Abstract
Purpose
To investigate the diagnostic value of serum APOC2 in patients with diabetes mellitus combined with pyogenic liver abscess.
Methods
From April 2023 to July 2023, 77 type 2 diabetes mellitus patients were included which divided into two groups: diabetes mellitus (n=55) and diabetes mellitus combined with pyogenic liver abscess (n=22). Additionally, 27 healthy individuals served as the control group. Serum APOC2 levels were detected and compared among the groups. ROC curve and logistic regression analysis were performed to evaluate the diagnostic value of serum APOC2.
Results
Serum APOC2 levels were significantly higher in diabetes mellitus patients compared to the healthy control group (P=0.008). In diabetes mellitus combined with pyogenic liver abscess patients, APOC2 levels were significantly reduced (P<0.001) while increased post-treatment (P<0.001). ROC curve analysis showed high diagnostic accuracy for serum APOC2 in diabetes mellitus combined with pyogenic liver abscess (AUC=0.945). Logistic regression analysis revealed that reduced serum APOC2 levels were a risk factor for diabetes mellitus combined with pyogenic liver abscess (OR=0.02, 95% CI=0.01~0.16, P=0.012). The diabetes mellitus combined with pyogenic liver abscess patients with lower APOC2 levels had higher ALT (P=0.038) and AST levels (P=0.007), suggesting that reduced serum APOC2 levels were associated with liver damage.
Conclusion
Serum APOC2 levels are significantly decreased in patients with diabetes mellitus combined with pyogenic liver abscess, serving as a potential marker for predicting the occurrence of this condition. Lower levels of APOC2 are strongly linked to liver function impairment.
Keywords: diabetes mellitus, pyogenic liver abscess, serum APOC2, liver damage
Introduction
Pyogenic liver abscess (PLA) is an intrahepatic infection caused by purulent bacteria with an incidence of 12~18 patients per 100,000 population annually in Asian countries and an estimated mortality rate of 2~31%.1 Typical PLA symptoms include upper right abdominal pain, fever and vomiting, along with nausea, vomiting, loss of appetite, and weight loss. The overuse of antibiotics and an ageing populations have altered the clinical manifestations of PLA, making it easy to miss or misdiagnose.2 Diabetes mellitus is one of the high-risk factors for PLA3,4 and when diabetes mellitus complicated with PLA, it often comes with vascular and neural complications which reduce the body’s sensitivity to pain, resulting in atypical local symptoms making early diagnosis more difficult.5 If not diagnosed and treated promptly, diabetes mellitus combined with PLA may lead to widespread suppurative infections, causing conditions such as endophthalmitis, uveitis, lung abscesses, brain abscesses, and suppurative meningitis, potentially leading to death.6 Therefore, finding early diagnostic markers for diabetes mellitus combined with PLA is essential for their treatment and prognosis evaluation.
APOC2 is a member of the apolipoprotein gene family found on triglyceride-rich lipoproteins (TRL), such as chylomicrons (CM) and very low-density lipoproteins (VLDL), and high-density lipoproteins (HDL). It can activate lipoprotein lipase (LPL) to hydrolyses triglycerides, providing free fatty acids.7 In addition, APOC3 acts as an inhibitor of LPL, thereby counteracting the function of APOC2; evaluating the balance or ratio between APOC2 and APOC3 may provide novel insights into triglyceride regulation in the setting of PLA.7,8 Furthermore, lecithin-cholesterol acyltransferase (LCAT), an enzyme that converts free cholesterol to cholesterol esters, often shows reduced activity in APOC2 deficiency, leading to an elevated ratio of free cholesterol to esterified cholesterol.9 Elevated serum APOC2 levels are closely linked with diabetes mellitus,10–12 atherosclerosis, and metabolic syndrome13,14 and are positively correlated with cardiovascular mortality.15
APOC2 is specifically expressed in the liver, and its expression levels are influenced by liver function.7 Studies have shown that elevated serum APOC2 levels are noted in diabetic mellitus patients,10,11 however, how its expression changes when diabetes mellitus is complicated by PLA, and whether it can serve as a marker for predicting the occurrence of PLA in diabetes mellitus patients, has not been studied. Therefore, this study evaluates serum APOC2 levels in diabetes mellitus patients at the First Affiliated Hospital of Fujian Medical University from April 2023 to July 2023, to determine its potential as an early diagnostic marker for diabetes mellitus combined with PLA.
Materials and Methods
Patients
This retrospective case-control study included 77 diabetes mellitus patients visited the First Affiliated Hospital of Fujian Medical University from April 2023 to July 2023, among which 22 were diabetes mellitus combined with PLA. Simultaneously, 27 healthy individuals from the hospital’s physical examination center served as the control group. The diabetes mellitus group comprised 30 males and 25 females, aged 59 (52.5~70.5) years. The diabetes mellitus combined with PLA group included 17 males and 5 females, aged 59 (52.25~67.75) years. The healthy control group consisted of 14 males and 13 females, aged 50 (44.5~54.5) years. There were no significant gender differences among the three groups.
Additionally, basic information (age, gender, hospitalization duration and underlying diseases), symptoms (fever and abdominal pain), laboratory tests, imaging studies (ultrasound and CT for lesion size), complications, and etiological examinations in diabetes mellitus patients combined with PLA were also collected.
Inclusion criteria for diabetes mellitus were met the 1999 WHO diagnostic criteria for type 2 diabetes mellitus. Diagnostic criteria for PLA: (1) typical imaging changes such as B-ultrasound, CT, or MRI showing liver abscess; (2) confirmed by liver puncture or surgical evidence; (3) in the absence of typical imaging and etiological evidence, abscess shrinks, disappears, and symptoms alleviate after antibiotic treatment.
Those patients with tuberculous liver abscess, amoebic liver abscess, hydatid disease of the liver, concomitant tumors, hematological system diseases, autoimmune diseases, chronic liver or kidney diseases and thyroid diseases were excluded. This study was authorized by the Ethics Committee of the First Affiliated Hospital of Fujian Medical University (approval number [2022]075). Informed consent was obtained from all participants.
Data Collection
Data were obtained from the hospital medical electronic records system. For each enrolled patient, the following clinical data were documented: demographic data (age and gender), clinical symptoms, underlying conditions, laboratory results, imaging findings and outcomes. Fasting venous blood of patients were extracted within 24 hours of admission and at discharge. Serum APOC2 levels at baseline and discharge were detected by Immune Turbidity Method using Apolipoprotein C-2 kit (BeiJing Strong Biotechnologies, Inc.) using Roche Cobas c 702 analyzer.
Statistical Analysis
Statistical analysis was performed using SPSS software. Normally distributed quantitative data are presented as Mean±SD, while non-normally distributed quantitative data are shown as median (Interquartile Range). The independent sample t-test was used for comparisons between two groups with normally distributed data, and one-way ANOVA for three groups. For non-normally distributed data, the Mann–Whitney U-test was used for two-group comparisons, and the Kruskal–Wallis H-test for three group comparisons. Categorical data are shown as case numbers (%), with group comparisons made using the χ2-test or Fisher’s exact test. P value of less than 0.05 was considered statistically significant.
Results
Demographic Data
The baseline data among the diabetes mellitus, diabetes mellitus combined with PLA, and the healthy control were compared as shown in Table 1. There were no significant differences in gender among the groups (P>0.05). Serum APOC2 levels in diabetes mellitus patients were significantly higher than those in healthy controls (4.681 (4.114~5.712) vs 3.490 (2.967~3.845) mg/dL, P=0.008). To minimize the systematic bias effect of age on APOC2 levels, we performed a subgroup analysis of age-matched diabetes mellitus patients and healthy controls (diabetes mellitus patients aged 48–54 years, n=22; healthy controls aged 46–54.5 years, n=23, Table S1). The results confirmed that serum APOC2 levels were still significantly higher in age-matched diabetes mellitus patients than in healthy controls (median: 4.785 mg/dL vs. 3.49 mg/dL, P<0.001), which is consistent with our original findings.
Table 1.
Comparison of Clinical Baseline Data Among the Diabetes Mellitus, Diabetes Mellitus Combined with PLA and Healthy Control
| Variables | Healthy Control (n = 27) |
Diabetes Mellitus (n = 55) |
Diabetes Mellitus Combined with PLA (n = 22) |
P1 | P2 | P3 |
|---|---|---|---|---|---|---|
| Gender, n (%) | 0.132 | 1 | 0.112 | |||
| Female | 13 (48.148) | 25 (45.455) | 5 (22.727) | |||
| Male | 14 (51.852) | 30 (54.545) | 17 (77.273) | |||
| Age (years), Median (Q1,Q3) | 50 (44.5, 54.5) | 59 (52.5, 70.5) | 59 (52.25, 67.75) | 0.002 | < 0.001 | 0.817 |
| TBIL (μmol/L), Median (Q1,Q3) | 10 (7.8, 11.1) | 9.5 (7.2, 13.9) | 8.6 (6.2, 29.2) | 0.943 | 0.834 | 0.761 |
| ALB (g/L), Median (Q1,Q3) | 44.7 (43.7, 47.8) | 43.1 (40.15, 45.1) | 34.1 (27.5, 37) | < 0.001 | < 0.001 | < 0.001 |
| ALT (U/L), Median (Q1,Q3) | 15 (13, 19) | 22 (14.25, 34) | 35 (26.5, 102.75) | < 0.001 | 0.002 | < 0.001 |
| AST (U/L), Median (Q1,Q3) | 18 (17, 18.5) | 22 (18, 28.75) | 34.5 (26.25, 57.5) | < 0.001 | 0.002 | < 0.001 |
| GGT (U/L), Median (Q1,Q3) | 17 (13, 21) | 23 (14, 40) | 131 (96.5, 191.75) | < 0.001 | 0.009 | < 0.001 |
| ALP (U/L), Median (Q1,Q3) | 68 (55, 76.5) | 69 (55, 82) | 156.5 (119.75, 221.25) | < 0.001 | 0.593 | < 0.001 |
| TCHO (mmol/L), Median (Q1,Q3) | 4.09 (3.835, 4.525) | 4.57 (3.85, 5) | 3.25 (2.985, 3.585) | < 0.001 | 0.054 | < 0.001 |
| Tg (mmol/L), Median (Q1,Q3) | 1.01 (0.785, 1.255) | 1.47 (1.105, 2.23) | 1.16 (0.85, 1.585) | < 0.001 | < 0.001 | 0.034 |
| HDL (mmol/L), Median (Q1,Q3) | 1.319 ± 0.142 | 1.207 ± 0.351 | 0.801 ± 0.293 | < 0.001 | 0.114 | < 0.001 |
| TG/HDL ratio, Median (Q1,Q3) | 0.769 (0.635, 1.02) | 1.219 (0.867, 2.22) | 1.55 (1.018, 2.643) | < 0.001 | < 0.001 | 0.404 |
| LDL (mmol/L), Median (Q1,Q3) | 2.62 (2.42, 2.985) | 2.67 (2.15, 3.24) | 1.92 (1.445, 2.335) | 0.001 | 0.798 | 0.001 |
| APOA1 (g/L), Median (Q1,Q3) | 1.42 (1.355, 1.535) | 1.335 (1.19, 1.53) | 0.68 (0.48, 0.765) | < 0.001 | 0.203 | < 0.001 |
| APOB (g/L), Median (Q1,Q3) | 0.83 (0.76, 0.925) | 0.985 (0.85, 1.192) | 0.85 (0.735, 0.995) | 0.002 | < 0.001 | 0.018 |
| APOC2 (mg/dL), Median (Q1,Q3) | 3.49 (2.967, 3.845) | 4.681 (4.114, 5.712) | 2.470 (2.202, 3.034) | < 0.001 | < 0.001 | < 0.001 |
| GLU (mmol/L), Median (Q1,Q3) | 4.55 (4.34, 4.885) | 7.29 (5.99, 8.59) | 6.535 (5.49, 9.75) | < 0.001 | < 0.001 | 0.594 |
| HBA1c (%), Median (Q1,Q3) | 5.6 (5.175, 6.225) | 7.4 (6.7, 8.8) | 7 (6.15, 8.8) | < 0.001 | < 0.001 | 0.48 |
Notes: P1: One-Way ANOVA of diabetes mellitus, diabetes mellitus with PLA, and healthy control group, P2: Comparison between diabetes mellitus and healthy control, P3: Comparison between diabetes mellitus and diabetes mellitus combined with PLA.
While, in diabetes mellitus combined with PLA, serum APOC2 levels were significantly lower than those in diabetes mellitus patients 2.470 (2.202~3.034) vs 4.681 (4.114~5.712) mg/dL, P<0.001) (Figure 1A). In patients with diabetes mellitus combined with PLA, paired t-tests showed a significant increase in serum APOC2 levels before and after treatment (2.470 (2.202~3.034) vs 4.323 (3.719~4.776) mg/dL, P<0.001) (Figure 1B). These results indicate that serum APOC2 levels significantly decrease when diabetes mellitus is combined with PLA but significantly increase and return to normal after treatment.
Figure 1.
(A) Serum APOC2 levels in healthy controls, diabetes mellitus, and diabetes mellitus combined with PLA. (B) Serum APOC2 levels in diabetes mellitus combined with PLA patients before and after treatment. Data are presented as the mean ± SEM, ****p<0.0001.
The Diagnostic Value of Serum APOC2 in Diabetes Mellitus Combined with PLA
The ROC curve analysis shows that APOC2 has an AUC of 0.94 (95% CI: 0.870~0.999) for diagnosing diabetes mellitus combined with PLA, with an optimal cutoff value of 3.403 mg/dL, and both sensitivity and specificity are 0.909 (Figure 2). Furthermore, through univariate and multivariate logistic regression analysis, it was found that after adjusting for gender and age, a decrease in serum APOC2 is a risk factor for PLA in diabetes mellitus patients (OR=0.02 (0.01, 0.16), P=0.012) (Table 2). However, owing to the small sample size, the multivariate result should be interpreted with caution, and that future studies with larger cohorts are needed to validate these findings.
Figure 2.
ROC curves of serum APOC2 for the prediction of PLA in diabetes mellitus patients.
Table 2.
Univariable and Multivariate Logistic Regression Analysis to Predict PLA in Diabetes Mellitus
| Baseline Variable | Univariate Analysis | Multivariate Analysis | ||
|---|---|---|---|---|
| OR (95% CI) | P Value | OR (95% CI) | P Value | |
| Gender | ||||
| Female | — | — | — | — |
| Male | 2.833(0.916–8.768) | 0.071 | 30.5(0.85–1113) | 0.12 |
| Age (years) | 1.007(0.973–1.043) | 0.671 | 1.07(0.97, 1.24) | 0.3 |
| TBIL (μmol/L) | 1.073(1.006–1.144) | 0.033 | — | — |
| ALB (g/L) | 0.661(0.542–0.806) | <0.001 | 0.41(0.14, 0.72) | 0.023 |
| ALT (U/L) | 1.038(1.015–1.062) | 0.001 | — | — |
| AST (U/L) | 1.062(1.017–1.109) | 0.006 | — | — |
| GGT (U/L) | 1.036(1.02–1.054) | <0.001 | — | — |
| ALP (U/L) | 1.042(1.02–1.064) | <0.001 | — | — |
| TCHO (mmol/L) | 0.154(0.057–0.418) | <0.001 | — | — |
| Tg (mmol/L) | 0.553(0.264–1.157) | 0.116 | — | — |
| HDL (mmol/L) | 0.013(0.001–0.124) | <0.001 | — | — |
| LDL (mmol/L) | 0.334(0.161–0.694) | 0.003 | — | — |
| APOA1 (g/L) | 0.001(0.001–0.003) | 0.001 | — | — |
| APOB (g/L) | 0.042(0.003–0.646) | 0.023 | — | — |
| APOC2 (mg/dL | 0.104(0.035–0.307) | <0.001 | 0.02(0.00, 0.16) | 0.012 |
| GLU (mmol/L) | 0.989(0.827–1.181) | 0.9 | — | — |
| HBA1c (%) | 0.952(0.717–1.263) | 0.731 | — | — |
Abbreviation: OR, Odds ratio.
Correlation Between Serum APOC2 Levels and Baseline Variables of Diabetes Mellitus Combined with PLA
Based on the median levels of APOC2, diabetes mellitus combined with PLA were divided into high and low APOC2 level groups. As shown in Table 3, in the low-APOC2 level group, ALT levels (101 (43.5~131.5) vs 31 (21~34) U/L, P=0.038) and AST levels were significantly higher (55 (39.5~103.5) vs 28 (24~34), U/L, P=0.007). Correlation analyses were further conducted between serum APOC2 levels and ALT or AST, with detailed results presented in Table S2. A negative correlation was observed between serum APOC2 expression and both ALT and AST, although the correlations did not reach statistical significance possibly due to the relatively small sample size of this study. Together, these findings further support that reduced serum APOC2 levels are closely associated with liver damage.
Table 3.
Clinical Characteristics of Diabetes Mellitus Combined with PLA Stratified According to Median Levels of Serum APOC2 (2.47 mg/dL)
| Variables | Total (n = 22) | APOC2<Median (n = 11) | APOC2>Median (n = 11) | P |
|---|---|---|---|---|
| Gender, n (%) | 0.311 | |||
| Female | 5 (22.727) | 4 (36.364) | 1 (9.091) | |
| Male | 17 (77.273) | 7 (63.636) | 10 (90.909) | |
| Age | 59.909 ± 11.731 | 55.455 ± 9.554 | 64.364 ± 12.412 | 0.075 |
| Duration of hospital stay (d) | 18.048 ± 7.883 | 20.182 ± 8.953 | 15.7 ± 6.111 | 0.194 |
| Hypertension, n (%) | 0.635 | |||
| No | 16 (72.727) | 9 (81.818) | 7 (63.636) | |
| Yes | 6 (27.273) | 2 (18.182) | 4 (36.364) | |
| Maximal body temperature (°C) | 38.214 ± 0.98 | 38.064 ± 1.155 | 38.38 ± 0.771 | 0.467 |
| Abdominal pain (%) | 0.199 | |||
| No | 12 (54.545) | 4 (36.364) | 8 (72.727) | |
| Yes | 10 (45.455) | 7 (63.636) | 3 (27.273) | |
| Vomit (%) | 0.149 | |||
| No | 16 (72.727) | 6 (54.545) | 10 (90.909) | |
| Yes | 6 (27.273) | 5 (45.455) | 1 (9.091) | |
| Maximal diameter of abscess (cm) | 5.5 (4.35, 6.45) | 5.7 (5.425, 6.55) | 5.025 (4.025, 5.575) | 0.14 |
| TBIL (μmol/L),Median (Q1,Q3) | 8.6 (6.2, 29.2) | 8.2 (6.7, 38.4) | 8.85 (5.95, 26.175) | 0.418 |
| ALB (g/L), Median (Q1,Q3) | 32.995 ± 5.495 | 32.391 ± 5.494 | 33.66 ± 5.713 | 0.611 |
| ALT (U/L), Median (Q1,Q3) | 35 (26.5, 102.75) | 101 (43.5, 131.5) | 31 (21, 34) | 0.038 |
| AST (U/L), Median (Q1,Q3) | 34.5 (26.25, 57.5) | 55 (39.5, 103.5) | 28 (24, 34) | 0.007 |
| GGT (U/L), Median (Q1,Q3) | 156.5 (119.75, 221.25) | 165 (126.5, 222.5) | 146 (113, 219) | 0.603 |
| ALP (U/L), Median (Q1,Q3) | 152.5 ± 88.114 | 140.818 ± 67.391 | 166.778 ± 111.111 | 0.55 |
| TCHO (mmol/L),Median (Q1,Q3) | 3.361 ± 0.818 | 3.048 ± 0.624 | 3.708 ± 0.899 | 0.087 |
| Tg (mmol/L),Median (Q1,Q3) | 1.16 (0.85, 1.585) | 1.015 (0.84, 1.22) | 1.27 (0.97, 1.93) | 0.211 |
| HDL (mmol/L),Median (Q1,Q3) | 0.801 ± 0.293 | 0.825 ± 0.329 | 0.776 ± 0.266 | 0.704 |
| TG/HDL ratio, Median (Q1,Q3) | 1.55 (1.018, 2.643) | 1.413 (0.988, 1.647) | 1.716 (1.25, 3.181) | 0.497 |
| LDL (mmol/L),Median (Q1,Q3) | 1.928 ± 0.844 | 1.851 ± 0.674 | 2.014 ± 1.037 | 0.694 |
| APOA1 (g/L), Median (Q1,Q3) | 0.641 ± 0.256 | 0.573 ± 0.2 | 0.717 ± 0.3 | 0.245 |
| APOB (g/L), Median (Q1,Q3) | 0.864 ± 0.187 | 0.844 ± 0.198 | 0.886 ± 0.183 | 0.64 |
| GLU (mmol/L),Median (Q1,Q3) | 6.535 (5.49, 9.75) | 7.105 (5.01, 9.93) | 6.535 (6.13, 8.38) | 0.579 |
| HBA1c (%),Median (Q1,Q3) | 7.86 ± 2.396 | 8.044 ± 2.512 | 7.583 ± 2.414 | 0.728 |
| CRP (g/L), Mean ± SD | 148.857 ± 99.837 | 165.415 ± 80.177 | 132.3 ± 117.898 | 0.451 |
| PCT (ng/L), Median (Q1,Q3) | 2.1 (0.54, 19.79) | 1.79 (0.68, 9.275) | 2.41 (0.47, 30.025) | 0.833 |
| WBC (109/L), Mean ± SD | 11.732 ± 4.034 | 12.519 ± 2.822 | 11.017 ± 4.92 | 0.398 |
| Neu (109/L), Mean ± SD | 9.945 ± 4.371 | 10.609 ± 3.048 | 9.341 ± 5.387 | 0.511 |
| Mono (109/L), Mean ± SD | 0.657 ± 0.328 | 0.799 ± 0.31 | 0.527 ± 0.3 | 0.056 |
| LYPMH (109/L), Mean ± SD | 1.026 ± 0.549 | 1.028 ± 0.566 | 1.025 ± 0.56 | 0.989 |
| NLR, Median (Q1,Q3) | 11.078 (5.29, 18.811) | 11.551 (7.599, 14.862) | 5.35 (4.385, 23.855) | 0.756 |
| RBC (1012/L), Mean ± SD | 3.915 ± 0.667 | 3.755 ± 0.862 | 4.061 ± 0.416 | 0.327 |
| Hb (g/L), Mean ± SD | 116.905 ± 18.069 | 111 ± 20.758 | 122.273 ± 14.093 | 0.169 |
| PLT (109/L), Mean ± SD | 252.286 ± 121.51 | 251.6 ± 145.001 | 252.909 ± 102.984 | 0.981 |
Discussion
PLA patients have a variety of clinical manifestations, and the classic triad of fever and right upper abdominal pain does not always show up, making early diagnosis a challenge for clinicians.4 Compared to patients without type 2 diabetes mellitus, those with type 2 diabetes mellitus are more prone to PLA and their clinical symptoms are less typical, mainly featuring chills and high fever rather than noticeable abdominal pain, leading to a higher rate of missed or incorrect diagnoses.5,16 With the rise in cases of diabetes mellitus combined with PLA, early diagnosis has become increasingly urgent and crucial. This study find that serum APOC2 levels are significantly decreased in diabetes mellitus patients combined with PLA compared to diabetes mellitus patients while APOC2 levels significantly increased post-treatment. In addition, ROC curve analysis and logistic regression analysis revealed that reduced serum APOC2 levels are a risk factor and had high diagnostic accuracy for diabetes mellitus combined with PLA. Therefore, APOC2 could be a potential marker for predicting the occurrence of PLA in diabetic patients, providing a new evidence for early diagnosis.
Since liver is the main source of APOC2 synthesis, in this study, diabetes mellitus combined with PLA patients are divided into two groups based on the levels of APOC2. PLA patients in low-APOC2 group have higher ALT and AST, which are the indication of liver damage. In addition, we find that the abscess diameter of the patients in the low-APOC2 group is larger than that in the high-APOC2 group. Our study indicates that PLA could affect the production of APOC2. Therefore, continuous dynamic monitoring APOC2 may provide references for the treatment and prognosis of diabetes mellitus combined with PLA.
This study has some limitations. Firstly, there are few cases of diabetes mellitus combined with PLA, and this study is single-centered. In the future, more multi-centered samples will be added to further clarify the diagnostic value of serum APOC2. Secondly, this study only collected serum APOC2 results within 24 hours of admission and at discharge, without continuous dynamic monitoring. Continuous follow-up results might better understand the relationship between APOC2 and infection process. Further, apolipoproteins may function as negative acute-phase proteins during acute infection.17 Accordingly, the observed reduction in APOC2 levels cannot be solely attributed to PLA-induced liver injury. We will therefore conduct further targeted studies to distinguish between these two distinct underlying mechanisms in our subsequent research. Lastly, the role of serum APOC2 in diabetes mellitus combined with PLA still need more in vitro/in vivo experiments to exemplify.
Conclusions
In conclusion, serum APOC2 is elevated in patients with diabetes mellitus and significantly reduced in those with diabetes mellitus complicated with PLA, with a more pronounced decrease in the presence of liver dysfunction. Serum APOC2 levels can recover to the normal range after treatment and clinical recovery, making it a potential biomarker for the early diagnosis and prognostic evaluation of diabetes mellitus complicated with PLA.
Acknowledgment
This paper has been uploaded to ResearchSquare as a preprint: https://www.researchsquare.com/article/rs-4800290/v1.
Funding Statement
This study was supported by National Natural Science Foundation of China (grant numbers: 82272420), Clinical Research Center for Traditional Chinese Medicine of Longyan City (grant number: 2025LYF1004) and Natural Science Foundation of Fujian Province, China (grant number: 2022J01228).
Abbreviations
ALB, Albumin; ALP, Alkaline Phosphatase; ALT, Alanine Aminotransferase; APOA1, Apolipoprotein A1; APOB, Apolipoprotein B; AST, Aspartate Aminotransferase; AUC, Area Under the Curve; CRP, C-reactive protein; GGT, Gamma-Glutamyl Transferase; GLU, Glucose; HBA1c, glycated hemoglobin; HDL, High-Density Lipoprotein; HGB, Hemoglobin; LDL, Low-Density Lipoprotein; LYMPH, Lymphocyte; MONO, Monocytes; Neu, Neutrophils; NLR, Neutrophil-to-Lymphocyte Ratio; PCT, Procalcitonin; PLA, Pyogenic liver abscess; RBC, Red Blood Cell; ROC, Receiver Operating Characteristic; TBIL, Total Bilirubin; TCHO, Total Cholesterol; TG, Triglyceride; TP, Total Protein; WBC, White Blood Cell.
Data Sharing Statement
The datasets and supporting materials of this article are available on reasonable request from corresponding author.
Ethical and Consent Statements
Approval of the research protocol: The study protocol has been approved by the Research Ethics Committee of the First Affiliated Hospital of Fujian Medical University and it conforms to the provisions of the Declaration of Helsinki. Written informed consent was obtained from all the patients for their consent to participate in this study and for their data to be used for research purposes and all private information of the included patients was erased. Approval date of Registry and the Registration No. of the study/trial: Research Ethics Committee of the First Affiliated Hospital of Fujian Medical University, Approval No. [2022]075, date: 02/08/2022.
Animal Studies: N/A.
Author Contributions
All authors significantly contributed to the reported work, including its conception, study design, execution, data acquisition, analysis, and interpretation. They participated in drafting, revising, or critically reviewing the article, gave final approval for the version to be published, agreed on the journal to which the article was submitted, and committed to being accountable for all aspects of the work.
Disclosure
The authors declare no conflicts of interest in this work.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The datasets and supporting materials of this article are available on reasonable request from corresponding author.