4.6 Article Proceedings Paper

Modulation of types I and II acute phase reactants with insulin-like growth factor-1/binding protein-3 complex in severely burned children

期刊

CRITICAL CARE MEDICINE
卷 30, 期 1, 页码 83-88

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00003246-200201000-00013

关键词

insulin-like growth factor-1; insulin-like growth factor binding protein-3; acute phase response; acute phase proteins; constitutive serum proteins; inflammatory cytokines; low-dose insulin-like growth factor-1/binding protein-3; pharmacological modulation; severe burns; pediatric burns

资金

  1. NIGMS NIH HHS [1 R01-GM56687-01] Funding Source: Medline
  2. NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM056687] Funding Source: NIH RePORTER

向作者/读者索取更多资源

Objective: To determine whether 0.5 mg/kg insulin-like growth factor (IGF)-1/binding protein (IGFBP)-3, given intravenously, effectively alters the acute phase response in severely burned children. Design: Longitudinal trial with each patient serving as their own control. Setting: University-affiliated pediatric burn center. Patients: Nine children, 15 yrs of age or less, with burns covering > 40% of the total body surface area. Interventions. Standard burn care with early burn wound excision and grafting. Blood sampled at defined time points before and after operative procedures. Measurements and Results: Determination of types I and II acute phase reactant proteins, constitutive serum proteins, serum cytokines, serum IGF-1, IGFBP-3, and growth hormone levels. Treatment with IGF-1/BP-3 attenuated increases in type I (complement 3, (alpha1-acidglycoprotein) and type II (haptoglobin, (alpha1-antitrypsin) acute phase proteins. Further, IGF-1/BP-3 increased constitutive serum protein levels (prealbumin, retinol binding protein, transferrin) and decreased serum IL-6 levels. Conclusions: Low-dose IGF-1/BP-3 effectively attenuated the type I and type 11 hepatic acute phase response, increased serum levels of constitutive proteins, and modulated the hypermetaoblic response.

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