Association between adenotonsillar hypertrophy and leptin, ghrelin and IGF-1 levels in children

Objective: Developmental and growth retardation is a condition that is often encountered among children with adenotonsillar hypertrophy (ATH). Leptin, ghrelin and IGF-1 are important factors in growth and development for children. The aim of the study was to investigate serum leptin, ghrelin and IGF-1 levels in children with ATH compare with healthy controls. Material method: 82 children between ages 6-12 were included in this study, divided into two groups. The first group being the study-group consisted of 42 children with obstructive adenotonsillar hypertrophy and the second group being the control-group consisted of 40 healthy children. At 08:30 a.m., peripheral blood samples were extracted from children from both groups to examine the serum levels, and kept in -40 degrees C until the Elisa test. Results: Leptin serum level of the control-group was found to be statistically significantly higher than the serum leptin level of the ATH group (p =0,049; p <0.05). Body mass indexes of the children with ATH were found to be statistically significantly lower than the body mass index (BMI) of the control group (p =0,001; p <0.05). In contrast, there was no statistically significant difference between ghrelin and IGF-1 levels between the ATH and control group (p = 0.193, p > 0.05 and p = 0.478, p > 0.05, respectively). Conclusion: Upper airway infections are common in children with ATH. Increased airway infections and obstructive enlarged adenotonsillar lymphoid tissue which are caused swallowing difficulties can lead to reduced oral intake and fat tissue. It has led us to think that, ghrelin levels may be increasing secondary to these problems in children with ATH. Furthermore, BMI and leptin would be lower in children with ATH, considering adipose tissue was lesser and leptin was being synthesized and oscillated out of the fat cells of the tissue in these children. (C) 2020 Oto-Rhino-Laryngological Society of Japan Inc. Published by Elsevier B.V. All rights reserved.