Levels Of Vascular Markers Research Articles

Use of Glycated Hemoglobin (A1c) as a Biomarker for Vascular Risk in Type 2 Diabetes: Its Relationship with Matrix Metalloproteinases-2, -9 and the Metabolism of Collagen IV and Elastin.

Background and objectives: HbA1c measurements may be useful not only in optimizing glycemic control but also as a tool for managing overall vascular risk in patients with diabetes. In the present study, we investigate the clinical significance of HbA1c as a biomarker for hyperglycemia-induced vascular damages in type 2 diabetes (T2D) based on the levels of matrix metalloproteinases-2, -9 (MMP-2, MMP-9), anti-collagen IV (ACIV), and anti-elastin (AE) antibodies (Abs) IgM, IgG, and IgA, and CIV-derived peptides (CIV-DP) reflecting collagen and elastin turnover in the vascular wall. The aim is to show the relationship of hyperglycemia with changes in the levels of vascular markers and the dynamics of this relationship at different degrees of glycemic control reported by HbA1c levels. Materials and Methods: To monitor elastin and collagen IV metabolism, we measured serum levels of these immunological markers in 59 patients with T2D and 20 healthy control subjects with an ELISA. Results: MMP-2, MMP-9, and the AEAbs IgA levels were significantly higher in diabetic patients than in control subjects, whereas those of the AEAbs IgM, ACIVAbs IgM, and CIV-DP were significantly lower. MMP-9 levels were significantly lower at HbA1c values >7.5%. Conclusions: A set of three tested markers (MMP-2, MMP-9, and AEAbs IgA) showed that vascular damages from preceding long-term hyperglycemia begin to dominate at HbA1c values ≥7.5%, which is the likely cut-point to predict increased vascular risk.

Differences in platelet-related parameters among patients with audiographically distinct sudden sensorineural hearing loss: A retrospective study.

We explored possible relationships between sudden sensorineural hearing loss (SSNHL) in patients differing in terms of audiographic data and the levels of vascular markers in routine blood data.We included 37 patients with low-frequency SSNHL (LF-SSNHL), 28 with high-frequency SSNHL (HF-SSNHL), 32 with all-frequency SSNHL (AF-SSNHL), 32 with total-deafness SSNHL (TD-SSNHL), and 31 age- and sex-matched healthy controls. Peripheral venous blood samples were collected, and routine blood parameters including platelet and lymphocyte count, mean platelet volume (MPV), and platelet-to-lymphocyte ratio (PLR) were measured. Each group was divided into recovery subgroup and unrecovery subgroup in accordance with hearing level after 1 month therapy, then compared the difference of platelet and lymphocyte count, MPV, and PLR between the 2 subgroups.No significant difference was observed between platelet count of all SSNHL patients and control group (all P > .05). MPV of AF-SSNHL and TD-SSNHL, PLR of all SSNHL patients were significantly higher than those of control group (all P < .05), while lymphocyte count of all audiographically distinct SSNHL patients was significantly lower than that of control group (all P < .05). However, the difference of platelet count, lymphocyte count, MPV, and PLR among audiographically distinct SSNHL patients was not significant (all P > .05). In HF-SSNHL patients, lymphocyte count of unrecovery subgroup was significantly lower, while MPV and PLR of the unrecovery subgroup were significantly higher than those of recovery subgroup (all P < .05). In AF-SSNHL patients, MPV of the unrecovery group was significantly higher than that of recovery subgroup (P < .05).Lymphocyte count, MPV, and PLR may be relative to SSSNHL, but they could not be used to distinct SSNHL audiographically. Lower lymphocyte, higher MPV, and PLR may be indicative for the prognosis of HF-SSNHL patients; higher MPV may be related to bad treatment outcome of AF-SSNHL patients.

AB0216 Serum Angiogenesis Markers and their Association with Ultrasound-Detected Synovitis in the Evaluation of Disease Activity in Juvenile Idiopathic Arthritis

BackgroundSynovial angiogenesis, defined as a complex process of developing new blood vessels from the existing microvascular bed, is considered to be an important early step in the course and pathogenesis...

Autoimmunity and Vascular Involvement in Systemic Sclerosis (SSc)

Endothelial injury, obliterative microvascular lesions, and increased vascular wall thickness are present in all involved organs in scleroderma. The vascular pathology is associated with altered vascular function with increased vasospasm, reduced vasodilatory capacity and increased adhesiveness of the blood vessels to platelets and lymphocytes. The extent of injury and dysfunction is reflected by changes in the circulating levels of vascular markers. The initial triggers for the vascular pathology are not known. Possible viral triggers are visited here, including cytomegalovirus in view of increased levels of anti-CMV antibodies in scleroderma, and the remarkable similarities between CM V vasculopathies and scleroderma vascular disease. Endothelial apoptosis in scleroderma may be related to viral infection, immune reactions to viral or environmental factors, reperfusion injury or to anti-endothelial antibodies. The impact of the vascular pathology on the evolution of tissue fibrosis is not known; still, cytokines (TGFβ, IL4), vascular factors (endothelin), and growth factors (PDGF) are possibly crucial signals that link the vascular disease to tissue fibrosis. Knowledge of the regulation of these and other factors will provide the opportunity to develop more rational therapeutic approaches to the disease