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      Prealbumin to fibrinogen ratio is closely associated with diabetic peripheral neuropathy

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          Abstract

          The aim of our study was to explore the diagnostic value of prealbumin to fibrinogen ratio (PFR) for predicting prognosis with the optimal cut-off value in diabetic peripheral neuropathy (DPN) patients. A total of 568 type 2 diabetes mellitus (T2DM) patients were enrolled in this study. The values including Toronto clinical neuropathy score (TCNS), nerve conduction velocity (NCV), vibration perception threshold (VPT), blood cells count, biochemical parameters, fibrinogen and PFR were recorded. The patients were divided into tertiles based on admission PFR value. First, clinical parameters were compared among the groups. Secondly, a logistic regression and ROC analysis were performed as the statistical model. The percentage of DPN, TCNS and VPT were significantly higher in the lowest PFR tertile than in the middle PFR tertile and the highest PFR tertile ( P < 0.01–0.001). NCV was significantly lower in lowest PFR tertile than in the middle PFR tertile and the highest PFR tertile ( P < 0.01–0.001). The Spearman correlation analysis showed that PFR was negatively correlated with TCNS and VPT ( P < 0.001), while PFR was positively correlated with median motor NCV ( P < 0.001), peroneal motor NCV ( P < 0.001), median sensory NCV ( P < 0.001), and peroneal sensory NCV ( P < 0.001). After adjusting these potentially related factors, PFR was independently related to DPN ( P = 0.007). The area under ROC curve was 0.627. This study finds the first evidence to suggest PFR may be the key component associated with DPN in T2DM, while PFR might underlie the pathophysiologic features of DPN.

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          Serum albumin: relationship to inflammation and nutrition.

          Hypoalbuminemia is the result of the combined effects of inflammation and inadequate protein and caloric intake in patients with chronic disease such as chronic renal failure. Inflammation and malnutrition both reduce albumin concentration by decreasing its rate of synthesis, while inflammation alone is associated with a greater fractional catabolic rate (FCR) and, when extreme, increased transfer of albumin out of the vascular compartment. A vicious cascade of events ensues in which inflammation induces anorexia and reduces the effective use of dietary protein and energy intake and augments catabolism of the key somatic protein, albumin. Hypoalbuminemia is a powerful predictor of mortality in patients with chronic renal failure, and the major cause of death in this population is due to cardiovascular events. Inflammation is associated with vascular disease and likely causes injury to the vascular endothelium, and hypoalbuminemia as two separate expressions of the inflammatory process. Albumin has a myriad of important physiologic effects that are essential for normal health. However, simply administering albumin to critically ill patients with hypoalbuminemia has not been shown to improve survival or reduce morbidity. Thus the inference from these clinical studies suggests that the cause of hypoalbuminemia, rather than low albumin levels specifically, is responsible for morbidity and mortality.
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            Plasma fibrinogen level and the risk of major cardiovascular diseases and nonvascular mortality: an individual participant meta-analysis.

            Plasma fibrinogen levels may be associated with the risk of coronary heart disease (CHD) and stroke. To assess the relationships of fibrinogen levels with risk of major vascular and with risk of nonvascular outcomes based on individual participant data. Relevant studies were identified by computer-assisted searches, hand searches of reference lists, and personal communication with relevant investigators. All identified prospective studies were included with information available on baseline fibrinogen levels and details of subsequent major vascular morbidity and/or cause-specific mortality during at least 1 year of follow-up. Studies were excluded if they recruited participants on the basis of having had a previous history of cardiovascular disease; participants with known preexisting CHD or stroke were excluded. Individual records were provided on each of 154,211 participants in 31 prospective studies. During 1.38 million person-years of follow-up, there were 6944 first nonfatal myocardial infarctions or stroke events and 13,210 deaths. Cause-specific mortality was generally available. Analyses involved proportional hazards modeling with adjustment for confounding by known cardiovascular risk factors and for regression dilution bias. Within each age group considered (40-59, 60-69, and > or =70 years), there was an approximately log-linear association with usual fibrinogen level for the risk of any CHD, any stroke, other vascular (eg, non-CHD, nonstroke) mortality, and nonvascular mortality. There was no evidence of a threshold within the range of usual fibrinogen level studied at any age. The age- and sex- adjusted hazard ratio per 1-g/L increase in usual fibrinogen level for CHD was 2.42 (95% confidence interval [CI], 2.24-2.60); stroke, 2.06 (95% CI, 1.83-2.33); other vascular mortality, 2.76 (95% CI, 2.28-3.35); and nonvascular mortality, 2.03 (95% CI, 1.90-2.18). The hazard ratios for CHD and stroke were reduced to about 1.8 after further adjustment for measured values of several established vascular risk factors. In a subset of 7011 participants with available C-reactive protein values, the findings for CHD were essentially unchanged following additional adjustment for C-reactive protein. The associations of fibrinogen level with CHD or stroke did not differ substantially according to sex, smoking, blood pressure, blood lipid levels, or several features of study design. In this large individual participant meta-analysis, moderately strong associations were found between usual plasma fibrinogen level and the risks of CHD, stroke, other vascular mortality, and nonvascular mortality in a wide range of circumstances in healthy middle-aged adults. Assessment of any causal relevance of elevated fibrinogen levels to disease requires additional research.
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              Inflammation in diabetic nephropathy: moving toward clinical biomarkers and targets for treatment.

              Diabetic nephropathy (DN) is a leading cause of end stage renal failure and there is an urgent need to identify new clinical biomarkers and targets for treatment to effectively prevent and slow the progression of the complication. Many lines of evidence show that inflammation is a cardinal pathogenetic mechanism in DN. Studies in animal models of experimental diabetes have demonstrated that there is a low-grade inflammation in the diabetic kidney. Both pharmacological and genetic strategies targeting inflammatory molecules have been shown to be beneficial in experimental DN. In vitro studies have cast light on the cellular mechanisms whereby diabetes triggers inflammation and in turn inflammation magnifies the kidney injury. Translation of this basic science knowledge into potential practical clinical applications is matter of great interest for researchers today. This review focuses on key pro-inflammatory systems implicated in the development of DN: the tumor necrosis factor(TNF)-α/TNF-α receptor system, the monocyte chemoattractant protein-1/CC-chemokine receptor-2 system, and the Endocannabinoid system that have been selected as they appear particularly promising for future clinical applications.
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                Author and article information

                Journal
                Endocr Connect
                Endocr Connect
                EC
                Endocrine Connections
                Bioscientifica Ltd (Bristol )
                2049-3614
                August 2020
                06 August 2020
                : 9
                : 8
                : 858-863
                Affiliations
                [1 ]Department of Endocrinology , Shanghai Fifth People’s Hospital, Fudan University, Shanghai, China
                [2 ]Department of Neurology , Shanghai Fifth People’s Hospital, Fudan University, Shanghai, China
                Author notes
                Correspondence should be addressed to H Ding: heyuan.ding@ 123456fudan.edu.cn
                Article
                EC-20-0316
                10.1530/EC-20-0316
                7487192
                32880377
                38ea65b9-05b8-4d1d-9c4a-6fd67cbe2617
                © 2020 The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : 30 July 2020
                : 06 August 2020
                Categories
                Research

                diabetes mellitus,type 2,prealbumin to fibrinogen ratio,diabetic peripheral neuropathy,vibrating perception threshold,nerve conduction velocity

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