Growth hormone secretion in growth retarded asthmatic children

Nigam, Pranesh; Laungia, S.; Goyal, B. M.; B, Dutt

doi:10.1007/bf02756664

Cited by 3 publications

(1 citation statement)

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“…Whereas the release of GH after stimulation was normal in all cases of short stature in children with atopic disorders, irrespective of having received steroids or not (David et al, 1991;Eastman and Lazarus, 1973;Ferguson et al, 1982;Nigam et al, 1977;Sanders and Norman, 1969), the investigations showed varying results for the spontaneous release of GH. It was in the normal range for 4 asthmatic patients of short stature (Eastman and Lazarus, 1973), but 3 out of 6 short children with atopic dermatitis exhibited reduced levels (David et al, 1991).…”

Section: Glucocorticoidsmentioning

confidence: 91%

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

Baum¹,

Schneyer²,

Lantzsch³

et al. 2002

Exp Clin Endocrinol Diabetes

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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.

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