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Kounis N.G.,Patras Highest Institute of Education and Technology
Clinical Therapeutics | Year: 2013

Background: When allergy or hypersensitivity and anaphylactic or anaphylactoid insults lead to cardiovascular symptoms and signs, including acute coronary events, the result might be the recently defined nosologic entity Kounis syndrome. Vasospastic allergic angina, allergic myocardial infarction, and stent thrombosis with occluding thrombus infiltrated by eosinophils and/or mast cells are the 3 reported variants of this syndrome. Objective: The purpose of this review was to highlight and consolidate the recent literature on allergic angina and allergic myocardial infarction and to propose new therapeutic modalities for stabilizing mast cells. Methods: A search for current literature on the pathophysiology, causality, clinical appearance, variance, prevention, and treatment of Kounis syndrome was conducted. Results: Kounis syndrome is caused by inflammatory mediators such as histamine; neutral proteases, including tryptase, chymase, and cathepsin-D; arachidonic acid products; platelet-activating factor; and a variety of cytokines and chemokines released during the mast-cell activation. Platelets with Fc γ receptor (FcγR) Ι, FcγRII, FcεRI, and FcεRII also have a role in the activation cascade. The same mediators released from the similar inflammatory cells are involved in acute coronary events of nonallergic etiology. These cells are not only present in the involved region before plaque erosion or rupture but also release their contents just before an acute coronary event. Pro-inflammatory mediators similar to those found in Kounis syndrome are found in some cases with nonallergic etiology, suggesting that this is a more general problem. The acute coronary and cerebrovascular events in Kounis syndrome may be prevented by the inhibition of mast-cell degranulation. Substances and natural molecules that protect the mast-cell surface and stabilize the mast-cell membrane are emerging as novel agents in the prevention of acute coronary and other arterial events. Conclusions: The 3 reported variants of Kounis syndrome-vasospastic allergic angina, allergic myocardial infarction, and stent thrombosis with occluding thrombus-are caused by inflammatory mediators. Agents that inhibit mast-cell degranulation may be efficacious in preventing the acute coronary and cerebrovascular events of Kounis syndrome. © 2013 Elsevier HS Journals, Inc.

Nikolakopoulou N.M.,Patras Highest Institute of Education and Technology
International Journal of Adolescent Medicine and Health | Year: 2010

The aim of this study was to assess the acceptance of H1N1 vaccination among parents in Greece. A sample of 850 parents participated in the present study. Interviews were performed using a structured questionnaire. The overall percentage of participants reporting that they had been administered the H1N1 vaccine was 0.35%. Only 1.18% of the respondents who had not been administered the vaccine were willing to accept it A significant barrier to H1N1 vaccination is concern about vaccine safety. © Freund Publishing House Ltd.

Cevik C.,Texas Tech University Health Sciences Center | Nugent K.,Texas Tech University Health Sciences Center | Shome G.P.,Texas Tech University Health Sciences Center | Kounis N.G.,Patras Highest Institute of Education and Technology
International Journal of Cardiology | Year: 2010

Kounis syndrome is potentially a life-threatening medical emergency with both a severe allergic reaction and acute coronary syndrome. Most of the information about this syndrome has come from the case reports. The management of these patients may be challenging for clinicians, and unfortunately guidelines have not been established yet. In this article, we review the current guidelines of acute coronary syndromes and anaphylaxis along with the published cases with Kounis syndrome secondary to beta-lactam antibiotics. We have summarized our recommendations for the work-up and treatment of Kounis syndrome from available data. Obviously, larger prospective studies are needed to establish definitive treatment guidelines for these patients. © 2010 Elsevier Ireland Ltd.

Kounis N.G.,Patras Highest Institute of Education and Technology | Soufras G.D.,University of Patras | Tsigkas G.,University of Patras | Hahalis G.,University of Patras
Clinical and Applied Thrombosis/Hemostasis | Year: 2015

Inflammation is a key feature of atherosclerosis and its clinical manifestations. The leukocyte count has emerged as a marker of inflammation that is widely available in clinical practice. Since inflammation plays a key role in atherosclerosis and its end results, discovering new biomarkers of inflammation becomes important in order to help diagnostic accuracy and provide prognostic information about coronary cardiac disease. In acute coronary syndromes and percutaneous coronary intervention, elevated levels of almost all subtypes of white blood cell counts, including eosinophils, monocytes, neutrophils, and lymphocytes, and neutrophil-lymphocyte ratio and eosinophil-leukocyte ratio constitute independent predictors of adverse outcomes. Eosinophil count and eosinophil-leukocyte ratio, in particular, emerge as novel biomarkers for risk stratification in patients with coronary artery disease. Since the presence of eosinophils denotes hypersensitivity inflammation and hypersensitivity associated with Kounis syndrome, this reality is essential for elucidating the etiology of inflammation in order to consider predictive and preventive measures and to apply the appropriate therapeutic methods. © The Author(s) 2014

Soufras G.D.,Saint Andrews State General Hospital | Kounis G.N.,Patras Highest Institute of Education and Technology | Kounis N.G.,Patras Highest Institute of Education and Technology
International Endodontic Journal | Year: 2014

Anaphylactic shock is a real and life threatening medical emergency which is encountered in every field of medicine. The coronary arteries seem to be the primary target of anaphylaxis resulting in the development of Kounis syndrome. Kounis syndrome is a pan-arterial anaphylaxis -associated syndrome affecting patients of any age, involving numerous and continuously increasing causes, with broadening clinical manifestations and covering a wide spectrum of mast cell activation disorders. Recently, Kounis-like syndrome affecting the cerebral arteries was found to be associated with mast cell activation disorders. In anaphylactic shock, the decrease of cerebral blood flow is more than what would be expected from severe arterial hypotension. This is attributed to the early and direct action of anaphylactic mediators on cerebral vessels. While adrenaline is a life saving agent in the treatment of anaphylactic shock, it contains sodium betabisulfite as preservative and should be avoided in sulfite allergic patients. Potential allergens encountered in endodotic practice include formocresol, zinc compounds thiurams, sodium dimethyldithiocarbamade, and mercaptobenzothiazole that might have synergistic action. All these agents together with analgesics, antibiotics, antiseptics, formaldehyde, latex, local anaesthetics and metals used in dental practice, in general, can induce anaphylactic shock. Practitioners should be aware of these consequences. A careful history of previous atopy and reactions is of paramount importance for safe and effective management. © 2013 International Endodontic Journal.

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