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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Systemic lupus erythematosus &#40;SLE&#41; is an autoimmune inflammatory disease of unknown origin that affects many organ systems&#46; It is characterized by chronic inflammation that can induce abnormal vasomotion by reducing nitric oxide production and increasing endothelin-1 release&#44; leading to endothelial injury and consequently to coronary artery spasm&#44; which can progress to acute myocardial infarction &#40;MI&#41;&#46; This could be the result of either increased C-reactive protein&#44; which induces significant expression of molecules associated with endothelial damage such as ICAM-1&#44; VCAM-1 and E-selectin&#44; or expansion of CD4 CD28 T cells&#44; which induce cytolysis in endothelial cells and&#47;or activation of macrophages and other related interacting cells such as mast cells&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">1</span></a> Therefore an association with Kounis mast cell activation-associated syndrome&#44; also known as coronary hypersensitivity disorder&#44;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">2</span></a> cannot be excluded&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">In the very interesting paper by de Matos Soeiro et al&#46; published in the <span class="elsevierStyleItalic">Journal</span><a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">3</span></a> concerning 11 patients with acute coronary syndromes&#44; it was concluded that coronary artery disease in young people with SLE due to premature atherosclerosis should be always be borne in mind because of its high mortality rate&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Indeed&#44; the following inflammatory substances and conditions that are associated with Kounis syndrome should be always considered in patients with lupus erythematosus&#44; including&#58;<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">1&#46;</span><p id="par0020" class="elsevierStylePara elsevierViewall">Interleukin-9&#44; a T-cell derived factor preferentially expressed by CD4&#43; T cells that has been characterized in human and murine systems&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">4</span></a></p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">2&#46;</span><p id="par0025" class="elsevierStylePara elsevierViewall">Mast cell tryptase&#44; which can be an indicator of type I hypersensitivity reaction and may serve as a surrogate marker of anaphylaxis&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">5</span></a></p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">3&#46;</span><p id="par0030" class="elsevierStylePara elsevierViewall">Macrophages and their polarization have been found to contribute to the initiation and perpetuation of SLE&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">6</span></a></p></li><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">4&#46;</span><p id="par0035" class="elsevierStylePara elsevierViewall">Hypereosinophilic syndrome&#44; which is associated with SLE&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">7</span></a></p></li><li class="elsevierStyleListItem" id="lsti0025"><span class="elsevierStyleLabel">5&#46;</span><p id="par0040" class="elsevierStylePara elsevierViewall">Mast cells&#44; macrophages and &#40;very few&#41; eosinophils are present in inflamed rheumatoid synovial tissue and sites of cartilage erosion in SLE and other autoimmune conditions&#44; including rheumatoid arthritis&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">8</span></a></p></li><li class="elsevierStyleListItem" id="lsti0030"><span class="elsevierStyleLabel">6&#46;</span><p id="par0045" class="elsevierStylePara elsevierViewall">Patients with SLE have higher risk of acute MI compared with non-SLE controls&#44; and this risk is more significant in females&#46; In addition&#44; SLE is an independent risk factor for post-acute MI mortality&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">9</span></a></p></li><li class="elsevierStyleListItem" id="lsti0035"><span class="elsevierStyleLabel">7&#46;</span><p id="par0050" class="elsevierStylePara elsevierViewall">Platelets bearing complement protein C4d &#40;P-C4d&#41; were initially determined to be specific for diagnosis of SLE and were later found to be associated with acute ischemic stroke in non-SLE patients&#46; P-C4d may identify a subset of SLE patients with a worse clinical prognosis and is associated with all-cause mortality and stroke in these patients&#46; P-C4d may be a prognostic biomarker as well as a pathogenic clue that links platelets&#44; complement activation&#44; and thrombosis&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">10</span></a></p></li><li class="elsevierStyleListItem" id="lsti0040"><span class="elsevierStyleLabel">8&#46;</span><p id="par0055" class="elsevierStylePara elsevierViewall">The R131 allele of the Fc gamma receptor IIa &#40;Fc&#947;RIIa&#41; is associated with SLE incidence and disease severity but also with coronary artery disease&#46; This finding implies that risk stratification of SLE patients and other high-risk patients with troponin-negative angina could be significantly improved by Fc&#947;RIIa genotyping&#46;<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">11</span></a></p></li><li class="elsevierStyleListItem" id="lsti0045"><span class="elsevierStyleLabel">9&#46;</span><p id="par0060" class="elsevierStylePara elsevierViewall">SLE nearly doubles mortality and event hazards in cardiovascular disease &#40;MI&#44; stroke&#44; or congestive heart failure&#41; compared to age- and sex-matched comparisons&#46; This raises research questions regarding delayed SLE diagnosis versus accelerated cardiovascular disease prior to SLE&#44; particularly in older-onset SLE&#46;<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">12</span></a></p></li><li class="elsevierStyleListItem" id="lsti0050"><span class="elsevierStyleLabel">10&#46;</span><p id="par0065" class="elsevierStylePara elsevierViewall">Cardiovascular events including acute MI and stroke in SLE patients are caused by multifactorial mechanisms&#44; including both traditional and disease-specific risk factors&#46; An overall evaluation with individual risk stratification based on both these features is important to correctly manage these patients in order to reduce negative outcomes&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">13</span></a></p></li></ul></p><p id="par0070" class="elsevierStylePara elsevierViewall">Consequently&#44; in order to elucidate the pathophysiology of the association of SLE and acute coronary syndromes and to discover potential therapeutic and preventive measures for acute coronary events&#44; a search for inflammatory cells and measurement of inflammatory cell mediators released from these cells should always be performed&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0075" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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Letter to the Editor
Inflammation, systemic lupus erythematosus and the Kounis mast cell activation-associated syndrome
Inflamação, lúpus eritematoso sistémico e síndrome de Kounis associada à ativação dos mastócitos
Nicholas G. Kounis
Department of Medical Sciences, Southwestern Greece Highest Institute of Education and Technology, Patras, Greece
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Systemic lupus erythematosus &#40;SLE&#41; is an autoimmune inflammatory disease of unknown origin that affects many organ systems&#46; It is characterized by chronic inflammation that can induce abnormal vasomotion by reducing nitric oxide production and increasing endothelin-1 release&#44; leading to endothelial injury and consequently to coronary artery spasm&#44; which can progress to acute myocardial infarction &#40;MI&#41;&#46; This could be the result of either increased C-reactive protein&#44; which induces significant expression of molecules associated with endothelial damage such as ICAM-1&#44; VCAM-1 and E-selectin&#44; or expansion of CD4 CD28 T cells&#44; which induce cytolysis in endothelial cells and&#47;or activation of macrophages and other related interacting cells such as mast cells&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">1</span></a> Therefore an association with Kounis mast cell activation-associated syndrome&#44; also known as coronary hypersensitivity disorder&#44;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">2</span></a> cannot be excluded&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">In the very interesting paper by de Matos Soeiro et al&#46; published in the <span class="elsevierStyleItalic">Journal</span><a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">3</span></a> concerning 11 patients with acute coronary syndromes&#44; it was concluded that coronary artery disease in young people with SLE due to premature atherosclerosis should be always be borne in mind because of its high mortality rate&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Indeed&#44; the following inflammatory substances and conditions that are associated with Kounis syndrome should be always considered in patients with lupus erythematosus&#44; including&#58;<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">1&#46;</span><p id="par0020" class="elsevierStylePara elsevierViewall">Interleukin-9&#44; a T-cell derived factor preferentially expressed by CD4&#43; T cells that has been characterized in human and murine systems&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">4</span></a></p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">2&#46;</span><p id="par0025" class="elsevierStylePara elsevierViewall">Mast cell tryptase&#44; which can be an indicator of type I hypersensitivity reaction and may serve as a surrogate marker of anaphylaxis&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">5</span></a></p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">3&#46;</span><p id="par0030" class="elsevierStylePara elsevierViewall">Macrophages and their polarization have been found to contribute to the initiation and perpetuation of SLE&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">6</span></a></p></li><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">4&#46;</span><p id="par0035" class="elsevierStylePara elsevierViewall">Hypereosinophilic syndrome&#44; which is associated with SLE&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">7</span></a></p></li><li class="elsevierStyleListItem" id="lsti0025"><span class="elsevierStyleLabel">5&#46;</span><p id="par0040" class="elsevierStylePara elsevierViewall">Mast cells&#44; macrophages and &#40;very few&#41; eosinophils are present in inflamed rheumatoid synovial tissue and sites of cartilage erosion in SLE and other autoimmune conditions&#44; including rheumatoid arthritis&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">8</span></a></p></li><li class="elsevierStyleListItem" id="lsti0030"><span class="elsevierStyleLabel">6&#46;</span><p id="par0045" class="elsevierStylePara elsevierViewall">Patients with SLE have higher risk of acute MI compared with non-SLE controls&#44; and this risk is more significant in females&#46; In addition&#44; SLE is an independent risk factor for post-acute MI mortality&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">9</span></a></p></li><li class="elsevierStyleListItem" id="lsti0035"><span class="elsevierStyleLabel">7&#46;</span><p id="par0050" class="elsevierStylePara elsevierViewall">Platelets bearing complement protein C4d &#40;P-C4d&#41; were initially determined to be specific for diagnosis of SLE and were later found to be associated with acute ischemic stroke in non-SLE patients&#46; P-C4d may identify a subset of SLE patients with a worse clinical prognosis and is associated with all-cause mortality and stroke in these patients&#46; P-C4d may be a prognostic biomarker as well as a pathogenic clue that links platelets&#44; complement activation&#44; and thrombosis&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">10</span></a></p></li><li class="elsevierStyleListItem" id="lsti0040"><span class="elsevierStyleLabel">8&#46;</span><p id="par0055" class="elsevierStylePara elsevierViewall">The R131 allele of the Fc gamma receptor IIa &#40;Fc&#947;RIIa&#41; is associated with SLE incidence and disease severity but also with coronary artery disease&#46; This finding implies that risk stratification of SLE patients and other high-risk patients with troponin-negative angina could be significantly improved by Fc&#947;RIIa genotyping&#46;<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">11</span></a></p></li><li class="elsevierStyleListItem" id="lsti0045"><span class="elsevierStyleLabel">9&#46;</span><p id="par0060" class="elsevierStylePara elsevierViewall">SLE nearly doubles mortality and event hazards in cardiovascular disease &#40;MI&#44; stroke&#44; or congestive heart failure&#41; compared to age- and sex-matched comparisons&#46; This raises research questions regarding delayed SLE diagnosis versus accelerated cardiovascular disease prior to SLE&#44; particularly in older-onset SLE&#46;<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">12</span></a></p></li><li class="elsevierStyleListItem" id="lsti0050"><span class="elsevierStyleLabel">10&#46;</span><p id="par0065" class="elsevierStylePara elsevierViewall">Cardiovascular events including acute MI and stroke in SLE patients are caused by multifactorial mechanisms&#44; including both traditional and disease-specific risk factors&#46; An overall evaluation with individual risk stratification based on both these features is important to correctly manage these patients in order to reduce negative outcomes&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">13</span></a></p></li></ul></p><p id="par0070" class="elsevierStylePara elsevierViewall">Consequently&#44; in order to elucidate the pathophysiology of the association of SLE and acute coronary syndromes and to discover potential therapeutic and preventive measures for acute coronary events&#44; a search for inflammatory cells and measurement of inflammatory cell mediators released from these cells should always be performed&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0075" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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