Insulinlike growth factor system in remission and flare of inflammatory bowel diseases.
Pol Arch Intern Med
; 127(12): 832-839, 2017 12 22.
Article
em En
| MEDLINE
| ID: mdl-29112184
ABSTRACT
INTRODUCTION Insulinlike growth factor 1 (IGF1) is involved in the modulation of immunity and inflammation. It also plays a role in regulating the migration of endothelial cells and production of vasoactive agents. OBJECTIVES This study assessed the concentrations of IGF1 and insulinlike growth factor-binding protein 3 (IGFBP3) and their relationships to disease activity in patients with inflammatory bowel disease (IBD). PATIENTS AND METHODS A total of 129 adult patients with IBD (69 with Crohn disease [CD] and 60 with ulcerative colitis [UC]) were involved in the study. The control group consisted of 31 healthy volunteers. Biochemical serum analyses were performed and the associations of IGF1 and IGFBP3 with inflammatory markers and disease activity were assessed. RESULTS IGF1 levels were decreased in patients with active UC compared with those with nonactive UC (mean [SD], 78.3 [22.7] ng/ml and 96.2 [24.5] ng/ml, respectively; P = 0.02) and controls (94.5 [26.5] ng/ml; P = 0.03). The IGF1 level was lower in patients with active CD compared with those with nonactive CD (mean [SD], 79.2 [24.9] ng/ml and 110.1 [43.4] ng/ml, respectively; P <0.001). The IGFBP3 level was lower in patients with active UC compared with those with nonactive UC (P = 0.04) and controls (P = 0.04). IGF1 correlated negatively with Creactive protein (CRP) levels (P <0.01), disease activity (P <0.05), and disease duration (P <0.05). IGFBP3 levels correlated negatively with CRP levels (P <0.05). CONCLUSIONS The IGF system is disrupted in patients with IBD. Systemic levels of the IGF axis components are related to disease activity and duration.
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Base de dados:
MEDLINE
Assunto principal:
Fator de Crescimento Insulin-Like I
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Doenças Inflamatórias Intestinais
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Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article