Delay of growth and development in children with bronchial asthma, atopic dermatitis and allergic rhinitis

Abstract

The elevated incidence of short stature (body height < (-)x - 2s), skeletal retardation and delayed puberty in children with bronchial asthma or atopic dermatitis is generally attributed to the severity of the disorder. However, a series of findings indicate a causal influence of the atopy and the existence of atopic skeletal retardation per se.The observation that children with atopic disorders, whether bronchial asthma, atopic dermatitis or allergic rhinitis, exhibit a rate of short stature that is twice to five times higher than normal indicates atopic and thus genetically determined influences. The elevated prevalence of short stature associated with allergic rhinitis is especially significant, as this disorder cannot be included among the severe chronic disorders. The fact that skeletal retardation is more prevalent in boys than in girls by a ratio of about 2:1 and that a significantly more marked retardation of bone maturation is found in atopic in comparisons with non-atopic asthmatics also lend support to this postulation. The clinical relevance of atopic growth retardation is also supported by the close interaction of pathophysiological basal mechanisms of bone metabolism and the atopy status. Thus the local growth factor prostaglandin E(2) (PGE(2)), which is important for bone metabolism, is also a messenger substance for the immediate and late allergic reaction. The platelet-activating factor (PAF), as one of the strongest mediators in the pathogenesis of allergic disorders, influences the PGE(2) synthesis in the osteoblasts. These relationships show that atopy-dependent imbalances in the complex system of local and systemic growth factors can certainly lead to disturbance of skeletal maturation which may delay growth and development in atopic children. In order to verify these assumptions it is necessary to research the interaction of local growth factors (particularly the roles of PGE(2), PAF and IGF I) in the skeletons of children of short stature suffering from atopic disorders. This should also include the possible effects on the overall hormonal factors influencing bone maturation. Atopy should be included in the differential diagnosis programme to clarify growth and development disturbances.

Impaired Growth during Childhood in Patients with Primary Ciliary Dyskinesia

“…In addition to malnutrition and chronic infections, which represent the most prevalent causes of acquired short stature worldwide, the significant nonendocrine causes of low growth rates in developed countries include inflammatory bowel disease, celiac disease, chronic renal failure, and chronic pulmonary disease [17–20]. In cystic fibrosis, growth failure can result from a combination of nutritional and pulmonary factors and from chronic inflammation.…”

Late Consequences of Chronic Pediatric Illness

“…Local growth factor prostaglandin E(2) (PGE(2)), which is important in bone mineralization, is a messenger substance for both the immediate and late allergic reaction. The platelet-activating factor (PAF) is one of the strongest mediators in the pathogenesis of allergic disorders and it influences the PGE(2) synthesis in osteoblasts [32]. Inhaled and nasal glucocorticoids rarely suppress adrenal function, though they may decrease prepubertal growth [33].…”

The prevention of eczema in infants and children: an overview of Cochrane and non‐Cochrane reviews

“…In 60–70% of children remission occurs by the age of 15, although some children relapse later. In the more severely affected child, development and puberty may be delayed (14). …”