| Biomarker | Hepatitis B core-related antigen (HBcrAg) | Full name | Hepatitis B core-related antigen | Molecular Type | Proteins |
| Molecular Formula | Human HBcrAg (HBcAg+HBeAg): C₄₁₂H₆₄₇N₁₁₉O₁₃₀S₄ | Molecular Weight | ~92 kDa | Core Functional Dimensions | Virus replication monitoring, prognosis assessment, recurrence prediction |
| Disease(or Constitution) | Viral Hepatitis | Disease Subtypes | Hepatitis B (HBV) | ||
| Organ | Liver | Test Sample / Technology Platform | Serum | ||
| Pathobiological Mechanisms | It contains HBcAg, HBeAg and other proteins, which are highly correlated with cccDNA levels and can reflect the viral replication status. It can predict the risk of liver fibrosis, cirrhosis and liver cancer, and guide the timing of drug withdrawal | ||||
| Clinical Availability Status | Clinical research phase (used in clinical practice in some areas) | ||||
| Notes and Dynamics | It is suitable for rapid detection in resource-limited areas. It is an important candidate marker for precise management of chronic hepatitis B, and needs to be further validated to establish a unified standard | ||||
| Biomarker | Serum HBV RNA | Full name | Serum Hepatitis B Virus RNA | Molecular Type | Nucleic acids |
| Molecular Formula | HBV RNA (genotype B): Variable sequence (typical ~3.2 kb) | Molecular Weight | ~1.06 MDa (per 3.2 kb strand) | Core Functional Dimensions | Virus replication monitoring, treatment response evaluation, prognosis prediction |
| Disease(or Constitution) | Viral Hepatitis | Disease Subtypes | Hepatitis B (HBV) | ||
| Organ | Liver | Test Sample / Technology Platform | Serum | ||
| Pathobiological Mechanisms | The transcription products directly derived from covalently closed circular DNA (cccDNA) can accurately reflect the transcription activity of cccDNA. It can predict HBeAg/HBsAg seroconversion, recurrence after treatment and the risk of HCC | ||||
| Clinical Availability Status | Clinical research phase | ||||
| Notes and Dynamics | As a non-invasive surrogate marker of cccDNA activity, it has important potential in the management of chronic hepatitis B and can make up for the shortage of existing markers. However, standardized detection methods are needed to promote clinical application | ||||
| Biomarker | Aspartate Aminotransferase (AST) | Full name | Aspartate Aminotransferase | Molecular Type | Enzymes |
| Molecular Formula | Human AST: C₁₁₁₃H₁₇₆₁N₂₉₅O₃₃₅S₆ | Molecular Weight | ~121 kDa | Core Functional Dimensions | Assessment of liver injury, disease staging, and prognosis |
| Disease(or Constitution) | Viral Hepatitis | Disease Subtypes | Hepatitis B (HBV), Hepatitis C (HCV), other viral hepatitis | ||
| Organ | Liver | Test Sample / Technology Platform | Serum | ||
| Pathobiological Mechanisms | It is widely distributed in liver, heart, muscle and other tissues, and is released into the blood when hepatocytes are injured. AST/ALT ratio > 1 indicates cirrhosis or severe liver injury, which is associated with liver cancer and all-cause mortality. It can assist in assessing the degree of liver fibrosis | ||||
| Clinical Availability Status | Routine clinical use | ||||
| Notes and Dynamics | The diagnostic value is slightly inferior to ALT, but combined with ALT and AST/ALT ratio can improve the ability to identify advanced liver disease, which is an important supplementary indicator for clinical comprehensive evaluation of liver health | ||||
| Biomarker | Alanine aminotransferase (ALT) | Full name | Alanine aminotransferase | Molecular Type | Enzymes |
| Molecular Formula | Human ALT: C₁₁₀₇H₁₇₅₃N₂₉₃O₃₃₁S₆ | Molecular Weight | ~120 kDa | Core Functional Dimensions | Liver injury detection, disease diagnosis and prognosis evaluation |
| Disease(or Constitution) | Viral Hepatitis | Disease Subtypes | Hepatitis B (HBV), Hepatitis C (HCV), other viral hepatitis | ||
| Organ | Liver | Test Sample / Technology Platform | Serum | ||
| Pathobiological Mechanisms | It is mainly expressed in the liver and released into the blood when hepatocytes are injured. It is a sensitive indicator of liver injury. It can reflect the degree of liver inflammation, and is related to viral replication and metabolic disorders. The fluctuation of its level can indicate the progression of disease and the response to treatment | ||||
| Clinical Availability Status | Markers are routinely used in clinical practice | ||||
| Notes and Dynamics | Although the classic and cost-effective core markers are affected by factors such as age and gender, they are still the key tools for early detection and efficacy monitoring of chronic liver disease, and the diagnostic accuracy should be optimized in combination with other indicators | ||||
| Biomarker | Serum antibodies (anti-Saccharomyces cerevisiae ASCA, ANCA, AEA, etc) | Full name | Serum antibodies (anti-Saccharomyces cerevisiae antibody, antineutrophil cytoplasmic antibody, anti-enterocyte antibody, etc) | Molecular Type | Proteins (immunoglobulins, e.g., IgG, IgA) |
| Molecular Formula | Human ASCA (IgG/IgA): C₆₃₂H₉８₄N₁₆₄O₁₉６S₈ (IgG), C₆₂０H₉６２N₁６０O₁９２S₈ (IgA); ANCA (IgG): C₆₃₂H₉８₄N₁₆₄O₁₉６S₈; AEA (IgG): C₆₃₂H₉８₄N₁₆₄O₁₉６S₈ | Molecular Weight | ~150 kDa (IgG), ~160 kDa (IgA) | Core Functional Dimensions | Identification of IBD subtypes (CD vs UC), assessment of disease susceptibility, and association of disease severity |
| Disease(or Constitution) | Inflammatory Bowel Disease (IBD) | Disease Subtypes | / | ||
| Organ | Intestine | Test Sample / Technology Platform | Serum (enzyme-linked immunosorbent assay ELISA, indirect immunofluorescence assay IIF, Western blot) | ||
| Pathobiological Mechanisms | The pathogenesis of IBD is closely related to intestinal flora imbalance and immune abnormalities: 1. Anti-saccharomyces cerevisiae antibody (ASCA) : Saccharomyces cerevisiae is a component of normal intestinal flora. Due to the damage of intestinal mucosal barrier, the yeast antigen enters the circulation of CD patients and induces the body to produce specific antibodies (mostly IgG/IgA), which is related to intestinal transmural inflammation, fistula formation and other complications of CD. 2. Antineutrophil cytoplasmic antibody (ANCA, mainly p-ANCA) : Due to the abnormal activation of neutrophils in UC patients, its cytoplasmic components are exposed and become autoantigens, inducing the body to produce autoantibodies, which is related to localized inflammation and mucosal erosion and ulcer in UC. Anti-enterocyte antibody (AEA) : The antibody against the surface antigen of intestinal epithelial cells can damage the intestinal barrier and aggravate inflammation. The positive rate of AEA in IBD patients is low, but it is positively correlated with the severity of the disease. | ||||
| Clinical Availability Status | Clinical use/guideline recommendation: as an important auxiliary indicator for the differentiation of IBD subtypes (CD vs UC), it has been included in the consensus on the diagnosis and classification of IBD, especially when the clinical manifestations are atypical and the subtypes are difficult to be distinguished by endoscopy and imaging, but it is not an independent diagnostic indicator. | ||||
| Notes and Dynamics | Serum antibodies (especially ASCA+ANCA combination) are the core auxiliary tools for the identification of IBD subtypes, which can effectively improve the accuracy of the identification of CD and UC, and provide reference for the selection of clinical treatment options (for example, CD is more likely to require biological agents, and UC can give priority to 5-aminosalicylic acid drugs). However, it should be noted that its sensitivity is limited (for example, the positive rate of ASCA in CD is about 40%-60%, and the positive rate of ANCA in UC is about 50%-70%), and it cannot be used alone for the diagnosis of IBD. In addition, some healthy people or patients with other autoimmune diseases (such as rheumatoid arthritis) may also have false positive results, which should be judged comprehensively by endoscopy, pathology and clinical symptoms. It is not recommended as a population screening index. | ||||
| Biomarker | Fecal Lactoferrin (FLF) | Full name | Fecal Lactoferrin | Molecular Type | Protein (iron-binding glycoprotein) |
| Molecular Formula | Human lactoferrin: C₆₉₀H₁₁₁₂N₁８８O₂₀₀S₄ | Molecular Weight | ~80 kDa | Core Functional Dimensions | Monitoring of intestinal inflammatory activity, early warning of disease recurrence, and evaluation of therapeutic effect |
| Disease(or Constitution) | Inflammatory Bowel Disease (IBD) | Disease Subtypes | / | ||
| Organ | Intestine | Test Sample / Technology Platform | Stool (enzyme-linked immunosorbent assay, immunoturbidimetric assay, colloidal gold assay) | ||
| Pathobiological Mechanisms | Lactoferrin is mainly synthesized by the secondary granules of neutrophils, and a small amount is secreted by mammary gland and intestinal epithelial cells. Lactoferrin has the functions of antibacterial, regulating intestinal mucosal immunity and maintaining intestinal barrier function. When inflammatory injury occurs in the intestinal mucosa of IBD patients, neutrophils accumulate and degranulate in large quantities, releasing lactoferrin into the intestinal lumen and excreted with feces. The level of lactoferricin in feces is positively correlated with the degree of neutrophil infiltration in the intestinal mucosa and the extent of inflammatory damage. It can sensitively reflect the dynamic changes of intestinal inflammation, which increases in the active stage of the disease, decreases in the remission stage, and increases in the early stage before recurrence, which can warn of disease fluctuations in advance. | ||||
| Clinical Availability Status | It has been included in the consensus on the diagnosis and treatment of IBD as an important auxiliary indicator for the monitoring of intestinal inflammatory activity, especially in primary medical institutions or in the absence of complex detection equipment. Some guidelines combine it with fecal calprotectin for the management of IBD. | ||||
| Notes and Dynamics | Fecal lactoferrin has the advantages of fast detection speed (such as 15-30 minutes for colloidal gold method) and low operation threshold, which is suitable for rapid clinical assessment of intestinal inflammation, especially for the follow-up monitoring and recurrence warning of IBD patients. However, compared with fecal calprotectin, its stability is slightly worse (greatly affected by the storage conditions of fecal samples), and its sensitivity is slightly lower in mild inflammation, so it should be combined with clinical symptoms when used alone. In addition, intestinal infection, ischemic bowel disease, etc., may also lead to its increase, which needs to be identified. | ||||
| Biomarker | Fecal Calprotectin (FCP) | Full name | Fecal Calprotectin | Molecular Type | Protein (calcium-binding protein) |
| Molecular Formula | Human calprotectin (S100A8/S100A9 heterodimer): C₁₈₄H₂₈₆N₄₈O₅₄S₄ | Molecular Weight | ~24 kDa | Core Functional Dimensions | Assessment of intestinal inflammatory activity, monitoring of disease activity, and differential diagnosis (organic vs. functional bowel disease) |
| Disease(or Constitution) | Inflammatory Bowel Disease (IBD) | Disease Subtypes | / | ||
| Organ | Intestine | Test Sample / Technology Platform | Stool (enzyme-linked immunosorbent assay ELISA, immunochromatography, latexenhanced immunoturbidimetry) | ||
| Pathobiological Mechanisms | Calprotectin is mainly synthesized and released by neutrophils, and a small amount of calprotectin is derived from monocytes and epithelial cells. Calprotectin has anti-inflammatory, antibacterial and immunomodulatory effects. During the onset of inflammatory bowel diseases (IBD, including ulcerative colitis (UC) and Crohn's disease (CD), the intestinal mucosa has an immune inflammatory response, and neutrophils infiltrate and activate in large numbers, releasing calprotectin into the intestinal lumen and excreted with feces. The level of calprotective protein in feces is directly related to the severity of intestinal mucosal inflammation and the number of neutrophil infiltration, which can reflect the activity of intestinal inflammation. It is not affected by extrintestinal inflammation (such as respiratory tract infection), and specifically points to local intestinal inflammation. | ||||
| Clinical Availability Status | It has become a core biomarker recommended by the guidelines for the diagnosis and treatment of IBD. It is widely used in the differentiation of IBD and irritable bowel syndrome (IBS), assessment of disease activity (such as guiding the timing of endoscopy), and monitoring of treatment response. | ||||
| Notes and Dynamics | Fecal calprotectin is a "landmark" marker in the clinical management of IBD. It has the advantages of non-invasive, convenient and high specificity (for local intestinal inflammation), which can reduce unnecessary endoscopy and reduce the burden of patients. However, it should be noted that intestinal infection (such as bacterial and parasitic infection), colorectal tumor and other diseases may also lead to a mild increase in fecal calprotective protein. Clinical diagnosis should be based on symptoms, medical history and other examinations. In addition, it has limited value in the identification of IBD subtypes (UC vs CD), so it should be used in combination with other indicators. | ||||
| Biomarker | IDH1 R132H Mut | Full name | Isocitrate Dehydrogenase 1 R132H Mutation | Molecular Type | Gene Mutation |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Prognosis |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Brain Tumor-Associated Epilepsy (BTRE) | ||
| Organ | Brain | Test Sample / Technology Platform | Tumor Tissue (NGS, Immunohistochemistry) | ||
| Pathobiological Mechanisms | Mutation leads to abnormal isocitrate dehydrogenase function, excessive production of D-2-hydroxyglutarate (D2HG), enhances neuronal excitability. | ||||
| Clinical Availability Status | Under clinical validation | ||||
| Notes and Dynamics | Incidence exceeds 70% in low-grade glioma patients; mutation carriers have a 3-fold higher preoperative epilepsy risk than wild-type. | ||||
| Biomarker | GABA-B R Ab | Full name | GABA-B Receptor Antibody | Molecular Type | Autoantibody |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Etiology |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Autoimmune Epilepsy | ||
| Organ | Brain | Test Sample / Technology Platform | Serum/Cerebrospinal Fluid (ELISA, Cell-based Assay) | ||
| Pathobiological Mechanisms | Binds to GABA-B receptors, inhibits inhibitory neurotransmission, leading to hyperexcitability of the neuronal network. | ||||
| Clinical Availability Status | Under clinical validation | ||||
| Notes and Dynamics | Often accompanied by limbic encephalitis, associated with refractory epilepsy; immunotherapy can improve prognosis. | ||||
| Biomarker | LGI1 Ab | Full name | Leucine-Rich Glioma-Inactivated 1 Antibody | Molecular Type | Autoantibody |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Etiology |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Autoimmune Epilepsy | ||
| Organ | Brain | Test Sample / Technology Platform | Serum/Cerebrospinal Fluid (Indirect Immunofluorescence, ELISA) | ||
| Pathobiological Mechanisms | Targets the neuronal surface LGI1 protein, disrupts the voltage-gated potassium channel complex, and induces limbic encephalitis-related seizures. | ||||
| Clinical Availability Status | Clinically available | ||||
| Notes and Dynamics | Specificity reaches 92%, sensitivity 88%; the response rate of immunoglobulin therapy in antibody-positive patients exceeds 70%. | ||||
| Biomarker | HMGB1 | Full name | High Mobility Group Box 1 Protein | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Prediction |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Temporal Lobe Epilepsy (TLE) | ||
| Organ | Brain | Test Sample / Technology Platform | Serum/Cerebrospinal Fluid (ELISA, Western Blot) | ||
| Pathobiological Mechanisms | Acts as a damage-associated molecular pattern (DAMP) binding to TLR4, activates the NLRP3 inflammasome, promotes IL-1β release, and enhances NMDA receptor activity. | ||||
| Clinical Availability Status | Under clinical validation | ||||
| Notes and Dynamics | Serum HMGB1 levels are significantly elevated in drug-refractory TLE patients; anti-HMGB1 monoclonal antibodies can reduce seizures in animal models. | ||||
| Biomarker | IL-1β | Full name | Interleukin-1β | Molecular Type | Cytokine |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Prognosis |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Temporal Lobe Epilepsy (TLE) | ||
| Organ | Brain | Test Sample / Technology Platform | Serum/Cerebrospinal Fluid (ELISA, qPCR) | ||
| Pathobiological Mechanisms | Activates the NF-κB/MAPK pathway, enhances glutamate release in the hippocampus, inhibits GABAₐ receptor function, and exacerbates neuronal hyperexcitability. | ||||
| Clinical Availability Status | Under clinical validation | ||||
| Notes and Dynamics | CSF IL-1β levels in refractory TLE patients are 2.1 times higher than those in drug-sensitive patients; the caspase-1 inhibitor VX-765 can reduce seizure frequency. | ||||
| Biomarker | Intestinal alkaline phosphatase (IAP) | Full name | Intestinal alkaline phosphatase | Molecular Type | Proteins (enzymes) |
| Molecular Formula | Human IAP: C₁₀₀₂H₁₅₄₈N₂₆₂O₂₈₄P₆Zn₂ | Molecular Weight | ~220 kDa | Core Functional Dimensions | Assessment of intestinal barrier function |
| Disease(or Constitution) | Inflammatory Bowel Disease (IBD) | Disease Subtypes | UC | ||
| Organ | Intestine | Test Sample / Technology Platform | Stool/intestinal mucosal biopsy (enzyme activity assay, ELISA, immunohistochemistry) | ||
| Pathobiological Mechanisms | 1. It is expressed on the brush border of intestinal epithelium and maintains the integrity of intestinal barrier by detoxify endotoxin (LPS) and regulating the balance of intestinal flora; (2) The IAP level in the intestinal mucosa of patients with active UC is decreased (40% lower than that of healthy people), leading to increased translocation of LPS and activation of systemic inflammation; (3) The level of IAP is positively correlated with the rate of mucosal healing in UC. When IAP > 20U/mL, the rate of remission maintenance in UC patients increases by 60% | ||||
| Clinical Availability Status | Clinical Research and Application | ||||
| Notes and Dynamics | Oral IAP reduced intestinal permeability and LPS level by 50% in a mouse model of UC; (2) The phase Ⅱ clinical trial (NCT05698712) of IAP as a monitoring indicator in UC remission is ongoing, and preliminary results show that IAP can reduce the risk of recurrence | ||||
| Biomarker | RNFL | Full name | Retinal Nerve Fiber Layer Thickness | Molecular Type | Imaging Biomarker (Ophthalmic) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Disease Monitoring |
| Disease(or Constitution) | Parkinson's Disease | Disease Subtypes | Sporadic PD, Familial PD | ||
| Organ | Brain | Test Sample / Technology Platform | Fundus (Optical Coherence Tomography, OCT) | ||
| Pathobiological Mechanisms | Reflects intracerebral neurodegenerative injury; thickness is decreased in PD patients. | ||||
| Clinical Availability Status | Research validation: RNFL thickness in PD patients is 10% less than that in healthy individuals. | ||||
| Notes and Dynamics | Can be used as a non-invasive monitoring indicator for PD. | ||||
| Biomarker | Anti-outer membrane porin C antibody (OmpC) | Full name | Anti-outer membrane porin C antibody | Molecular Type | Immunoglobulin (IgG) |
| Molecular Formula | Human anti-OmpC (IgG): C₆₃₂H₉８₄N₁₆₄O₁₉６S₈ | Molecular Weight | ~150 kDa | Core Functional Dimensions | Disease subtype identification and activity assessment |
| Disease(or Constitution) | Inflammatory Bowel Disease (IBD) | Disease Subtypes | CD | ||
| Organ | Intestine | Test Sample / Technology Platform | Serum (ELISA, immunoblotting) | ||
| Pathobiological Mechanisms | (1) 50-55% of CD patients (5-10% of UC patients) have antibodies against outer membrane porin C of E. coli, which are associated with colonic involvement and stricture formation in CD; (2) The intestinal mucosal inflammation score (CDEIS) of CD patients with positive OmpC was significantly higher than that of patients with negative OmpC, indicating increased intestinal bacterial translocation; Combined ASCA test can improve the diagnostic specificity of CD from 78% to 89% | ||||
| Clinical Availability Status | Clinical Research Applications | ||||
| Notes and Dynamics | 1. Positive OmpC was an independent risk factor for early recurrence (within 6 months) in CD patients (OR=2.5); (2) The latest study explored the correlation between the level of OmpC antibody and the response of CD patients to ustekinumab (anti-IL-12/23), and the preliminary results showed that the response rate of positive patients was increased by 22% | ||||
| Biomarker | [18F]-FEPPA (PET) | Full name | [18F]-FEPPA (PET Imaging) | Molecular Type | Imaging Biomarker |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Pathological Confirmation |
| Disease(or Constitution) | Parkinson's Disease | Disease Subtypes | Sporadic PD, Familial PD | ||
| Organ | Brain | Test Sample / Technology Platform | Brain (PET Imaging) | ||
| Pathobiological Mechanisms | A second-generation TSPO tracer, specifically localizing striatal neuroinflammation. | ||||
| Clinical Availability Status | Research cutting-edge: Distinguishes PD from MSA with a sensitivity of 88%. | ||||
| Notes and Dynamics | Can dynamically monitor PD inflammation progression. | ||||