Mild or moderate severity of persistent bronchial asthma should be treated with long-acting supportive agents, which include NSAIDs, inhaled glucocorticoids, theophylline depot preparations, long-acting b2-adrenostimulants and leukotriene modulators.   

NSAIDs for bronchial asthma in children

Cromoline and nedocromil inhibit the manifestations of the early and late phases of an allergic asthmatic reaction and can relieve bronchospasm caused by physical effort. Both drugs belong to the first line of defense of children with mild persistent bronchial asthma. They are practically devoid of side effects, but they need to be administered at least 2-4 times a day, and in terms of effectiveness they are inferior to the substances of the other two main groups of supporting agents – inhaled glucocorticoids and leukotriene modulators. 

Therefore, at present they are referred to as alternative means . Cromoline and nedocromil relieve bronchospasm caused by physical exertion, and can be used instead of b-adrenostimulants, especially if the latter cause side effects (for example, tremors or tachycardia), as well as in combination with them, if bronchospasm associated with physical exertion is not removed only fast p-adrenostimulants. 

Glucocorticoids in childhood bronchial asthma

Glucocorticoids are available in forms suitable for inhalation, oral administration and parenteral administration. They represent the most active and effective means of treating both acute (with systemic administration) and chronic (with local application) manifestations of bronchial asthma. 

Inhaled glucocorticoid therapy

The development of inhalation devices that ensure the delivery of glucocorticoids to the respiratory tract has made this method the main one in the treatment of persistent bronchial asthma. Inhaled glucocorticoid therapy alleviates asthma symptoms, improves lung function and reduces bronchial irritability. In addition, with mild asthma or moderate illness in children, such therapy reduces the need for fast-acting b2-adrenostimulants and prednisone, and also almost halves the number of medical calls and hospitalizations. 

Large epidemiological studies show that low-dose inhaled glucocorticoid therapy also reduces the frequency of fatal asthma attacks. Inhaled glucocorticoid therapy meets all the goals of asthma treatment and is therefore the “gold standard”.  

According to the recommendations of NAEPP , low-dose inhaled glucocorticoid therapy should be carried out in all cases of persistent bronchial asthma. However, its need for a mild illness in children is in doubt. Proponents of its use in all patients with persistent asthma substantiate their opinion by the fact that it reduces inflammation of the respiratory tract, reduces the sensitivity of the bronchi and reduces morbidity and mortality associated with asthma. Opponents, however, emphasize the insecurity of this method of treatment and suggest limiting its use only to cases of persistent asthma of moderate severity or severe. 

Some studies have shown that the later inhaled glucocorticoid therapy begins, the weaker its therapeutic effect. This only emphasizes the fact that bronchial asthma is a progressive disease that requires the use of anti-inflammatory drugs that would prevent the restructuring of the airways and reduce their sensitivity to therapeutic effects.  

Currently, the US FDA has approved the use of five inhaled glucocorticoid drugs. There are glucocorticoid metering inhalers (not containing substances that deplete the ozone layer), powdered inhalation preparations, and also solutions used with a nebulizer. All of them are effective for bronchial asthma. 2nd generation drugs – fluticasone propionate, mometasone furoate and (to a lesser extent) budesonide – have a greater local and less systemic property than other inhaled glucocorticoids, which increases their therapeutic effect.  

This is due to their rapid destruction already at the first passage through the liver. It is recommended to start with high doses of inhaled glucocorticoids, gradually reducing them as the symptoms of the disease stop. It has been repeatedly shown that after achieving compensation for bronchial asthma, it is enough to use only part of the initial dose of these drugs. Doses of inhaled glucocorticoids should be high enough to prevent asthma symptoms, and at the same time low enough so that no side systemic effects occur. You can use these drugs only 1-2 times a day.  

Long-term inhaled glucocorticoid therapy in children is treated with concern, primarily because of its possible side effects. However, when using the recommended doses, clinically significant side effects of such therapy are extremely rare. The risk of their occurrence depends on the dose and frequency of inhalation of glucocorticoids and increases with the frequent (for example, 4 times a day) use of high doses (1000 mcg / day).  

Most often, with inhaled glucocorticoid therapy , local side effects develop – candidal stomatitis and dysphonia (hoarseness). The cause of candidal stomatitis is local immunosuppression, and dysphonia is myopathy of the vocal cords. These effects are dose-dependent and most often occur with high-dose inhaled and / or oral glucocorticoid therapy. Their frequency can be minimized by using special inhalation devices (dispensers), which dramatically reduce the deposition of inhaled substances on the mucous membrane of the oral cavity and pharynx. After inhalation of any glucocorticoid, it is recommended to rinse the mouth thoroughly. Of particular concern is the possible growth retardation of children with chronic use of inhaled glucocorticoid therapy.  

However, it is often forgotten that with insufficient treatment, bronchial asthma can in itself slow down the growth of a child. According to a study conducted in the framework of the Childhood Asthma Management Program, over 4.3 years, children with mild or moderate asthma who received budesonide at a dose of 400 mcg / day increased by an average of 22.7 cm, then how those who received placebo grew by 23.8 cm, and this difference of 1.1 cm fell mainly on the first year of therapy. In other words, stunting was a transient and non-progressive phenomenon. According to another study, the final growth in patients with asthma who received inhalation of budesonide (400 mcg / day) for more than 9 years did not differ from expected. Transient growth retardation in the first year of therapy was also noted here. Thus, judging by the results of these two lengthy studies, inhaled glucocorticoid therapy has only a weak and transient effect on the development of the skeleton and practically affects the final growth.  

No effect of such therapy on bone mineral density was found . Although on the basis of the conducted studies it is impossible to exclude the possibility of developing osteoporosis in adulthood (after 30 years of inhaled glucocorticoid therapy), it should be remembered that improving the condition of patients should eventually reduce the need for glucocorticoids. Summing up, we can conclude that the available data do not confirm fears regarding the adverse effect of long-term inhaled glucocorticoid therapy on the final growth and bone mineral density in patients with bronchial asthma. However, these data relate only to the use of budesonide at a dose of 400 μg / day, the effects of higher doses of inhaled glucocorticoids may be more dangerous.