Clinical Characteristics of Hospitalized Patients with Dengue Fever in Guangzhou, China

Abstract

Background

While the WHO has outlined specific dengue clinical phases, detailed real-world comparisons across different clinical phases remain valuable for clinical management. This study evaluates clinical features of dengue hospitalizations during the 2024 outbreak in Guangzhou, China, where recent tracking confirmed a predominant circulation of highly homologous DENV-1.

Methods

This is a retrospective study of hospitalized patients with dengue virus infection from May to October 2024 in Guangzhou. Both descriptive and inferential statistics were utilized to compare symptoms and laboratory results among patients in different clinical phases.

Results

Of 151 hospitalized dengue cases, 101 (66.9%), 42 (27.8%), and 8 (5.3%) patients were in the febrile phase, critical phase and recovery phases at admission, respectively. The mean age was 44 years, with 76 (50%) female patients. Fifty-two (34%) patients had comorbidities. Median time from symptom onset to hospital admission was 1 day (IQR: 1–4), with a consequent median hospital length of stay of 5.2 days (3.8–6.5). While fever was the dominant symptom in the febrile phase (67%, P < 0.001), while rash prevalence peaked in the recovery phase (62.5%, P=0.009). Compared to the febrile phase, the critical phase exhibited significantly lower white blood cells (P=0.008), platelets (P<0.001), blood urea nitrogen (P=0.008), fibrinogen (P=0.043), and prothrombin time (P<0.001), but significantly elevated alanine aminotransferase (P=0.028), aspartate aminotransferase (P=0.001), and lactate dehydrogenase (P=0.001).

Conclusion

Despite the limitation of lacking specific viral etiology identification, this descriptive study delineates the distinct symptomatology and macroscopic laboratory kinetics of dengue patients across different WHO clinical stages during the 2024 outbreak. The high prevalence of rash and altered laboratory parameters in the later stages indicate that additional care is required in the later stages of the disease.

Introduction

As one of the most prevalent arboviral diseases globally, dengue fever infections (DENV) has expanded dramatically over the past two decades, marked by a ten-fold surge in globally reported cases from approximately 500,000 in 2000 to 5.2 million in 2019, which stood as an unprecedented peak spanning 129 countries. Following this historical trajectory, the annual infection count approximately doubled each year from 2021 to 2023, with over 14 million cases reported in 2024 – more than twice the 6.5 million cases reported in 2023.¹ According to the World Health Organization (WHO), nearly 75% of the global disease burden from dengue was borne by populations in Southeast Asia and Western Pacific regions.²

The clinical manifestations of DENV are systemic and dynamic, involving three distinct clinical phases as classified by the WHO) in 2009 to facilitate the clinical management of dengue cases.² During the febrile phase, patients experience sudden-onset high fever, accompanied by facial flushing, generalized body pain, headache, and possible mild hemorrhage. Hepatomegaly (liver enlargement) is common, and white blood cell counts decline progressively over 2–7 days. As patients enter the critical phase, the fever subsides, but capillary permeability increases, leading to elevated hematocrit levels and plasma leakage. Concurrently, leukopenia and thrombocytopenia may occur, potentially causing shock, organ damage, or severe hemorrhage. Survivors of the critical phase transition to the recovery phase, during which extravascular fluid is reabsorbed. Physical improvement is marked by hematocrit stabilization, rising leukocyte counts, and delayed platelet recovery, though residual symptoms like rash, pruritus (itching), and bradycardia may continue to persist. The WHO classification of clinical phases of DENV has been adopted in the management of dengue cases in China and other region with significant dengue burden, including Thailand³ and Brazil.⁴ In addition, the clinical course of dengue may also differ by viral serotypes,⁵ host immune competence,⁶ and underlying chronic conditions.⁷

Although dengue is not endemic in China, cases tend to occur very frequently during the main epidemic season from June to October.⁸ Dengue outbreaks were mostly observed in Guangdong, Guangxi, Fujian, Yunnan, and other southern provinces.⁹ As the capital and largest city of Guangdong province, Guangzhou has a long history of dengue epidemics, with the first outbreak occurred in 1978.¹⁰ Subsequently, Guangzhou experienced three major epidemics: in 1980 (452,674 cases; 7,899.36 cases/million), 1986 (118,881 cases; 1,887.09 cases/million), and 2014 (45,189 cases; 421.71 cases/million), with the 2014 outbreak being the most severe recent surge that drew intense domestic and international attention. During the 2024 epidemic season, virological and epidemiological tracking revealed that outbreaks in this region, including neighboring Shenzhen, were predominantly driven by DENV-1. Genomic sequencing demonstrated that these cases shared high homology with viruses found in adjacent cities, strongly indicating a homologous regional circulation, including Guangzhou.¹¹ While large-scale epidemiological studies have contributed immensely to characterizing DENV strains and transmission dynamics in Guangzhou,^12,13 clinical feature analyses of dengue cases also provides both distinct and complementary values, offering clinicians important insights for effective case management.

While a previous study characterized the clinical characteristics of dengue infections in Fuzhou, China,¹⁴ a systematic comparison between cases at different clinical stages has not been made. In this study, we aim to evaluate the clinical and laboratory features across clinical phases to provide insight into the clinical management of dengue cases.

Methods

Study Setting and Participants

We recruited all hospitalized patients diagnosed with Dengue fever between May and October 2024 from The First Affiliated Hospital of Guangzhou University of Chinese Medicine, a Grade A tertiary hospital in Guangzhou. The study was conducted in accordance with the Declaration of Helsinki and was approved by the Ethics Committee of The First Affiliated Hospital of Guangzhou University of Chinese Medicine studies. Through a consecutive sampling strategy, all eligible patients admitted during the 2024 epidemic season were enrolled in this study.

The diagnosis of dengue fever was based on epidemiological evidence (eg, recent travel history), clinical manifestations, and laboratory testing results. All dengue cases included in this study were laboratory-confirmed by meeting at least one of the following criteria: (1) A positive result for the DENV-specific nonstructural glycoprotein-1 Antigen (GUANGZHOU WONDFO BIOTECH CO.LTD.¹⁵) in an acute-phase serum sample (collected within 6 days following onset of symptom); (2) Detection of IgM antibodies via enzyme-linked immunosorbent assay (ELISA) in a recovery-phase serum sample (collected ≥ 7 days after symptom onset); (3) A positive result from a quantitative Real-time polymerase chain reaction (RT-PCR) test for DENV RNA.^2,16,17

Data Collection

Demographical, epidemiological, and clinical data were collected from patients’ electronic medical records, including sex, age, body mass index (BMI), comorbidities, travel history, date of hospital admission and discharge, and symptoms/signs of dengue observed upon hospitalization. The baseline laboratory data from the patient’s very first blood draw at the date of hospitalization were retrieved, including white blood cell (WBC), platelet count (PLT), hematocrit (HCT), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBil), lactate dehydrogenase (LDH), creatine Kinase (CK), creatine kinase isoenzymes (CK - MB), troponin (Tn), blood urea nitrogen (BUN) creatinine (Cre), fibrinogen (Fib), prothrombin time (PT), activated partial thromboplastin time (APTT), and plasma D-dimer (DD).

Case Classification

The symptom onset date of dengue fever infection was defined as the initial fever onset date provided by the patients upon hospitalization. Based on the time interval between symptom onset and hospital admission, patients were categorized into different clinical phases in accordance with Dengue guidelines, for diagnosis, treatment, prevention, and control, jointly published by the WHO and the Special Programme for TDR:² the febrile phase (days 1–3 after disease onset), the critical phase (day 4 to day 6), and the recovery phase (days ≥ 7). Patients could be in any of these clinical phases at the time of admission.

Statistical Analysis

For descriptive statistical analysis, the denominator of each frequency calculation was the number of patients with available data for the corresponding variable. Frequency of categorical variables were compared between groups using the chi-square test or Fisher’s exact test. For continuous variables, one-way analysis of variance (ANOVA) was used. When the assumptions for parametric tests were not met, Kruskal–Wallis ANOVA was applied to assess differences between groups. The Bonferroni correction is adopted for adjusting the p-value in multiple comparisons. Statistical significance was defined as a two-tailed P < 0.05.

Results

Patient Characteristics

The descriptive statistics were shown in Table 1. Of the 151 patients hospitalized with dengue fever, 75 (49.7%) were male (Table 1). The mean age of the study participants was 44 years (range: 1–88 years), with the majority (75.5%) aged 19–64 years, predominantly hypertension (17.2%), followed by diabetes (8.6%) and cerebrovascular disease (8.6%). Based on the time since symptom onset, patients were categorized into different clinical phases: 101 in the febrile phase, 42 in the critical phase and 8 in the recovery phase. The median length of hospital stay was 5.2 days [IQR: 3.8–6.5], and the time from symptom onset to hospital admission of the patient was primarily concentrated at 1 day, with an interquartile range of 1 to 4 days. Only one patient had a documented history of outbound travel a few days before the hospital presentation.

Table 1.

Clinical Signs and Symptoms in 151 Hospitalized Dengue Patients Between May and October 2024

Variables	Hospitalizations Diagnosed with Dengue Fever (n = 151)
Age, mean (SD)	46.3 (19.3)
Age group, n (%)
≤ 18 yrs	14 (9.3)
19 ~ 64 yrs	114 (75.5)
≥ 65 yrs	23 (15.2)
Sex, n (%)
Male	75 (49.7)
Female	76 (50.3)
Clinical stage, n (%)
Febrile phase	101 (66.9)
Critical phase	42 (27.8)
Recovery phase	8 (5.3)
BMI category, n (%)
Underweight	17 (11.3)
Normal	74 (49.0)
Overweight	37 (24.5)
Obesity	17 (11.3)
Not available	6 (3.9)
Comorbidities, n (%)
Any Comorbidity	52 (34.4)
Hypertension	26 (17.2)
Diabetes	13 (8.6)
Cancer	3 (2.0)
Cerebrovascular disease	13 (8.6)
Autoimmune disease	5 (3.3)
Renal disease	1 (0.7)
Travel history, n (%)	1 (0.7)
Length of hospital stay (days), median (IQR)	5.2 (3.8–6.5)
Duration between first symptom onset and hospital admission (days), median (IQR)	1 (1–4)

Notes: Data are presented as mean (SD), median (IQR), or n (%).

Clinical Manifestations at Hospital Admission

Among hospitalized dengue patients, the predominant signs (in descending order) during febrile phase were fever (67%), fatigue (35.9%), myalgia (33%), and headache (31.1%); in patients during the critical phase: fatigue (50%), rash (47.5%), myalgia (27.5%), fever (25%), nausea (23.1%) and vomiting (15.4%); and in the recovery phase: fatigue (75%), rash (62.5%), myalgia (50%), and headache (37.5%) (Table 2). Overall inter-group comparisons revealed significant differences in the frequencies of fever (P < 0.001), rash (P = 0.009), and headache (P = 0.039) across the three clinical phases. Post-hoc pairwise comparisons with Bonferroni correction demonstrated that, compared to the febrile phase, fever was significantly less frequent in both the critical phase (25.0%, P < 0.05) and the recovery phase (12.5%, P < 0.05). Conversely, rash was significantly more frequent in the recovery phase (62.5%, P < 0.05) than in the febrile phase. No other symptoms exhibited statistically significant pairwise differences compared with the febrile phase.

Table 2.

Comparison of Clinical and Laboratory Characteristics of Hospitalized Dengue Patients in the Clinical Stages of Dengue Recommended by the World Health Organization (Febrile Phase: 1–3 Days, Critical Phase: 4–6 Days, and Recovery Phase: ≥ 7 Days)

Variables	Clinical Phases at Admission			P value#
	Febrile Phase (n =103)	Critical Phase (n = 40)	Recovery Phase (n = 8)
Symptoms, n (%)
Fever	69 (67.0)	10 (25.0)*	1 (12.5)*	<0.001
Myalgia	34 (33.0)	11 (27.5)	4 (50.0)	0.428
Headache	32 (31.1)	5(12.5)	3 (37.5)	0.039
Rash	22 (21.4)	15 (37.5)	5 (62.5) *	0.009
Vomiting	12 (11.7)	6 (15.4)	2 (25.0)	0.834
Abdominal pain	9 (8.7)	0 (0.0)	1 (12.5)	0.067
Mucosal bleeding	6 (5.8)	4 (10.0)	0 (0.0)	0.696
Fatigue	37 (35.9)	20 (50.0)	6 (75.0)	0.053
Nausea	18 (17.5)	9 (23.1)	2 (25.0)	0.609
Laboratory characteristics†, mean (range)
WBC (×109 cells/L)	4.18 (1.07–17.6), (n = 103)	3.42 (1.15–15.83)*, (n = 40)	2.50 (1.39–4.24), (n = 8)	0.008
PLT (×109 cells/L)	152.66 (40–300), (n = 103)	98.88 (25–255)*, (n = 40)	109.25 (37–181), (n = 8)	<0.001
HCT (L/L)	0.4 (0.13–0.49), (n = 103)	0.42 (0.31–0.53), (n = 38)	0.41 (0.29–0.47), (n = 8)	0.279
ALT (U/L)	41.48 (6–289), (n = 102)	59.92 (13–339)*, (n = 40)	73.63 (20–387), (n = 8)	0.028
AST (U/L)	56.59 (18–217), (n = 102)	81.97 (22–463)*, (n = 40)	87.00 (41–304), (n = 8)	0.001
TBil (μmol/L)	7.42 (1.5–20.1), (n = 100)	7.07 (2.9–17.2), (n = 39)	9.83 (3.6–19.2), (n = 8)	0.246
LDH (U/L)	264.52 (142–539), (n = 64)	429.65 (135–2797)*, (n = 31)	309.2 (264–384), (n = 5)	0.001
CK (U/L)	226.16 (52–1471), (n =65)	404.87 (38–4868), (n = 31)	448 (39–1450), (n = 6)	0.521
CK-MB (U/L)	21.41 (0.9–257), (n = 66)	20.47 (8–52), (n = 30)	21.50 (10–42), (n = 6)	0.132
Tn (ng/mL)	0.01 (0–0.08), (n = 53)	0.00 (0–0.01), (n = 21)	0.01 (0.00–0.02), (n = 4)	0.054
BUN (mg/mL)	4.64 (1.39–27.56), (n = 97)	3.50 (1.84–6.1)*, (n = 35)	3.01 (2.2–4.17)*, (n = 7)	0.008
Cre (μmol/L)	89.27 (27–895), (n = 97)	72.00 (44–122), (n =35)	70.86 (40–98), (n = 7)	0.309
Fib (g/L)	2.60 (1.68–4.31), (n = 99)	2.37 (1.68–3.59)*, (n = 39)	2.83 (2.34–4.49), (n = 8)	0.043
PT (second)	11.56 (9.6–28.6), (n = 99)	10.59 (9.3–13.3)*, (n = 39)	10.54 (10.1–11.2)*, (n = 8)	<0.001
APTT (second)	34.18 (23.9–52), (n = 98)	36.40 (24.5–64.6), (n = 39)	31.88 (26.6–37.8), (n = 8)	0.460
DD (mg/L)	1.12 (0.08–8.34), (n = 98)	1.09 (0.13–8.33), (n = 38)	0.59 (0.19–1.17), (n = 8)	0.501

Notes: Data are presented as n (%) or mean (range). ^#Overall P-values across the three clinical phases were calculated exclusively using Fisher’s exact test for all categorical variables (necessitated by expected cell frequencies < 5) and the Kruskal–Wallis H-test for all continuous variables (due to deviations from normality). Statistically significant results are indicated in bold. *Significantly different from febrile phase. The Bonferroni correction is adopted for adjusting the p-value in multiple comparisons. ^†Data were presented and compared for patients who underwent the laboratory test.

Laboratory Characteristics

Significant overall differences across the three clinical phases were observed in the levels of WBC (P = 0.008), PLT (P < 0.001), ALT (P = 0.028), AST (P = 0.001), LDH (P = 0.001), BUN (P = 0.008), Fib (P = 0.043), and PT (P < 0.001). Post-hoc pairwise comparisons revealed that, compared to the febrile phase, patients in the critical phase had significantly lower levels of WBC, PLT, BUN, and PT, accompanied by significantly higher levels of liver and tissue injury markers, including ALT, AST, and LDH. When comparing the recovery phase to the febrile phase, only PT remained significantly shorter; no other laboratory variables showed significant post-hoc pairwise differences.

Notably, several key laboratory parameters followed a distinct dynamic pattern across the three phases. PLT values fell significantly during the critical phase (mean 98.88 ×10⁹/L; range 25–255) compared with the febrile phase (152.66 ×10⁹/L; 40–300), and subsequently began to rebound in the recovery phase (109.25 ×10⁹/L; 37–181). Conversely, transaminases and tissue enzymes surged during disease progression. ALT was mildly elevated in the febrile period (41.48 U/L; 6–289), increased significantly during the critical period (59.92 U/L; 13–339), and remained elevated during recovery (73.62 U/L; 20–387). LDH mirrored this exacerbation pattern: levels rose from 264.52 U/L (142–539) in the febrile phase to a striking peak of 429.65 U/L (135–2797) in the critical phase, before trending downward toward baseline in the recovery phase (309.2 U/L; 264–384).

Discussion

Symptom Progression and Clinical Implications

Dengue fever, an acute vector-borne infectious disease, has been exhibiting increasingly active epidemics in South China. In this study, we compared the frequencies of symptoms and clinical characteristics of hospitalized dengue cases, classified according to the WHO clinical staging criteria. Our study suggests that fever was the most frequently observed symptom in the febrile phase compared to other phases. As the febrile phase progressed to the critical phase, the frequency of rash significantly increased, becoming the predominant notable sign during recovery.

Current research on dengue causing persistent fatigue may be related to genetics, disease, personality traits, and psychological problems.¹⁸ A previous study has shown that plasma leakage and most laboratory markers did not predict fatigue following infection.¹⁹ In our patient sample, fatigue was highly prevalent across all clinical phases (ranging from 35.9% to 75.0%), without statistically significant differences between stages. The disappearance of the rash was significantly associated with the development of fatigue after dengue infection, while no significant association was found between fatigue and dengue severity.¹⁸ Although the association was not explicitly explored in this study, a reduction in rash was found to be accompanied by a reduction in the occurrence of fatigue in patients.

As the within-host viral load decreases, the body’s immune response to the virus fades, leading to a reduced fever.^20,21 After the recovery period, the pathophysiological processes in hospitalized patients gradually stabilize. The inflammatory response further subsides, allowing the body to repair the damaged tissues and organs, while body temperature normalizes, and fever symptoms naturally diminish.²²

Overall, this study presents the clinical characteristics of hospitalized dengue patients. These findings emphasize the importance for physicians to monitor changes in liver and heart functions, as well as specific clinical signs like abnormal bleeding and rapid heart rate during treatment to promote patient recovery.

Laboratory Abnormalities and Their Pathophysiological Mechanisms

The transition from the febrile phase to the critical phase was characterized by a significant decrease in WBC, PLT, BUN, and PT, alongside a marked increase in ALT, AST, and LDH. In the recovery phase, the frequency of rash was significantly higher, while PT remained significantly shorter compared to the febrile phase. In dengue patients progressing from the febrile phase to the recovery phase, the observed decrease in WBC and PLT can be attributed to the direct invasion of bone marrow hematopoietic cells and hepatocytes by the dengue virus, and the massive elimination of leukocytes during the immune response.²² Enzymes such as ALT and AST in damaged hepatocytes are released into the bloodstream, elevating the activity of these enzymes in the blood.²³ Consistent with previous studies, the elevation of AST is often more prominent than that of ALT. Because ALT is predominantly a liver-specific enzyme, whereas AST is also released following damage to cardiac and skeletal muscle, this specific transaminase pattern suggests that the elevated enzyme levels in dengue likely originate from both hepatic and extrahepatic tissue injury.²⁴

A decrease in albumin, which is essential for maintaining plasma colloid osmotic pressure, may cause hemodilution, subsequently affecting WBC concentration. The decrease in Fib is primarily due to the infection-induced systemic microvascular damage, which increases vascular permeability and triggers hyperactivation of the coagulation system,²⁵ leading to quicker consumption of coagulation factors such as Fib.²⁶

PT is an indicator of the function of the exogenous coagulation system and is typically prolonged due to the reduction of Fib and the excessive consumption of other coagulation factors. However, it shortened even as Fib levels decreased after disease progression. This may reflect a transient hypercoagulable state during early disseminated intravascular coagulation. Specifically, endothelial injury and tissue factor release can trigger a temporary shortening of PT prior to the typical prolongation caused by eventual factor depletion.²⁷ Additionally, this phenomenon may be due to microthrombosis²⁸ or liver failure.²⁹

Organ Dysfunction and Prognostic Indicators

Abnormalities in the liver, kidneys, and heart may also help explain the unusual changes observed in laboratory factors.

Renal function: In dengue hospitalized patients during the hospital phase of treatment, BUN levels declined in hospitalized patients during treatment. Previous studies have shown that renal involvement during DENV infection frequently results in elevated BUN levels, which may be the result of glomerular injury or hypotension.³⁰ This suggests that as the disease progresses, DENV infection may affect renal tubular reabsorption, which may reduce BUN accumulation.

Cardiac function: Although Tn levels showed slight variations, the overall difference across phases was not statistically significant (P = 0.054). According to the WHO guidelines,² severe organ damage including myocarditis can occur in patients with severe dengue, but individual variability in disease progression and clinical presentation (including myocarditis development) leads to varied extents of myocardial damage—some cases may have mild damage not sufficient to cause a significant increase in Tn value. Furthermore, a comprehensive review indicates that clinically significant myocarditis in dengue is relatively rare and predominantly associated with severe dengue hemorrhagic fever or dengue shock syndrome (DHF/DSS).³¹ This aligns perfectly with our observation that Tn levels did not show significant inter-phase differences in our predominantly non-severe study population. Additionally, direct infection of the virus in the heart fibers has been proposed as at least a partial contributing mechanism for cardiac dysfunction.²⁸ However, it remains unclear whether Tn elevation is a reliable indicator of heart damage, and the absence of severe dengue patients in this study further limits the persuasiveness of findings on cardiac damage. Given these uncertainties and the limited number of severe cases, further research on cardiac involvement in dengue infection is warranted.

Liver and multi-organ function: LDH is mainly found in the myocardium, liver, kidneys, and other tissues. When the tissues experience hypoxia or metabolic disorders, LDH catalyzes the conversion between lactic acid and pyruvic acid, leading to increase LDH activity in the blood, and this reflects changes in the liver, kidneys, and heart of the patients hospitalized with dengue fever. Several studies have also shown that the dengue virus impairs liver function.^25,28,30

However, this study has several limitations. First, this is a single-center study involving a relatively small sample size, which may limit the generalizability of the study finding. Second, severe dengue patients or patients with warning signs of severe outcomes were not identified in the study participants; therefore, our finding may only be applicable to dengue cases with mild symptoms. Third, we did not have access to data on the serotype of dengue virus, and the cases in our study may be infected by different serotypes. However, according to the previous study, DENV-1 is the most predominant serotype in Guangzhou.³² This is further corroborated by recent 2024 epidemiological tracking, which revealed that the dengue outbreak in neighboring Shenzhen was predominantly caused by DENV-1, with genomic sequences showing high homology to viruses found in adjacent cities.¹¹ A previous study demonstrated that patients infected with DENV-1 commonly showed non-severe clinical manifestations compared with those infected by other serotypes.⁵ Additionally, due to limited data accessibility, we did not have information on the vaccination status and history prior infection of dengue (with only one documented secondary infection). The predominant homologous DENV-1 circulation and the rarity of secondary infections likely explain the absence of severe dengue cases in our study. Finally, only eight patients were identified as in the recovery phase of infection, which limited the statistical power. Future studies may expand the sample size, adopt prospective research methods, and collaborate with multiple institutions to further explore the relationship between the pathogenesis and clinical course of dengue fever in-depth, providing a more accurate basis for clinical treatment.

In conclusion, our work provides insights into the clinical features of the hospitalized dengue cases during the 2024 dengue outbreaks in Guangzhou. The finding that patients in different WHO clinical stages present with unique symptomatology underscores the distinct physiological trajectory of the disease. For clinical practice, our findings are helpful for clinicians to prioritize monitoring for pronounced rash and trending laboratory values such as platelet count and liver enzymes, as these were key indicators of progression to the critical and recovery phases. While limited by the lack of specific viral etiology identification, these data provide a descriptive foundation for improving routine patient monitoring and clinical management during future dengue outbreaks.

Funding Statement

This study was supported by the Project of Guangdong Provincial Department of Science and Technology (No.: 2023A1515110849, 2025A1515011256), the project of Guangdong Provincial Health Commission-Guangdong Province (No: B2024112), the joint project of Guangzhou University of Chinese Medicine and Zhongshan Hospital of Chinese Medicine (No.: GZYZS2024G09), and the project of Traditional Chinese Medicine Research Platform of Guangdong Provincial Administration of Chinese Medicine (No.: 20254040). SZ was supported by the National Natural Science Foundation of China (No.: 12401648), the Young Elite Scientists Sponsorship Program by CAST (No.: 2024QNRC001), and Tianjin Medical University start-up funding.

Abbreviation

BMI, body mass index; WBC, white blood cell; PLT, platelet count; HCT, hematocrit; ALT, alanine aminotransferase; AST, aspartate aminotransferase; TBil, total bilirubin; LDH, lactate dehydrogenase; CK, creatine kinase; CK – MB, creatine kinase isoenzymes; Tn, troponin; BUN, blood urea nitrogen; Cre, creatinine; Fib, fibrinogen; PT, prothrombin time; APTT, activated partial thromboplastin time; DD, plasma-dimer.

Data Sharing Statement

The original database containing confidential patient information cannot be made publicly available. The anonymized data were available by reasonable request to Zhilin Chen.

Ethical Statement

The study was conducted in accordance with the Declaration of Helsinki and was approved by the Ethics Committee of the First Affiliated Hospital of Guangzhou University of Chinese Medicine for studies. Institutional Review Board (IRB) approval number: k-2022-066.

Patient Consent Statement

A signed informed consent form was obtained from each of the included patients or their legal guardians.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

Ying Wang, Fang Fang, and Qiaoge Chi are co-first authors for this study. The authors report no conflicts of interest in this work.