Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 60-year-old male was bitten by a venomous snake (Vipera ammodytes) and gradually developed signs of an allergic reaction including generalized itching, generalized rash, and chest discomfort. This was followed by severe retrosternal pain with electrocardiographic evidence of an inferior myocardial ischemia progressing to acute myocardial infarction. Cardiac enzymes and troponin, serum tryptase, and histamine were elevated. Coronary arteriography showed normal coronary arteries. This is a characteristic type I variant 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 reactions. This is the first report to show that viper bites can induce allergic angina and/or allergic myocardial infarction.
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PMID:Hypersersensitivity and Kounis syndrome due to a viper bite. 1661 60

Kounis syndrome is the concurrence of acute coronary syndromes with conditions associated with activation of interacting inflammatory cells including allergic or hypersensitivity and anaphylactic or anaphylactoid insults. It is caused via inflammatory mediators released during inflammatory cell activation. A variety of conditions, drugs, and environmental exposures can induce Kounis syndrome. A patient suffering from coronary artery disease and taking metoprolol and aspirin was stung by wasps and developed cutaneous allergic signs including rash, urticaria and orbital oedema. This was followed by retrosternal pain, chest discomfort and electrocardiographic changes compatible with acute myocardial ischemia. Cardiac enzymes, troponins and blood pressure remained normal but serum tryptase was raised. The clinical implications and pathophysiology of this rare association are discussed.
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PMID:Hymenoptera sting-induced Kounis syndrome: effects of aspirin and beta-blocker administration. 1709 68

A 38-year-old cocaine abuser was admitted to the Emergency Department with a one hour history of precordial chest pain associated with shortness of breath and extreme discomfort. On admission his blood pressure was 90/60 mmHg, the resting 12-lead ECG showed ventricular tachycardia at about 300 beats per minute, and oxygen saturation was 86 percent in room air. After electrical cardioversion, the 12-lead ECG revealed sinusal rhythm and a significative ST segment elevation in leads I, aVL and V1-V6, that was about 0.5 mV in leads I and aVL and more than 1 mV in leads V2, V3 and V4. Laboratory determinations showed elevated creatine-chinase MB (CK-MB) and troponin I. An emergency coronary angiogram was normal. Cocaine use is a major cause of acute myocardial infarction in patients with normal epicardial coronary arteries but the exact mechanism still remains unclear. We hypothesize a non-IgE mediated mast-cell activation, with a direct action played by cocaine, and consequent massive expression of several factors effecting the microcirculatory system, including pro-inflammatory cytokines and chemokines. Our hypothesis is supported by an elevated serum tryptase levels in the patient.
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PMID:High serum tryptase value in massive acute myocardial infarction with ventricular arrhythmia exortion in a cocaine abuser. 1950 5