Histamine fish poisoning and acute coronary syndrome.

Introduction: Histamine fish poisoning (scombroid poisoning) is a foodborne disease caused by histamine toxicity that results from eating specific types of spoiled fish. This syndrome, typically benign, such an allergic reaction, in some cases, can lead to development of life-threatening anaphylactic reactions or acute organ involvements, such as acute coronary syndrome. Acute coronary syndrome, resulting from allergic reaction or pseudo-allergic reaction like histamine fish poisoning, also referred to Kounis syndrome, was rarely described and not completely understood. Case report: A 22 year-old woman presented mild itching, nausea, diaphoresis and weakness, after eating a meal with canned tuna. Within 30 minutes, her symptoms intensified, she develops headache and sweating, she also became pale, and her forehead, chin and neck were erythematous. Admitted to the hospital, in emergency department, her clinical exam was unremarkable. The patient had a past medical history with reported foods intolerances, without any cardiovascular risk. She reported that canned tuna was homemade, and that it had remained open for several days. Laboratory parameters and chest X ray were normal. Electrocardiogram reveals sinus tachycardia, normal atrioventricular conduction. It was been administered O2 insufflation, volume expanders, hydrocortisone 1 mg/kg IV and H1- H2 antihistamines, (diphenhydramine 2 mg/kg and ranitidine 1 mg/kg IV) with improvement of clinical outcomes. Her facial erythema was subsided. Within one hour after the meal, she developed chest retrosternal constrictive pain with a feeling of impending doom, became hypotensive (BP 70/30 mmHg) with shortness of breath and a recurrence of urticarial plaques in her forehead. It was been administered epinephrine IM in escalating dose, oxygen therapy with advanced oxygen managment. Another Electrocardiogram was suggestive of subendocardial ischemia in infero-anterior-lateral leads. Bedside echocardiography shown apical and infero-antero septal ipokinesis. Increase in myocardial necrosis biomarkers values: TroponinI 2 ng/ml; Creatine kinase-MB 19 ng/ml; and Myoglobin 212 ng/ml. We started the administration of aspirin, low-molecular-weight heparin. Admitted in CCU, emergency coronary angiography promptly performed with normal findings at epicardial arteries. Allergic or hypersensitivity reactions may have been involved in this clinical presentation, as a trigger for vasospastic reaction. High histamine concentration was found in tuna leftover (> 5000 ppm). No other pathogens were isolated. On the third day, electrocardiogram and echocardiographic study shown normal pattern, as well as values of myocardial necrosis biomarkers. The patient was discharged on the sixth day, asymptomatic. Conclusion: In this case, a patient with normal coronary arteries, after an acute release of inflammatory mediators develops coronary artery spasm progressing to acute myocardial infarction with raised cardiac enzymes and troponins. This syndrome can represent a life threatening, if not promptly and early known. There is not a gold standard in pharmacological treatment, but antihistamines drugs represent first line treatment in this case. Cardiologists must have this knowledge, because only circumspect anamnesis can lead to correct and prompt diagnosis and maybe safe a life.