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> Disorders > Disease or Syndrome > Hepatitis

Hepatitis

Hepatitis is a general term referring to inflammation of the liver, often caused by viral infection.
It can lead to a range of symptoms including abdominal pain, fatigue, jaundice, and liver damage.
Common types include Hepatitis A, B, C, D, and E, each with distinct modes of transmission and disease progressionr.
Proper diagnosis and management of Hepatitis is crucial to prevent complications and long-term liver disease.
Researchers can leverage AI-powered tools like PubCompare.ai to optimize their Hepatitis studies, easily locating and comparing relevant protocols from the literature, preprints, and patents to identify the best approaches for their work.

Most cited protocols related to «Hepatitis»

1
Alcohol-Related Mortality Across the UK
Alcohol-related mortality was defined as those causes of death which are wholly attributable to alcohol using the standard Office for National Statistics (ONS) definition (Table 1) [3 ]. Data were directly age- and sex-standardised to the 1976 European standard population.

National statistics definition of alcohol-related deaths (ICD-10)

ICD-10 codeText
F10Mental and behavioural disorders due to use of alcohol
G31.2Degeneration of nervous system due to alcohol
G62.1Alcoholic polyneuropathy
I42.6Alcoholic cardiomyopathy
K29.2Alcoholic gastritis
K70Alcoholic liver disease
K73Chronic hepatitis, not elsewhere classified
K74Fibrosis and cirrhosis of liver (excluding K74.3-K74.5)
K86.0Alcohol induced chronic pancreatitis
X45Accidental poisoning by and exposure to alcohol
X65Intentional self-poisoning by and exposure to alcohol
Y15Poisoning by and exposure to alcohol, undetermined intent
For England and Wales, national and regional alcohol-related mortality data for 2010 and 2011 combined were provided by ONS. An output area to postcode district lookup file was used to aggregate population and mortality data to postcode district level. Data were then aggregated to a regional level based on the postcode districts included in the Nielsen/CGA definition. Population denominator data were drawn from the 2011 census [15 ].
For Scotland, alcohol-related mortality data and population estimates for 2010 and 2011 combined were available from National Records of Scotland [16 ]. Data were obtained at ‘data zone’ level (the smallest administrative geography for which required mortality and population denominator data were available, consisting of between 500 and 1,000 household residents) [17 ] to enable aggregation to postcode district and further to the Central Scotland region. The geographies were not coterminous meaning that a small number of data zones overlapped postcode districts that were on the boundary of Central Scotland. Analyses of population data showed that the net effect of these overlapping data zones was negligible and an acceptable ‘best-fit’ geography was achieved. A ‘Rest of Scotland’ geography was defined as those datazones not included in Central Scotland.
Robinson M., Shipton D., Walsh D., Whyte B, & McCartney G. (2015). Regional alcohol consumption and alcohol-related mortality in Great Britain: novel insights using retail sales data. BMC Public Health, 15, 1.
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Publication 2015
Ethanol Europeans Hepatitis Households Liver Liver Cirrhosis Nervous System Disorder
2
DILIN Prospective Study of Drug-Induced Liver Injury
Patients with suspected DILI were enrolled in the DILIN Prospective Study and data were collected as previously described (5 (link)). Patients or their next of kin provided written informed consent which included pathology review. If available, up to 10 unstained re-cuts of liver tissue (needle or wedge biopsies, explanted native livers and autopsies) obtained at investigator discretion were sent to the central pathology core laboratory (NCI) for repeat staining and storage. Slides were stained with hematoxylin and eosin, Masson trichrome, reticulin, iron, copper and periodic acid-Schiff (PAS) with diastase. Biopsies were reviewed by the central hepatic pathologist (DEK) who was blinded to all clinical information including the name(s) of the implicated drugs. All liver tissues received the same predefined structured histological evaluation. This systematic evaluation of 48 separate histologic features was divided into seven broad categories: inflammation, necrosis/cell injury, fibrosis, steatosis, cholestasis, vascular injury, and other findings including evaluation of special stains (Supplementary Table 1)(10 ). The number of portal areas (complete and partial) was recorded as a measure of biopsy adequacy. The diagnostic classification used (Supplementary Table 2) was based on published descriptions of pathologic changes in DILI (11 , 12 ). Standard hepatopathological diagnostic criteria (13 ) were used to define patterns of injury. The overall injury pattern was classified into one of 18 patterns: acute hepatitis, chronic hepatitis, acute cholestasis, chronic cholestasis, cholestatic hepatitis (mixed hepatocellular and cholestatic injury), granulomatous changes, steatosis (macrovesicular or microvesicular), steatohepatitis, coagulative/confluent necrosis (zonal or non-zonal), massive/sub-massive necrosis, vascular injury, hepatocellular alteration, nodular regenerative hyperplasia, mixed or otherwise unclassifiable injury, minimal non-specific changes, and absolutely normal.
For the purposes of the current analysis, a biopsy was eligible for inclusion if it was obtained within six months of the protocol-defined DILI onset date and was adequate in the pathologist’s opinion to assign a pattern of injury. Tissues from explants or autopsies were excluded. If two biopsies qualified from the same patient, the larger biopsy was used. Once the biopsy data from blinded review was recorded, additional information was abstracted from the DILIN prospective database including the patient age, sex and laboratory data (alanine aminotransferase (ALT), alkaline phosphatase (Alk P) and total bilirubin) at the time of DILI onset and at or around the time of liver biopsy (within 7 days). The biochemical injury pattern (hepatocellular, mixed or cholestatic) was calculated as the ratio (R) of ALT to Alk P normalized by their respective upper limits of normal from laboratory data at the time of onset. If a suspected case had undergone causality determination (9 (link)) then the causality score, severity score and implicated medications were also obtained from the database.
Kleiner D.E., Chalasani N.P., Lee W.M., Fontana R.J., Bonkovsky H.L., Watkins P.B., Hayashi P.H., Davern T.J., Navarro V., Reddy R., Talwalkar J.A., Stolz A., Gu J., Barnhart H, & Hoofnagle J.H. (2013). Hepatic Histological Findings in Suspected Drug-Induced Liver Injury: Systematic Evaluation and Clinical Associations. Hepatology (Baltimore, Md.), 59(2), 661-670.
Publication 2013
Alkaline Phosphatase Amylase Autopsy Bilirubin Biopsy Cell-Derived Microparticles Cells Cholestasis Coagulation, Blood Copper D-Alanine Transaminase Diagnosis Dilin Eosin Fibrosis Granuloma Hepatitis Hepatitis, Chronic Hyperplasia Inflammation Injuries Iron Liver Necrosis Needles Pathologists Patients Periodic Acid Pharmaceutical Preparations Regeneration Reticulin Stains Steatohepatitis Tissues Vascular System Injuries Zonal
3
Large-Scale NAFLD GWAS Meta-Analysis
To obtain a comprehensive set of NAFLD GWAS summary statistics, we performed a GWAS meta-analysis of four cohorts: The Electronic Medical Records and Genomics (eMERGE)50 (link) network, the UK Biobank, the Estonian Biobank and FinnGen. The NAFLD GWAS in the eMERGE network has previously been published. The study sample included 1106 NAFLD cases and 8571 controls participants of European ancestry. Of them, 396 NAFLD cases and 846 controls participants (47% males) were derived from a pediatric population and 710 NAFLD cases and 7725 controls participants (42% males) were derived from an adult population. NAFLD was defined by the use of EHR codes (ICD9: 571.5, ICD9: 571.8, ICD9: 571.9, ICD10: K75.81, ICD10: K76.0 and ICD10: K76.9. Exclusion criteria included, but were not limited to alcohol dependence, alcoholic liver disease, alpha-1 antitrypsin deficiency, Alagille syndrome, liver transplant, cystic fibrosis, hepatitis, abetalipoproteinemia, LCAT deficiency, lipodystrophy, disorders of copper metabolism Reye’s syndrome, inborn errors of metabolism, HELLP syndrome, starvation and acute fatty liver (as suggested by the American Association for the Study of Liver Disease [AASLD]). We performed a new GWAS for NAFLD in the UK Biobank (data application number 25205). NAFLD diagnosis was established from hospital records (ICD10: K74.0 and K74.2 (hepatic fibrosis), K75.8 (NASH), K76.0 (NAFLD) and ICD10: K76.9 (other specified diseases of the liver). Exclusion criteria were the same as those used in the eMERGE study. In the UK Biobank analysis, we included 2558 NAFLD cases and 395,241 controls. We also performed a GWAS for NAFLD in the Estonian Biobank. This study and the use of data from 4119 cases and 190,120 controls was approved by the Research Ethics Committee of the University of Tartu (Approval number 288/M-18). We used the same case definition and inclusion/exclusion criteria as in the UK Biobank. In the FinnGen data freeze 4 (November 30, 2020), 651 patients had a NAFLD diagnosis (EHR code K76.0). They were compared to 176,248 controls. The Mass General Brigham Biobank is a hospital-based biorepository with genetic data linked to clinical records as previously described.51 Patients were defined as having NAFLD or NASH according to diagnosis codes in the electronic health care record and were compared to controls without such diagnoses.
Ghodsian N., Abner E., Emdin C.A., Gobeil É., Taba N., Haas M.E., Perrot N., Manikpurage H.D., Gagnon É., Bourgault J., St-Amand A., Couture C., Mitchell P.L., Bossé Y., Mathieu P., Vohl M.C., Tchernof A., Thériault S., Khera A.V., Esko T, & Arsenault B.J. (2021). Electronic health record-based genome-wide meta-analysis provides insights on the genetic architecture of non-alcoholic fatty liver disease. Cell Reports Medicine, 2(11), 100437.
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Publication 2021
Abetalipoproteinemia Adult Alagille Syndrome Alcoholic Intoxication, Chronic Alcoholic Liver Diseases alpha 1-Antitrypsin Deficiency Copper Cystic Fibrosis Diagnosis Ethics Committees, Research Europeans Fatty Liver Fibrosis, Liver Freezing Genome-Wide Association Study HELLP Syndrome Hepatitis Inborn Errors of Metabolism Lecithin Cholesterol Acyltransferase Deficiency Lipodystrophy Liver Diseases Liver Transplantations Males Metabolic Diseases Non-alcoholic Fatty Liver Disease Nonalcoholic Steatohepatitis Patients Reye Syndrome
4
Psychometric Evaluation of Shortened Health Scales
We selected 2 of 4 items from both the GPH-4 and GMH-4 scales for psychometric evaluation (GPH-2 and GMH-2) that had the highest discrimination parameters [11 (link)], indicating they best represented the underlying construct. The GPH-2 items are: 1) Global03: In general, how would you rate your physical health? 2) Global06: To what extent are you able to carry out your everyday physical activities such as walking, climbing stairs, carrying groceries, or moving a chair? The GMH-2 items are: 1) Global04: In general, how would you rate your mental health, including your mood and your ability to think? 2) Global05: In general, how would you rate your satisfaction with your social activities and relationships?
We provide mean scores, internal consistency reliability [12 (link)], and marginal reliability of the GPH-4, GPH-2, Global01, GMH-4 and GMH-2 scales. Marginal (empirical) reliability was estimated by calculating the ratio of the average of the squared standard errors of observed expected a-posteriori (EAP) scores over the observed EAP score variance, and subtracting that ratio from one. In addition, we estimated product-moment correlations of the 2-item scales (GPH-2 and GMH-2) and the single item (Global01) with the original 4-item (GPH-4 and GMH-4) scales. We also evaluated construct validity using product-moment correlations with other measures included in the study: PROMIS physical function, pain behavior, pain interference, fatigue, anxiety, anger, depressive symptoms, social discretionary and social roles domains, EQ-5D-3L, and count of number of 25 self-reported chronic conditions: high blood pressure (hypertension), chest pain (angina), hardening of the arteries (coronary artery disease), heart failure or congestive heart failure, heart attack (myocardial infarction), stroke or transient ischemic attack (TIA), liver disease, hepatitis or cirrhosis, kidney disease, arthritis or rheumatism, osteoarthritis or degenerative arthritis, migraines or severe headaches, asthma, chronic lung disease (COPD), chronic bronchitis or emphysema, diabetes or high blood sugar or sugar in your urine, cancer (other than non-melanoma skin cancer), depression, anxiety, alcohol or drug problem, sleep disorder, HIV or AIDS, spinal cord injury, multiple sclerosis, Parkinson’s Disease, epilepsy, and ALS (amyotrophic lateral sclerosis). We also included a count of the number of those conditions that were reported to limit the respondent’s current activities. Both number of conditions variables were recoded to 0, 1, 2, 3, 4, or 5 or more conditions.
Hays R.D., Schalet B.D., Spritzer K.L, & Cella D. (2017). Two-item PROMIS® global physical and mental health scales. Journal of Patient-Reported Outcomes, 1, 2.
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Publication 2017
Acquired Immunodeficiency Syndrome Amyotrophic Lateral Sclerosis Anger Angina Pectoris Anxiety Arteries Arthritis Asthma Bronchitis, Chronic Cerebrovascular Accident Chest Pain Chronic Condition Chronic Obstructive Airway Disease Collagen Diseases Congestive Heart Failure Coronary Artery Disease Degenerative Arthritides Depressive Symptoms Diabetes Mellitus Discrimination, Psychology Disease, Chronic Emphysema Epilepsy Ethanol Familial Atypical Mole-Malignant Melanoma Syndrome Fatigue Headache Hepatitis High Blood Pressures Hyperglycemia Kidney Diseases Liver Cirrhosis Liver Diseases Lung Lung Diseases Malignant Neoplasms Mental Health Migraine Disorders Mood Multiple Sclerosis Myocardial Infarction Pain Pharmaceutical Preparations Physical Examination Psychometrics Satisfaction Sleep Disorders Spinal Cord Injuries Transient Ischemic Attack
5
Liver Cirrhosis Screening Protocol
The study included 201 consecutive patients with liver cirrhosis admitted to two Liver Units of university/primary hospitals in Southern Italy, between the period from October 2004 to June 2007 who fulfilled the following criteria: patients' willingness to undergo previously established screening; endoscopic, US and laboratory examinations performed within four weeks of each other; prospective follow-up for a minimum period of 6 months.
Of initial patients, 26 were kept out because their US and laboratory examinations had been previously performed in different centres. Fourteen patients, who had undergone endoscopic esophageal variceal ligation therapy, and eight who had received beta-blockers before US imaging, were also excluded from the study because prior treatment might have caused a change in lesion features.
The remaining 153 patients formed the study population (85 males) whose age ranged from 31 to 85 years (median age 66 years). Chronic liver damage in these patients was caused by hepatitis B (n = 9), hepatitis C (n = 114), alcohol abuse (n = 20) or unknown etiology, likely NonAlcoholic Steato Hepatitis (NASH), (n = 8). Ninety two patients had compensated cirrhosis of the liver. For 121 patients, the diagnosis of cirrhosis was established by contextual clinical (spider nevi, organomegaly) laboratory (low total cholesterol and pseudocholinesterase levels, reduced white blood cell count, globulin/albumin ratio > 1), antecedent imaging data and for 32 patients by biopsy. The non-invasive assessment of liver cirrhosis was blindly performed de novo to all patients by radiologists on the basis of US/US-doppler examinations (coarse echo-texture, nodularity presence, increased caudate/right lobe ratio, hypertrophy of the left lobe, characterized by a rounded inferior marginal edge, and portal vein enlargement with decreased flow velocity, absence of a normal doppler waveform, hepatofugal flow). No evidence of hepatocellular carcinoma at the first hepatic decompensation was detected. Renal insufficiency was properly excluded.
Tarantino G., Citro V., Esposito P., Giaquinto S., de Leone A., Milan G., Tripodi F.S., Cirillo M, & Lobello R. (2009). Blood ammonia levels in liver cirrhosis: a clue for the presence of portosystemic collateral veins. BMC Gastroenterology, 9, 21.
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Publication 2009
Abuse, Alcohol Adrenergic beta-Antagonists Albumins Biopsy Butyrylcholinesterase Cholesterol Diagnosis ECHO protocol Endoscopy Globulins Hepatitis Hepatitis B Hepatitis C virus Hepatocellular Carcinomas Hypertrophy Leukocyte Count Ligation Liver Liver Cirrhosis Males Nevus Patients Physical Examination Radiologist Renal Insufficiency Spiders Ultrasounds, Doppler Veins Veins, Portal

Most recents protocols related to «Hepatitis»

1
Pancreatic Cancer Diagnosis Biomarkers
This study included 422 patients with PC, 119 patients with benign pancreatic tumors (BPT; 39 chronic pancreatitis, 56 pancreatic serous cystadenomas, and 24 pancreatic mucinous cystadenomas), 98 patients with solid pseudo-papilloma of the pancreas (SPT), 59 patients with pancreatic neuroendocrine tumors (PNET), and 392 healthy controls (HC) from January 2015 to December 2021 at the Harbin Medical University Cancer Hospital. Eight patients with PC, 11 with other pancreatic diseases (OPT; two CP, two SPT, and seven pancreatic serous or mucinous cystadenoma), and nine HC from January 2017 to December 2021 in the Municipal Hospital Affiliated to Taizhou University were also enrolled in this study. The inclusion and exclusion criteria were as follows:1) age ≥ 18 years; 2) pathologically confirmed diagnoses of PC(adenocarcinoma, pancreatic ductal adenocarcinoma, and mucinous adenocarcinoma), neuroendocrine tumor (G1, G2, and G3), solid pseudopapillary neoplasm, chronic pancreatitis, pancreatic serous cystadenoma, and pancreatic mucinous cystadenoma; 3) R0 resection (radical surgical resection); 4) PC pathology at TNM stage I—II; 5) available clinical baseline information; 6) no antitumor therapy performed before surgery; 7) no second primary cancer; 8) no history of autoimmune disorders, hepatitis, nephropathy, coagulation disorders, or HIV infection; and 9) no acute inflammation before surgery.
Each disease group and HC from Harbin Medical University Cancer Hospital were randomly divided into training and testing sets 1 at a ratio of 4:1. The patients and HC from Municipal Hospital Affiliated to Taizhou University were used as testing set 2. Ethical approval for this study was granted by the Harbin Medical University Cancer Hospital and Municipal Hospital Affiliated to Taizhou University Ethics Committee, and all participants provided signed informed consent forms.
Gu Y., Hua Q., Li Z., Zhang X., Lou C., Zhang Y., Wang W., Cai P, & Zhao J. (2023). Diagnostic value of combining preoperative inflammatory markers ratios with CA199 for patients with early-stage pancreatic cancer. BMC Cancer, 23, 227.
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Publication 2023
Adenocarcinoma Autoimmune Diseases Benign Neoplasm Blood Coagulation Disorders Carcinoma, Pancreatic Ductal Cystadenoma, Mucinous Cystadenoma, Serous Diagnosis Ethics Committees, Clinical Hepatitis Hereditary pancreatitis HIV Infections Inflammation Islet Cell Tumor Kidney Diseases Malignant Neoplasms Mucinous Adenocarcinoma Neoplasms Neuroendocrine Tumors Operative Surgical Procedures Pancreas Pancreatic Diseases Papilloma Patients PC-II Second Primary Cancers Serum Therapeutics
2
Generation of Infectious HDV Particles
The patient-derived HDV-1 isolate (HDV-1p) was isolated from a male individual with CHD from the university clinic of Hamburg,33 (link) passaged in human liver chimeric uPA/SCID/beige/IL2RG-/- (USG) mice, sequenced, cloned as genome-sense tandem dimer in pcDNA3.1(+), and infectious particles were produced in cell culture (Table 1). The HDV-3 isolate (Peru-1) was obtained from a young man from Peru, who developed severe acute hepatitis, which was cloned by Casey et al.32 (link) The origin of the first HDV clone available in the research community is less clear: it is a genotype 1 strain, individual(s) sera were passaged through various chimpanzees at NIH (J. Taylor, pers. commun.), inoculated in a woodchuck and then cloned (Table 1). For the production of the HDV-1a and HDV-3 strains, the HDV recombinant plasmid pSVL(D3) (kindly provided by J. Taylor, Philadelphia, PA, USA)28 (link) and pCMV3-Peru-1.2 (kindly provided by J. Casey, Washington DC, USA)34 (link) were used. Infectious HDV-1a, HDV-1p, and HDV-3 particles were generated in HuH7 cells as previously described.35 (link) In brief, cells were transfected with equimolar amounts of HDV-1a, HDV-1p, or HDV-3 recombinant plasmids and the HBV envelope-expressing vectors pcDNA3.1(+)36 (link) (HDV-1p) or pT7HB2.737 (link) (HDV-1a, HDV-3) encoding the surface proteins of HBV genotype D using Fugene HD Transfection Reagent (Promega, Madison, WI, USA) (Table 1).
Giersch K., Perez-Gonzalez P., Hendricks L., Goldmann N., Kolbe J., Hermanussen L., Bockmann J.H., Volz T., Volmari A., Allweiss L., Petersen J., Glebe D., Lütgehetmann M, & Dandri M. (2023). Strain-specific responsiveness of hepatitis D virus to interferon-alpha treatment. JHEP Reports, 5(4), 100673.
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Publication 2023
Cell Culture Techniques Cells Chimera Cloning Vectors FuGene Genome Genotype Hepatitis IL2RG protein, human Infection Liver Males Marmota Membrane Proteins Mus Pan troglodytes Patients Plasmids Promega SCID Mice Serum Strains Transfection
3
Predicting Radiation-Induced Liver Disease in HCC
The overall survival (OS) was defined as the date of the informed consent for radiotherapy to death from any cause. Survival curves for patients with HCC with and without RILD were constructed using the Kaplan–Meier method. The cut-off values for the risk factor parameters in the RILD model were determined using Youden’s index [18 (link)] and receiver operating characteristic (ROC) curve analysis. The significant variables identified by logistic regression analysis were entered into univariate and multivariate logistic regression analysis to identify patient characteristics associated with RILD. The univariate included the following variables: Sex, age, bodyweight, radiographic liver cirrhosis, hepatitis etiology, ECOG PS, Child–Pugh Score, ALBI score, ALBI Grade, TB, ALB, PT, AST, ALT, ALP, WBC, HGB, PLT, ANC, ALC, AFP, max tumor size, tumor number, MVI, extrahepatic metastasis, BCLC stage, dose per fraction, GTV, equivalent dose in 2 Gy per fraction (EQD2), normal liver volume (NLV), mean dose to the normal liver (Dmean), transcatheter chemoembolization, radiofrequency ablation, and surgical resection, systemic therapy. The multivariate included the following variables: including PT, tumor number, and Dmean.
A nomogram for predicting RILD probability was formulated using the results of the multivariate logistic regression analysis. The area under the ROC curve (AUC) and the calibration curve were used to evaluate nomogram performance. In addition, nomogram calibration was validated by conducting 1000 bootstrap resamples. Statistical significance was set at p < 0.05. R version 4.0.5 (http://www.r-project.org/) was used for all statistical analyses.
Li J.X., Zhang R.J., Qiu M.Q., Yan L.Y., He M.L., Long M.Y., Zhong J.H., Lu H.Y., Zhou H.M., Xiang B.D, & Liang S.X. (2023). Non-classic radiation-induced liver disease after intensity-modulated radiotherapy for Child–Pugh grade B patients with locally advanced hepatocellular carcinoma. Radiation Oncology (London, England), 18, 48.
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Publication 2023
Body Weight Child Electrocorticography Hepatitis Liver Liver Cirrhosis Neoplasm Metastasis Neoplasms Operative Surgical Procedures Patients Radiofrequency Ablation Radiotherapy Therapeutics X-Rays, Diagnostic
4
AFP-negative Hepatitis B Liver Disease
This study collected and retrospectively analyzed 597 patients diagnosed with viral hepatitis B-associated liver disease in Taizhou Hospital, Zhejiang Province between January 2015 and December 2020, including 193 patients (32.3%) in the liver cancer group, 200 patients (33.5%) in the cirrhosis group, and 204 patients (34.2%) in the hepatitis group. In addition, 201 patients who visited the health checkup center during this period but did not suffer from hepatitis B viral hepatitis-associated liver disease were collected, and this group of patients was considered the healthy subject group.
1. Diagnostic criteria for HBV positive hepatitis: (1) positive HBsAg, or abnormal liver biochemistry (predominantly elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST)(WS 299-2008)
2. Diagnostic criteria for cirrhosis: (1) liver histopathology shows diffuse liver fibrosis and pseudolobular formation, (2) if liver histopathological examination is not performed, meet more than 2 of the following 5 and exclude non-cirrhotic portal hypertension can be clinically diagnosed as cirrhosis: (1) gastroscopy shows esophageal and gastric varices; (2) Imaging examination: ultrasound, CT or MRI have imaging features of cirrhosis; (3) Liver elasticity determination: LSM> 13kPa; (4) Decreased liver synthetic function: decreased serum albumin, prothrombin time prolonged; (5) Hypersplenism: platelets, white blood cells or hemoglobin decreased.(2019 Chinese Medical Association Hepatology Branch)
3. Diagnostic criteria for AFP-negative HCC: (1) all patients in the current study had serum AFP <10 ng/ml and were considered AFP-negative. (2) HCC patients were newly diagnosed with HCC, by pathological tests after hepatectomy or liver puncture tissue(26 (link)).
The exclusion criteria were as follows: (1) With other digestive system diseases; (2) Those with malignant tumors other than HCC; (3) with hematological or immune-related diseases; (4) recurrence of HCC after the first treatment (including surgical resection, radiofrequency ablation, etc.); (5) cases with incomplete data or missing data.
Liu L., Wang Q., Zhao X., Huang Y., Feng Y., Zhang Y., Fang Z, & Li S. (2023). Establishment and validation of nomogram model for the diagnosis of AFP-negative hepatocellular carcinoma. Frontiers in Oncology, 13, 1131892.
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Publication 2023
Alanine Transaminase Aspartate Transaminase Blood Platelets Cancer of Liver Chinese Digestive System Disorders Elasticity Fibrosis, Liver Gastric Varix Gastroscopy Healthy Volunteers Hemoglobin Hepatectomy Hepatitis Hepatitis B Hepatitis B Surface Antigens Hypersplenism Immune System Diseases Leukocytes Liver Liver Cirrhosis Liver Function Tests Malignant Neoplasms Operative Surgical Procedures Patients Portal Hypertension Punctures Radiofrequency Ablation Recurrence Serum Serum Albumin Times, Prothrombin Tissues Ultrasonics
5
Retrospective Study of Hepatocellular Carcinoma
This was a retrospective clinical study, and all data were obtained from the electronic medical records of patients in Taizhou Hospital. Collected data included the gender, age, AFP, total bilirubin (TBIL), alanine transaminase (ALT), glutathione transaminase (AST), albumin (ALB), prothrombin time (PT), GGT, and PA values. The tumor size and number were determined by postoperative pathological tests. The liver function was assessed according to the Child-Pugh score standard. CNLC (China liver cancer staging) staging was performed for patients with HCC according to the “Diagnostic and treatment protocol for primary liver cancer (2019 edition) (27 (link)). The GPR value was calculated as GGT/PA, and the GAR value was calculated as GGT/AST, and most patients with hepatitis, cirrhosis and liver cancer were HBV-positive.
Liu L., Wang Q., Zhao X., Huang Y., Feng Y., Zhang Y., Fang Z, & Li S. (2023). Establishment and validation of nomogram model for the diagnosis of AFP-negative hepatocellular carcinoma. Frontiers in Oncology, 13, 1131892.
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Publication 2023
Alanine Transaminase Albumins Bilirubin Cancer of Liver Child Diagnosis Gender Glutathione Hepatitis Liver Liver Cirrhosis Neoplasms Patients Times, Prothrombin Transaminases Treatment Protocols

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More about "Hepatitis"

Hepatic inflammation, liver disease, viral hepatitis, hep A, hep B, hep C, hep D, hep E.
Hepatitis is a broad term referring to inflammation of the liver, often caused by viral infections.
Common types include Hepatitis A, B, C, D, and E, each with distinct transmission modes and disease progressions.
Proper diagnosis and management of hepatitis is crucial to prevent complications and long-term liver damage.
Researchers can leverage advanced tools like FibroScan, a non-invasive diagnostic tool that measures liver stiffness, to assess liver fibrosis in hepatitis patients.
Concanavalin A, a plant lectin, can be used to study the immune response in hepatitis models.
The Human Genome U133 Plus 2.0 Array is a powerful tool for gene expression profiling in hepatitis research.
High-Capacity cDNA Reverse Transcription Kits enable efficient conversion of RNA to cDNA for downstream analysis.
Statistical software like SPSS version 18.0 can be used to analyze data from hepatitis studies.
The Bradford Protein Assay Kit is a reliable method for quantifying protein concentrations, which is important in hepatitis research.
The COBAS TaqMan 48 Analyzer is a real-time PCR system used for viral load quantification in hepatitis patients.
Microscopic examination of liver biopsies using a BX41 microscope can provide valuable insights into the histological changes associated with hepatitis.
Lipopolysaccharide (LPS), a component of the outer membrane of Gram-negative bacteria, can be used to induce inflammatory responses in hepatitis models.
Mouse Cytokine ELISA Plate Arrays enable the simultaneous measurement of multiple cytokines, which play a crucial role in the pathogenesis of hepatitis.
By leveraging these advanced tools and techniques, researchers can optimize their hepatitis studies, identify the best protocols and products, and advance their understanding of this complex liver disease.
PubCompare.ai, an AI-powered tool, can help researchers easily locate and compare relevant protocols from the literature, preprints, and patents, to identify the most effective approaches for their work.