| Biomarker | IL - 6, sCD163 | Full name | Interleukin-6, soluble CD163 | Molecular Type | Protein (cytokines/macrophage marker) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Inflammation monitoring and disease progression assessment | ||
| Disease(or Constitution) | Chronic pancreatitis (CP) | Disease Subtypes | Chronic pancreatitis (CP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (ELISA, immunoassay) | ||
| Pathobiological Mechanisms | IL - 6 mediated chronic inflammation, reflect sCD163 macrophage activation, the participation of the CP process of chronic inflammation, fibrosis | ||||
| Clinical Availability Status | Clinical study phase: persistently elevated in CP patients and associated with disease progression | ||||
| Notes and Dynamics | It can be used to monitor the inflammatory activity of CP and evaluate the control effect of treatment on inflammation. It is expected to be included in the clinical monitoring system | ||||
| Biomarker | MMP-9/TIMP-1 ratio | Full name | Matrix metalloproteinase-9/Tissue inhibitor of metalloproteinase-1 ratio | Molecular Type | Protein (matrix metalloproteinases/inhibitor) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Fibrosis monitoring and prognosis | ||
| Disease(or Constitution) | Acute pancreatitis (AP) | Disease Subtypes | Acute pancreatitis (AP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (ELISA, Immunoblotting) | ||
| Pathobiological Mechanisms | MMP-9 is involved in pancreatic tissue remodeling, and TIMP-1 inhibits its activity. The increased ratio of MMP-9 to TIMP-1 indicates an increased risk of pancreatic fibrosis progression | ||||
| Clinical Availability Status | Clinical research phase: Ratio abnormalities have been identified in patients with AP and used to assess the risk of fibrosis | ||||
| Notes and Dynamics | It can predict the risk of AP transformation to chronic pancreatitis and provide a basis for early intervention. At present, it is being verified by expanding the sample size | ||||
| Biomarker | Lipase | Full name | Lipase | Molecular Type | Proteins (enzymes) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis and condition monitoring | ||
| Disease(or Constitution) | Acute pancreatitis (AP) | Disease Subtypes | Acute pancreatitis (AP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (Colorimetry, enzyme-linked immunosorbent assay) | ||
| Pathobiological Mechanisms | Pancreatic acinar cells secrete enzymes and specificity, increase damage after release, specificity is higher than the amylase, more accurately reflect the pancreas injury | ||||
| Clinical Availability Status | Clinical routine use: AP core markers, diagnostic specificity is better than that of amylase, is one of the diagnostic gold standard | ||||
| Notes and Dynamics | It has a certain correlation with the severity of AP, and can be used to identify non-pancreatic abdominal pain and guide clinical diagnosis | ||||
| Biomarker | Amylase | Full name | Amylase | Molecular Type | Protein (enzyme) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis and disease monitoring | ||
| Disease(or Constitution) | Acute pancreatitis (AP) | Disease Subtypes | Acute pancreatitis (AP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (colorimetry, enzyme-linked immunosorbent method) | ||
| Pathobiological Mechanisms | Pancreatic acinar cells, which are released into the blood after injury, are the classic diagnostic marker of AP and reflect the degree of pancreatic parenchymal injury | ||||
| Clinical Availability Status | Diagnostic criteria, clinical routine use: into the AP for early diagnosis and a dynamic monitoring | ||||
| Notes and Dynamics | Diagnostic sensitivity but the specificity is insufficient, need combined with lipase and clinical symptoms, avoid miscalculation | ||||
| Biomarker | TNF alpha | Full name | Tumor necrosis factor alpha | Molecular Type | Proteins (cytokines) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Inflammation monitoring, prognosis | ||
| Disease(or Constitution) | Acute pancreatitis (AP) | Disease Subtypes | Acute pancreatitis (AP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (immunoassay, ELISA) | ||
| Pathobiological Mechanisms | The key factors of early inflammatory response activate the NF-κB pathway, promote the release of pro-inflammatory factors, and aggravate pancreatic and systemic tissue damage | ||||
| Clinical Availability Status | Commonly used in clinical practice (inflammation monitoring) : It is widely used to evaluate the inflammatory activity of AP and to monitor the efficacy of anti-inflammatory treatment | ||||
| Notes and Dynamics | AP is elevated in the early stage and can quickly reflect the activation of inflammation, but its specificity is low, so it needs to be used in combination with other markers | ||||
| Biomarker | IL-6 | Full name | Interleukin-6 | Molecular Type | Proteins (cytokines) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Inflammation monitoring, prognosis | ||
| Disease(or Constitution) | Acute pancreatitis (AP) | Disease Subtypes | Acute pancreatitis (AP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (immunoassay, ELISA) | ||
| Pathobiological Mechanisms | In the systemic inflammatory response induced by AP, macrophages and other immune cells are secreted in large quantities, which mediate the inflammatory cascade and promote pancreatic tissue damage | ||||
| Clinical Availability Status | Commonly used in clinical practice (inflammation monitoring) : Routinely used to assess the severity of inflammation in AP and guide treatment decisions | ||||
| Notes and Dynamics | Positively related to the severity of AP, it is one of the core indicators of systemic inflammation clinical evaluation, dynamically monitoring the efficacy of treatment | ||||
| Biomarker | tRF-36 | Full name | tRNA-derived fragment 36 | Molecular Type | Trna-derived small RNA (tsRNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis and Prognosis | ||
| Disease(or Constitution) | Acute pancreatitis (AP) | Disease Subtypes | Acute pancreatitis (AP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (RNA sequencing, RNA pull - down) | ||
| Pathobiological Mechanisms | Interact with IGF2BP3, targeting the p53 mRNA m6A modification site, enhance its stability, and promote pancreatic acinar cell ferroptosis, aggravating the AP | ||||
| Clinical Availability Status | Cutting-edge research: clinical serum samples to rise significantly, expressed in cells in the model on inflammatory factor levels after low | ||||
| Notes and Dynamics | High stability, strong specificity, is expected to become a noninvasive biomarkers in early diagnosis of AP, its related pathways can be used as therapeutic targets | ||||
| Biomarker | tRF3-Thr-AGT | Full name | tRNA-derived fragment 3-Thr-AGT | Molecular Type | Trna-derived small RNA (tsRNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis and Prognosis | ||
| Disease(or Constitution) | Acute pancreatitis (AP) | Disease Subtypes | Acute pancreatitis (AP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (RNA sequencing, qRT-PCR) | ||
| Pathobiological Mechanisms | ZBP1 inhibits NLRP3-mediated pyroptosis and inflammation by binding to its 3'-UTR region, and its down-regulation will aggravate AP inflammatory injury | ||||
| Clinical Availability Status | Cutting-edge research: already validation functions in the cell and animal models, clinical samples showed abnormal expression | ||||
| Notes and Dynamics | It can affect the progression of AP by regulating pancreatic acinar cell pyroptosis, which is a potential non-invasive diagnostic marker and therapeutic target | ||||
| Biomarker | RAR (red blood cell distribution width-albumin ratio) | Full name | RDW-albumin ratio | Molecular Type | Composite index (hematology index + protein) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Assessment of prognosis and severity | ||
| Disease(or Constitution) | Acute pancreatitis (AP) | Disease Subtypes | Acute pancreatitis (AP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Whole blood (blood routine + serum albumin detection) | ||
| Pathobiological Mechanisms | RDW reflect systemic inflammation and oxidative stress, albumin reflects the status of nutrition and inflammation, the combination can be comprehensive evaluation AP inflammation degree and prognosis | ||||
| Clinical Availability Status | Clinical validation: was validated through a number of retrospective study, used for AP mortality and severe degree of prediction | ||||
| Notes and Dynamics | Operation is simple, low cost, and can be obtained from routine blood test, rapid risk stratification for limited resources scene, although flair than traditional grading system, but the advantage is quick and easy | ||||
| Biomarker | APOE ε4 | Full name | Apolipoprotein E ε4 allele | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Susceptibility | ||
| Disease(or Constitution) | Acute pancreatitis (AP) | Disease Subtypes | Acute pancreatitis (AP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Whole blood (genotyping) | ||
| Pathobiological Mechanisms | Influence of lipid metabolism, reduce A beta removal efficiency, carriers AP related neurological complications increased risk and the time in advance | ||||
| Clinical Availability Status | Clinical available (risk assessment) : conventional genetic tests available, but only for risk assessment, not for diagnosis, involves ethical issues | ||||
| Notes and Dynamics | It is the core variable in establishing the risk stratification model of neurological complications of AP. Important stratification factor is related to treatment trials | ||||
| Biomarker | GFAP | Full name | Glial fibrillary acidic protein | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Susceptibility, early diagnosis | ||
| Disease(or Constitution) | Acute pancreatitis (AP) | Disease Subtypes | Acute pancreatitis (AP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Plasma (SIMOA) | ||
| Pathobiological Mechanisms | The markers of astrocyte activation are activated in the early inflammatory response of AP, which is earlier than some traditional inflammatory markers | ||||
| Clinical Availability Status | Cutting-edge research: a lot of evidence that its phase before symptoms or have change, is a potential risk early warning markers | ||||
| Notes and Dynamics | High correlation with the AP early inflammatory pathology and possible earlier than p - tau reflect systemic inflammation caused by activation of glial cells | ||||
| Biomarker | Nerve filament light chain (NfL) | Full name | Neurofilament light chain | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Monitoring, prognosis | ||
| Disease(or Constitution) | Acute pancreatitis (AP) | Disease Subtypes | Acute pancreatitis (AP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | CSF/Plasma (SIMOA) | ||
| Pathobiological Mechanisms | Axon damage after the release of cytoskeleton proteins, is a specific neurons damage marks, the AP caused by systemic inflammation can result in the release | ||||
| Clinical Availability Status | Research/clinical monitoring tools: widely used in clinical trials for effectiveness monitoring indicators; Clinically used to assess the progression of nerve injury | ||||
| Notes and Dynamics | It is elevated in a variety of diseases such as AP, MS, ALS, and can be used to evaluate the degree of AP-related nerve damage and treatment response | ||||
| Biomarker | p-tau (181, 217) | Full name | Phosphorylated tau (181, 217) | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, Prognosis | ||
| Disease(or Constitution) | Acute pancreatitis (AP) | Disease Subtypes | Acute pancreatitis (AP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | CSF/Plasma (SIMOA, IP-MS) | ||
| Pathobiological Mechanisms | Tau protein phosphorylation cause nerve fiber entanglement, cytoskeleton damage neurons, the nerve injury induced by abnormal expression and AP | ||||
| Clinical Availability Status | Clinical validation/guideline recommendation: CSF p-tau is the core marker for the diagnosis of related nerve injury; Plasma P-tau 217 has excellent diagnostic performance | ||||
| Notes and Dynamics | P - tau217 specificity is higher than p - tau181 is AP related nerve complications, evaluate the potential of molecular | ||||
| Biomarker | Aβ42/40 ratio | Full name | Amyloid-beta 42/40 ratio | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, susceptibility | ||
| Disease(or Constitution) | Acute pancreatitis (AP) | Disease Subtypes | Acute pancreatitis (AP) | ||
| Organ | Pancreas | Test Sample / Technology Platform | CSF/plasma (SIMOA, ELISA) | ||
| Pathobiological Mechanisms | Aβ42 aggregates into oligomers and plaques leading to neurotoxicity, while Aβ40 is relatively stable. The reduction of Aβ40 ratio is more reliable than A single indicator to reflect Aβ pathology and indirectly related to the mechanism of pancreatic inflammatory injury | ||||
| Clinical Availability Status | Study validation/early clinical: CSF testing was included in the study criteria; Plasma testing is being validated on a large scale | ||||
| Notes and Dynamics | Plasma Aβ42/40 is A hot spot for early screening and population screening, which is expected to enter clinical practice and provide a supplement for early diagnosis of AP | ||||
| Biomarker | PR | Full name | Progesterone receptor | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis differential | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Mucous sex cystic neoplasm (MCN) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Tissue (immunohistochemistry) | ||
| Pathobiological Mechanisms | Progesterone receptor, type in ovarian interstitial abnormal expression in MCN, to participate in the regulation of tumor cell proliferation | ||||
| Clinical Availability Status | Clinical research stage: it is a specific diagnostic marker for MCN and can distinguish MCN from other pancreatic cystic lesions | ||||
| Notes and Dynamics | Has tissue specificity, identification is of important value to the diagnosis of MCN, especially in imaging the atypical cases | ||||
| Biomarker | MUC5AC+MUC2+MUC1 | Full name | Mucin 5AC + Mucin 2 + Mucin 1 | Molecular Type | Protein combination |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | A premalignant lesion progression prediction | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Mucinous cystic neoplasm (MCN) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Tissue (immunohistochemistry) | ||
| Pathobiological Mechanisms | Members of the family of mucin MUC5AC and MUC2 expression in noninvasive MCN, (MUC1) expression is associated with invasive characteristics | ||||
| Clinical Availability Status | Clinical research phase: used to assess the risk of progression of MCN, guiding surgical intervention in time | ||||
| Notes and Dynamics | It can be used to distinguish non-invasive and invasive MCN, provide molecular basis for clinical decision-making, and avoid overtreatment or undertreatment | ||||