Insulin-like growth-factor-binding proteins (BPs) in serum interfere with the measurement of insulin-like growth factor-I (IGF-I). Various assays have been developed to overcome this interference. We evaluated an immunoradiometric (IRMA) assay and compared it with the radioimmunoassay (RIA) using bo
Insulin-like growth factor I (IGF-I) as a sensitive biomarker of catabolism in patients with gastrointestinal diseases
✍ Scribed by Olgica Nedić; Vesna Malenković; Judith Anna Nikolić; Ivona Baričević
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 121 KB
- Volume
- 21
- Category
- Article
- ISSN
- 0887-8013
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✦ Synopsis
Abstract
Gastrointestinal ailments evoke changes in the hypothalamic‐pituitary‐adrenal (HPA) axis and modulation of hepatic protein synthesis. We examined the catabolic effect of certain primary gastrointestinal diseases and surgery on the concentration of insulin‐like growth factor I (IGF‐I). Blood samples from patients with gastric cancer (GC), cholecystitis (CC), or inguinal hernia (IH) were taken before and after surgery. The concentrations of IGF‐I, IGF binding protein‐1 (IGFBP‐1), insulin, cortisol, and glucose were determined. In GC patients the concentration of IGF‐I was reduced and the concentrations of IGFBP‐1 and cortisol were elevated preoperatively; after surgery, IGFBP‐1 normalized. In CC patients the concentration of IGF‐I was low and the concentration of IGFBP‐1 was high before cholecystectomy; after surgery IGFBP‐1 returned to normal and the concentration of cortisol increased. In IH patients the concentration of IGF‐I was low and the concentrations of IGFBP‐1 and cortisol were high before surgery; after laparotomy IGFBP‐1 returned to normal. The metabolic changes were present in all analyzed patient groups, regardless of the severity of disease and nutrition. The concentration of IGF‐I was reduced before surgery and remained reduced after, recommending IGF‐I as a metabolic marker in both pre and postoperative examination of patients. J. Clin. Lab. Anal. 21:335–339, 2007. © 2007 Wiley‐Liss, Inc.
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