Interactions between growth hormone (GH), insulin-like growth factor-1 (IGF-1), and the immune system are complex, bidirectional, but not fully explained. Current reviews based on numerous studies have indicated that chronic inflammation could suppress the GH/IGF-1 axis via several mechanisms such as relative GH and/or IGF-1 insufficiency, peripheral resistance to GH and/or IGF-1 resulting from down-regulation of GH and IGF-1 receptors, disruption in the GH/IGF-1 signalling pathways, dysregulation of IGF binding proteins (IGFBPs), reduced IGF bioavailability, and modified gene regulation due to changes in the microRNA system. It is well-known that relationships between the immune system and the GH/IGF-1 axis are mutual and GH as well as IGF-1 could modulate inflammatory response and the activity of systemic inflammation. Available data indicate that the GH/IGF-1 axis exerts both pro-inflammatory and anti-inflammatory effects. Pro-inflammatory cytokines such as interleukin-6 (IL-6), tumour necrosis factor- (TNF-), and interleukin-1(IL-) are some of the most significant factors, besides malnutrition, chronic stress, and prolonged use of glucocorticoids, which impair the activity of the GH/IGF-1 axis, and consequently lead to growth retardation in children suffering from childhood-onset chronic inflammatory diseases. In this review, we discuss the mechanisms underlying the impact of chronic inflammation on the GH/IGF-1 axis and growth processes during childhood and adolescence, based on a number of experimental and human studies.

Obesity and thyroid function are closely related. Thyroid hormones are involved in the regulation of metabolism, thermogenesis, food intake, and fat oxidation. In obese children the most frequent hormonal abnormalities are slight hyperthyrotropinaemia and moderate increases in total T3 and/or fT3 concentrations. Those abnormalities are usually considered a cause of obesity, but according to recent studies, they should actually be considered an adaptation process aimed at increasing resting energy expenditure and total energy expenditure. Those abnormalities do not require any treatment and normalise after substantial weight loss. The mechanisms of those changes are dependent on leptin, thyroid hormone resistance, and mitochondrial dysfunction. The present paper describes the abovementioned mechanisms based on the latest research. We also present a review of some recent original studies evaluating thyroid function in overweight and obese children, including thyroid ultrasound. A thyroid ultrasound scan in obese children frequently shows increased thyroid volume, which correlates with moderately increased TSH levels and a hypoechoic pattern typical of autoimmune thyroiditis, but without antithyroid autoantibodies. Alterations of thyroid function in overweight and obese patients cause an increase in energy expenditure, which facilitates weight loss and prevents further weight gain. Therefore, normalisation of TSH and fT3 after weight loss could explain difficulties in maintaining reduced weight. (Endokrynol Pol 2017; 68 (1): 54–60) Obesity and thyroid function are closely related. Thyroid hormones are involved in the regulation of metabolism, thermogenesis, food intake, and fat oxidation. In obese children the most frequent hormonal abnormalities are slight hyperthyrotropinaemia and moderate increases in total T3 and/or fT3 concentrations. Those abnormalities are usually considered a cause of obesity, but according to recent studies, they should actually be considered an adaptation process aimed at increasing resting energy expenditure and total energy expenditure. Those abnormalities do not require any treatment and normalise after substantial weight loss. The mechanisms of those changes are dependent on leptin, thyroid hormone resistance, and mitochondrial dysfunction. The present paper describes the abovementioned mechanisms based on the latest research. We also present a review of some recent original studies evaluating thyroid function in overweight and obese children, including thyroid ultrasound. A thyroid ultrasound scan in obese children frequently shows increased thyroid volume, which correlates with moderately increased TSH levels and a hypoechoic pattern typical of autoimmune thyroiditis, but without antithyroid autoantibodies. Alterations of thyroid function in overweight and obese patients cause an increase in energy expenditure, which facilitates weight loss and prevents further weight gain. Therefore, normalisation of TSH and fT3 after weight loss could explain difficulties in maintaining reduced weight. (Endokrynol Pol 2017; 68 (1): 54–60)

Introduction: In the majority of countries, autoimmune thyroiditis is the main cause of acquired hypothyroidism in children. Typically, the natural course of the disease is initially insidious and the diagnosis is incidental. There are some children who develop severe hypothyroidism without a proper diagnosis. The aim of the study was to analyze the clinical and biochemical profiles of children with severe primary hypothyroidism due to autoimmune thyroiditis. Materials and Methods: We analyzed the records of 354 patients diagnosed between 2009 and 2019 with autoimmune thyroiditis. Only patients with TSH above 100 μIU/mL, associated with decreased free thyroxine and the presence of antithyroid antibodies, were enrolled in the study. The analysis encompassed clinical symptoms, thyroid and biochemical status, bone age, and imaging. Results: Twenty-six children were enrolled in the study. The mean age at diagnosis was 10.26 ± 3.3 years, with a female preponderance of 1.8:1. The most frequent symptom was growth impairment (77%) and weight gain (58%). Goiters were present in 42% of patients. Less common findings were pituitary hypertrophy (four patients) and hypertrichosis (three patients). Median values at the time of diagnosis were TSH 454.3 uIU/ml (295.0–879.4), anti-TPO antibodies 1,090 IU/ml, and anti-Tg antibodies 195 IU/ml. Anti-TSHR ab were evaluated only in six out of the 26 patients. The characteristic biochemical profile was correlated with the grade of hypothyroidism, and the strongest correlations were found with CBC parameters, lipid profile, aminotransferases, and creatine. Conclusion: In children with severe hypothyroidism, the most sensitive symptoms are growth arrest and weight gain despite the fact that, in some children, the auxological parameters at presentation could be within normal values for the population. The specific biochemical profile closely correlates to the severity of thyroid hormone deficiency and involves mostly erythropoiesis, liver function, and kidney function. Pituitary enlargement should be considered in each child with severe hypothyroidism. It is necessary to conduct prospective studies evaluating the actual frequency of anti-TSHR antibodies and pituitary enlargement in children with extremely high TSH, especially those presenting without goiters.