A Case of Type I Kounis Syndrome Caused by Double Allergens
Kounis syndrome, first described in 1991 by Kounis and Zavras, is a condition characterized by acute coronary syndrome (ACS) triggered by allergic reactions. It is caused by the activation and degranulation of mast cells in the heart, leading to coronary artery spasm, myocardial ischemia, or even myocardial infarction. The syndrome is classified into three types based on clinical presentation and underlying coronary pathology. This article presents a detailed case report of a 42-year-old man diagnosed with type I Kounis syndrome, highlighting the role of double allergens in its pathogenesis.
The patient, a 42-year-old Chinese man, experienced a brief loss of consciousness while cycling outdoors after being stung by a bee on his nasal root. He fell and sustained head trauma, following which he was rushed to the emergency room. Upon arrival, he exhibited symptoms of anaphylactic shock, including sweating, dizziness, headaches, chest tightness, shortness of breath, and urinary incontinence. His blood pressure was critically low at 74/47 mmHg, blood oxygen saturation was reduced to 81%, and his pulse rate was elevated to 149 beats per minute. Physical examination revealed mental confusion, bilateral pupil diameter of 3 mm with slight insensitivity to light, and a rigid abdomen. Immediate treatment with 25 mg promethazine and 10 mg dexamethasone was administered.
The patient had no prior history of cardiovascular disease or related risk factors. However, he had a history of bee stings without any significant complications in the past. An electrocardiogram (ECG) showed sinus tachycardia (152 beats per minute), ST-segment depression in leads II-III, and ST-segment elevation in lead aVR. Echocardiography and chest X-ray revealed no abnormalities. Laboratory tests indicated a white blood cell count of 17.06 × 10^9/L (normal range: 3.5–9.5 × 10^9/L), an elevated eosinophil count of 0.73 × 10^9/L (normal range: 0.02–0.52 × 10^9/L), and increased levels of creatine kinase-MB (CK-MB) at 29.5 ng/L (normal range: 0–5 ng/L). Cardiac troponin I levels were within the normal range (<0.5 ng/mL), but myoglobin levels were significantly elevated at 249.1 ng/mL (normal range: 0–70 ng/mL). Coronary angiography showed no significant abnormalities.
Further investigation by a dermatologist included specific immunoglobulin E (S-IgE) tests, which revealed a high sensitivity to a tree combination (willow/poplar/elm) with an S-IgE level of 11.4 kU/L (normal range: 0–0.35 kU/L). The patient’s condition improved after the administration of anti-allergy medications and fluid infusion, and follow-up ECGs and myocardial enzyme levels normalized. The patient was advised to avoid exposure to allergens, and no similar episodes were reported during a one-year follow-up period.
Kounis syndrome is classified into three types. Type I, as seen in this case, occurs in patients with no prior coronary artery disease. The acute release of inflammatory mediators, such as histamine, leukotrienes, and cytokines, induces coronary artery spasm, leading to angina or myocardial infarction. Coronary angiography typically shows no significant abnormalities, and the condition is primarily driven by an allergic mechanism. Type II Kounis syndrome occurs in patients with pre-existing coronary artery disease, where allergic reactions exacerbate underlying atherosclerotic lesions, leading to plaque rupture or thrombosis. Type III is associated with stent thrombosis in patients who develop anaphylaxis after coronary stenting.
The pathogenesis of Kounis syndrome involves the activation of mast cells, which release a cascade of inflammatory mediators. These mediators cause coronary artery spasm, endothelial dysfunction, and platelet activation, leading to myocardial ischemia. The condition can be triggered by various factors, including physical stimulation, mental stress, foods, drugs, chemical agents, and insect venom. In this case, the patient’s exposure to two allergens—bee venom and tree pollen—likely contributed to the development of Kounis syndrome.
The patient’s history of bee stings without prior complications suggests that the combination of allergens played a critical role in triggering the syndrome. The onset occurred during spring, a season when willow and poplar trees release pollen, and the patient’s S-IgE levels indicated a high sensitivity to these allergens. The simultaneous exposure to bee venom and tree pollen likely caused a severe allergic reaction, leading to mast cell activation and subsequent coronary artery spasm.
Treatment of Kounis syndrome requires a combination of anti-allergic and anti-thrombotic therapies. Corticosteroids, histamine H1- and H2-receptor blockers, and vasodilators are commonly used to manage the allergic component, while antiplatelet agents and anticoagulants address the thrombotic risk. In this case, the prompt administration of promethazine and dexamethasone, along with fluid resuscitation, effectively managed the patient’s symptoms and prevented further complications.
The rarity of Kounis syndrome and its overlap with ACS often lead to underdiagnosis or misdiagnosis. Healthcare professionals should maintain a high index of suspicion for Kounis syndrome in patients presenting with ACS symptoms and a history of allergic reactions or exposure to potential allergens. Early recognition and appropriate management are crucial to improving patient outcomes.
In conclusion, this case highlights the importance of considering Kounis syndrome in patients with ACS symptoms and a history of allergic exposure. The combination of bee venom and tree pollen as double allergens underscores the complex interplay between allergic reactions and cardiovascular pathology. Increased awareness and understanding of Kounis syndrome among healthcare professionals are essential for timely diagnosis and effective management.
doi.org/10.1097/CM9.0000000000000684
Was this helpful?
0 / 0