate asthma, but the causal relationship between sinusitis and asthma remains controversial. The aim of this study is to evaluate the influence of sinusitis on bronchial responsiveness in asthmatic children. Bronchial provocation test with methacholine were performed in the ast,hmatics with sinusitis before and after t,reatment of sinusitis and the concoulratins of methecholine causing a 20% fall in forced expiratory volume one second(PC) were determined. The PC was increased significantly in asthmatics with sinusitis after treat,ment of sinusitis. These data suggest that sinusitis may increase the bronchial responsiveness of asthmatics and treatment of sinusitis may be important in the control of asthma.

Tolune diisocynate(TDI) is the most com- mon cause of occupational asthma in Korea as well as other industrialized countries. The pathogenetic mechanism of TDI-induced occu- pational asthma is still unclear. Immunological mechnism, such as IgE-medicated type I hypersensitivity, was thought to be involved in some TDI asthma patients. Other immulogical and non-immunological mechanisms have been suggested. To evaluate a possible role of circulating immune complex(CIC) in the development of TDI asthma, we measured C3- containing CIC in 21 TDI-induced asthmatics, which were confirmed by TDI-bronchoprovocation test, and they were compared with those of14 atopic asthma patients and 26 controls with no exposure history to TDI. Serum specific IgE antibodies to TDI-human serum albumin (HAS) conjugate were detected by RAST technique. The mean level of C3 contsining IgG-CIC tended to be higher in TDI asthma patients than those of atopic asthma and controls with no statistical significance(p=0.42). The IgG- CIC level correlated well with the percent fall of FEV, during the TDI brochoprovocation test(r=0.69, p=0.005), but poorly correlated with methacholine PC20. TDI asthma patients with high TDI-specific IgE antibody showed higher IgG-CIC level than those without specific IgE antibody(p=0.018). These data suggest that C3 containing IgG- CICs have a possible role in induction of inflammatory responses in TDI-induced occupational asthma.

Grain dust-induced occupational asthma is commonly found in western countries. To the best of our knowledge, these are the first cases of grain dust-induced occupational asthma in this country. Their pathogenetic mechanisms still remains to be defined. Here we report six cases of occupational asthma induced by grain dust which was confirmed by bronchoprovocation test with grain dust extracts derived from their workplace. In order to further understand pathogenetic mechsnisms of grain dust-induced occupational asthma, we detected serum specific IgE, IgG and IgG antibodies to grain dust, and studied the direct activation of grain dust on basophils from them. Bronchoprovocstioan test showed tat early asthmatic response was the most commonly found one(5 patients) and dual asthmatic  response was noted in one patient. The PC20 methacholine ranged from 2.5 to 40mg/ml. High specific IgE antibodies to grain dust were detected in three(50%) patients. All had high specific IgG antibodies and all but one had high specific IgG, antibody. Basophil histamine release test revealed that grain dust extracts directly released significant amounts of histamirle from basophils as well as IgE- mediated rneohanisms. Minimal amounts of histamine release by anti-IgG antibodies was noted. These results suggested that grain dust can induce IgE-mediated bronchoconstrictions in exposed workers and grain dust may contain some potent active substances that can activate basophil.

Familial cold urticaria is a rare abnormal cutaneous and systemic reaction to cold with autosomal dominant inheritance, distinctive clinical features, and unknown etiology. A 21  year  old male patient presented with generalized erythematous macules and papules accompanied by burning, chills and arthralgia after cold exposure since early childhood. Autosomsl dominant inheritance was revealed on the examination of his pedigree. Autosomal dominant inheritance was revealed on the examination of his pedigree. Cold room challenge induced the same lesions after a delay of 20 min. Histopathologic findings showed a perivascular polymorphonuclear leukocytic infiltrstion with some eosinophils. He was treated with several antihistamines, but unsatisfaetory. We report a patient with a familial cold urticaris showing typical cutaneous manifests- tions and general symptoms with a consistent familial history through his five generations.