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Volume 145, Issue 5, Pages 657-661 (November 2004)


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Peripheral inflammatory and fibrinolytic markers in adolescents with growth hormone deficiency: Relation to postprandial dyslipidemia

Roberto Lanes, MDCorresponding Author Informationemail address, Mariela Paoli, MD, Eduardo Carrillo, MD, Omar Villaroel, MSc, Anselmo Palacios, MD

Received 25 March 2004; received in revised form 24 June 2004; accepted 16 July 2004.

Objective

To determine whether peripheral inflammatory and fibrinolytic markers are elevated in growth hormone-deficient (GHD) adolescents and associated with increased postprandial lipoproteins.

Study design

Fifteen GHD children on GH treatment with a chronologic age of 12.7 ± 2.5 years and 10 untreated GHD adolescents with a chronologic age of 13.0 ± 2.6 years were studied. Triglycerides (TG), C-reactive protein (CRP), fibrinogen, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α) were measured in the fasting state and 4 hours after ingesting a high-fat meal; 15 healthy adolescents served as controls.

Results

Fasting and postprandial TG of untreated GHD children were higher than those in treated subjects and healthy controls. Fasting TNF-α, CRP, and fibrinogen concentrations of untreated GHD adolescents were higher than those in healthy controls, but similar to those of GH-treated GHD adolescents. Although fibrinogen levels increased after a high-fat meal in GHD adolescents, CRP, TNF-α, and IL-6 concentrations did not increase further. Fasting and postprandial TG of untreated GHD adolescents were positively associated with fasting and postprandial CRP, and with postprandial TNF-α and IL-6 concentrations. Fasting TG also correlated positively with fasting fibrinogen concentrations in untreated and treated GHD adolescents.

Conclusions

The pronounced inflammatory response seen in GHD adolescents seems to be associated with the presence of elevated levels of fasting and postprandial TG, which may result in an increased susceptibility for premature atherosclerosis.

From Pediatric Endocrine Unit, Hospital de Clinicas Caracas; Division of Endocrinology, Hospital Universitario de Los Andes, Merida; Division of Endocrinology, Hospital Central Dr Carlos Arvelo; and Division of Endocrinology, Clinica Avila, Caracas, Venezuela.

Corresponding Author InformationReprint requests: Roberto Lanes, MD, M-209, PO Box 020010, Miami, FL 33102.

 Generous contributions by Pfizer and Glaxo-Smith-Kline of Venezuela allowed us to purchase the laboratory material for this study.

PII: S0022-3476(04)00677-8

doi:10.1016/j.jpeds.2004.07.037


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