Serum IgE levels are associated with coronary artery disease severity

Guo, Xiaoxiao; Yuan, Shinsheng; Liu, Yongtai; Zeng, Yong; Xie, Hongzhi; Liu, Zhenyu; Zhang, Shuyang; Fang, Quan; Wang, Jing; Shen, Zhujun

doi:10.1016/j.atherosclerosis.2016.05.020

Cited by 40 publications

(32 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…6 Elevated serum IgE can be caused by allergic reactions, infections, and other immune conditions, including the hyper-IgE syndrome, 7 a rare primary immunodeficiency disease characterized by recurrent skin and pulmonary abscesses and extremely elevated IgE serum levels. In addition, IgEs might be increased in acute myocardial infarction, stable and unstable angina, further correlating with plaque destabilization and severity of acute myocardial infarction, 1,8 and elevated IgE levels may be a risk factor for increased cardiovascular mortality. 9 Increased IgE Levels: Cause or Consequence of Acute Coronary Events?…”

Section: Causes Of Ige Releasementioning

confidence: 99%

Humanized Monoclonal Antibodies Against IgE Antibodies as Therapy for IgE-Mediated Coronary Syndromes: Are We There Yet?

Kounis

Koniari²,

Tsigkas

et al. 2020

Canadian Journal of Cardiology

View full text Add to dashboard Cite

See article by Liu et al., pages 966.e5-966.e6 of this issue. Immunoglobulin E (IgE) antibodies are synthesized and released by B lymphocytes as a result of a complex interplay between genes, cytokines, and environmental antigen exposure. IgE antibodies participate in atopic diseases and systemic anaphylaxis, constituting components of a protein network implicated in signalling response to antigens and allergens. 1 IgEs are very short lived in plasma (w 1 day), but receptorbound IgE can remain fixed to cells in tissues for weeks or months. Their biologic activity is mainly dependent on binding to specific fragment crystallisable region (FcR) receptors high-affinity FCεRI and FCgRI and low-affinity FCεRII and FCgRII situated on the surface, mainly of mast cells, but also of basophils, eosinophils, monocytes, and epithelial and dendritic cells. 2 The IgE binding to FcR increases cell survival and causes up-regulation of the above receptors. Interactions mediated by IgEs bound on mast cells with corresponding antigens/allergens on the surface of mast cells leads to mast cell degranulation and release of a variety of preformed and newly formed substances acting as mediators. Degranulation and mediator release occur when IgE antibodies bridged with antigens/allergens reach the critical number of 2000, forming 1000 bridges for a maximum of w 500,000-1,000,000 IgE antibodies on the cell surface! 3 Mediator release can induce coronary artery spasm, independently from the existence of underlying atherosclerotic disease, manifesting as Kounis type I syndrome (Table 1) and myocardial infarction with nonobstructive coronary arteries (MINOCA). 4 The mediators might contribute to the critical progression, erosion, and rupture of atherosclerotic plaque, inducing thrombotic complications resulting from platelet activation and fibrinolytic system impairment, and further

show abstract

Section: Causes Of Ige Releasementioning

confidence: 99%

Humanized Monoclonal Antibodies Against IgE Antibodies as Therapy for IgE-Mediated Coronary Syndromes: Are We There Yet?

Kounis

Koniari²,

Tsigkas

et al. 2020

Canadian Journal of Cardiology

View full text Add to dashboard Cite

show abstract

“…In this issue of Atherosclerosis, Guo et al [4] measured total serum IgE concentrations in 708 consecutive patients admitted to coronary angiography laboratory, and assessed the severity of coronary artery disease by the number of diseased vessels showing !50% diameter stenosis and quantified by Gensini scores. They found that total serum IgE levels were significantly increased in patients with multi-vessel disease compared to those with singlevessel disease, were independent predictors for an increased risk of multi-vessel disease, and contributed to discriminating coronary artery disease severity independently of traditional cardiovascular risk factors.…”

mentioning

confidence: 99%

“…When IgE levels were above 200 kU/L, the incidence of non-fatal myocardial infarction was even higher. 4 In another prospective clinical study [8], 55 patients with acute myocardial infarction, unstable angina and stable angina pectoris were compared with 15 healthy controls. IgE levels were serially measured on days 1, 3, 7, 21 after admission and 3 months later in the acute myocardial infarction and unstable angina groups and only once in the stable angina pectoris and healthy controls.…”

mentioning

confidence: 99%

Serum IgE levels in coronary artery disease

Kounis

Hahalis

2016

Atherosclerosis

View full text Add to dashboard Cite

The development and progression of atherosclerosis and its predisposition for unstable angina, myocardial infarction and stroke is associated with traditional risk factors such as family history, cigarette smoking, hypertension, dyslipidemia, diabetes mellitus, obesity, imbalance of the hemostatic/fibrinolytic system and sedentary lifestyle. However, much of the variability in atherosclerosis and its manifestations still remains unexplained. Nowadays, there is increasing evidence that immunologic mechanisms play a major role in etiology, prediction of coronary plaque instability and foreseeing severe reaction leading to an actual coronary event. Cells of the immune system such as macrophages, mast cells and T-lymphocytes are major components of human atheromatous plaque. These cells participate in a vicious immune cycle and activate each others via bidirectional stimuli. For example, mast cells can activate macrophages and may enhance T-cell activation. Inducible macrophage protein 1a may activate mast cells, while CD169+ macrophages activate CD8 T cells. T cells may mediate mast-cell activation and proliferation and regulate macrophage activity. Mediators secreted by these cells, including histamine, neutral proteases, arachidonic acid products, platelet activating factor and a variety of cytokines and chemokines, can induce coronary artery spasm and atheromatous plaque erosion and rupture, culminating in the development of acute coronary syndromes.

show abstract

“…Further studies by others indicated that high serum IgE levels might be related to myocardial infarction, coronary arterial disease, cerebral arterial stenosis, coronary artery aneurysms and other CVDs 9 - 14 . Furthermore, we and our colleagues found that serum IgE levels were significantly higher in multi-vessel disease compared to single-vessel disease (61.80 vs. 32.45 kU/L, p = 0.003) independently of traditional cardiovascular risk factors, indicating that serum IgE levels might be associated with coronary artery disease severity 15 . Another study reported by us showed that IgE was able to stimulate arterial cell apoptosis and cytokine expression and promote atherosclerosis by enhancing Na+/H+ exchanger 1 (NHE1) activity on macrophages 16 .…”

Section: Introductionmentioning

confidence: 57%

The Relationship of Serum Antigen-Specific and Total Immunoglobulin E with Adult Cardiovascular Diseases

Wang

Guo

et al. 2018

Int. J. Med. Sci.

Self Cite

View full text Add to dashboard Cite

Background: The relationship of serum antigen-specific immunoglobulin E (IgE) with cardiovascular diseases (CVDs) remains poorly understood. This study aimed to explore the association of antigen-specific and total IgE with CVDs using data derived from the National Health and Nutrition Examination Survey (NHANES) 2005-2006.Methods and Results: The association of serum total or antigen-specific IgE levels with CVDs was analyzed by survey-weighted logistic regression modeling, adjusted by age, sex, race, education, body mass index, blood pressure, total cholesterol, C-reactive protein, homocysteine, diabetes, smoking, and alcohol consumption. 4953 subjects were included. Coronary heart disease was significantly related to serum total IgE levels. The association of serum total IgE levels with coronary heart disease was further validated by negative, ≥1 and 1-6 positive antigen-specific IgE. Myocardial infarction was positively associated with serum total IgE levels only when all antigen-specific IgE were negative, but inversely associated with serum total IgE when plant-specific IgE test results were positive. More specifically, myocardial infarction was also inversely related to positive oak, birch, or peanut-specific IgE. In addition, serum total IgE are positively associated with angina when at least one specific IgE were positive.Conclusions: Serum antigen-specific IgE, as well as total IgE, is significantly associated with CVDs independently of a long list of established cardiovascular risk factors, which is more informative than total IgE per se.

show abstract

Serum IgE levels are associated with coronary artery disease severity

Cited by 40 publications

References 31 publications

Humanized Monoclonal Antibodies Against IgE Antibodies as Therapy for IgE-Mediated Coronary Syndromes: Are We There Yet?

Humanized Monoclonal Antibodies Against IgE Antibodies as Therapy for IgE-Mediated Coronary Syndromes: Are We There Yet?

Serum IgE levels in coronary artery disease

The Relationship of Serum Antigen-Specific and Total Immunoglobulin E with Adult Cardiovascular Diseases

Contact Info

Product

Resources

About