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Kounis syndrome: first series in Turkish patients.

After the first report of acute myocardial infarction during a prolonged allergic reaction to penicillin was published in 1950 (1), the concurrence of allergic reactions and acute coronary syndromes called Kounis syndrome (KS) has gained acceptance as a new cause of coronary artery spasm (1-3). Kounis Syndrome was firstly described in 1991 as “the allergic angina syndrome” which could progress to acute myocardial infarction, which was named “allergic myocardial infarction” (2-4). There are several causes that have been reported as capable of inducing KS (5). These include a number of drugs (antibiotics, analgesics, antineoplastics, contrast media, corticosteroids, intravenous anesthetics, nonsteroidal anti-inflammatory drugs, skin disinfectants, thrombolytics, anticoagulants, proton pump inhibitors), various conditions (angio-edema, bronchial asthma, urticaria, food allergy, exercise induced allergy, mastocytosis, serum sickness), and environmental exposures (stings of ants, bees, wasps, jellyfish, grass cutting, millet allergy, poison ivy, latex contact, shellfish eating, viper venom poisoning). In this report, we describe 6 patients (5 male, average age 27.7 years) with KS who were admitted or referred to our hospital in the last two years with acute-onset chest pain, accompanied by allergic symptoms, electrocardiographic changes and elevated cardiac enzymes. The characteristics of the patients who developed KS are given in Table 1. Our patients consisted of 4 children and 2 adults, presented with acute-onset chest pain, accompanied by allergic symptoms, electrocardiographic changes and elevated cardiac enzymes. The reasons of KS were drugs in four, bee sting in one and wasp sting in the other patient. They did not have previous history of allergy, bronchial asthma, dermatitis, eczema, diabetes or coronary artery disease. Complete blood count, D-dimer, antithrombin III, lipoprotein (a), brain natriuretic peptide, serum cholesterol levels, antistreptolysin-O (ASO) titer, C3 and C4 levels and antinuclear antibody, anti-DNA tests were within normal limits. The serologic tests for viral etiology were also negative. Echocardiographic examination and coronary angiography was performed in all patients. While echocardiography showed segmental wall motion abnormality, coronary angiography revealed normal coronary arteries in first five patients and non-critical plaques in the left anterior descending and circumflex arteries in the sixth patient. Kounis syndrome is characterized by the concurrence of acute coronary syndrome with mast cell activation induced by inflammatory mediators released during allergic reaction (5). Mast cell degranulation follows after antibody antigen reaction or sometimes direct action against the mast cell can happen (6, 7). Following mast cell degranulation several vasoconstricting and collagen degrading compounds are released locally and in the peripheral circulation. These compounds include preformed mediators such as, histamine, neutral proteases (tryptase, chymase), platelet activating factor and newly synthesized mediators such as an array of cytokines and chemokines and others by the metabolism of arachidonic acid through activation of a phospholipase (6, 7). Tryptase level, which has a half-life of 90 minutes, was elevated in all patients. However, subsequent daily estimations of serum tryptase were within normal limits. The increased levels of tryptase suggest an acute allergic reaction, where tryptase has been incriminated to induce coronary artery spasm and/or plaque erosion or rupture (5, 7). Total immunoglobulin (Ig) E levels were also elevated in four patients. Amoxicillin spesific IgE antibodies were negative in the second patient, but it does not exclude mast cell degranulation because as above-mentioned, sometimes direct action against the mast cell can happen (7). This applies especially for drugs. Hymenoptera venoms mainly contain peptides, proteins, and vasoactive amines including histamine, acetylcholine, norepinephrine and dopamine (8). These substances are responsible for direct venom cardiotoxicity and several of the proteins and peptides are allergenic. The major allergen of honeybee venom is phospholipase A2. Other allergens include