(27-07-16) Endothelial Dysfunction as a Link between Cardiovascular Risk Factors and Peripheral Neuropathy in Diabetes.
Roustit M1, Loader J1, Deusenbery C1, Baltzis D1, Veves A1.
Abstract
CONTEXT:
Cardiovascular risk factors are well-known predictors of the development of diabetic peripheral neuropathy (DPN), which has traditionally been considered as a manifestation of diabetes-associated microangiopathy. As endothelial dysfunction is strongly associated with all cardiovascular risk factors, we hypothesized that it may be a link between cardiovascular risk factors and DPN.
OBJECTIVE:
The primary objective of this study was to test whether endothelial dysfunction is a predictor of DPN.
DESIGN AND SETTING:
This is a cross-sectional analysis of a cohort composed of patients followed at the Microcirculatory laboratory, Beth Israel Deaconess Medical Center.
PATIENTS:
Participants with diabetes without DPN (n=192) and with DPN (n=166), subjects with prediabetes (n=75) and non-diabetic controls (n=59) were included.
INTERVENTIONS:
Endothelial function was assessed with FMD of the brachial artery. Inflammatory cytokines and biomarkers of endothelial function (Intercellular Cell Adhesion Molecules, ICAM) were quantified using a multiplex bead-based immunoassay. Neurological assessment included the Neuropathy Disability Score (NDS).
MAIN OUTCOME MEASURE:
The relationship between FMD and NDS assessed using multiple linear regression.
RESULTS:
In addition to already known risk factors of DPN, FMD was strongly associated with NDS (β=-0.24; P<0.001). Sensitivity analysis that removed FMD from the model provided similar results for ICAM, another biomarker of endothelial function. Confirmatory factor analysis further showed that endothelial dysfunction is a significant mediator between HbA1c and diabetes duration, and diabetic complications.
CONCLUSIONS:
This study shows that endothelial dysfunction occurs early in the pathophysiology of diabetes and is a link between cardiovascular risk factors and DPN.
Fonte: J Clin Endocrinol Metab. 2016 Jul 11:jc20162030.
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