First Report of Moxifloxacin-Induced Type II Kounis Syndrome: A Case Study and Comprehensive Literature Review

doi:10.21203/rs.3.rs-5232115/v1

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Case Report

First Report of Moxifloxacin-Induced Type II Kounis Syndrome: A Case Study and Comprehensive Literature Review

https://doi.org/10.21203/rs.3.rs-5232115/v1

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Background

Kounis syndrome is a distinct form of acute coronary syndrome that is precipitated by allergic or hypersensitivity reactions. Although this syndrome is infrequently observed in clinical practice, it can result in severe cardiovascular events and represents a significant threat to patient life when it occurs. Consequently, enhancing the understanding, diagnosis, and management of this condition is essential. We present a case of Type II Kounis syndrome induced by intravenous moxifloxacin.

Case Summary

A 71-year-old female patient with no prior history of coronary artery disease developed hypotension and chest pain thirty minutes after the intravenous administration of moxifloxacin. Electrocardiography revealed T-wave inversion in leads I and aVL, accompanied by elevated levels of troponin I. Coronary angiography indicated 80% stenosis in the mid-segment of the left anterior descending artery (LAD), 99% stenosis at the ostium of the diagonal branch, and localized 60% stenosis in the proximal segment of the left circumflex artery (LCx). Subsequent echocardiography demonstrated segmental wall motion abnormalities, with a left ventricular ejection fraction (LVEF) of 52%. The diagnosis was moxifloxacin-induced Type II Kounis syndrome, presenting as acute non-ST-segment elevation myocardial infarction.

Conclusion

Kounis syndrome is a potentially life-threatening emergency that necessitates prompt intervention. Although primarily documented in case studies, the actual incidence of Kounis syndrome may be underreported. Clinicians should remain vigilant for the possibility of allergic reactions in patients presenting with acute coronary syndrome (ACS). For patients with known allergies, particularly those suspected of experiencing systemic allergic reactions, it is crucial to monitor for cardiac symptoms, perform electrocardiograms, conduct cardiac enzyme tests, and, if indicated, carry out coronary angiography. Early recognition and appropriate management of Kounis syndrome can significantly enhance patient prognosis.

Moxifloxacin

Kounis Syndrome

Allergy

Acute coronary syndrome

clinical case

Kounis syndrome is a rare yet severe allergic coronary condition typically triggered by allergic or hypersensitivity reactions. It is characterized by coronary artery spasm or acute coronary syndrome induced by these reactions, which may manifest as angina, myocardial infarction, or even life-threatening arrhythmias. Kounis syndrome represents a distinct type of acute vascular syndrome that affects the coronary, cerebral[1, 2], mesenteric[2], peripheral[3], and venous systems[], all precipitated by allergic or hypersensitive reactions. Although infrequently diagnosed, clinical practice necessitates a high degree of suspicion for this syndrome. When diagnosed, it can lead to serious cardiovascular events that significantly endanger the patient's life. Therefore, enhancing the understanding, diagnosis, and management of this condition is crucial. This paper presents a case of Kounis syndrome and reviews its epidemiology, etiology, pathogenesis, diagnostic methods, and treatment strategies to raise awareness and improve management of this condition among clinicians.

A 71-year-old woman was admitted to the hospital on February 23, 2024, with complaints of fever and fatigue lasting for five days, which had worsened over the preceding day. Initially, she experienced a fever of 38.5°C, fatigue, muscle and joint aches, and a loss of appetite, but reported no respiratory symptoms. After self-administering oseltamivir, her symptoms temporarily improved. However, the day before admission, she felt increasingly fatigued, and her body temperature rose to 37.5°C, prompting her to seek medical attention. Physical examination revealed a temperature of 37.6°C, blood pressure of 128/64 mmHg, heart rate of 89 beats per minute, and mild edema in both lower limbs. Her past medical history included hyperlipidemia, but there was no history of diabetes, hypertension, or coronary artery disease. Laboratory tests returned negative results for COVID-19 and influenza A and B viruses. Routine blood tests indicated a white blood cell count of 12.91*10^9/L (reference range: 4.5 ~ 9.5), a neutrophil percentage of 79.2% (reference range: 40 ~ 75), and a C-reactive protein (CRP) level of 21.67 mg/L (reference range: 0 ~ 10). The creatinine level was 69 µmol/L (reference range: 44 ~ 115). Cardiac enzyme levels were normal. The electrocardiogram showed sinus rhythm [Figure 1], and chest CT revealed inflammation in both lower lungs. She was diagnosed with community-acquired pneumonia and hyperlipidemia, and was treated with 0.4 g of intravenous moxifloxacin.

Thirty minutes after the intravenous administration of moxifloxacin, the patient reported experiencing chest pain localized behind the sternum, accompanied by left shoulder pain. Additionally, there was a significant drop in blood pressure to 80/56 mmHg. The heart rate was elevated at 114 beats per minute, and oxygen saturation (SpO2) fluctuated between 92% and 95%.Immediate treatment included intravenous dexamethasone and fluid resuscitation. An electrocardiogram (ECG) revealed sinus rhythm with T-wave inversion in leads I and aVL (see Fig. 2). Laboratory results indicated a Troponin I (TnI) level of 1.6 ng/ml (reference range: 0.010–0.023 ng/mL), suggesting the presence of acute coronary syndrome. The Killip classification for heart failure was determined to be Killip II, with a GRACE-II score of 164.

Immediate treatment included 300 mg of aspirin, 300 mg of clopidogrel, 20 mg of atorvastatin, and 0.4 ml of low-molecular-weight heparin calcium. Coronary angiography revealed 80% stenosis in the mid-segment of the LAD, 99% stenosis from the origin to the proximal segment of the first diagonal branch, and 60% focal stenosis in the proximal segment of the LCx.Balloon dilation angioplasty was conducted on the proximal LAD (see green arrow in Fig. 3), while drug-coated balloon dilatation angioplasty was performed from the origin of the first diagonal branch to its proximal end (see yellow arrow in Fig. 3). No residual stenosis was observed in the posterior vessels.The patient was transferred back to the ward with improved symptoms.

Echocardiography revealed segmental wall motion abnormalities, with a left ventricular ejection fraction (LVEF) of 52%. On the second postoperative day, the patient's repeat troponin and D-dimer tests returned normal values, and the electrocardiogram showed a return to baseline. The patient's condition was stable. Ongoing treatment focused on enhancing myocardial perfusion, stabilizing the plaque, administering antiplatelet therapy, switching antibiotics to cefuroxime, and providing antispasmodic and bronchodilator therapy. Six days later, the patient's condition stabilized, and he was discharged from the hospital. The discharge diagnosis included: (1) community-acquired pneumonia; (2) delayed drug allergic reaction (moxifloxacin) complicated by type II Kounis syndrome; (3) coronary atherosclerotic heart disease with acute non-myocardial infarction, specifically ST-segment elevation myocardial infarction, Killip grade II.

We report, for the first time, a case of acute coronary syndrome (ACS) triggered by an allergic reaction to moxifloxacin, a phenomenon known as Kounis syndrome, also referred to as allergic angina[5]. kounis syndrome is an acute coronary syndrome mediated by allergic mechanisms. First described by Kounis and Zavras in 1991, it involves mast cell activation, which can lead to conditions ranging from coronary artery spasm to myocardial infarction[6]. While most ACS cases are typically caused by the erosion or rupture of atherosclerotic plaques followed by thrombosis, kounis syndrome encompasses three main types[5].

Type I: Allergic coronary artery spasm occurs in patients without underlying coronary atherosclerotic disease, resulting in myocardial ischemia due to coronary artery spasm. This phenomenon is primarily attributed to the release of inflammatory mediators, such as histamine and tryptase, during an allergic reaction, which triggers the spasm.

Type II: Allergic Myocardial Infarction. In patients with pre-existing atherosclerotic coronary disease, allergic reactions can trigger plaque rupture or erosion, mediated by inflammatory factors, resulting in acute coronary syndrome (ACS). This type is characterized by the instability of atherosclerotic plaques and a significant inflammatory response.

Type III: Allergic stent thrombosis can be further categorized into two subtypes: IIIa and IIIb. (1) Type IIIa refers to coronary artery stent thrombosis (in situ thrombosis) occurring without pre-existing atherosclerosis, triggered by hypersensitivity reactions such as allergies or anaphylaxis. This subtype is observed in patients with implanted stents, where allergic reactions lead to thrombus formation in otherwise normal coronary arteries. (2) Type IIIb involves coronary artery stent thrombosis (in situ thrombosis) occurring in the presence of underlying atherosclerosis, which becomes complicated by an allergic or hypersensitivity reaction. In these cases, pre-existing atherosclerosis is exacerbated by the hypersensitivity reaction, ultimately leading to stent thrombosis. Patients who have undergone coronary stenting may experience stent thrombosis as a result of allergic reactions to medications, stent materials, or contrast agents, which can precipitate acute coronary events.

Among all cases of Kounis syndrome, Type I accounts for 72.6%, Type II for 22.3%, and Type III for 5.1% [7]. We conducted a comprehensive search of databases, including PubMed and CNKI, utilizing the keywords "Kounis syndrome" and "antibiotics," which yielded 68 case reports to date. Of these, 49 cases provided coronary angiography findings, which we have compiled into Table 1. This case highlights the critical importance of recognizing Kounis syndrome, particularly in patients presenting with acute coronary syndrome (ACS) symptoms following exposure to potential allergens. Early diagnosis and appropriate management are essential for improving outcomes in these patients.

Table 1

Summary of Literature Containing Kounis Syndrome Angiography Results.
PMID	Doi	Kounis type	Coronary arteriography
16025365[8]	10.1007/s00380-004-0804-6.	I	not significant coronary stenosis
15999477[9]	10.2143/AC.60.3.2005015.	I	not significant coronary stenosis
17707099[10]	10.1016/j.ijcard.2007.06.029. Epub 2007 Aug 16.	I	not significant coronary stenosis
17360053[11]	10.1016/j.ijcard.2006.11.165. Epub 2007 Mar 13.	I	not significant coronary stenosis
19166448[12]	10.1111/j.1532-5415.2008.01912.x.	I	not significant coronary stenosis
19428133[13]	doi: 10.1016/j.ijcard.2009.04.026. Epub 2009 May 9.	I	not significant coronary stenosis
18632172[14]	10.1016/j.ijcard.2008.04.064. Epub 2008 Jul 15.	I	not significant coronary stenosis
18632173[15]	10.1016/j.ijcard.2008.03.069. Epub 2008 Jul 15.	II	RCA, LAD and LCx had multiple critical lesions,
19203807[16]	10.1016/j.ijcard.2009.01.031. Epub 2009 Feb 8.	I	not significant coronary stenosis
20223532[17]	10.1016/j.ijcard.2010.02.066. Epub 2010 Mar 12.	II	a thrombotic lesion in the origin of the first LAD diagonal branch
21894822[18]	10.1080/ac.66.4.2126625.	I	not significant coronary stenosis
20471121[19]	10.1016/j.ijcard.2010.04.069. Epub 2010 May 14.	III	an intrastent stenosis (80%) of mid RCA,followed by a total thrombotic occlusion of the stent
20605239[20]	10.1016/j.ijcard.2010.04.086. Epub 2010 Jun 3.	I	not significant coronary stenosis
23363946[21]	10.5543/tkda.2012.54077.	I	not significant coronary stenosis
22892496[22]	10.2169/internalmedicine.51.7852. Epub 2012 Aug 15.	I	not significant coronary stenosis
21996416[23]	10.1016/j.ijcard.2011.09.075. Epub 2011 Oct 11.	II	critical (90%) left main stem stenosis
23954011[24]	10.1016/j.ijcard.2013.07.209. Epub 2013 Jul 29.	II	subocclusion of anterior interventricular artery and LCx in middle tracts
23623347[25]	10.1016/j.ijcard.2013.03.158. Epub 2013 Apr 25.	I	normal coronary arteries
24998115[26]	10.1016/j.bjane.2013.06.015. Epub 2013 Oct 23.	I	not significant coronary stenosis
25459048[27]	10.1016/j.jcin.2014.05.031. Epub 2014 Nov 17.	III	residual thrombus and stent struts well covered by neointima
25080953[28]	10.5543/tkda.2014.92891.	I	not significant coronary stenosis
25266187[29]	10.5144/0256-4947.2014.250.	I	not significant coronary stenosis
25464452[30]	10.1016/j.ijcard.2014.11.049. Epub 2014 Nov 6.	I	no stenosis or atherosclerotic plaque.
26363750[31]	10.5543/tkda.2015.44567.	I	not significant coronary stenosis
26800128[32]	10.1016/j.ijcard.2016.01.103. Epub 2016 Jan 11.	I	diffuse multivessel vasospasm
27872436[33]	doi: 10.14744/AnatolJCardiol.2016.7335.	I	not significant coronary stenosis
28532437[34]	10.1186/s13256-017-1310-7.	I/II	Case1:not significant coronary stenosis .Case 2: total occlusion of mid-LAD
28345355[35]	10.1177/2048872617701885. Epub 2017 Mar 27.	I	revealed severe spasm of the left main coronary artery (LMCA)
29534969[36]	10.1016/j.jiph.2018.02.009. Epub 2018 Mar 10.	I	not significant coronary stenosis
29486927[37]	10.1016/j.therap.2017.12.010. Epub 2018 Feb 7.	III	acute stent thrombosis in a sirolimus eluting stent after wasp sting
30305804[38]	10.1186/s12948-018-0099-2. eCollection 2018.	I	normal coronary arteries
30073957[39]	10.18176/jiaci.0248.	I	severe right coronary spasm
29428243[40]	10.1016/j.jaip.2018.01.033. Epub 2018 Feb 8.	II	a medial stenosis of the right coronary artery (75% degree)
32026020[41]	10.1186/s40981-019-0269-3.	I	normal coronary arteries
31014971[42]	10.1016/j.jemermed.2019.03.026. Epub 2019 Apr 20.	I	not significant coronary stenosis
31467731[43]	10.1155/2019/5185716. eCollection 2019.	I	not significant coronary stenosis
31419012[44]	10.1111/1742-6723.13377. Epub 2019 Aug 16.	II	50% stenosis of the LAD, minor disease of the circumflex, 60% stenosis mid-right coronary artery and 99% stenosis distal right coronary artery
31341482[45]	10.1155/2019/6317956. eCollection 2019.	I/II	case 1: a significant stenosis of the right proximal coronary artery, due to coronary spasm;case 2:a subocclusion of the anterior descending branch of the LAD
31003822[46]	10.1016/j.jemermed.2019.03.001. Epub 2019 Apr 16.	I	normal coronary arteries
29902529[47]	10.1016/j.jaip.2018.05.030. Epub 2018 Jun 11.	I	not significant coronary stenosis
33711934[48]	10.1186/s12872-021-01936-4.	I	not significant coronary stenosis
33172656[49]	10.1016/j.redar.2019.06.009. Epub 2020 Nov 7.	II	moderate distal injury (40%) and distal occlusion of the LCx
34100733[50]	10.5152/AnatolJCardiol.2020.36422.	I	normal coronary arteries
32963159[51]	10.2169/internalmedicine.5548-20. Epub 2020 Sep 19.	I	normal coronary arteries
36270738[52]	10.1136/bcr-2022-251820.	II	severe stenosis in the LAD
35888574[53]	10.3390/medicina58070855.	III	complete thrombotic stent occlusion in the LCx
35744022[54]	10.3390/medicina58060759.	I	not significant coronary stenosis
37039056[55]	10.52964/AMJA.0933.	II	the presence of coronary artery occlisions
37294099[56]	10.18176/jiaci.0921. Epub 2023 Jun 9.	I	not significant coronary stenosis

Currently, research on Kounis syndrome, both domestically and internationally, primarily comprises case reports and reviews. Alongside the presented case, we offer an overview of the epidemiology, pathogenesis, diagnosis, and treatment of Kounis syndrome.

Epidemiology

The incidence of Kounis syndrome was primarily estimated through a three-year retrospective study, which reported 226 individuals experiencing 246 severe allergic reactions, predominantly characterized by cardiovascular symptoms. The annual incidence was estimated to be between 7.9 and 9.6 per 100,000 individuals[57], with three deaths attributed to allergic reactions, resulting in a mortality rate of 0.0001%. Recent studies indicate that the incidence is higher in males than in females[58]. Kounis syndrome can occur across all age groups, ranging from 2 to 90 years, but is most commonly observed in individuals aged 40 to 70 years[59]. With increased awareness among healthcare professionals, more cases are being reported globally. A prospective study found a prevalence of 3.4% among emergency patients presenting with allergic reactions, suggesting that Kounis syndrome is not rare[60].

Etiology and Pathogenesis

Various conditions can trigger Kounis syndrome, including drug use, environmental exposures, insect stings, dietary factors, and the presence of coronary drug-eluting stents[6]. Among these, drugs are the most common trigger; a meta-analysis conducted by Raschi et al. identified that out of 252 case reports, 142 were drug-induced[61]. Frequently implicated medications include nonsteroidal anti-inflammatory drugs[62], antibiotics[57], anticancer agents[63], contrast media[64], corticosteroids[65], and proton pump inhibitors[66]. Specifically, the antibiotics most commonly associated with kounis syndrome are vancomycin, cephalosporins, amoxicillin/clavulanic acid, and penicillin[67]. In addition to moxifloxacin, other fluoroquinolones have also been reported to trigger Kounis syndrome. Levofloxacin and ciprofloxacin, both of which are commonly used fluoroquinolones[62], have been implicated in several cases documented in the literature. These cases further underscore the potential of fluoroquinolones to induce allergic reactions that may lead to coronary artery spasms or acute myocardial infarction, particularly in susceptible individuals. The recognition of this association across multiple drugs within this class highlights the necessity for vigilance when prescribing fluoroquinolones, especially in patients with a history of allergic reactions or cardiovascular risk factors.To mitigate or prevent the incidence of KS, pre-treatment with antihistamines, corticosteroids, and nonsteroidal anti-inflammatory drugs, as well as reducing infusion rates, is recommended[61].

The exact pathogenesis of Kounis syndrome remains incompletely understood. It is thought to involve inflammatory mediators such as histamine, platelet-activating factor (PAF), products of arachidonic acid, and neutral proteases released during allergic activation.[68]. Mast cells are central to this pathogenesis, serving as key players in allergic reactions. They are located in proximity to blood vessels, lymphatics, and peripheral nerves, with a notable increase in mast cell density observed in the cardiac systems of patients with coronary artery disease.[69]. During allergic reactions, mast cells interact with other inflammatory cells, releasing substances such as PAF, histamine, metabolites of arachidonic acid, proteases, and various cytokines and chemokines. These mediators contribute to coronary artery spasm, which is integral to the disease's pathogenesis. [7, 68].Additionally, platelet activation significantly influences the clinical manifestations of Kounis syndrome, occurring through binding to receptors on their surface (FcγRI, FcγRII, FcεRI, FcεRII). [70]. his interaction triggers a cascade of inflammatory pathways and cytokine responses[71]. Many inflammatory mediators are synthesized de novo and released locally during allergic reactions, particularly within the coronary arteries. [72].he underlying mechanism involves the release of mediators by mast cells and other immune cells, leading to coronary spasm, plaque erosion or rupture, and subsequent thrombosis[71]. Furthermore, systemic vasodilation, reduced venous return, increased vascular permeability, and decreased cardiac output during allergic reactions culminate in coronary hypoperfusion, vasoconstriction, and myocardial injury.

Diagnosis

Kounis syndrome presents with a diverse range of clinical manifestations, including chest pain, palpitations, dyspnea, rash, urticaria, and fluctuations in blood pressure. An accurate and timely diagnosis is essential for effective treatment. The diagnostic process includes clinical evaluation, laboratory tests, electrocardiography (ECG), and imaging studies. Kounis syndrome should be considered in patients experiencing concurrent allergic reactions and cardiac symptoms. It is recommended to measure serum tryptase and cardiac enzymes, such as troponin and creatine kinase (CK)[73], as tryptase has a half-life of approximately 90 minutes and should be assessed early in the diagnostic process[74].

ECG is also critical, and echocardiography and coronary angiography should be performed if possible. ECG findings in kounis syndrome often include transient ST-segment elevation, but can be normal[75]. ST-segment elevation in kounis syndrome-related vasospasm is usually transient[76]. Patients can be classified based on ECG:

Persistent ST-segment elevation (> 20 minutes) with chest pain suggests acute coronary occlusion, requiring immediate percutaneous coronary intervention (PCI).

Non-persistent ST-segment elevation includes transient elevation (vasospasm), transient or persistent ST-segment depression, T-wave inversion, T-wave flattening, or pseudonormalization, warranting elective PCI.

Treatment and Prognosis

There are currently no established clinical guidelines for the treatment of Kounis syndrome, and most available information is derived from case reports and series. The management of Kounis syndrome presents challenges due to the conflicting requirements of therapies for cardiovascular and allergic reactions. While fluid resuscitation can alleviate hypotension, it may simultaneously increase cardiac load and the risk of heart failure. In cases of anaphylactic shock, vasopressors are essential to counteract peripheral vasodilation, whereas vasodilators are necessary to address coronary spasm, necessitating a complex therapeutic balance. An initial assessment should ascertain whether the symptoms are predominantly allergic, which would require immediate administration of epinephrine, or indicative of acute coronary syndrome (ACS), which would necessitate the use of calcium channel blockers. Additionally, the presence of coronary occlusion and the potential need for revascularization should be thoroughly evaluated[77].

Anti-allergic treatment can alleviate symptoms in most patients with Type I Kounis syndrome[78]. Epinephrine is the first-line medication for anaphylactic shock; however, it may exacerbate ischemia, prolong QT intervals, and induce coronary spasm and arrhythmias in acute coronary syndrome (ACS),particularly among elderly and hypertensive patients[79].Consequently, epinephrine should be reserved for cases of anaphylactic shock and laryngeal edema in Kounis syndrome[80]. Calcium channel blockers are preferred for treating ischemia in Kounis syndrome, as their mechanism aligns with the pathophysiology of vasospasm[79].Patients with Type II Kounis syndrome should be managed according to ACS protocols, which include corticosteroids and antihistamines[78]. It is important to note that β-blockers may exacerbate coronary spasm, while vasodilators such as nitrates and calcium channel blockers can worsen hypotension. Opioids like morphine, which may aggravate allergic reactions, should be avoided in favor of fentanyl and its derivatives[81].Type III kounis syndrome patients should receive urgent myocardial infarction treatment and stent thrombectomy.

In conclusion, the management of Kounis syndrome necessitates the control of systemic allergic reactions alongside the management of potential cardiovascular complications.Early intervention with anti-allergic medications and meticulous management of cardiovascular symptoms is essential. Additionally, coronary angiography is advised in suitable circumstances to facilitate the early detection and treatment of coronary artery disease.

This report presents the first documented case of moxifloxacin-induced Type II Kounis syndrome. Kounis syndrome is a life-threatening emergency that necessitates prompt intervention; however, specific guidelines for its management are currently lacking. While primarily documented in case studies, Kounis syndrome exhibits a notable incidence.The overlapping clinical features of allergic reactions and myocardial ischemia further complicate both diagnosis and treatment.Emergency physicians should consider the possibility of Kounis syndrome in patients presenting with acute coronary syndrome (ACS) alongside allergic symptoms.In cases of suspected systemic allergic reactions,it is essential to monitor cardiac symptoms and perform ECG and cardiac enzyme tests, with coronary angiography conducted as necessary. Early recognition and appropriate treatment can significantly enhance outcomes for patients affected by Kounis syndrome.

Clinical trial number: not applicable.

Availability of data and materials：Ethical approval for this study was provided by the NAC of Beijing Electric Power Hospital of State Grid Corporation of China on May 27, 2020, and the ethics approval number is KY-2020-009-01.

Competing interests：Not applicable

Funding:Not applicable.

Authors' contributions:

Qiqi Chen:Conceptualization, Methodology, Software;

Junyue Xu: Data curation, Writing- Original draft preparation;

Ming Zhang: Visualization, Investigation.

Yanna Yang:Supervision;

Lili Dai: Software, Writing- Reviewing and Editing;

Hongxia Niu:The corresponding author is responsible for ensuring that the descriptions are accurate and agreed by all authors.

Acknowledgements:All authors disclosed no relevant relationships

Authors' information:

Qiqi Chen¹;Junyue Xu²;Ming Zhang³;Yanna Yang¹;Lili Dai¹;Hongxa Niu¹;

1.Department of Emergency,Capital medical university electric power teaching hospital (State Grid Corporation of China Beijing electric power hospital);Beijing 100073，China;

2.Department of Laboratory,Capital medical university electric power teaching hospital (State Grid Corporation of China Beijing electric power hospital);Beijing 100073，China.

3.Department of Cardiovascular Medicine,Capital medical university electric power teaching hospital (State Grid Corporation of China Beijing electric power hospital);Beijing 100073，China.

Corresponding Author：

Name:Hongxia Niu

Email:[email protected]

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Declarartions.

No competing interests reported.

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First Report of Moxifloxacin-Induced Type II Kounis Syndrome: A Case Study and Comprehensive Literature Review

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