Takehiko Matsui

Japanese pediatric guidelines for the treatment and management of bronchial asthma 2008

The fourth version of the Japanese Pediatric Guidelines for the Treatment and Management of Bronchial Asthma 2008 (JPGL 2008) was published by the Japanese Society of Pediatric Allergy and Clinical Immunology in December 2008. In JPGL 2008, the recommendations were revised on the basis of the JPGL 2005. The JPGL 2008 is different to the Global Initiative for Asthma guideline in that it contains the following items: a classification system of asthma severity; recommendations for long‐term management organized by age; a special mention of infantile asthma; and an emphasis on prevention and early intervention. Here we show a summary of the JPGL 2008 revising our previous report concerning JPGL 2005.

Japanese pediatric guideline for the treatment and management of bronchial asthma 2012: Pediatric guideline for asthma

A new version of the Japanese pediatric guideline for the treatment and management of bronchial asthma was published in Japanese at the end of 2011. The guideline sets the pragmatic goal for clinicians treating childhood asthma as maintaining a “well‐controlled level” for an extended period in which the child patient can lead a trouble‐free daily life, not forgetting the ultimate goal of obtaining remission and/or cure. Important factors in the attainment of the pragmatic goal are: (i) appropriate use of anti‐inflammatory drugs; (ii) elimination of environmental risk factors; and (iii) educational and enlightening activities for the patient and caregivers regarding adequate asthma management in daily life. The well‐controlled level refers to a symptom‐free state in which no transient coughs, wheezing, dyspnea or other symptoms associated with bronchial asthma are present, even for a short period of time. As was the case in the previous versions of the guideline, asthmatic children younger than 2 years of age are defined as infantile asthma patients. Special attention is paid to these patients in the new guideline: they often have rapid exacerbation and easily present chronic asthmatic conditions after the disease is established.

Hospitalizations Associated with Pandemic Influenza A (H1N1) 2009 in Asthmatic Children in Japan

BACKGROUND The pandemic influenza A (H1N1) 2009 [pdm (H1N1) 2009] spread through the world in 2009, producing a serious epidemic in Japan. Since it was suggested early that asthma is a risk factor for an increased severity of the infection, the Japanese Society of Pediatric Allergy and Clinical Immunology (JSPACI) organized a working group for countermeasures, and investigated asthmatic children admitted to the hospitals for pdm (H1N1) 2009 infection. METHODS An appeal was made on the home page of the JSPACI to medical practitioners to input clinical information about asthmatic and non-asthmatic children (0-19 years) admitted to the hospital with pdm (H1N1) 2009 infection. RESULTS A total of 862 children (390 with asthma, and 472 without asthma) from 61 medical centers were registered, and the data of 333 asthmatic children and 388 non-asthmatic children in all were entered in the analyses. The mean age was 7.4 ± 2.9 years in the asthma group and 6.9 ± 3.8 years in the non-asthma group. The percentage of children admitted for respiratory symptoms was significantly higher in the asthma group than in the non-asthma group (p < 0.001). There was no significant difference in the frequency of admission to the ICU or need for mechanical ventilation support between the two groups. No definite trend was detected in the relationship between the severity of asthma and the intensity of asthma attack. Antiviral drugs were administered within 24 hours in about 85% of the patients in both groups. CONCLUSIONS Asthma may not be a risk factor for severe pdm (H1N1) 2009 infection in children.

ASTHMA DEATH IN JAPANESE CHILDREN. THE COMMITTEE REPORT IN 1997

The causes of asthma death were studied on 137 patients, 85 male and 52 female, age ranged from 0 to 28 years old, from 1990 to 1997. Eight cases were excluded because of non-asthma death such as car accident. Twenty six cases (19.1%) have mild asthma, 30 cases (22.1%) moderately severe, 41 cases (30.1%) severe, and 39 cases (28.7%) unknown or undescribed. Seventy eight cases (58%) died in hospitals but 5 and 6 cases with age of 13 years old or above died more frequently on the way to hospital and in the ambulance cars respectively. The contributory factors to asthma death were delay by patients and/or families in seeking help in 69.3% and unexpected sudden exacerbation in 67.9%. The delay in seeking help when condition begin to deteriorate was made by their families in 48.9% and by patients in 47.4%, and strong dependence on beta-stimulant by metered dose inhaler (MDI) was seen in 29.2%. The possible causes of deaths were overtreatment with drugs in 19 cases, and 12 of them were beta-stimulants by MDI. Eight of them were reported to be fenoterol by MDI.

The prognosis of asthma in children

The prognosis in 1000 asthmatic children who were followed up 5 to 15 years after the first attack was studied. Sex made no difference in the prognosis. Severity of asthma and treatment seemed to play some role in the prognosis of asthma. Mild cases and the specific hyposensitization group had a better prognosis. In the mild group none died. On the other hand in the moderately severe group 0.3% were dead and in the severe group 3.4% were dead.

Cell‐mediated and Humoral Immune Respose Following Mycoplasma Pneumoniae Infection in Children

To investigate the effects of mycoplasma pneumoniae infection on cell-mediated and humoral immunity, we studied 16 children with pneumonia associated with mycoplasma pneumoniae infection. Cell-mediated immune response was examined by skin testing for delayed hypersensitivity to purified protein derivative (PPD), phytohemagglutinin (PHA), streptokinase-streptodornase (SK-SD), and candida antigens. As showed in Fig. 1 , 10 of 14 cases had a negative tuberculin reaction when first tested and 9 out of 10 children with a negative tuberculin reaction in the early phase of the illness had a positive skin test when retested 3-5 weeks after the onset of illness. Other skin reactions also decreased during the first 3-5 weeks after the clinical onset. These results suggest that there was a transient depression of cell-mediated immunity during the acute phase of mycoplasma pneumoniae infection. .*. L N*n“lYI or OhIM. .LY( -0,-I”