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IGF-I, IGF-BP3, and GH serum levels after stimulation tests in prepubertal allergic boys
A Guelpa Hauache1, A Spinola-Castro, V Lourenzi
1Division of Allergy, Clinical Immunology and Rheumatology-Dept of Pediatrics, Federal University of São Paulo-Escola Paulista de Medicina, São Paulo, SP, Brazil.
Insights
Growth hormone (GH) deficiency does not appear to cause short stature in children with respiratory allergies. Studies show normal GH response to exercise and clonidine tests in allergic children with short stature.
Area of Science:
- Pediatric Endocrinology
- Allergology
Background:
- Short stature (SS) affects 2-10% of children with respiratory allergies.
- The cause of SS in these children remains unclear despite research.
- This study investigates growth hormone (GH) levels in prepubertal boys with SS and respiratory allergies.
Purpose of the Study:
- To evaluate serum growth hormone (GH) levels in response to standardized exercise and clonidine stimulation tests.
- To determine if GH deficiency contributes to short stature in children with mild, untreated respiratory allergies.
Main Methods:
- Prepubertal boys with SS were divided into allergic (A) and non-allergic (NA) groups.
- GH levels were measured after standardized exercise and clonidine administration.
- Insulin-like growth factor I (IGF-I) and IGF-binding protein 3 (IGF-BP3) levels were also assessed.
Main Results:
- Most allergic and non-allergic children showed a positive GH response to at least one stimulation test.
- Serum IGF-I and IGF-BP3 levels were generally within the normal range.
- Bone age was delayed relative to chronological age but appropriate for height age in all participants.
Conclusions:
- GH deficiency does not appear to be the primary cause of short stature in the studied pediatric population.
- Further research is needed to elucidate the etiology of short stature in children with respiratory allergies.
Abstract:
The prevalence of short stature (SS, < 3rd percentile NCHS) among children with respiratory allergy (asthma and/or rhinitis) varies from 2% to 10%. In spite of several studies, the etiology of SS in those patients remains unknown. We evaluated growth hormone (GH) serum levels in response to two stimulating tests (standardized exercise and clonidine) in prepubertal boys (G1P1, Tanner; 8 years and 5 months to 14 years) with SS, 14 of them with respiratory allergy (A, positive skin prick test to D. pteronyssinus) and 5 nonallergic children (NA). Other causes of SS were excluded in both groups. Patients had mild asthma and/or rhinitis, and they had never received inhaled or systemic corticosteroid at any time. Tests were performed on different days, at least 1 week apart. [To prevent exercise-induced asthma, 30 min before the exercise test, allergic children inhaled disodium cromoglycate (2 mg)]. GH serum levels (Immunoassay, AIA-PACK HGH, Tosoh Co, Japan) were determined at the following times: exercise (E)--basal, 5, 15, and 30 min after exercising for 6 min; clonidine (C)--basal, 30, 60, and 90 min after clonidine (0.15 mg/m2 body surface) ingestion. A response was considered positive when GH serum levels reached the minimum of 10 ng/ml. Among (the allergic) A patients, four responded to both tests, five to C (clonidine) alone, four to E (exercise) alone and one had no response. Among NA, four had a positive response to both tests and one to C (clonidine) alone. The serum levels of insulin-like growth factor I (IGF-I) (DSL-5600 Active TM IGF-I Coated-Tube IRMA [DSL Lab Inc, USA]) and its binding protein (IGF-BP3) (DSL-6600 Active TM IGF-BP3 Coated-Tube IRMA [DSL Lab Inc, USA]) were within the normal range except for one A child. Bone age was delayed in relation to chronological age in all children, but adequate for height age. All children had delayed skeletal age in relation to chronological age, but bone age was normal for height. We concluded that in the children studied a deficiency of GH does not seem to be responsible for SS.
