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At least 19 recordsLinked to original sources
PubMed2026

Network pharmacological and experimental validation of the mechanism of Chaihu Guizhi Ganjiang decoction regulating T helper cell 17/regulatory T cell balance to improve autoimmune hepatitis.

OBJECTIVE: To elucidate the therapeutic efficacy and mechanism of action of Chaihu Guizhi Ganjiang decoction (, CGGD) in autoimmune hepatitis. METHODS: CGGD components and potential target genes were extracted from previously published databases. The autoimmune hepatitis (AIH)-related regulatory genes were obtained from the DisGeNET database. Intersections were taken, and enrichment analyses were performed on the extracted data. Concanavalin A (ConA)-induced AIH model mice were treated with CGGD via gavage. The results of network pharmacological analysis were experimentally validated. RESULTS: Network pharmacology revealed 228 genes at the intersection of AIH and CGGD. Kyoto Encyclopedia of Genes and Genomes analysis revealed that CGGD primarily regulates the phosphoinositide 3-kinase (PI3K)/ protein kinase B (AKT) signaling pathway and cellular metabolism in AIH. Gene Ontology enrichment analysis revealed that CGGD modulates inflammation through transcription factor-mediated signaling pathways. As predicted, CGGD attenuated ConA-induced AIH in a dose-dependent manner by activating the PI3K/AKT signaling pathway. Histopathological assessment confirmed the protective effects of CGGD against ConA-induced AIH. Further investigation revealed that CGGD regulated the T helper cell 17 (Th17)/regulatory T cell (Treg) balance by modulating the PI3K/Akt/ nuclear factor kappa-B (NF-κB) pathway. CONCLUSIONS: This study demonstrated the therapeutic effect of CGGD on AIH through a combination of network pharmacological prediction and experimental validation. Its mechanism of action involves PI3K/Akt/ NF-κB-mediated regulation of Th17/Treg cells.

Animals↗
PubMed1979

[Atypical antibody against liver cell cytoplasm in virus induced autoimmune hepatitis (author's transl)].

A high titer (1:500) antibody against liver cell cytoplasm was found in one case of atypical viral hepatitis. The central areas of the rat liver lobule react more intensive than the periphery. Inconstantly it was found a reaction also with the parietal cells of the stomach, with the 3rd segment of proximal rat kidney tubules, and with smooth muscle. Possibly, this antibody is a marker of a virus induced autoimmune hepatitis.

Animals↗
PubMed2026

Mendelian Randomization Using a Japanese GWAS Identifies an HLA-Linked Causal Effect of Chronic Hepatitis B on Cholangiocarcinoma Risk.

BACKGROUND: Cholangiocarcinoma (CCA) is a highly malignant cancer that develops in the bile ducts. Its incidence is particularly high in East Asian populations, but the underlying genetic factors remain unclear. To investigate potential risk factors for CCA, we conducted a Mendelian randomization study to infer causality. METHODS: Using large-scale genome-wide association study data from the BioBank Japan resource, we systematically investigated the causal effects of genetic predisposition to seven conditions, chronic hepatitis B (CHB), chronic hepatitis C, autoimmune hepatitis, type 1 diabetes, type 2 diabetes, chronic gastritis, and chronic pancreatitis, on CCA risk. RESULTS: Our analysis reveals a significant association between genetic susceptibility to CHB with a 24% higher likelihood of developing CCA than non-susceptible individuals (Inverse-Variance Weighted Odds Ratio = 1.24, 95% Confidence Interval: 1.08-1.42; p = 0.002). This genetic association is significantly driven by instrumental variables enriched in the immune-regulatory HLA class II region (6p21), suggesting a plausible biological mechanism. For the primary outcome (CCA), statistical significance was assessed across seven exposures at a Bonferroni-corrected threshold (two-sided p<0.0071). Notably, the CHB-CCA association remains significant after correction. This primary finding is strongly supported by comprehensive sensitivity analyses that showed no evidence of confounding by horizontal pleiotropy or heterogeneity. Conversely, no significant causal effects on CCA were identified for the other six conditions. CONCLUSIONS: Our MR analysis supports a causal role of HBV infection in CCA development, highlighting the importance of targeted HBV screening and surveillance.

Female↗
PubMed1978

[Hepatology and immunology].

Immunologic diseases of the liver are exogenous mostly initiated by virus or endogenous initiated by autoaggression. All virus-induced kinds of hepatitis are due to an immune response against inocculated hepatocytes. Therefore the hepatitis is limited to the period of complete elimination of virus-infected cells. A strong immune response therefore corresponds with an acute and short hepatitis whilest a weak immune response develops a chronic hepatitis. In contrast, autoimmune hepatitis based on a disorder of the immune system with some genetic background is always unlimited. Each cirrhosis developing from immunologic hepatitis is also an immunologic disease; a special variant is the autoimmune primary biliary cirrhosis. All in all, the number of immunologic liver diseases surmounts the remaining liver diseases due to intoxication of metabolic disorders.

Antibodies, Viral↗
PubMed2024

Identifying a therapeutic window of opportunity for people living with primary sclerosing cholangitis: Embryology and the overlap of inflammatory bowel disease with immune-mediated liver injury.

Primary sclerosing cholangitis (PSC) is a variably progressive, fibrosis-causing autoimmune disorder of the intrahepatic and extrahepatic bile ducts of unclear etiology. PSC is commonly (in 60%-90% of cases) associated with an inflammatory bowel disease (IBD) like PSC-IBD and less commonly with an autoimmune hepatitis (AIH) like PSC-AIH or AIH-overlap disorder. Hepatologists and Gastroenterologists often consider these combined conditions as distinctly different from the classical forms in isolation. Here, we review recent epidemiologic observations and highlight that PSC-IBD and PSC-AIH overlap appear to represent aspects of a common PSC clinico-pathological pathway and manifest in an age-of-presentation-dependent manner. Particularly from the pediatric experience, we hypothesize that all cases of PSC likely originate from a complex "Early PSC"-"IBD"-"AIH" overlap in which PSC defines the uniquely and variably associated "AIH" and "IBD" components along an individualized lifetime continuum. We speculate that a distinctly unique, "diverticular autoimmunity" against the embryonic cecal- and hepatic diverticulum-derived tissues may be the origin of this combined syndrome, where "AIH" and "IBD" variably commence then variably fade while PSC progresses with age. Our hypothesis provides an explanation for the age-dependent variation in the presentation and progression of PSC. This is critical for the optimal targeting of studies into PSC etiopathogenesis and emphasizes the concept of a "developmental window of opportunity for therapeutic mitigation" in what is currently recognized as an irreversible disease process. The discovery of such a window would be critically important for the targeting of interventions, both the administration of current therapies and therapeutic trial planning.

Humans↗
PubMed1979

[Guillain-Barré syndrome associated to a type B acute hepatitis (author's transl)].

A 42-year-old male patient suffers an acute hepatitis with positive HBs Ag and approximately 2 months after its onset, an acute polyneuritis with lessening of conduction velocity and albumino-cytologic dissociation appeared. Both conditions recuperated synchronously in a few months. This association has been only slightly referred to previously, and the majority of cases lacked facts important to the establishment of a diagnosis. The polyneuritis is possibly secondary to the viral alteration, either directly or due to an ensuing immunological alteration. Besides, there is the possibility that a clinical or sub-clinical demyelinizing neuropathy that does not fill the criteria of a Guillain-Barré syndrome may complicate a hepatitis, or that an acute polyneuritis may associate itself to an autoimmune hepatitis.

Acute Disease↗
PubMed1976

Weber-Christian panniculitis and auto-immune disease: a case report.

A case is described of Weber-Christian panniculitis accompanied by a gammaglobulin disturbance which preceded by five years the diagnosis of an autoimmune hepatitis and pancytopenia. Also associated was the onset of diabetes mellitus, found at necropsy to be related to pancreatic islet amyloid deposition. This case reinforces the view that Weber-Christian panniculitis may be an adipose response to a variety of immunological stimuli.

Adipose Tissue↗
PubMed1977

[The kinetoplast immunofluorescence technic using Crithidia luciliae, a simple test for the detection of DNA-antibodies].

The kinetoplast immunofluorescence test for the detection of antibodies against desoxynucleic acid (DNA) utilizes as a substrate the native double-stranded DNA containing kinetoplast of the hemoflagellate Crithidia luciliae, which is nonpathogenic in human beings. By studying the sera of 279 patients with dermatological and internal diseases, as well as the sera of 80 blood donors, this technique was assessed for its usefulness in routine diagnosis. DNA-antibodies were found most frequently in the sera of patients with systemic lupus erythematosus (34/53). Additionally DNA-antibodies were demonstrated in some patients with cicatrical pemphigoid (1/1), autoimmune hepatitis (4/25) and myasthenia gravis (1/3). According to the experience thus far the kinetoplast immunofluorescence test appears to be a specific and well reproducible method to demonstrate DNA-antibodies in a simple way.

Antibodies, Antinuclear↗
PubMed2026

A genetic signal at 8q12.3 modulates GGT levels via the Runx1-CYP7B1 axis in female ethnic minorities from Guizhou.

Gamma-glutamyl transferase (GGT) regarded as a biomarker of liver dysfunction or excessive alcohol consumption; however, existing genome-wide association studies (GWAS) have been conducted predominantly in European populations and East Asian populations from Japan and the Taiwan region, with limited investigation in ethnic minorities from Guizhou Province. Previous genetic studies have demonstrated that Guizhou ethnic minorities share an East Asian genetic background while exhibiting specific genetic structures, a pattern that is also confirmed by our principal component analysis (PCA) results. We therefore performed a GWAS in this population and identified a genome-wide significant signal at 8q12.3 in female ethnic minorities from Guizhou. Fine-mapping and functional annotation analyses suggest that a regulatory pathway involving Runt-related transcription factor 1 (Runx1)-Cytochrome P450 family 7 subfamily B member 1 (CYP7B1)-cholesterol-reactive oxygen species (ROS)-glutathione (GSH) may contribute to the regulation of GGT levels. Mendelian randomization (MR) analyses further supported a causal relationship between GGT levels and autoimmune hepatitis (AIH). These findings uncover a genetic mechanism underlying GGT variation at 8q12.3 in female ethnic minorities from Guizhou, implicating a pathway linked to cholesterol metabolism and oxidative stress, and providing potential targets and insights for precision prevention and treatment of related diseases.

Female↗
PubMed1977

[Liver pathology in juvenile chronic polyarthritis].

Besides lymphodenopathy and splenomegaly, hepatomegaly may also be detected in 25-50% of children with juvenile rheumatoid arthritis. This is particularly evident in patients with complete Still's syndrome. The hepatomegaly increases during relapse situations and disappears during remissions. Transient icterus, elevation of aminotransferases and delayed bromsulfalein excretion have been reported, particularly in patients with complete Still's syndrome, and indicate impairment of liver function. Liver biopsies have been performed only rarely and show nonspecific infiltrations of portal fields with lymphocytes and, in a few cases, "autoimmune" hepatitis and even cirrhosis with portal hypertension. Plasma cell hepatitis with affection of joints can be readily differentiated from juvenile rheumatoid arthritis: the synovitis is merely transiet and disappears with institution of steroid therapy. As in the adult, severe liver dysfunction leads to remission of arthritis. Amyloidosis should be considered in every case of long-lasting hepatomegaly.

Amyloidosis↗
PubMed1978

Diagnosis of autoimmune chronic active hepatitis a simplified method for the detection of liver membrane autoantibodies (LMA).

A simplified method for the detection of liver membrane autoantibodies (LMA) in patient's serum is presented. Hepatocytes are isolated from the liver of young rabbits. A calcium-free solution without enzymes is injected into the portal vein with a normal syringe. The liver is then cut into small pieces in a solution with calcium, shaken in a water bath, filtered and washed in Eagle's medium. The isolated hepatocytes are incubated first in patient's serum and secondly in FITC labeled antihuman IgG. The test requires three hours and allow the detection of LMA, antinuclear and antimitochondrial antibodies simultaneously. The detection of LMA is valuable in the diagnosis of autoimmune chronic active hepatitis.

Animals↗
PubMedDate not supplied

[Splenectomy in chronic hepatitis with an autoimmune component].

The authors present a synthesis of studies performed on the role of the spleen in chronic active-digestive hepatitis with auto-immune participation. The study was based on a group of 48 patients out of which a lot of 20 patients was selected, with histological diagnosis of chronic active and aggressive hepatitis, in whom the presence of AgAu was ascertained, as well as of antiliver antibodies. From the immunological viewpoint, the effect of splenectomy was manifested, by a rapid and significant decrease of anti-liver antibodies mainly produced by the spleen, immediately following the intervention. In most of the patients the IgM antibodies disappeared somewhat later. At the same time the chronic hepatitis lesions were stabilized, the biological signs were improved and the clinical evolution of the patients was good. The authors consider that splenectomy in this category of hepatopathies is an immuno-suppressive therapy that may arrest the evolution towards cirrhosis.

Adult↗
PubMed1976

Genetic factors and autoimmunity in viral hepatitis.

Whether a patient develops the HBsAg carrier state may depend on his genome. HBsAg subtypes may reflect the viral genome and may be of prognostic significance. Different subtypes predominate in different populations throughout the world. Altered immune response, as in patients with Down's syndrome, may increase the HBsAg carrier rate. Autoantibodies have been used to differentiate various types of hepatitis. There is an increased incidence of histocompatibility antigen HL-A1 and HL-A8 in patients who have chronic aggressive hepatitis. In primary hepatic carcinoma, the HBsAg carrier rate is increased. Because of the suggestion that neonatal hepatitis, biliary atresia and choledochal cyst may all result from infantile obstructive cholangiopathy, with the precise outcome depending on whether other conditions such as alpha 1-antitrypsin deficiency are also present, we have determined HBsAg in 166 children with a variety of diseases, among them Reye's syndrome, alpha 1-antitrypsin deficiency, and renal disorders. The HBsAg carrier rate in the sera of these patients was normal.

Autoantibodies↗
PubMed1976

Autoimmune reaction to a liver specific membrane antigen during acute viral hepatitis.

Lymphocyte cytotoxicity for isolated hepatocytes has been demonstrated in 93% of cases of acute viral hepatitis tested within two weeks of the onset of symptoms. The frequency of cytotoxicity during this time was similar for HBsAg positive and negative cases. However, after this time it was significantly higher in HBsAg positive than negative cases, 90% and 25% respectively (P less than 0-01). Cytotoxicity was found in B-cell, but not T-cell, enriched fractions of lymphocytes, compatible with an antibody-dependent K-cell mediated reaction. In two cases the assay remained positive on retesting six months later, and follow-up liver biopsies showed the features of chronic aggressive hepatitis. These findings suggest that, in addition to the known immunological reactions against viral antigens that occur during the acute phase of viral hepatitis, an autoimmune reaction directed against a liver specific protein is also initiated; and if this reaction persists then chronic hepatitis may develop.

Acute Disease↗