食物相关Kounis综合征：来自一例病例报告及已发表病例系统定性综合的临床谱与诊断考量。
完整摘要 · 中文译文
库尼斯综合征（Kounis syndrome，KS）是一种与超敏反应相关的急性冠脉综合征。与食物相关的KS仍缺乏充分描述，且其临床表现可能被非免疫性食物相关毒性反应所模拟。旨在描述食物相关KS中所报告的食物暴露情况、临床与心血管表现、变态反应学评估、潜在协同因素、KS表型、处理方式及预后。检索了PubMed、Scopus和Web of Science核心合集，检索时间从建库至2026年8月22日。纳入原始病例报告、病例系列及信息量足够的会议报告，这些报告描述了与食物或食物源性暴露时间相关的客观冠状动脉受累情况。对患者层面数据进行了定性综合。分别评估了KS诊断确定性、冠状动脉表型、食物因果关系及推定机制。计划中的敏感性分析将综合范围限制于确诊或疑似食物过敏、明确或可能KS，以及冠状动脉发病或首次客观记录前未使用肾上腺素的患者。综合共纳入50篇出版物或报告，涉及53例独特患者。食物相关机制包括：20例确诊食物过敏，26例临床疑似食物过敏，6例鲭鱼中毒，1例墨汁鬼伞（Coprinopsis atramentaria）与酒精相互作用。所报告的冠状动脉表现谱系从一过性血管痉挛和非阻塞性表现，到斑块相关性心肌梗死、原位冠状动脉血栓形成，以及支架或桥血管血栓形成。I型最为常见。 频繁指定的表型。过敏学评估、急性期与基线类胰蛋白酶配对测量、治疗时间顺序及长期随访的报告不一致。主要心血管模式在预设的敏感性分析中保持广泛一致。食物相关KS涵盖了过敏性冠脉表现的异质性谱系。临床上相似的非免疫性食物相关毒性反应，包括鲭鱼中毒，应被识别为鉴别诊断，并与真正的过敏性KS分开分析。诊断需整合暴露时间顺序、客观心血管发现、冠脉基础病变、过敏学证据、潜在协同因素及竞争性暴露。肌注肾上腺素仍是过敏反应的一线治疗，时间上的先后关系不应被解释为肾上腺素导致冠脉事件的证据。
完整摘要 · 英文原文
Kounis syndrome (KS) is a hypersensitivity-associated acute coronary syndrome. Food-associated KS remains poorly characterized, and its clinical presentation may be mimicked by non-immune food-related toxic reactions. To characterize the food exposures, clinical and cardiovascular presentations, allergological assessment, potential cofactors, KS phenotypes, management, and outcomes reported in food-associated KS. PubMed, Scopus, and Web of Science Core Collection were searched from inception to August 22, 2026. Original case reports, case series, and sufficiently informative conference reports describing objective coronary involvement temporally associated with a food or food-derived exposure were included. Patient-level data were synthesized qualitatively. KS diagnostic certainty, coronary phenotype, food causality, and presumed mechanism were assessed separately. Planned sensitivity analyses restricted the synthesis to confirmed or suspected food allergy, definite or probable KS, and cases without epinephrine administration before coronary onset or its first objective documentation. The synthesis included 50 publications or reports describing 53 unique patients. Food-related mechanisms comprised confirmed food allergy in 20 patients, clinically suspected food allergy in 26, scombroid poisoning in six, and a Coprinopsis atramentaria-alcohol interaction in one. The reported coronary spectrum ranged from transient vasospasm and nonobstructive presentations to plaque-related myocardial infarction, native-coronary thrombosis, and stent or graft thrombosis. Type I was the most frequently assigned phenotype. Allergological assessment, paired acute and baseline tryptase measurements, treatment chronology, and long-term follow-up were inconsistently reported. The main cardiovascular patterns remained broadly consistent across the planned sensitivity analyses. Food-associated KS encompasses a heterogeneous spectrum of allergic coronary presentations. Clinically similar non-immune food-related toxic reactions, including scombroid poisoning, should be recognized as differential diagnoses and analyzed separately from true allergic KS. Diagnosis requires integration of exposure chronology, objective cardiovascular findings, coronary substrate, allergological evidence, potential cofactors, and competing exposures. Intramuscular epinephrine remains the first-line treatment for anaphylaxis, and temporal precedence should not be interpreted as evidence that epinephrine caused the coronary event.