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Short-term effects of GH treatment on coagulation, fibrinolysis, inflammation biomarkers, and insulin resistance status in prepubertal children with GH deficiency



Short-term effects of GH treatment on coagulation, fibrinolysis, inflammation biomarkers, and insulin resistance status in prepubertal children with GH deficiency



European Journal of Endocrinology 167(2): 255-260



The aims of this study was to determine whether prepubertal GH deficiency (GHD) children showed any impairment in coagulation- and fibrinolysis-related parameters and in inflammatory and insulin resistance markers and to evaluate the effect of short-term GH therapy on these parameters. This was a 6-month, prospective, observational, case–control study (36 prepubertal children with GHD and 38 healthy prepubertal children with no differences in BMI). Comparison of study parameter values in GHD and control groups at baseline and after 6 months of GH treatment in the GHD group. The following were analyzed: glucose, insulin, fibrinogen, absolute plasminogen activator inhibitor type 1 (aPAI-1), von Willebrand factor (vWF), homeostasis model assessment for insulin resistance (HOMA-IR) index, C-reactive protein (CRP), and interleukin 6 (IL6) levels. Children with GHD showed higher baseline levels of aPAI-1 and fibrinogen and lower levels of glucose, insulin, and HOMA-IR index than healthy controls. No intergroup differences were found for vWF. After 6 months of treatment, aPAI-1 levels were lower but no changes were observed in fibrinogen or vWF levels, which were similar to those of controls. Glucose levels increased, though not significantly, while insulin levels and HOMA-IR index rose to normal levels. A positive correlation was found between changes in insulin status/HOMA-IR index and levels of aPAI-1, fibrinogen, vWF, CRP, and IL6. At early ages, GH therapy appears to exert beneficial effects on the amount of aPAI-At the same time, it increases the state of insulin resistance (HOMA-IR index) without modifying the levels of fibrinogen, vWF, CRP, and IL6.

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Accession: 036501497

Download citation: RISBibTeXText

PMID: 22645201

DOI: 10.1530/EJE-12-0214


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