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Published on: February 2, 2017
Cluster of cardiometabolic risk factors in children with GH deficiency: a prospective, case-control study
Donatella Capalbo1, Giuseppina Mattace Raso, Andrea Esposito
1Pediatric Endocrinology Unit, Department of Translational Medical Sciences, University "Federico II" of Naples, Naples, Italy.
Insights
Children with growth hormone deficiency (GHD) show early cardiovascular risk factors. Growth hormone (GH) therapy improves these risk factors, including reduced waist-to-height ratio and improved cholesterol levels.
Area of Science:
- Pediatric Endocrinology
- Cardiovascular Risk Assessment
- Metabolic Disorders
Background:
- Adult growth hormone deficiency (GHD) is linked to increased cardiovascular (CV) risk.
- Early CV risk factors in children with GHD are documented but inconsistent.
- Understanding these factors in children is crucial for long-term health.
Purpose of the Study:
- To evaluate cardiometabolic risk factors in children with GHD.
- To assess the impact of growth hormone (GH) therapy on these risk factors.
- To analyze a large cohort of children with GHD.
Main Methods:
- Assessed waist-to-height ratio (WHtR), lipids, atherogenic index (AI), homocysteine, leptin, adiponectin, hsCRP, and fibrinogen.
- Compared 71 children with GHD to 71 healthy controls.
- Evaluated changes after 2 years of GH therapy.
Main Results:
- GHD children had higher WHtR, triglycerides, total cholesterol, LDL cholesterol, AI, homocysteine, leptin, and fibrinogen than controls.
- GH therapy significantly reduced WHtR, total cholesterol, LDL cholesterol, homocysteine, leptin, and fibrinogen.
- GH therapy significantly increased adiponectin levels.
Conclusions:
- Children with untreated GHD present with a cluster of early cardiovascular risk factors.
- GH treatment demonstrates beneficial effects on these cardiometabolic abnormalities.
- This supports early intervention for GHD in children to mitigate CV risk.
Objective:
Growth hormone (GH) deficiency (GHD) in adults is associated with increased cardiovascular (CV) risk. Although some authors have documented the presence of early CV risk factors in untreated GHD children, results are still inconsistent. Aim of this study was to evaluate the effects of GHD and GH therapy on early cardiometabolic risk factors in a large cohort of children.
Subjects And Methods:
Waist-to-height ratio (WHtR), triglycerides, total-, low-density lipoprotein (LDL), high-density lipoprotein (HDL) cholesterol, atherogenic index (AI = total /HDL cholesterol), homocysteine, leptin, adiponectin, high-sensitivity C-reactive protein (hsCRP) and fibrinogen were evaluated in seventy-one GHD children (9·8 ± 3·6 years) before and after 2 years of GH therapy. Seventy-one healthy controls comparable with patients for age, sex and body mass index (BMI) were enrolled.
Results:
Compared with controls, GHD children at study entry had higher WHtR (0·52 ± 0·05 vs 0·45 ± 0·19, P = 0·004), triglycerides (0·44 ± 0·98 vs -0·03 ± 0·73 SDS, P = 0·012), total cholesterol (0·28 ± 1·08 vs -0·46 ± 0·98 SDS, P < 0·001), LDL cholesterol (0·20 ± 0·90 vs -0·39 ± 1·06 SDS, P = 0·007), AI (3·19 ± 0·73 vs 2·77 ± 0·53, P = 0·001), homocysteine (8·45 ± 1·8 vs 7·72 ± 1·6 μm, P = 0·003), leptin (8·03 ± 4·2 vs 5·09 ± 1·9 ng/ml, P = 0·001) and fibrinogen (292·6 ± 33 vs 268 ± 31·4 mg/dl, P = 0·011). No differences were found in adiponectin or hsCRP. GH therapy was associated with a significant reduction in WHtR (P < 0·001), total cholesterol (P < 0·001), LDL cholesterol (P = 0·002), homocysteine (P = 0·044) leptin (P = 0·022) and fibrinogen (P = 0·001). Moreover, GH therapy was associated with a significant increase in adiponectin levels (P = 0·001).
Conclusions:
Our data suggest that children with untreated GHD exhibit a cluster of early cardiovascular risk factors and that GH treatment exerts beneficial effects on these abnormalities.
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