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Cluster of cardiometabolic risk factors in children with GH deficiency: a prospective, case–control study
Author(s) -
Capalbo Donatella,
Mattace Raso Giuseppina,
Esposito Andrea,
Di Mase Raffaella,
Barbieri Flavia,
Meli Rosaria,
Bruzzese Dario,
Salerno Mariacarolina
Publication year - 2014
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/cen.12393
Subject(s) - medicine , endocrinology , body mass index , adiponectin , leptin , homocysteine , cholesterol , prospective cohort study , fibrinogen , insulin resistance , insulin , obesity
Summary 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 ( WH t R ), 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 (hs CRP ) 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 WH t R (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 μ m , 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 hs CRP . GH therapy was associated with a significant reduction in WH t R ( 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.