Liver Pathological Features Research Articles

ACLY as a modulator of liver cell functions and its role in Metabolic Dysfunction-Associated Steatohepatitis

BackgroundNon-alcoholic Fatty Liver Disease (NAFLD), now better known as Metabolic (Dysfunction)-Associated Fatty Liver Disease (MAFLD) and its progression to Nonalcoholic Steatohepatitis (NASH), more recently referred to as Metabolic (Dysfunction)-Associated Steatohepatitis (MASH) are the most common causes of liver failure and chronic liver damage. The new names emphasize the metabolic involvement both in relation to liver function and pathological features with extrahepatic manifestations. This study aims to explore the role of the immunometabolic enzyme ATP citrate lyase (ACLY), with a critical function in lipogenesis, carbohydrate metabolism, gene expression and inflammation.MethodsACLY function was investigated in TNFα-triggered human hepatocytes and in PBMC-derived macrophages from MASH patients. Evaluation of expression levels was carried out by western blotting and/or RT-qPCR. In the presence or absence of ACLY inhibitors, ROS, lipid peroxidation and GSSG oxidative stress biomarkers were quantified. Chromatin immunoprecipitation (ChIP), transient transfections, immunocytochemistry, histone acetylation quantitation were used to investigate ACLY function in gene expression reprogramming. IL-6 and IL-1β were quantified by Lumit immunoassays.ResultsMechanistically, ACLY inhibition reverted lipid accumulation and oxidative damage while reduced secretion of inflammatory cytokines in TNFα-triggered human hepatocytes. These effects impacted not only on lipid metabolism but also on other crucial features of liver function such as redox status and production of inflammatory mediators. Moreover, ACLY mRNA levels together with those of malic enzyme 1 (ME1) increased in human PBMC-derived macrophages from MASH patients when compared to age-matched healthy controls. Remarkably, a combination of hydroxycitrate (HCA), the natural ACLY inhibitor, with red wine powder (RWP) significantly lowered ACLY and ME1 mRNA amount as well as IL-6 and IL-1β production in macrophages from subjects with MASH.ConclusionCollectively, our findings for the first time highlight a broad spectrum of ACLY functions in liver as well as in the pathogenesis of MASH and its diagnostic and therapeutic potential value.Graphical

Modulation of Dietary Choline Uptake in a Mouse Model of Acid Sphingomyelinase Deficiency.

Acid sphingomyelinase deficiency (ASMD) is a lysosomal storage disorder caused by mutations in the gene-encoding acid sphingomyelinase (ASM). ASMD impacts peripheral organs in all patients, including the liver and spleen. The infantile and chronic neurovisceral forms of the disease also lead to neuroinflammation and neurodegeneration for which there is no effective treatment. Cellular accumulation of sphingomyelin (SM) is a pathological hallmark in all tissues. SM is the only sphingolipid comprised of a phosphocholine group linked to ceramide. Choline is an essential nutrient that must be obtained from the diet and its deficiency promotes fatty liver disease in a process dependent on ASM activity. We thus hypothesized that choline deprivation could reduce SM production and have beneficial effects in ASMD. Using acid sphingomyelinase knock-out (ASMko) mice, which mimic neurovisceral ASMD, we have assessed the safety of a choline-free diet and its effects on liver and brain pathological features such as altered sphingolipid and glycerophospholipid composition, inflammation and neurodegeneration. We found that the choline-free diet was safe in our experimental conditions and reduced activation of macrophages and microglia in the liver and brain, respectively. However, there was no significant impact on sphingolipid levels and neurodegeneration was not prevented, arguing against the potential of this nutritional strategy to assist in the management of neurovisceral ASMD patients.

From the Editor’s desk…

From the Editor’s desk…

Clinicopathological analysis in patients with chronic hepatitis B virus infection in immune tolerant phase

Objective: To analyze the liver pathology, clinical characteristics and influence factors in patients with chronic hepatitis B virus (HBV) infection in immune tolerant phase (IT). Methods: The clinical data of 273 patients in IT phase who underwent liver biopsy from January 2015 to December 2019 were included in this study. The correlation between liver pathological changes and clinical features was analyzed. Results: There were 43 cases (15.75%) with liver histologic activity ≥ G2, 30 cases (10.99%) with liver fibrosis ≥ S2, and 55 cases (20.15%) with liver pathology ≥ G2 and/or ≥ S2. A total of 17.95% patients had liver steatosis. The majority (98.17%) of tissue samples were positive for HBsAg staining, while only 79.49% were positive for HBcAg. The characteristics of liver pathology were comparable in men from women patients. The differences of G and S were not statistically significant according to different HBsAg positivity, while those were statistically significant according to different HBcAg positivity. By univariate and multivariate analysis, the independent risk factors of pathological severity were HBcAg intensity, HBeAg level, and age. However, the differences of liver histologic activity and fibrosis were not statistically significant between those younger than 30 years old group from those older than 30 years old, neither between those younger or older than 40. Although the diagnostic value of liver inflammation and fibrosis 5 (LIF-5) was better than that of aspartate aminotransferase-to-platelet ratio index (APRI) and fibrosis 4 score (FIB-4), three diagnostic models for predicting the pathological severity were not strong enough (all area under the curves<0.8). Only the specificity of LIF-5 for predicting≥ G2, ≥ G2 and/or ≥ S2 was over 80%. Conclusions: Approximately 20% patients with chronic HBV infection in IT phase have progressive liver inflammation or fibrosis. The intensity of liver HBcAg and HBeAg level are negatively correlated with the severity of disease. The diagnostic models or most clinical indicators have low predictive effect for chronic HBV infections in IT phase.

Protective Effects of Bone Marrow Mesenchymal Stem Cells (BMMSCS) Combined with Normothermic Machine Perfusion on Liver Grafts Donated After Circulatory Death via Reducing the Ferroptosis of Hepatocytes.

BackgroundTo improve the quality of liver grafts from extended-criteria donors donated after circulatory death (DCD), this study explored whether bone marrow mesenchymal stem cells (BMMSCs) combined with normothermic machine perfusion (NMP) have protective effects on DCD donor livers and the effects of ferroptosis in this procedure.Material/MethodsTwenty-four male rat DCD donor livers were randomly and averagely divided into normal, static cold storage (SCS), NMP, and NMP combined with BMMSCs groups. Liver function, bile secretion, and pathological features of DCD donor livers were detected to evaluate the protective effects of NMP and BMMSCs on DCD donor livers. Hydrogen peroxide was used to induce an oxidative stress model of hepatocyte IAR-20 cells to evaluate the protective effects of BMMSCs in vitro.ResultsLivers treated with NMP combined with BMMSCs showed better liver function, relieved histopathological damage, reduced oxidative stress injury and ferroptosis, and the mechanism of reduction was associated with downregulation of intracellular reactive oxygen species (ROS) and free Fe2+ levels. BMMSCs showed significant protective effects on the ultrastructure of DCD donor livers and ROS-induced injury to IAR-20 cells under electron microscopy. BMMSCs also significantly improved the expression level of microtubule-associated protein 1 light chain 3 (LC3)-II in both DCD donor livers and ROS-induced injured IAR-20 cells, including upregulating the expression of ferritin.ConclusionsBMMSCs combined with NMP could reduce the level of ROS and free Fe2+ in oxidative stress damaged rat DCD donor livers, potentially reduce the ferroptosis in hepatocytes, and repair both morphology and function of DCD donor livers.

Clinicopathological features of Caroli disease/Caroli syndrome: an analysis of 21 cases

Objective: To summarize and compare clinicopathological features of Caroli disease and Caroli syndrome. Methods: A total of 21 patients diagnosed with Caroli disease or Caroli syndrome in Beijing Friendship Hospital, Capital Medical University, from January 2015 to December 2018 were included. Through the clinical manifestations and comparative analysis of the differences between different clinical types, the liver pathological features of these patients were described. Results: Of all patients included, 8 were male and 13 were female, and the medium age was 13.5 year old. The initial symptom was fever in 6 cases (28.6%), gastrointestinal bleeding in 6 cases (28.6%) and hepatosplenomegaly in 9 cases (42.8%). Caroli disease accounted for 6 cases (28.6%) and Caroli syndrome 15 cases (71.4%). The total bilirubin [6.7 (4.7, 15.0) vs 16.0(10.9, 33.0)μmol/L] and direct bilirubin [1.3(0.9,6.4)vs 3.5(2.7, 16.2)μmol/L] were significantly lower in Caroli disease group in comparison to those in Caroli syndrome group(both P<0.05). The hemoglobin [117.0 (106.0, 126.2) vs 85.0 (74.0, 103.0) g/L] and platelet count [286.0 (149.8, 467.5)×10(9)/L vs 76.1(55.0,123.0)×10(9)/L] in Caroli disease group were significantly higher than those in Caroli syndrome group (both P<0.05). There were 10 patients (47.6%) who underwent liver transplantation. Child-Pugh-Turcotte Score (liver function reserve) were significantly higher than that in the non-liver transplantation group[8.0(8.0, 10.2)vs 5.0 (5.0, 6.0), P<0.05]. Conclusions: Early symptoms of Caroli disease/Caroli syndrome are atypical and prone to misdiagnosis and misdiagnosis. The diagnosis is usually based on pathology and may be supplemented by laboratory examination and imaging analysis.

Grading fatty liver and detecting liver pathological features - Is there consensus between sonographers and radiologists?

Introduction Hepatic steatosis is the leading cause of chronic liver disease. Reliable detection and staging of liver disease is important to facilitate diagnosis and treatment. The aim of this study was to evaluate the interobserver agreement between trainee sonographers, qualified sonographers and radiologists in grading non-alcoholic fatty liver disease (NAFLD) and detecting common liver pathological features in B-mode images. Methods 150 B-mode liver ultrasound images from 50 adult patients referred for an abdominal ultrasound were obtained retrospectively from a PACS system. The images were independently graded for the severity of hepatic steatosis (normal, mild, moderate or severe) and the detection of incidental 0findings, focal fatty sparing, liver surface irregularity and rounded liver edge (present or absent) by 17 qualified, six trainee sonographers and six radiologists. Fleiss’ kappa statistics were used to calculate interobserver agreement among participants in grading common liver pathological features. Intraclass correlation coefficient (ICC) were used to calculate the level of absolute agreement among participants in grading NAFLD. Results The interobserver agreement rates among trainee sonographers for the detection of incidental findings, focal fatty sparing, liver surface irregularity and rounded liver edge were: κ = 0.243, 0.486, 0.155 and 0.079 respectively. Among qualified sonographers, the agreement rates were: κ = 0.323, 0.428, 0.167 and 0.152 respectively. Among radiologists, the agreement rates were: κ = 0.156, 0.266, 0.015 and 0.154 respectively. The intraclass correlation coefficient average scores among trainee sonographers, qualified sonographers, all the sonographers combined and radiologists were: 0.927, 0.978, 0.985 and 0.954 respectively. Conclusion Visual assessment of common liver pathology in B-mode imaging has low interobserver agreement among sonographers and radiologists, but excellent inter-rater reliability in grading NAFLD. The low agreement levels are likely caused by a lack of standardised assessment criteria. The development of a standardised criteria for staging NAFLD and common liver pathological features are recommended.

Grading fatty liver and detecting liver pathological features - Is there consensus between sonographers and radiologists?

Grading fatty liver and detecting liver pathological features - Is there consensus between sonographers and radiologists?

Research advances in clinicopathological features of patients with chronic HBV infection and normal alanine aminotransferase level

It was generally considered that patients with chronic HBV infection and normal alanine aminotransferase ( ALT) level had no or mild liver pathological changes, but in recent years, a large number of studies have found that such patients may also have marked inflammation and fibrosis in the liver. This article discusses the association between clinical features and liver pathological features in patients with chronic HBV infection and normal ALT level and points out that age, sex, HBeAg status, HBV DNA load, ALT level, and liver stiffness measurement are associated with liver pathological changes. Monitoring of these clinical indices helps with early detection of liver pathological changes in patients with chronic HBV infection and normal ALT level.

Is There Consensus among Sonographers and Radiologists in Grading Fatty Liver Disease and Detecting Liver Pathological Features in B-Mode Images?

Hepatic steatosis is the leading cause of chronic liver disease. Reliable detection and staging of liver disease using ultrasound is important to facilitate diagnosis and treatment. The aim of this study was to evaluate the interobserver agreement between trainee sonographers, qualified sonographers and radiologists in grading non-alcoholic fatty liver disease (NAFLD) and detecting common liver pathological features on B-mode images. 150 B-mode liver ultrasound images from 50 adult patients referred for abdominal ultrasound were obtained retrospectively from a PACS system. The images were independently graded for the severity of hepatic steatosis (normal, mild, moderate or severe) and the detection of incidental findings, focal fatty sparing, liver surface irregularity and rounded liver edge (present or absent) by 17 qualified, six trainee sonographers and six radiologists. Fleiss’ kappa statistic was used to calculate interobserver agreement. The interobserver agreement rates among trainee sonographers for the detection of incidental findings, focal fatty sparing, liver surface irregularity and rounded liver edge were: κ = 0.243, 0.486, 0.155 and 0.079 respectively. Among qualified sonographers, the agreement rates were: κ = 0.323, 0.428, 0.167 and 0.152 respectively. Among radiologists, the agreement rates were: κ = 0.156, 0.266, 0.015 and 0.154 respectively. Visual assessment of NAFLD and common liver pathology in B-mode imaging has low interobserver agreement among sonographers and radiologists. The low agreement levels are likely caused by a lack of standardised assessment criteria. The development of standardised criteria for staging common liver pathological features are recommended.

Clinical features of drug-induced autoimmune hepatitis and drug-induced liver injury: a comparative analysis

To investigate the clinical features of drug-induced autoimmune hepatitis (DIAIH) and its therapeutic strategies, and to provide a reference for early diagnosis and treatment of this disease and prevention of chronicity. The clinical data of 116 patients with drug-induced liver injury (DILI) or DIAIH confirmed by medical history, liver biochemistry, and liver biopsy were analyzed retrospectively. Among these patients, 13 had DIAIH and 103 had simple DILI (30 patients in the hepatocyte-type group and 73 in the cholestasis/mixed-type group). The population characteristics, major drugs inducing the diseases, clinical manifestations, liver biochemical parameters, liver pathological features, and clinical outcome were compared between groups. The Kruskal-wallis H test was used for comparison and the Mann-Whitney U test was used for comparison between any two groups. The chi-square test was used for comparison of categorical data, and the R×C chi-square test was used for comparison of rates between the three groups; in the case of significant differences, the R×C contingency table was used for comparison between any two groups. The patients with DIAIH had a mean age of 53.54±8.28 years, and the mean age was 35.13±13.46 and 46.99±14.82 years for the hepatocyte-type group and cholestasis/mixed-type group, respectively. The disease was mainly induced by a combination of various drugs. The patients with DIAIH had significantly higher serum levels of alanine aminotransferase, aspartate aminotransferase, γ-glutamyltransferase, and alkaline phosphatase and a significantly higher positive rate of anti-nuclear antibody than those with DILI (all P < 0.05). In patients with DIAIH, the liver pathological features and the features of response to treatment were as follows: obvious interface hepatitis, proliferation of small bile ducts, and mixed inflammatory cell infiltration in the portal area, including eosinophils and plasma cells, and the short-term corticosteroid therapy had a good therapeutic effect. DIAIH has a low incidence and is more common in the female population, with the features of tissue injury in both DILI and autoimmune hepatitis. The short-term corticosteroid therapy can prevent disease progression and reduce chronicity.

Effects of Polygonum multiflorum Thunb. water extraction by different processed temperature on acute liver injury induced by CCl4 in mice

Objective To explore the effects of Polygonum multiflorum Thunb. by different processed temperature on acute liver injury induced by CCl4 in mice. Methods A total of 140 KM mice were randomly divided into the control group, the positive drug group, the model group, the 100 ℃, 110 ℃, and 120 ℃ processed group and crude drug group, all the groups above were in sequence given the equal normal saline, silymarin (10 mg/kg), 100 ℃ extract (100 mg/kg), 110 ℃ extract (100 mg/kg), 120 ℃ extract (100 mg/kg) and crude drug extract (100 mg/kg) each day, respectively. After 7 days, apart of the control group, the other groups were established the acute liver injury model by the carbon tetrachloride. The blood and liver of mice were taken after 24 h post-model made. The levels of AST, ALT, Alb, TP, IL-6, TNF-a, IL-1, SOD, MDA and GSH-Px were detected, and liver pathological features of each group were observed. Results Compared with the model group, the levels of ALT (132.14 ± 19.66 U/L, 81.55 ± 12.67 U/L, 169.37 ± 24.18 U/L vs. 261.84 ± 31.61 U/L), AST (231.57 ± 38.38 U/L, 181.73 ± 36.52 U/L, 318.36 ± 39.68 U/L vs. 624.79 ± 49.98 U/L), IL-6 (10.35 ± 1.62 pg/ml, 6.26 ± 1.36 pg/ml, 12.57 ± 1.88 pg/ml vs. 18.73 ± 5.54 pg/ml), TNF-α (243.74 ± 13.02 pg/ml, 189.36 ± 9.85 pg/ml, 273.13 ± 14.64 pg/ml vs. 314.36 ± 29.67 pg/ml), IL-1 (235.36 ± 30.14 pg/ml, 208.07 ± 9.33 pg/ml, 48.21 ± 33.15 pg/ml vs. 264.76 ± 32.55 pg/ml) in the 100 ℃, 110℃, 120 ℃ group significantly decreased (P<0.05). The levels of TP (69.16 ± 2.96 g/L, 74.14 ± 3.17 g/L, 65.73 ± 2.22 g/L vs. 62.06 ± 2.65 g/L), Alb (35.86 ± 2.64 g/L, 36.67 ± 2.81 g/L, 34.06 ± 2.64 g/L vs. 32.16 ± 2.05 g/L) in the 100 ℃, 110 ℃, and 120 ℃ group significantly increased (P<0.05). The levels of SOD (82.94 ± 6.21 U/mg, 101.33 ± 9.16 U/mg, 71.32 ± 5.15 U/mg vs. 66.22 ± 1.13 U/mg), GSH-Px (153.39 ± 15.23 U, 199.25 ± 12.04 U, 159.26 ± 17.18 U vs. 64.79 ± 32.56 U) in the 100 ℃, 110℃, and 120 ℃ group significantly increased (P<0.05), while the level of MDA (0.96 ± 0.22 nmol/mg, 0.69 ± 0.13 nmol/mg, 1.29 ± 0.13 nmol/mg vs. 1.71 ± 0.33 nmol/mg) in the 100 ℃, 110 ℃, and 120 ℃ group significantly decreased (P<0.05). Conclusions Different processed temperature of Polygonum Multiflorum Thunb. water extract on liver injury in mice caused by carbon tetrachloride is not the same. The 110 ℃ processed temperature showd the best liver protection. Key words: Processing (TCD); Fallopia multiflora; Carbon tetrachloride; Liver injury; Mice

Steatohepatitis Secondary to Long-Term Glucocorticoid Treatment for Congenital Adrenal Hyperplasia: A Potential Diagnostic Pitfall

A 24-year-old woman with congenital adrenal hyperplasia (CAH) was referred for evaluation of elevated liver enzyme activities over the preceding 6 months. The patient was diagnosed with CAH at the age 12 when she presented with irregular menses and hirsutism. Since then, she had been on dexamethasone to maintain a normal menstrual cycle and prevent hirsutism and acne. She had no history of chronic liver disease and drank alcohol socially. An extensive workup for other treatable causes of liver disease was unrevealing. Therefore, a liver biopsy was performed, which revealed extensive ballooned degenerative hepatocytes containing Mallory-Denk hyalines. The ballooned hepatocytes were located predominantly in centrilobular areas and without any accompanying steatosis. Even though the histopathologic features are most compatible with alcoholic and/or nonalcoholic steatohepatitis, it was not supported by the patient's medical history and clinical presentation. The patient had a normal body mass index and only occasional alcohol use. Based on the biopsy finding and clinical presentation, we postulated that the abnormal liver enzyme and pathological features seen on the liver biopsy were secondary to CAH and long-term use of glucocorticoid. A few studies have shown that patients with CAH often develop metabolic abnormalities and insulin resistance, particularly women treated with glucocorticoid for several years. To our knowledge, this is the first report describing steatohepatitis secondary to CAH and prolonged glucocorticoid treatment. It is important to be aware that steatohepatitis can develop in these patients due to long-term glucocorticoid use and potentially lead to progressive liver damage. Furthermore, in patients with CAH who develop abnormal liver enzyme activities a liver biopsy is warranted to assess for steatohepatitis and any associated fibrosis. If indeed fibrosis is already present, a consultation with the endocrinologist should be undertaken in an effort to lower the dose of the glucocorticoids as much as possible while still controlling the symptoms of the disease.

A high‐fat diet and multiple administration of carbon tetrachloride induces liver injury and pathological features associated with non‐alcoholic steatohepatitis in mice

The aim of the present study was to establish a progressive steatohepatitis mouse model because few reported animal models of non-alcoholic steatohepatitis (NASH) show the progression from fatty liver to steatohepatitis. C57BL/6N mice were fed a high-fat diet (HFD) to develop obesity and were either administered carbon tetrachloride (CCl4 ) eight times (0.05mL/kg, s.c., once, followed by 0.1mL/kg, s.c., seven times) or not. Serum parameters and hepatic histopathology were examined. In a separate experiment, CCl4 was administered subcutaneously from 0 to eight times to HFD-fed obese mice to investigate progressive changes. Markers of oxidative stress, inflammation and apoptosis, as well as histopathological changes in the liver, were analysed. The HFD-fed obese mice showed fatty liver but not steatohepatitis. In contrast, HFD-fed mice administered CCl4 eight times showed histopathological features of steatohepatitis (fatty liver, inflammation, hepatocellular ballooning and fibrosis) and increased serum alanine aminotransferase levels. However, the multiple administration of CCl4 to obese mice reduced the ratio of reduced glutathione to oxidized glutathione, superoxide dismutase activity and mitochondrial DNA copy number, leading to the development of chronic oxidative stress, increased numbers of apoptotic cells and increased levels of both tumour necrosis factor-α and transforming growth factor-β mRNA. The resulting inflammation led to increased hydroxyproline content in the liver and fibrosis. The present study demonstrates that multiple administration of CCl4 to HFD-fed obese mice induces chronic oxidative stress that triggers inflammation and apoptosis and leads to the development of fibrosis in the liver, resulting in progression from fatty liver to steatohepatitis. This murine model will be useful in the research of hepatic disorders.

PP-108 Investigation on serum HBV viral loads and the changes of liver pathological features in 158 patients with chronic hepatitis B

PP-108 Investigation on serum HBV viral loads and the changes of liver pathological features in 158 patients with chronic hepatitis B

An Evaluative Study on Sidoarjo Mud Flow after Phytoremediation Treatment in Milk Fish (Chanos Chanos) Liver

A sudden discharge of Sidoarjo mud flow into the water bodies would disturb aquatic biota, the fisheries culture. The aim of this research is to evaluate the availability of phytoremediated water of Sidoarjo mud flow (abbreviated: pwmf) as a milkfish culture media using liver histological approach. After two weeks acclimatization period, the juvenile and adult of milkfish were exposed the pwmf at the sub lethal concentration and an acute static bioassay at 96 hours. Control fishes were reared in the artificial brackish water. Each treatment of pwmf exposure was done in three replicates. After exposure, the liver fishes were removed and histologically processed using paraffin method and HE staining. Histopathology change was assessed semi quantitative scoring. The result of the histological analyses suggested the liver pathological features such as vacuolation of hepatocytes, the loss of sinusoid integrity from mild to severe occurrence and necrosis.

Alpers syndrome presenting with anatomopathological features of fulminant autoimmune hepatitis

A 6-month-old girl with normal psychomotor development presented with fulminant hepatitis. Interestingly, liver biopsy demonstrated features of autoimmune hepatitis, whereas autoantibodies and raised immunoglobulin G (IgG) were absent. There was extensive centrolobular necrosis with bridging (Fig. 1a) and ductular reaction (Fig. 1b). There were numerous lymphocytes and plasmocytes (polyclonal on kappa and lambda stain) (Fig. 1c). Biochemical investigations excluded alternative causes of fulminant hepatitis. Steroid treatment was started, but the patient soon evolved to liver failure and received a liver transplantation. Three months posttransplant, the patient developed myoclonic and generalized tonic-clonic fits. Computed tomography (CT) scan, normal at presentation, revealed evolution toward severe brain atrophy. Mitochondrial assays on postmortem muscle biopsy revealed normal activity of respiratory chain complex II and decreased I, III, and IV activity. This is indicative of mitochondrial DNA (mtDNA) depletion in this clinical setting (Hargreaves et al. 2002). DNA analysis revealed two known POLG mutations (p.Ala467Thr and p. Gly848Ser), diagnostic for Alpers syndrome. We show here for the first time that a mtDNA-depletion syndrome can present with the anatomopathological features of autoimmune hepatitis. Alpers syndrome therefore should not be excluded from the differential diagnostic list based on these features. Whether this is also the case in older children, or even adults, presenting with cryptogenic acute liver failure and pathological features of autoimmune hepatitis remains to be determined.

Study on the relationship of serum vitamin E and liver pathological features in the patients with chronic hepatitis B

To study on the relationship of serum vitamin E and liver pathological features in the patients with chronic hepatitis B. Sixty-six patients with chronic hepatitis B and ten healthy controls were enrolled in this present study. The serum vitamin E level was measured spectrophotometrically. Comparisons of liver function test, HBeAg and HBV DNA level were conducted among different liver pathological features including inflammatory grading and fibrosis staging. Compared with healthy controls, the serum level of vitamin E was significantly decreased in the patients with chronic hepatitis B, especially in those with elevated ALT activity. In comparison between HBeAg positive group and HBeAg negative group, the serum level of vitamin E of the former group did not significantly changed (P > 0.05). Furthermore, the serum level of vitamin E has been demonstrated to be negatively associated with the inflammation grading in the patients with chronic hepatitis B. However, there was no significant association between the serum vitamin E and liver fibrosis staging. Vitamin E, as one of the important anti-oxidants, was demonstrated to be implicated in the progression of liver inflammation in the patients with chronic hepatitis B. Furthermore, the supplement of vitamin E would be a potential therapy for attenuate the inflammatory response.