The relationship between cytokine concentrations and wound healing in chronic venous ulceration

Abstract

Wound fluid collection volume correlates with ulcer size. Ulcer healing correlated with increased concentrations of TGFbeta(1), possibly reflecting increased fibrogenesis in the proliferating wound. Aside from this, there was a large variation in wound and serum cytokine levels that largely limits their usefulness as markers of healing.

Wound Fluid Diagnostics in Diabetic Foot Ulcers

“…Furthermore, huge inter-patient variability in cytokine concentrations -possibly due to technical problems during wound fluid aspiration from under occlusive Tegaderm ® dressings-was observed in one study (Gohel et al 2008). …”

“…Various modifications of this technique have been described with respect to used materials, patient preparation and time scales, as well as with respect to wound bed preparation (Trengove et al 1999;Trengove, Bielefeldt-Ohmann, and Stacey 2000;Yager et al 1996;Wysocki and Grinnell 1990;James et al 2000;Wallace and Stacey 1998;Chen et al 1997;Wysocki et al 1999;Gohel et al 2008). Even very comprehensive protocols aiming for standardisation have been proposed, including the prior fasting of patients for eight hours as well as grading their hydration status by drinking one litre of water while hanging down the leg (Trengove, Langton, and Stacey 1996).…”

Computational Approach To Characterize Causative Factors and Molecular Indicators of Chronic Wound Inflammation

“…Yet, it has not been firmly established whether the expression of the same genes is altered in humans during disease, questioning the validity of such indicators. Any human study of chronic inflammatory diseases takes place well after the disease has already progressed and, thus, fails to provide insights into the factors triggering the chronic state (9,(18)(19)(20)(21)(22). Although chronic inflammation can be present in many pathological conditions, it is not causative to disease unless exacerbated by additional genetic and environmental factors (11).…”

Venous leg ulceration pathophysiology and evidence based treatment

“…15,29,31 The regulation of MMP production and function in VLU pathogenesis is not fully understood, but is likely linked to inflammatory cells, cytokines, urokinase-type plasminogen activator (uPA), extracellular MMP inducer CD147 (EMMPRIN), plateletderived growth factor (PDGF-AA), and the mitogen-activated protein kinase pathway (MAPK). 15,[32][33][34][35][36][37][38][39][40][41] MMPs exert many of their effects in degrading the extracellular matrix and chronic inflammation within the VLU environment, perpetuating MMP degradation of the provisional matrix and persistent VLU. 16,31 Pro-inflammatory cytokines are considered as potent inducers of MMP expression in chronic wounds.…”