Leukotriene receptor antagonist is now one of the choice as a controller medicine for childhood bronchial asthma. We assessed the inhibitory effects of a single dose of pranlukast hydrate on exercise-induced bronchoconstriction (EIB). Subjects were 9 children who showed a postexercise fall of FEV₁ of at least 30%. Exercise challenges were performed with or without oral administration of pranlukast hydrate (3.5mg/kg) 5hr in advance. The mean maximal % fall in FEV₁ and PEF without medication were 45.1±14.0% and 48.7±14.6% respectively, which were reduced significantly to 23.9±20.1% and 22.7±22.1% respectively with the administration of pranlukast hydrate. The degree of inhibitory effect of pranlukast hydrate was various in each subject, being remarkable (>60%) in 5 subjects, whereas being ineffective (<5%) in 2. The former showed a tendency to lower serum eosinophil cationic protein (ECP). The study demonstrated the potency of pranlukast hydrate administered before the exercise to attenuate EIB in childhood asthma.

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The case was a nine-year-old boy hospitalized due to bronchial asthma. We began to administer him cefaclor because Group A streptococci had been detected by throat culture. Then, he fell into the anaphylactic shock with a cyanotic, hypotension and laryngeal edema 15 minutes later. Symptoms disappeared after subcutaneous injection of epinephrine, intravenous infusion of aminophylline, hydroxyzine, and hydrocortisone with inhalation of oxygen.
Cefaclor induces anaphylactic shock easily compared with other oral antibiotics. The case fell into anaphylaxis although he had lacked the past history of drug hypersensitivity and had taken cefaclor before. We need to pay better attention to prescribe cefaclor to the allergic constitution.

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Asthmatic children sometimes receive inhalation therapy during sleep. However, inhalation while sleeping is not effective because patients inspire aerosol spontaneously through their noses, but not forcedly through their mouths. The efficiency of inhalation can be estimated according to the rate of urinary excretion of disodium cromoglycate (DSCG) after DSCG inhalation by using high performance liquid chromatography (HPLC). Therefore, we measured the urinary excretion of DSCG in 13 asthmatic children after inhalation in two different conditions; while sleeping and while awake. Six cases inhaled DSCG with “MILLICON N” and 10 cases with “OMRON NE-U22”. Three children used both devices. In every case, urinary excretion of DSCG after inhalation was less during sleep than while awake. The rate of the urinary excretion of DSCG>1% was shown in 2 cases of 6 using MILLICON N during sleep, and 9 cases of 10 using OMRON NE-U22. The younger children (1-4 years old) more frequently inhaled DSCG during sleep in the evening than did the elder children (more than 4 years old). Although OMRON NE-U22 was relatively useful for inhalation during sleep, asthmatic children should be educated to perform inhalation therapy while awake, not during sleep.

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To analyze the determinants involved in the development of allergic diseases early in infancy, we examined the following factors that might affect the induction of the allergic diseases during the infancy by questionnaire: the maternal history both during the pregnancy and during the child-bearing period, childhood history of the diseases, the vaccinations, the nutrition and the environment, and the allergic diseases in their family members. Maternal fever, cough, and pharyngitis during pregnancy were significantly related to the development of asthma plus atopic dermatitis, asthma alone, and atopic dermatitis alone in their infants, respectively. Moreover, the frequency of the maternal infection was associated with a significant increased risk of allergy in their infants. The prevalence of maternal allergy after their delivery was positively associated with the allergic symptoms in their children. The incidence of allergic children was related to the numbers of allergic individuals in their family. The numbers of immunization with the diphteria-pertussis-tetanus (DPT) vaccine were inversely correlated with the development of allergy, while BCG vaccination significantly inhibited them. These results suggested that pre- and post-natal maternal factors, immunization history of early in life, and the genetic predisposition might modify the development of allergy in infancy.

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The prevalence of allergic diseases in school children was examined both in 1992 (46, 718 children) and in 2002 (36, 228 children) in 11 western districts of Japan. Both studies were conducted with the same questionnaire in the same districts.
Results:
1) The study in 2002 established prevalence rate of 20.5% in allergic rhinitis (AR), 13.8% in atopic dermatitis (AD), 9.8% in allergic conjunctivitis (AC), 6.5% in bronchial asthma (BA), 5.7% in Japanese cedar pollinosis (P), 5.3% in wheeze, respectively. These rate were higher than those of 10 years ago except AD.
2) The prevalence rate of allergic diseases was 31.3% in 1992 and 34.1% in 2002. The cumulative rate was 45.5% in 1992 and 56.3% in 2002.
3) Higher prevalence rates were found in children who lived in urban area, but area's differences in 2002 survey were smaller than those in 1992 survey.
Higher prevalence rates of AR, AC and P were found in elder children, and W was found in younger children. No differences were found in AD or BA.
4) There was slight difference among nutrition during infancy, indoor smoking, type of heating or air conditioning.
5) Higher prevalence were found in children who had family history of allergic diseases and early history of lower respiratory infectious diseases.

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[in Japanese]

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[in Japanese]

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The causes of asthma death were analyzed on 180 children, aged from 0 to 28 years old, from 1988 to 2001. Subjects studied were divided in two groups by the year when they died between 1988 to 1997 and between 1998 to 2001, to observe the recent change of causes of asthma death. The annual number of asthma death registered in this committee decreased since 1988. Sex ratio (male:female) was 95:60 in the former group and 12:11 in the later group. The severity of asthma prior to their death were mild (17.9%), moderate (20.5%), severe (29.5%) and unknown or not described (32.1%) in the former group and mild (13.0%), moderate (21.7%), severe (21.7%)and unknown or not described (43.5%) in the later group.
The main contributing factors to asthma death were the unexpected sudden exacerbation in 70% and delayed decision on medical help in 68% in the former group and 45%in the later group. Medications given in the last one month was analyzed. Steroid inhalation therapy was given in 15% and 26% respectively, reflecting the recent asthma therapy trend.
The longitudinal changes of the growth in height and weight were studied.

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Cysteinyl leukotrienes (cysLTs), arachidonate 5-lipoxygenase products, play significant roles in the pathogenesis of bronchial asthma in children. In these 15 years several lines of evidence have demonstrated that the production of cysLTs is controlled by molecular mechanisms induced by external and internal bioactive substances. A direct evidence is that levels of cysLTs and LTB4 in BALF were markedly increased in asthmatic children with acute exacerbation. Peripheral polymorphonuclear leukocytes obtained from asthmatic children produced higher levels of cysLTs and LTB4 than those from controls, which also supported this hypothesis. The increased production of cysLTs and LTB4 is attributable to transcriptional and/or post-transcriptional up-regulation of LT-synthetic enzymes, 5-lipoxygenase, LTA4 hydrolase and LTC4 synthase. Activity of cysLT-catabolic enzymes in vivo is also determined by degradation of cysLTs. LTC4 is metabolized to less bioactive LTE4 via LTD4 by two consecutive catabolic enzymes, gamma-glutamyl leukotrienase (gamma-glutamyl transpeptidase related enzyme; GTPRE) and dipeptidase. GTPRE was found to be transcriptionally up-regulated by glucocorticosteroid (GCS) in transformed human bronchial epithelial cells. Accelerated conversion of LTC4 to LTE4 by GCS-induced GTPRE explains, in part, the efficacy of GCS in the treatment of bronchial asthma. Thus, leukotriene metabolism is controlled by transcriptional and/or post-transcriptional regulatory mechanisms at various steps of synthetic and catabolic enzymes, which contributes to pathophysiology of childhood asthma.

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