Lecithin-bound iodine (LBI) has been reported to be a potential candidate for one of the therapeutic modalities for children with bronchial asthma. In in-vitro study, it suppressed the production of interleukin-4 (IL-4) from mitestimulated patients' lymphocytes and conversely, it enhanced the secretion of interferon-γ (IFN-γ) from them. In addition to the in-vitro effect, treatment with LBI for 8 weeks effectively upregulated IFN-γ production by the patients' lymphocytes. Therefore, LBI may reduce the signs of bronchial asthma by upregulating the synthesis of IFN-γ that is a representative Th1 cytokine.

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We examined plasma concentrations of disodium cromoglycate (DSCG) on 6 healthy adults skilled with inhalation therapy using 3 types of nebulizer (NE-U07 as a formal type of ultrasonic nebulizer, NE-U14 as a handy type of ultrasonic nebulizer, and Voyage as a compressed air nebulizer) to estimate differences of drug amounts accessible to the lung among three types of nebulizers. The mean plasma concentration of DSCG by NE-U07 was the highest and that by Voyage was the lowest at any times after inhalation. The mean Area Under the Curve up to 480 min after inhalation was 2197.46min·ng/ml by NE-U07, and 1170.59min·ng/ml by NE-U14, but by Voyage, it was 441.10min·ng/ml, which was lower than that by NE-U07 significantly (p=0.03). Plasma concentration of DSCG exceeded 4ng/ml, which was reported to be more effective to protect asthmatic attacks, in all subjects using NE-U07, in almost half numbers of subjects using NE-U14, but in only one subject using Voyage. We estimated that the amount of DSCG accessible to the lung using ultrasonic nebulizers might be more than that using a compressed air nebulizer. Moreover, the formal type of ultrasonic nebulizer showed the possibility to obtain larger amount of DSCG accessible to the lung than the handy type of ultrasonic nebulizer.

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Although the combination of nebulized sodium cromoglycate (SCG) and beta2-agonists has been reported as an effective treatment for children with moderate to severe asthma, there has been concern that regular use of beta2-agonists might worsen asthma itself. Therefore, we evaluated if the combination therapy with SCG and beta2-agonists is more useful for the treatment of milder asthma compared with SCG alone. Young children aged 0 to 8 year-old with mild to moderate persistent asthma were randomly divided into the following groups; SCG alone and the mixture of SCG and one of beta2-agonists, procaterol. Children inhaled these medications by a jet nebulizer twice a day for 24 weeks. The asthma symptom scores of the combination treatment group significantly decreased after 4-week treatment, whereas in the single treatment group a significant difference was found only after 8-week treatment. After 12-week treatment, there was no difference in the symptom scores between two groups. No patients reported adverse effects, and the combination therapy did not show any deterioration of their asthma symptoms during 24-week period. From these results, we concluded that the combination of nebulized SCG and procaterol is effective and safe in the long-term treatment of children with mild to moderate asthma.

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The effects of inhaled fluticasone and pranlukast on bronchial reactivities in 36 mild persistent or moderate persistnet asthma patients aged 7-15 years (22patients treated with inhaled fluticasone and 14 patients with pranlukast) were studied. All patients were treated with those drugs for more than 6 months and showed no asthmatic attacks for more than 5 months. Those patients were also treated only with sustained released theophylline and dosage of inhaled fluticasone, pranlukast and theophylline on each patients were not changed. At the beginning of anti-inflammatory drug treatments and at 6 months after the biginning of the treatments, bronchial reactivities (provocation concentration, PC20) were studied with methacholine. Geometric averages of PC20 in patients who treated with inhaled fluticasone were 243.5μg/mL at the biginning of the treatment and 2074.6μg/mL after 6 months treatments, whereas those of PC20 in patients treated with pranlukast were 238.1μg/mL and 862.7μg/mL, respectively. Both treatments showed statistically significant changes in PC20.
Between before and after treatments, PC20 in 13 patients in 22 patients treated with inhaled fluticasone increased more than 8 times, whereas those in 3 patients in 14 patients treated with pranlukast showed more than 8 times increments (p=0.0611). Among 19 patients who showed high bronchial reactivities (PC20≤196μg/mL) before those drugs treatments, their differences were significant (p=0.0238).
These results suggested that influences of treatments with inhaled fluticasone or pranlukast on bronchial reactivities in asthma children who did not suffer from asthmatic attacks for more than 5 months after treatments were different, and inhaled fluticasone showed stronger influences in asthma patients' bronchial reactivities than pranlukast.

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