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. 2025 Sep 26;25:682. doi: 10.1186/s12872-025-05099-4

Acute myocardial injury induced by pheochromocytoma: a case report

Guangxing Li 2,#, Shuwan Xu 3,#, Shangyan Shi 1,#, Xilin Ouyang 2, Peibiao Mai 3, Huanji Zhang 3, Niansang Luo 2,✉, Kun Zhang 1,✉
PMCID: PMC12465244  PMID: 41013238

Abstract

Background

Pheochromocytomas (PCC) are neuroendocrine tumors derived from neural crest cells. PCC typically develop within the adrenal medulla and are known for their catecholamine hypersecretion, leading to acute myocardial injuries and cardiac dysfunction, such as acute heart failure, pulmonary embolism, cardiogenic shock, and tachyarrhythmia. In the clinic, the rarity of these conditions often results in diagnostic challenges, which can delay crucial treatment interventions.

Case presentation

A 37-year-old woman presented with headache, chest discomfort, hypertension, and was detected myocardial injury. Chest computed tomography revealed a mass inside the left adrenal limb. The elevation of methoxy-catecholamines in urine confirmed the diagnosis of PCC. After a left adrenal mass resection, the plasma catecholamine level was recovery to normal. At the telephone follow-up, the patient complained of occasional episodes of palpitation, but no pain or other discomfort.

Conclusions

We present a case of acute myocardial injury caused by PCC and conduct a relevant literature review to provide experience for the clinic. In young patients lacking cardiovascular risk factors presenting with episodes of hypertension and chest tightness, it is recommended to perform CT imaging to differentiate between PCC and cardiovascular diseases. All patients with PCC are advised to refine genetic testing.

Keywords: Pheochromocytoma, PCC, Acute myocardial injury

Background

Pheochromocytomas (PCC) are neuroendocrine tumors originating from neural crest cells. These tumors often secrete excessive catecholamines, leading to hypertension [1]. This may consequently result in complications affecting the cardiovascular, cerebral, and renal vascular systems, as well as induce changes in metabolic processes [2]. PCC is a rare condition, with an international incidence of merely 3 to 8 individuals per million each year [3]. This infrequency often precipitates in diagnostic challenges, leading to either overlooked cases or misdiagnoses, thereby postponing critical interventions [4]. Presented herein is a distinctive clinical report of acute myocardial injury precipitated by PCC, a notably rare manifestation. Accompanying this report is an extensive literature review, which aims to enrich the understanding and augment future methodologies in both diagnosing and managing such exceptional cases associated with this condition.

Case presentation

The patient, a 37-year-old female, was admitted to the hospital on September 11, 2021, with the main reason of “headache for 5 days, aggravated for 2 days”. Five days before admission, the patient experienced persistent vague pain in the right temporal region firstly. And she suffered from more severe headache 3 days later with pain in the left lower abdomen, pale face, tinnitus, vertigo, blurred vision, muscle pain in both upper arms, along with chest tightness, nausea and vomiting once. Symptoms were slightly relieved after she took ibuprofen. She had no other significant medical or family history and was not receiving any other medication. There were no prodromal symptoms of virus infection in the past 1–3 weeks, or psychological trauma in the past six months.

At the time of presentation, the patient’s blood pressure was 158/82 mmHg and the heart rate was 92 beats per minute (bpm). Emergency head CT indicated no obvious abnormalities. The electrocardiograph (ECG) and laboratory results indicated myocardial injury (Fig. 1; Table 1). Considering the possibility of acute myocardial infarction (AMI) or myocarditis, the patient was suggested to undergo coronary angiography, but she refused. Subsequent coronary Computed Tomography Angiography (CTA) examination ruled out coronary artery disease (Fig. 2). In addition, we found a mass in the medial extremity of the left adrenal gland (not included) after chest CT examination. Therefore, the patient was admitted to the cardiovascular intensive care unit (CCU) to further investigate the cardiac condition.

Fig. 1.

Fig. 1

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The electrocardiograph (ECG) on first medical contact. The emergency ECG showed sinus rhythm, flat or inverted T wave in leads III and aVF, and ST segment depression in leads V2-V5 by 0.05mV

Table 1.

The changes of the myocardial enzymes during hospitalization

11/09 12/09 13/09 14/09 15/09 16/09 19/09 Reference ranges Units
creatine kinase (CK) 1214 644 210 120 92 77 69 26-174 U/L
creatine kinase isoenzyme (CK-MB) 168 74 39 57 49 42 24 0-24 U/L
high-sensitivity cardiac troponin T (cTnT) 2263 1154 904 823 678 169 20 0-14 pg/ml
N-terminal pro-B-type Natriuretic Peptide (NT-proBNP) 1490 797 708 429 0-125 pg/ml
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Fig. 2.

Fig. 2

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The coronary Computed Tomography Angiography (CTA) examination. The image indicates that there is no significant calcification or stenosis in the left and right coronary, and their branches

When admitted to the CCU, the patient’s blood pressure was 136/70mmHg, with the heart rate of 56 bpm, and no obvious abnormality was found in other physical examinations. Blood test showed an increased leukocytes count of 14.39*10^9/L, a mild increased neutrophil percentage of 74.5%, and significant elevation of myocardial injury markers (Table 1). The levels of blood glucose, serum lipids, electrolyte and the function of liver and kidney were all within the normal range. Re-examination of the ECG showed no significant changes compared with before admission (Fig. 3). Admission echocardiogram revealed mild enlargement of left atrium (36 mm), mitral valve prolapse with moderate regurgitation, and normal left ventricular ejection function (LVEF 70%). In order to further elucidate the characteristics of the mass in the left adrenal gland, a precise CT scan of the adrenal gland was conducted.It revealed an obscured normal structure of the left adrenal gland and identified a localized solid tumor measuring approximately 40.6 mm x 35.9 mm x 31.9 mm. It suggested the possibility of left adrenergic pheochromocytoma (Fig. 4). Overall, the patient’s preliminary diagnosis is hypertension with adrenal mass (possibly adrenal pheochromocytoma), and phentolamine was given temporarily to control blood pressure.

Fig. 3.

Fig. 3

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The rechecked electrocardiograph (ECG). The first re-examination of the ECG after admission showed sinus rhythm, flat or inverted T waves in leads II, III, and aVF, and ST-segment depression in leads V2-V5 of 0.05mV, which had no significant changes compared with before admission

Fig. 4.

Fig. 4

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The adrenal CT imaging. The enhanced CT scan showed heterogeneous enhancement, with a small non-enhancing necrotic area in the center (CT attenuation values ranged from 30 to 60 Hounsfield units), and the rest showed moderate enhancement, suggesting the possibility of left adrenergic pheochromocytoma

The enhanced CT scan showed heterogeneous enhancement, with a small non-enhancing necrotic area in the center (CT attenuation values ranged from 30 to 60 Hounsfield units), and the rest showed moderate enhancement, suggesting the possibility of left adrenergic pheochromocytoma.

In-hospital course

On the first day of CCU admission, after urinating in the morning, the patient experienced chest tightness, palpitations, nausea, upper limb aches, pain in the left lower abdomen and pale complexion, with the blood pressure as high as 167/90mmHg, and heart rate as high as 100 bpm. Phentolamine was given immediately for controlling blood pressure. The symptoms of the patient were significantly relieved after 20 min of administration, as well as the blood pressure was stabilized. Myocardial enzymology was urgently checked, and the results showed that CK was 644U/L, CK-MB was 74U/L, cTNT was 1154pg/ml, which were all lower than before, with a significantly increased NT-proBNP of 1490.0pg/ml. Further tests related to the function of the adrenal mass were determined (Table 2). The dexamethasone suppression test, parathyroid hormone, calcitonin and aldosterone in the both supine and standing position were measured to exclude other causes of secondary hypertension. The results supported the diagnosis of pheochromocytoma.

Table 2.

Pheochromocytoma and paraganglioma-related examinations:

Parameter 2nd day of admission 4th day of admission 8th day of admission Reference ranges
Urine
 Metanephrine 5.62umol/L↑ 1.20–1.90
 Normetanephrine 2.47umol/L 3.00-3.80
 3-Methoxytyramine 0.33umol/L /
 Vanilla mandelic acid 49.50 mg/24 h↑ 0.00–12.00
 Vanilla mandelic creatinine ratio 18.45↑ 0.00–10.00
Plasma
 Neuron-specific enolase 67.20ng/mL↑ ≤ 16.30
 Metanephrine 18.25 nmol/L↑ 2.66nmol/L ↑ 0.30–0.60
 Normetanephrine 36.89 nmol/L↑ 8.13nmol/L ↑ 0.60–0.90
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On the third day of admission at night, the patient complained again of the above symptoms. During the onset of symptoms, the blood pressure increased from 119/58 mmHg to 151/68 mmHg, with a maximum heart rate of 92 bpm. The review electrocardiogram showed T-wave inverted in leads II, III and aVF, as well as ST-segment depressed in leads V3-V5 by 0.1 mV (Fig. 5). Urapidil was given to control the blood pressure and metoprolol succinate to lower the heart rate. After stabilization of blood pressure, phenoxybenzamine 10 mg q8h was bridged to oral antihypertensive therapy and metoprolol succinate 12.5 mg qd to control heart rate. On the 6th day after admission, the patient no longer complained of dizziness, headache and other discomfort, and occasionally experienced precordial discomfort, so the dosage of phenoxybenzamine was adjusted to 20 mg (8am), 10 mg (4pm), 10 mg (0am) (40 mg per day in total). On the 9th day after admission, the patient experienced transient chest pain and headache again, with blood pressure of 133/77mmHg and heart rate of 82 bpm. Phentolamine was given immediately to control blood pressure and the symptoms were relieved quickly. The dosage of phenoxybenzamine was adjusted upward to 20 mg (8am), 10 mg (4pm), 20 mg (0am) three times a day (50 mg per day in total). Myocardial enzymatic changes of the patient during hospitalization are shown in Fig. 6.

Fig. 5.

Fig. 5

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The electrocardiograph during chest tightness on September 14, 2021. The review electrocardiogram of the patient on the third day of admission showed T-wave inverted in leads II, III and aVF, as well as ST-segment depressed in leads V3-V5 by 0.1 mV

Fig. 6.

Fig. 6

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Myocardial enzymatic changes of the patient during hospitalization

Considering the gradual recovery of myocardial injury, the patient underwent the resection of the left adrenal mass on October, 18, 2021, 2 weeks after oral administration of phenoxybenzamine.

Subsequent histopathological examination of the surgical specimen confirmed the diagnosis of pheochromocytoma (PCC). It showed that most of the tissues had coagulation necrosis, accompanied by proliferation of fibers and histiocytes, many lymphocytes infiltrated, and some cells with small round nuclei and clear cytoplasm could be seen growing in small nests, sheets or nets. On immunohistochemical staining, the necrotic tissue was positive for chromogranin A (CgA) and CD56, weakly positive for synaptophysin (Syn), S-100 protein and somatostatin receptor 2 (SSTR2), and negative for E-cadherin (E-cad), Cytokeratin (CK), and neuron-specific enolase (NSE); In clear cytoplasmic cells, CgA, Syn, CD56, NSE, S-100 protein, and STTR2 were positive, E-cad, a-inhibin, MelanA, Human Melanoma Black-45 (HMB-45), Wilms Tumor Protein (WT-1), and erythroblast transformation-specific related gene (ERG) were negative, P53 was partly weakly positive, The Ki-67 proliferation index was about 2%; CD68 was expressed in histiocytes (Fig. 7).

Fig. 7.

Fig. 7

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Histopathological examination of the surgical specimen. a. The resected mass had a dark brown to gray surface and measured 6.8×5.5×3.8 cm.b. On histologic examination of the hematoxylin and eosinstained specimen (magnification, 100×), cells with small round nuclei and clear cytoplasm are observed to be arranged in a nested pattern (Zellballen structure). c. Positive immunohistochemical staining for CgA in the necrotic tissue (magnification, 200×). d. Positive immunohistochemical staining for CD56 in the necrotic tissue (magnification, 200×). e. Positive immunohistochemical staining for NSE in the tumor cells (magnification, 200×). f. Positive immunohistochemical staining for synaptophysin in clear cytoplasmic cells (magnification, 200×). g. Positive immunohistochemical staining S-100 protein for in clear cytoplasmic cells (magnification, 200×). h. Positive immunohistochemical staining for SSTR-2 in clear cytoplasmic cells (magnification, 200×). i. The positive rate of Ki-67 proliferation index was about 2% (magnification, 200×)

After the operation, the blood pressure and the heart rate were stabilized; hence, the administration of adrenergic blockers was stopped. A month after the resection, the patient’s plasma catecholamine hormones level returned to normal (NSE: 11.4 ng/mL, MN: 0.09 nmol/L, NMN: 0.56 nmol/mL). At the second and the fifth month postoperative follow-ups, the patient complained of occasional palpitations. Self-measured heart rate was 100 bpm and the blood pressure fluctuated around 110/70mmHg during the attack, without chest tightness, chest pain, headache or dizziness.

Discussion

Pheochromocytoma is a sort of neuroendocrine tumor that originates from the adreno-medullary chromaffin cells. It is commonly grouped together with paraganglioma which derived from extra-adrenal chromaffin cells of the sympathetic paravertebral ganglia of thorax, abdomen, and pelvis as Pheochromocytoma and Paraganglioma (PPGL) [3, 5]. These rare neuroendocrine chromaffin-derived tumors are diagnosed on average between the ages of 40 and 50, with 10–20% of people diagnosed during childhood [4]. In the general population, the annual incidence of PCC is 3 to 8 cases per 1 million people [6]. The impact of PCC on physiological functions primarily stems from the excessive catecholamine secretion by these tumors, which can lead to substantial episodic or sustained elevations in blood pressure [3]. The most common triad of hypertensive episodes are headache, palpitations and hyperhidrosis [7]. The specificity of headache is low, while palpitations and hyperhidrosis are specific [8] and can induce adverse cardiovascular events in severe cases, such as myocarditis, cardiomyopathy, myocardial infarction, and tachyarrhythmia or bradyarrhythmia [9]. Among these complications, the incidence of myocardial injury due to PCC can reach to 32%−65.4% [10].

Plasma and urine MN and NMN concentrations are preferred for the diagnosis of PCC, while 3-methoxytyramine, VMA and NSE may also assist in the diagnosis of PCC [3]. CT is generally used for localization of PCC [11]. Pathological diagnosis is the gold standard for the diagnosis of PCC [12]. The immunohistochemistry of the patient after adrenal mass resection is consistent with that of PCC [13, 14]. Pheochromocytoma with hemorrhage and necrosis may be accompanied by a poor prognosis [15], but judging whether PCC is benign or malignant is still based on its biological behavior. At least one-third of patients with PCC carry pathogenic mutations, and PCC is often seen as part of certain genetic syndromes, such as multiple endocrine neoplasia type 2 (MEN2), Von Hipple-Lindau (VHL) syndrome, and neurofibromatosis type 1 (NF1). Therefore, all patients with PCC should be genetically tested [16], and it is recommended that all patients with metastatic PCC should be genetically tested for SDHB [3].

The pathogenesis of myocardial damage in this case may include four main mechanisms. Firstly, catecholamines can directly cause myocardial toxicity, and cause pathological changes such as contractile zone necrosis through mechanisms such as α-receptor-mediated vasoconstriction and oxygen free radical damage, resulting in myocardial cell membrane damage and death [17]. Secondly, catecholamines stimulate β-adrenergic receptors, resulting in increased myocardial oxygen demand, which further causes relative insufficiency of coronary artery perfusion [18]. Thirdly, inflammatory cells infiltrate into the tissue [19]. Fourthly, catecholamines affect the extracellular matrix through collagen deposition and subsequent myocardial fibrosis, which may further aggravate myocardial injury [17]. Clinical data show that myocardial injury usually has a good prognosis if the primary disease is successfully treated [10].

The main differential diagnoses to consider in this case are Takotsubo cardiomyopathy, myocarditis, and myocardial infarction with non-obstructive coronary arteries (MINOCA). Mayo Clinic guidelines use PCC as an exclusion criterion for the diagnosis of Takotsubo cardiomyopathy. Takotsubo cardiomyopathy is a syndrome characterized by a series of clinical symptoms including chest pain, apical and ventricular regional wall-motion abnormalities, minor elevations of cardiac enzyme and biomarker levels, and electrocardiographic ST-segment changes. Its pathogenesis is related to catecholamines[21]. Therefore, PCC needs to be differentiated from Takotsubo cardiomyopathy in this case. Another literature review pointed out that patients with PCC complicated with Takotsubo-like cardiomyopathy are younger than patients with Takotsubo cardiomyopathy, and have a higher incidence of complications and poorer prognosis. Therefore, it is recommended that the presence of PCC complicated by Takotsubo-like cardiomyopathy should be clarified in younger patients and in patients without significant psychological shock [20]. However, in this case, left ventricle angiography was not completed, and whether Takotsubo-like cardiomyopathy occurred concurrently during the attack could not be ruled out. Catecholamine myocarditis caused by PCC is similar to acute myocarditis and needs to be differentiated. The infiltrated leukocytes in the myocardial tissue of PCC patients are secondary to the focal contractile zone necrosis caused by the excessive release of catecholamines from sympathetic nerve endings [21, 22], which is different from the recruitment of inflammatory cells to myocardial tissue caused by myocarditis due to viral infection resulting in myocardial necrosis. Although the MRI features of catecholamine cardiomyopathy are similar to myocarditis, with the evolution of the disease, the damage of catecholamine cardiomyopathy in MRI is difficult to restore to the normal state, and myocardial fibrosis will persist even after surgery [17]. In this case, echocardiography has been performed to clarify the degree of myocardial injury, and it is clear that the patient has no changes such as abnormal ventricular wall motion and decreased ejection fraction, so that there was no evidence to prove that the patient is complicated by catecholamine cardiomyopathy. According to the guidelines of the European Society of Cardiology, PCC is not considered as a differential diagnosis of MINOCA [23]. However, there was a case report of a patient with recurrent myocardial infarction who had segmental wall motion abnormalities and decreased ejection fraction, but no obvious abnormalities were found on coronary angiography [24]. The initial diagnosis was MINOCA, and then multiple endocrine neoplasia type 2 was found. At 6-month follow-up after resection of bilateral pheochromocytomas, the patient had remission of symptoms and no decline in ejection fraction without other treatment. Therefore, it is considered that PCC needs to be differentially diagnosed with MINOCA. In this case, after diagnostic treatment with α-receptor blockers, the myocardial enzymes decreased, the original ECG changes were restored, and symptoms such as chest tightness, elevated blood pressure, and rapid heart rate were significantly improved compared with before. At the same time, each episode of chest tightness and palpitations lasted less than 1 h, so we did not consider MINOCA (Table 3).

Table 3.

Summary of differential diagnosis of PCC associated myocardial injury

Differences
PCC

*left ventricle angiography was not completed, and it is unable to ensure if there is any abnormality in apical and ventricular structure

#without changes such as abnormal ventricular wall motion and decreased ejection fraction

✝α-receptor blockers are effective in treatment
Takotsubo *between60–70 years of age, with an identifiable preceding stressor, apical and ventricular regional wall-motion abnormalities
Myocarditis #the damage in MRI is difficult to restore to the normal state, and myocardial fibrosis will persist even after surgery
MINOCA ✝Treatments including anticoagulation for thromboembolism, calcium channel blockers for vasospasm and so on
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*Myocardial Injury Induced by PCC vs. Takotsubo cardiomyopathy

#Myocardial Injury Induced by PCC vs. Myocarditis

✝Myocardial Injury Induced by PCC vs. MINOCA

Regarding the management of this case, for hypertensive crisis due to PCC, rapid blood pressure control with phentolamine, which has a short half-life, was mainly used, and phentolamine was discontinued once the blood pressure returned to normal and bridged to phenoxybenzamine for long-term blood pressure control [3]. When using phenoxybenzamine to manage blood pressure, due to its non-selective α-receptor blocking effects, it can increase the heart rate influenced by autonomic control and regulate central sympathetic outflow. Consequently, metoprolol is prescribed to further manage heart rate and decrease myocardial oxygen demand. It is critical not to initiate β-blocker therapy prior to α-blockade to prevent acute cardiac insufficiency [3]. When the side effects of phenoxybenzamine are severe, doxazosin and calcium channel antagonists are recommended [25]. Currently, most experts support the view that there is little need for adrenoceptor blockade for nonfunctional PCC or for those that only produce dopamine. Nevertheless, there have been some case reports describing hypertensive crisis or spells during the surgery in apparently “biochemically silent pheochromocytoma” [26]. Since negative biochemical test results cannot be used alone to determine whether a PCC is nonfunctional, and given the associated difficulties in defining a PCC as biochemically silent, there is need for considerable caution when assessing whether such patients should receive adrenoceptor blockade. At the same time, avoid the use of glucocorticoids, metoclopramide, atropine, tramadol and other drugs [27, 28], which can easily lead to the emergence of hypertensive crisis. Studies have shown that the tumor-derived factors of PCC cooperate with catecholamines to cause myocardial remodeling [29], so tumor removal has a good prognosis for both metastatic and non-metastatic PCC. However, emergency resection of PCC has a high complication rate and mortality rate [30, 31], so phenoxybenzamine and metoprolol are taken orally before surgery to control blood pressure and heart rate for more than 2 weeks [32]. For the perioperative management of PCC, the primary purpose is to stabilize blood pressure and heart rate. At the same time, it is necessary to actively expand effective blood volume, improve metabolic status, and prevent catecholamine storms [33]. Various symptoms can be significantly relieved after mass resection [34], but it is still recommended that all PCC patients should be screened for genetic alterations and life-long surveillance, especially recommended for patients with mutations leading to an increased risk of PCC development. In accordance with contemporary guidelines for individualized management of PCC, different gene phenotypes are closely related to the development process, treatment strategies and prognosis of the disease. Krebs cycle/VHL/EPAS1-related cluster 1 tumors need close follow-up due to the risk of metastasis and recurrence. However, kinase signaling-related cluster 2 tumors generally have a less aggressive course. Wnt signaling-related cluster 3 tumors seem to have aggressive behavior. So it is imperative that patients with a history of PCC, along with asymptomatic carriers harboring pertinent genetic mutations, undergo sustained, lifelong surveillance [35]. This monitoring regimen should be meticulously individualized, taking into account the distinct genetic aberrations and the particular clinical manifestations of their condition [35]. In cases where surgery is not an option or the disease has metastasized, options for systemic therapy encompass chemotherapy, radionuclide therapy, and tyrosine kinase inhibitors [35]. While not yet a standard in regular clinical practice, a treatment approach based on genetic cluster-specific therapy appears to be a promising and logical advancement [35].

Conclusion

When young patients lacking cardiovascular risk factors have episodic hypertension and chest tightness, it is recommended to perform CT imaging to check whether there is an adrenal mass and check for metanephrines to rule out extra-adrenal lesions. When a PCC patient develops chest tightness and pain, it is necessary to promptly rule out whether there is a concurrent circulatory system disease. In non-metastatic PCC and in some cases with loco-regional but resectable metastatic disease, surgical treatment is recommended. Regarding the prognosis, all PCC patients especially those with metastatic disease are recommended to complete genetic testing, including SDHB genetic testing.

Acknowledgements

Not applicable.

Abbreviations

AMI

Acute myocardial infarction

bpm

Beats per minute

CCU

Cardiovascular intensive care unit

CgA

Chromogranin A

CK

Creatine kinase

CK-MB

Creatine kinase isoenzyme

CTA

Computed Tomography Angiography

cTnT

Cardiac troponin

E-cad

E-cadherin

ECG

Electrocardiograph

ERG

erythroblast transformation-specific related gene

HMB-45

Human Melanoma Black-45

LVEF

Left ventricular ejection fraction

PCC

Pheochromocytoma

PPGL

Pheochromocytoma and paraganglioma

SSTR2

Somatostatin receptor 2

Syn

Synaptophysin

WT-1

Wilms Tumor Protein

MEN2

Multiple endocrine neoplasia type 2

MINOCA

Myocardial infarction with non-obstructive coronary arteries

MN

Metanephrine

NF1

Neurofibromatosis type 1

NMN

Normetanephrine

NSE

Nerve-specific enolase

NT-proBNP

N-terminal pro-B-type Natriuretic Peptide

VHL

Von Hipple-Lindau

VMA

Vanillylmandelic acid

Authors’ contributions

GXL, SWX, SYS and XLOY participated in data collection, writing, and revision of the manuscript. KZ, NSL and HJZ participated in the treatment of the patient, data collection, writing, and revision of the manuscript. PBM participated in data collection (histologic examination). All authors read and approved the final manuscript.

Funding

This work was supported by The National Natural Science Foundation of China (81600351) to Kun Zhang. It was also supported by The Natural Science Foundation of Guangdong Province (2020A1515010216), and the public health project of Shenzhen Futian (FTWS2020010) to Huanji Zhang. The funding support had no role in the study design, in the collection, analysis, and interpretation of data, or in the writing of this manuscript.

Data availability

Not applicable. All data supporting the conclusions are presented in the manuscript.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images.

Competing interests

The authors declare no competing interests.

Footnotes

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Guangxing Li, Shuwan Xu and Shangyan Shi contributed equally to this work.

Contributor Information

Niansang Luo, Email: luons@mail.sysu.edu.cn.

Kun Zhang, Email: zhangk65@mail.sysu.edu.cn.

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Data Availability Statement

Not applicable. All data supporting the conclusions are presented in the manuscript.

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