Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hymenoptera stings can induce acute coronary syndromes by different pathogenetic mechanisms including direct action of the venom constituents on the coronary endothelium or allergic reaction with mediators acting on the coronary vasculature. Two patients were stung by wasps and honeybees and developed Kounis syndrome as a consequence of allergic reaction. Kounis syndrome is the concurrence of acute coronary syndromes with mast cell activation induced by allergic or hypersensitivity and anaphylactic of anaphylactoid reactions. It is caused via inflammatory mediators released through mast cell activation. The patients had pre-existing coronary artery disease (type II variant of Kounis syndrome) and the allergic reaction induced by hymenoptera stings seems to have triggered inflammatory mediator release. The pathophysiology and clinical implications of this association are discussed.
Int J Cardiol 2007 Jan 08
PMID:Kounis syndrome associated with hypersensitivity to hymenoptera stings. 1664 68

The inflammatory cytokine tumor necrosis factor alpha (TNFalpha) is controversially discussed in ischemia/reperfusion damage of the heart. Purpose of this study was to elucidate cellular sources of TNFalpha and parameters which possibly influence its release in the heart following ischemia. Isolated hearts of mice were subjected to 15 min of global ischemia and 90 min of reperfusion. We employed hearts of various mice knock-out strains (interleukin-6(-/-), matrix metalloprotease-7(-/-), mast-cell deficient WBB6F1-Kit(W)/Kit(W-v), TNF-R1(-/-)) and wildtype mice, the latter perfused without and with infusion of cycloheximide or TNFalpha-cleaving-enzyme inhibitor (TAPI-2). Normoxic control hearts showed basal release of TNFalpha during the whole experiment. Immunohistology identified cardiac mast cells, macrophages and endothelial cells as main sources. TNFalpha release was stimulated during postischemic reperfusion, occurring in a two-peak pattern: directly after ischemia (0-10 min) and again after 60-90 min. The first peak mainly reflects tissue washout of TNFalpha accumulated during ischemia. The second, protracted peak arose continuously from the basal level and was abolished by protein synthesis inhibitor cycloheximide. Both properties are characteristic for de novo synthesis of TNFalpha, e.g., in cardiac muscle cells. However, immunohistological staining for TNFalpha failed in cardiomyocytes after 90 min of reperfusion. In contrast to hearts of TNF-R1(-/-) and Kit(W/W-v)-mice, those of IL-6(-/-) and MMP-7(-/-) mice lacked the late TNFalpha peak. TAPI did not suppress release of TNFalpha. While autostimulation via TNF-R1 also does not seem obligatory and mast cell can be ignored as source of the second peak, IL-6 may support de novo synthesis of TNFalpha. Additionally, TNFalpha release may essentially involve cleavage of membrane bound TNFalpha by MMP-7.
J Mol Cell Cardiol 2007 Jan
PMID:Insights from knock-out models concerning postischemic release of TNFalpha from isolated mouse hearts. 1710 Nov 48

A 70-year-old man experienced an amoxycillin-induced anaphylactic reaction complicated by acute inferior myocardial infarction with transient ST-segment elevation. There was a spontaneous resolution of ST-segment elevation and the patient was treated for anaphylaxis. Coronary angiography showed severe obstructive coronary atherosclerosis, but not involving the infarct-related artery. Percutaneous coronary intervention of the affected artery was then performed and the patient was discharged three days later. Acute ST-elevation myocardial infarction has been described as one of the severe, still rare cardiovascular complications of anaphylaxis. In the present case, according to the previous reports, the main pathogenetic mechanism involved appears to have been coronary vasospasm probably caused by the release of potent vasoactive mast cell derived mediators in the setting of anaphylaxis.
Int J Cardiol 2007 Apr 12
PMID:Acute ST-segment elevation myocardial infarction complicating amoxycillin-induced anaphylaxis: a case report. 1730 66

Myocardial injury and acute coronary syndrome have been rarely associated with amoxicillin/clavulanic acid intake. The responsible pathogenetic mechanism is described by an amplified mast cell degranulation inducing coronary artery spasm and/or acute myocardial infarction in susceptible individuals which is called Kounis syndrome. We report here a case of Kounis syndrome presented with acute coronary syndrome due to amoxicillin/clavulanic acid use. All other etiologies, including ischemic reinfarction were appropriately ruled out.
Int J Cardiol 2008 Feb 20
PMID:Kounis syndrome secondary to amoxicillin/clavulanic acid use. 1770 99

The use of drug-eluting stents (DES) for the treatment of coronary stenosis has increased sharply and now accounts for more than 75% of all coronary stents utilized. However, concern has been increasing that DES could be associated with stent thrombosis, paradoxical coronary vasoconstriction, and hypersensitivity reactions. Components of currently used DES have been reported to induce, either separately or synergistically, hypersensitivity reactions and possibly lead to cardiac events. DES-activated intracoronary mast cells could release histamine, arachidonic acid metabolites, proteolytic enzymes, as well as a variety of cytokines, chemokines, and platelet-activating factor (PAF) leading to local inflammation and thrombosis. These events may be more common than suspected because it is hard to document them, unless they become systemic, in which case they manifest themselves as the "Kounis syndrome," characterized by the concurrence of acute coronary events with hypersensitivity reactions. Recognition of this problem may lead to better vigilance, as well as new DES with mast cell blocking molecules that may also be disease modifying.
J Interv Cardiol 2007 Oct
PMID:Coronary stents, hypersensitivity reactions, and the Kounis syndrome. 1788 Mar 27

A patient with severe coronary disease, who underwent inguinal hernia repair, suffered a cardiovascular collapse after anaesthetic induction and died. He had Kounis syndrome, which is the concurrence of acute coronary syndrome (ACS) with conditions associated with mast cell activation. We measured the serum tryptase level in this patient and in a group of ten other patients admitted to hospital with the diagnosis of ACS with ST elevation in order to determine the origin of these events.
Int J Cardiol 2009 Jan 24
PMID:Serum tryptase levels in acute coronary syndromes with ST elevation. 1798 53

Acute coronary syndromes have been described as potential complications of any type of anaphylactic reaction. The real pathogenic mechanism inducing acute myocardial ischemia in the setting of anaphylaxis is not yet completely understood. Some pathogenic mechanisms, like coronary vasospasm, plaque activation and systemic hypotension, have been suggested. The hypothesis of a central role of mast cell and inflammatory cell activation and release of potent vasoactive mediators, inducing the mechanisms mentioned above, is the mainstay of so-called "cardiac anaphylaxis". We report two cases of anaphylaxis-induced acute ST-segment elevation myocardial ischemia which occurred during coronary angiography. The first one was probably related to contrast media contact, the second one to latex glove contact. Both of them were treated with percutaneous coronary intervention that immediately resolved the myocardial ischemia.
J Invasive Cardiol 2008 Mar
PMID:Anaphylaxis-induced acute ST-segment elevation myocardial ischemia treated with primary percutaneous coronary intervention: report of two cases. 1831 36

Kounis syndrome is the concurrence of acute coronary syndromes with conditions associated with mast cell activation including allergic or hypersensitivity and anaphylactic or anaphylactoid insults. We present a case of acute myocardial infarction associated with an allergic reaction in a 73-year-old Italian woman with recent implantation of stents.
Int J Cardiol 2009 May 15
PMID:Acute myocardial infarction and Kounis syndrome. 1837 25

Mast cells have diverse roles throughout the body as evidenced by their heterogeneous nature. In the heart, cardiac mast cells have been implicated in left ventricular (LV) remodeling in response to elevated myocardial stress. Accordingly, the purpose of this study was to use mast cell deficient rats (Ws/Ws) to delineate the interaction between cardiac mast cell activation and LV remodeling. LV matrix metalloproteinase (MMP) activity, fibrillar collagen, TNF-alpha levels, and LV diameter were compared in Ws/Ws and wild type (WT) rats subjected to 5 d (n=3/group) and 8 weeks (n=4/group) of aortocaval fistula-induced volume overload. In contrast to attenuation of myocardial remodeling in the Ws/Ws group: 1) MMP-2 activity was significantly increased in the WT group at 5 days; 2) there was marked degradation of the extracellular collagen matrix in WT at 5 days and 8 weeks; 3) the percent increase in LV diameter from baseline was significantly greater in WT at 2, 4, 6, and 8 weeks post-fistula; and 4) myocardial TNF-alpha levels were markedly elevated in the WT group at 5 days post-fistula. These results underscore the importance of cardiac mast cells in mediating MMP activation, collagen degradation and LV dilatation and suggest that mast cell-derived TNF-alpha plays a role in early myocardial remodeling.
J Mol Cell Cardiol 2008 Jul
PMID:Protection from adverse myocardial remodeling secondary to chronic volume overload in mast cell deficient rats. 1853 42

A 58-year-old man with no history of cardiac diseases or cardiovascular risk factors was stung by honeybees. Soon after, he gradually developed signs of an allergic reaction followed by severe retrosternal pain. Electrocardiographic, echocardiographic evidence and positive biochemical markers were consistent with an acute anterolateral myocardial infarction. Coronary arteriography showed a left anterior descending artery thrombotic lesion. This is a case of Kounis syndrome, which is the concurrence of acute coronary syndromes with conditions associated with mast cell activation including allergic or hypersensitivity reactions as well as anaphylactic or anaphylactoid insults. The clinical implications and pathophysiology of this dangerous association are discussed.
Int J Cardiol 2009 May 29
PMID:Acute anterior myocardial infarction after multiple bee stings. A case of Kounis syndrome. 1855 34


<< Previous 1 2 3 4 5 Next >>