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Type 1 Kounis-syndrome: case reportA 38-year-old man developed type 1 Kounis syndrome during treatment with paracetamol for infectious diarrhoea [dosage and exact time to reaction onset not stated].The man, who consumed raw foods, presented to a rural hospital with a 3-days history of lightheadedness, stomachache, diarrhoea and blood stains. He was admitted with a diagnosis of infectious diarrhoea. His medical history included heavy smoking, diabetes and hyperlipidaemia. Upon admission, he started receiving treatment with paracetamol infusion, and shortly thereafter, he experienced hypotension, chest discomfort and dyspnoea. Electrocardiogram revealed posterior and anterolateral ST elevation and depressed ST segments in leads aVR, V1, V2, V3, V3R, V4R with no q waves. His hs-Troponin T level was noted to be elevated. Other tests were unremarkable. A diagnosis of acute myocardial infarction was made, and he was referred to another hospital. A repeat electrocardiogram was performed, 6h after the angina attack, which showed no ST-T alterations, sinus rhythm with no q waves at any of the leads. The blood concentrations of D-dimer and hs-Troponin T were noted to be increased. The diagnosis of type 1 Kounis syndrome was confirmed, and he was referred to other cardiology centre. On arrival to hospital (12h after the angina attack) his EKG was observed to be negative, along with normal transthoracic echocardiography. He was admitted for planned coronary angiography. The left ventricular function was 71%, and no pericardial effusion was observed. The blood IgE concentration was found to be increased. Coronary angiography findings showed no stenosis, right coronary dominance and no wall motion abnormalities in left ventriculography. He was then discharged with an uneventful hospital course.
Type 1 Kounis-syndrome: case reportA 38-year-old man developed type 1 Kounis syndrome during treatment with paracetamol for infectious diarrhoea [dosage and exact time to reaction onset not stated].The man, who consumed raw foods, presented to a rural hospital with a 3-days history of lightheadedness, stomachache, diarrhoea and blood stains. He was admitted with a diagnosis of infectious diarrhoea. His medical history included heavy smoking, diabetes and hyperlipidaemia. Upon admission, he started receiving treatment with paracetamol infusion, and shortly thereafter, he experienced hypotension, chest discomfort and dyspnoea. Electrocardiogram revealed posterior and anterolateral ST elevation and depressed ST segments in leads aVR, V1, V2, V3, V3R, V4R with no q waves. His hs-Troponin T level was noted to be elevated. Other tests were unremarkable. A diagnosis of acute myocardial infarction was made, and he was referred to another hospital. A repeat electrocardiogram was performed, 6h after the angina attack, which showed no ST-T alterations, sinus rhythm with no q waves at any of the leads. The blood concentrations of D-dimer and hs-Troponin T were noted to be increased. The diagnosis of type 1 Kounis syndrome was confirmed, and he was referred to other cardiology centre. On arrival to hospital (12h after the angina attack) his EKG was observed to be negative, along with normal transthoracic echocardiography. He was admitted for planned coronary angiography. The left ventricular function was 71%, and no pericardial effusion was observed. The blood IgE concentration was found to be increased. Coronary angiography findings showed no stenosis, right coronary dominance and no wall motion abnormalities in left ventriculography. He was then discharged with an uneventful hospital course.
Background: Kounis syndrome is defined as a combination of acute coronary syndrome and allergic reactions. Objective: In this review, we aim to describe the etiological, clinical, and diagnostic characteristics of Kounis syndrome. Methods: A literature search using PubMed was conducted for the past 32 years using keywords, resulting in the selection of 761 scientific papers. From these, 217 articles describing 235 clinical cases were selected. Patients under 18 years of age or without a confirmed diagnosis were excluded. Results: Among the 235 patients, type I Kounis syndrome was observed in 49.7%, type II in 27.2%, type III in 5.9%, and a combination of types I and II in 1.0%; in 16.2%, it was not possible to classify the type of Kounis syndrome. The median age was 57 years, and 68.5% of the patients were male. The most common causes were antibiotics (32.3%) and non-steroidal anti-inflammatory drugs (24.3%). The clinical features included chest pain (59.1%), hypotension (74.2%), itching (30.6%), and dyspnea (30.6%). Electrocardiographic monitoring revealed ST-segment elevation in 42.9% and was normal in only 5.5% of patients. Coronary angiography was performed in 80.4% of the patients, revealing unchanged coronary arteries in 50.3% of cases. Сonclusion: Allergic myocardial infarction is a serious complication of drug therapy
Kounis syndrome is a multisystem and multidisciplinary disease affecting the circulatory system that can be manifested as spasm and thrombosis. It can occur as allergic, hypersensitivity, anaphylactic, or anaphylactoid reactions associated with the release of inflammatory mediators from mast cells and from other interrelated and interacting inflammatory cells, including macrophages and lymphocytes. A platelet subset with high- and low-affinity IgE surface receptors is also involved in this process. Whereas the heart, and particularly the coronary arteries, constitute the primary targets of inflammatory mediators, the mesenteric, cerebral, and peripheral arteries are also vulnerable. Kounis syndrome is caused by a variety of factors, including drugs, foods, environmental exposure, clinical conditions, stent implantation, and vaccines. We report a unique case of a 60-year-old male with a past medical history of allergy to human albumin, alcoholic cirrhosis, and esophageal varices, who was admitted due to multiple episodes of hematemesis. Due to low hemoglobin levels, he was transfused with 3 units of red blood cells and fresh frozen plasma without any adverse reactions. On the third day of hospitalization, severe thrombocytopenia was observed and transfusion of platelets was initiated. Immediately following platelet infusion, the patient developed chest discomfort, skin signs of severe allergic reaction, and hemodynamic instability. The electrocardiogram revealed ST segment elevation in the inferior leads. Given the strong suspicion of Kounis syndrome/allergic coronary spasm, the patient was treated with anti-allergic treatment only, without any anti-platelet therapy. The clinical status of the patient gradually improved and the electrocardiographic changes reverted to normal. Based on these findings, Kounis hypersensitivity-associated acute coronary syndrome, specifically, type I Kounis syndrome, was diagnosed. Although platelet transfusion can be a life-saving therapy, each blood transfusion carries a substantial risk of adverse reactions. The aims of this report are to expand the existing knowledge of patient responses to blood transfusion and provide information on the incidence of various severe transfusion reactions to all blood components and especially to platelets. To the best of our knowledge, Kounis syndrome induced by platelet transfusionhas never been previously reported. Hypersensitivity to platelet external membrane glycoproteins in an atopic patient seems to be the possible etiology. Despite that Kounis syndrome remains an under-diagnosed clinical entity in everyday practice, it should always be considered in the differential diagnosis of acute coronary syndromes.
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