Plasma Resistin Levels in Patients with Acute Aortic Dissection: A Propensity Score-Matched Observational Case-Control Study

Liu, Xintian; Zheng, Xuan; Su, Xi; Tian, Wei; Hu, Yuanyang; Zhang, Zhiping

doi:10.12659/msm.909469

Cited by 6 publications

(3 citation statements)

References 21 publications

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“…AAD is a fatal cardiovascular disease [ 13 ]. Since the underlying mechanisms of the development and progression of spontaneous AAD cases remain unclear, a screening or prevention strategy for these patients has yet to be developed [ 14 ]. In previous studies, preoperative creatinine, uric acid, serum tenascin-C, and inflammatory factors were all associated with postoperative mortality following AAD [ 10 , 15 – 17 ].…”

Section: Discussionmentioning

confidence: 99%

Serum sodium on admission affects postoperative in-hospital mortality in acute aortic dissection patients

Huang

Wang

et al. 2021

PLoS ONE

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Background Acute aortic dissection (AAD) is very fatal without surgical treatment. Higher serum sodium can increase in-hospital mortality of many diseases; however, the effect of serum sodium on postoperative in-hospital mortality in AAD patients remains unknown. Methods We collected a total of 415 AAD patients from January 2015 to December 2019. Patients were classified into four categories (Q1-Q4) according to the admission serum sodium quartile. The cox proportional hazards model evaluated the association between serum sodium and in-hospital mortality. All-cause in-hospital mortality was set as the endpoint. Results By adjusting many covariates, cox proportional hazards model revealed the in-hospital mortality risk of both Q3 and Q4 groups was 3.086 (1.242–7.671, P = 0.015) and 3.370 (1.384–8.204, P = 0.007) respectively, whereas the risk of Q2 group was not significantly increased. Univariate and multiple Cox analysis revealed that Stanford type A, serum glucose, α-hydroxybutyrate dehydrogenase and serum sodium were risk factors correlated with in-hospital death in AAD patients. Conclusion The study indicates that the admission serum sodium of AAD patients has a vital impact on postoperative hospital mortality.

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Section: Discussionmentioning

confidence: 99%

Serum sodium on admission affects postoperative in-hospital mortality in acute aortic dissection patients

Huang

Wang

et al. 2021

PLoS ONE

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“…In order to strengthen our hypothesis, it is essential that we develop further/future studies on larger groups of patients. Also, they must include other markers of acute inflammation, with a special interest for those reportedly correlated with resistin during acute cardiovascular events: tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP) and other proinflammatory cytokines [34]. Resistin promotes the production of TNF-α, IL-1β, IL-6 and other cytokines [12,35].…”

Section: Discussionmentioning

confidence: 99%

Resistin and Cardiac Arrest—A Prospective Study

Tat

Golea

Rahaian

et al. 2019

JCM

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The systemic response to ischemia-reperfusion that occurs after a cardiac arrest (CA) followed by the return of spontaneous circulation leads to endothelial toxicity and cytokine production, both responsible for the subsequent occurrence of severe cardiocirculatory dysfunction and early death. Resistin is emerging as a biomarker of proinflammatory status and myocardial ischemic injury and as a mediator of endothelial dysfunction. The study aimed to analyze the possible associations between several clinical and biological variables and the serum levels of resistin in CA survivors. Forty patients with out-of-hospital resuscitated CA, were enrolled in the study. Demographic, clinical and laboratory data (including serum resistin measurements at admission and at 6, 12, 24, 48 and 72 h) were recorded. For resistin, we calculated the area under the curve (AUC) using the trapezoidal method with measurements from 0 to 12 h, 0 to 24 h, 0 to 48 h and 0 to 72 h. Fifteen (37.5%) patients died in the first 72 h after CA. Cardiovascular comorbidities were present in 65% of patients. The majority of patients had post-CA shock (29 (72.5%)). Resistin serum levels rose in the first 12–24 h and decreased in the next 48–72 h. In univariate analysis, advanced age, longer duration of resuscitation, high sequential organ failure assessment score, high lactate levels, presence of cardiovascular comorbidities and the post-CA shock were associated with higher resistin levels. In multivariate analysis, post-CA shock or cardiovascular comorbidities were independently associated with higher AUCs for resistin for 0–12 h and 0–24 h. The only identified variable to independently predict higher AUCs for resistin for 0–48 h and 0–72 h was the presence of post-CA shock. Our data demonstrate strong independent correlation between high serum resistin levels, cardiac comorbidities and post-CA shock. The impact of the post-CA shock on serum concentration of resistin was greater than that of cardiac comorbidities.

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“…Numerous studies have shown that resistin can antagonize insulin to prevent cells from taking up glucose, resulting in decreased glucose tolerance in patients with T2DM, and that it can cause obesity by promoting blood sugar elevation and stimulating fat cell proliferation [115]. It is also involved in the inflammatory response, stimulating the release of endothelin-1 and monocyte chemotactic protein-1 by vascular endothelial cells, and promoting atherosclerosis, thereby leading to endothelial dysfunction [116,117]. While reducing weight and fat accumulation through exercise, which is an effective treatment for obesity and its complications, also has a positive effect on resistin concentrations, the relationship between the two is not clear.…”

Section: The Physiological Function Of Resistinmentioning

confidence: 99%

Effects of different obesity-related adipokines on the occurrence of obstructive sleep apnea

2020

Endocr J

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Obstructive sleep apnea (OSA), characterized by recurrent episodes of apnea during sleep and daytime sleepiness, seriously affects human health and may lead to systemic organ dysfunction. The pathogenesis of OSA is complex and still uncertain, but multiple surveys have shown that obesity is an important factor, and the incidence of OSA in people with obesity is as high as 30%. Adipokines are a group of proteins secreted from adipocytes, which are dysregulated in obesity and may contribute to OSA. Here, we review the most important and representative research results regarding the correlation between obesity-related adipokines including leptin, adiponectin, omentin-1, chemerin, and resistin and OSA in the past 5 years, provide an overview of these key adipokines, and analyze possible intrinsic mechanisms and influencing factors. The existing research shows that OSA is associated with an increase in the serum levels of leptin, chemerin, and resistin and a decrease in the levels of adiponectin and omentin-1; the findings presented here can be used to monitor the development of OSA and obesity, prevent future comorbidities, and identify risk factors for cardiovascular and other diseases, while different adipokines can be linked to OSA through different pathways such as insulin resistance, intermittent hypoxia, and inflammation, among others. We hope our review leads to a deeper and more comprehensive understanding of OSA based on the relevant literature, which will also provide directions for future clinical research.

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Plasma Resistin Levels in Patients with Acute Aortic Dissection: A Propensity Score-Matched Observational Case-Control Study

Cited by 6 publications

References 21 publications

Serum sodium on admission affects postoperative in-hospital mortality in acute aortic dissection patients

Serum sodium on admission affects postoperative in-hospital mortality in acute aortic dissection patients

Resistin and Cardiac Arrest—A Prospective Study

Effects of different obesity-related adipokines on the occurrence of obstructive sleep apnea

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