Methacholine

The high incidence of airway hyperreactivity in members of asthmatic families is well known. In our previous study a significantly higher bronchial sensi­tivity and reactivity was present in “healthy” parents of asthmatic children with allergic rhinitis and/or airflow limitation in small airways compared with nonatopic parents of asthmatic children. In the pres­ent study, atopic children of asthmatic parents also demonstrated higher bronchial sensitivity and reactiv­ity than the nonatopic children (Fig 2, Table 1). However, the airway hyperreactivity in our atopic adults is about ten times higher than in the atopic children. In nonatopic parents and children of asth­matic families, no difference in bronchial response to methacholine was observed (Table 3).

Our results indicate that exposure to specific and/ or nonspecific irritants with age results in a marked increase in bronchial sensitivity and reactivity in atopic members of asthmatic families. This finding may explain the development of “late onset asthma” in patients with a history of allergic rhinitis and/or sinusitis following an acute upper respiratory tract infection. Since airway hyperreactivity is known to be present in “healthy” children of asthmatic families, and since, according to results from our previous study, it increases with age, the question arises whether antiasthmatic drugs (cromolyn, steroids, and ketotifen) can change nonspecific airway hyperreactiv­ity in healthy persons, as in asthmatic and atopic patients. canadian discount drugs

Table 3—Bronchial Response in Children of Asthmatic Parents in Comparison to Barents of Asthmatic Children with and without Atopy

No.

Mean Bronchial Sensitivity, mg

Mean Bronchial

Reactivity, Percent Decrease in SCaw/mg

Allergic

Children

8

1.3±0.5*

10.5 ±5*

rhinitis

Parents

9

0.14 ±0.05*

75 ±20*

No atopy

Children

13

2.7±l.lt

4.8±1.7t

Normal PFT

Parents

11

1.3±0.45t

4.5±1.5t

In our study, six weeks of treatment with cromolyn sodium during the same period of year decreased airway hyperreactivity significantly only in children with allergic rhinitis, while no change was observed in children with no atopy and normal results of PFTs, despite an increased BHR.

No change in BHR after treatment with cromolyn sodium was reported also by Lowhagen and Rak in atopic asthmatic patients not exposed to relevant allergens (defined by Lowhagen and Rak as “primary”

BHR), while cromolyn sodium blocked the increase in BHR in the same patients during birch pollen season (“secondary” BHR). Our results are in accor­dance with those of Lowhagen and Rak, ie, cromolyn sodium decreases airway hyperreactivity induced by allergen or by spontaneous release of mediators in “secondary” BHR, but it does not change the “pri­mary” BHR that exists in nonatopic members of asthmatic families. As our results show, the “primary” BHR does not change with age, and may thus reflect the inherited characteristics of bronchial asthma, ie, an increased bronchial smooth muscle tone.

In view of our results, children of asthmatic families with known atopies should have yearly BPTs per­formed and in case of further increase in BHR should receive prophylactic treatment.