INTRODUCTION: Portal hypertension progression can be relieved after controlling the etiology of liver cirrhosis. Whether beta-blockers could additionally enhance the effects during treatment, particularly for small esophageal varices (EV), was unclear. This study aims to assess the efficacy of add-on carvedilol to delay EV progression during anti-hepatitis B virus (HBV) treatment in HBV-related cirrhosis. METHODS: This randomized controlled trial enrolled patients with virologically suppressed HBV-compensated cirrhosis and small/medium EV. The participants were randomly assigned to receive nucleos(t)ide analog (NUC) or carvedilol 12.5 mg plus NUC (1:1 allocation ratio). The primary end point was the progression rate of EV at 2 years of follow-up. RESULTS: A total of 238 patients (small EV, 77.3%) were randomized into 119 NUC and 119 carvedilol plus NUC (carvedilol [CARV] combination group). Among them, 205 patients (86.1%) completed paired endoscopies. EV progression rate was 15.5% (16/103) in the NUC group and 12.7% (13/102) in the CARV combination group (relative risk = 0.79, 95% confidence interval 0.36-1.75, P = 0.567). Subgroup analysis on medium EV showed the CARV combination group had a more favorable effect in promoting EV regression (43.5% vs 13.1%, P = 0.022) than NUC alone, but not in small cases (P = 0.534). The incidence of liver-related events (decompensation, hepatocellular carcinoma, or death/liver transplantation) within 2 years was similar between the 2 groups (11.2% vs 10.4%, P = 0.881). DISCUSSION: The overall results did not show statistically significant differences between the added carvedilol strategy and NUC monotherapy in preventing EV progression in patients with virologically suppressed HBV-compensated cirrhosis. However, the carvedilol-added approach might offer improved outcomes specifically for patients with medium EV (NCT 03736265).

Viral hepatitis, caused by its etiology, hepatitis virus, is a public health problem globally. Among all infections caused by hepatitis-associated viruses, hepatitis B virus (HBV) infection remains the most serious medical concern. HBV infection particularly affects people in East Asia and Africa, the Mediterranean region, and Eastern Europe, with a prevalence rate of > 2%. Currently, approximately 1 billion people worldwide are infected with HBV, and nearly 30% of them experience chronic infection. Chronic HBV infection can lead to chronic hepatitis B (CHB), liver cirrhosis, and hepatocellular carcinoma (HCC), resulting in the related death of approximately 1 million people annually. Although preventative vaccines and antiviral therapies are currently available, there is no cure for this infection. Clinical testing is not only the gateway for diagnosis of HBV infection, but also crucial for judging the timing of medication, evaluating the effect of antiviral therapy, and predicting the risk of relapse after drug withdrawal in the whole follow-up management of hepatitis B infected persons. With advances in detection technology, it is now possible to measure various viral components in the blood to assess the clinical status of HBV infection. Serum viral products of HBV infection, such as HBV DNA, HBV RNA, hepatitis B surface antigen, hepatitis B e-antigen, and hepatitis B core-related antigen, are non-invasive indicators that are critical for the rapid diagnosis and management of related diseases. Improving the sensitivity of monitoring of these products is essential, and the development of corresponding detection technologies is pivotal in achieving this goal. This review aims to offer valuable insights into CHB infection and references for its effective treatment. We provide a comprehensive and systematic overview of classical and novel methods for detecting HBV serum viral products and discusses their clinical applications, along with the latest research progress in this field.

慢性乙型肝炎病毒(hepatitis B virus,HBV)感染可导致诸多肝脏问题,共价闭合环状DNA(covalently closed circular DNA,cccDNA)的存在是造成HBV持续感染、难以清除的主要原因.cccDNA检测依赖于肝活检,限制了其临床广泛应用,而HBV感染者血清中的HBV RNA主要为前基因组RNA(pregenomic RNA,pgRNA),由cccDNA转录产生,可以反映cccDNA的转录活性,在评估抗病毒治疗效果以及预测停药后复发风险等方面具有较好的指示性,故本文就血清HBV RNA的相关临床研究进展作一综述.

目前尚无关于溃疡性结肠炎(ulcerative colitis,UC)患者感染 SARS-CoV-2 的风险、相互间的影响、治疗策略等的指南及共识.为进一步做好UC患者合并 COVID-19 的诊疗工作,本文结合近期收治的 2 例典型临床病例及相关文献对 UC 患者合并 COVID-19 的风险及诊疗进行总结分析,希望能对此类患者的临床诊疗提供参考.

Background Liver fibrosis is a critical part of the clinical process of liver disease that progresses to cirrhosis and even liver cancer, and effective treatment and clinical biomarkers are urgently needed to manage liver fibrosis. Ferroptosis, a notable biological phenomenon that has received attention because of the role it performs in liver fibrosis. The objective of this research is in order to identify key ferroptosis genes related to advanced liver fibrosis/cirrhosis. Methods Gene expression differences were analyzed in liver fibrosis liver tissue of hepatitis B virus(HBV)infection patients, non-alcoholic steatohepatitis (NASH) patients and alcoholic hepatitis (AH) patients to obtain overlapping ferroptosis-related genes that are significantly up-regulated. A multigroup comparison was performed to evaluate the diagnostic clinical importance of ferroptosis-related genes of patients in differential degrees of liver fibrosis, and confirmed via gene expression trend analysis. The differential expression of candidate ferroptosis-related genes through classical carbon tetrachloride (CCl 4 ) induced advanced liver fibrosis mice model were validated by real-time quantitative PCR (qPCR). Correlation analysis was conducted to tentatively identify the connections between hepatic ferroptosis-related genes and key genes participating in functional pathways relevant to liver fibrosis. Results We screened and obtained 10 genes related to ferroptosis, all of which were significantly up-regulated in liver tissue from liver fibrosis patients of different etiologies, and identified acyl-CoA synthetase long chain family member 4 ( ACSL4 ) was transcriptomic enriched in patients with HBV infection, NASH, AH-associated advanced liver fibrosis and cirrhotic tissue adjacent to hepatocellular carcinoma (HCC). In CCl 4 induced advanced liver fibrosis mice model, the hepatic ACSL4 expression was significantly up-regulated when compared to normal controls. In our study, we also suggest a significant association between ACSL4 and representative genes in liver fibrosis-related pathway. Conclusion We found that ACSL4 mRNA can effectively differentiate the severity of liver fibrosis, suggesting its potential clinical diagnostic value in patients with liver fibrosis regardless of its etiology. ACSL4 may be a promising biomarker, which deserves further research.

血尿在临床上很常见,但肝硬化胃底静脉曲张预防性治疗后出现血尿在临床上非常罕见,尤其还伴有凝血因子Ⅴ缺乏.本文介绍1例肝硬化胃底静脉曲张Ⅱ期预防治疗后血尿的病例.

Background and Aims: The prevalence of high-risk varices (HRV) is low among compensated cirrhotic patients undergoing EGD. Our study aimed to identify a novel machine learning (ML)-based model, named ML EGD, for ruling out HRV and avoiding unnecessary EGDs in patients with compensated cirrhosis. Methods: An international cohort from 17 institutions from China, Singapore, and India were enrolled (CHESS2001). The variables with the top 3 importance scores (liver stiffness, platelet count, and total bilirubin) were selected by the Shapley additive explanation and input into a light gradient-boosting machine algorithm to develop ML EGD for identification of HRV. Furthermore, we built a web-based calculator for ML EGD, which is free with open access (http://www.pan-chess.cn/calculator/MLEGD_score). Unnecessary EGDs that were not performed and the rates of missed HRV were used to assess the efficacy and safety for varices screening. Results: Of 2794 enrolled patients, 1283 patients formed a real-world cohort from 1 university hospital in China used to develop and internally validate the performance of ML EGD for varices screening. They were randomly assigned into the training (n Z 1154) and validation (n Z 129) cohorts with a ratio of 9:1. In the training cohort, ML EGD spared 607 (52.6%) unnecessary EGDs with a missed HRV rate of 3.6%. In the validation cohort, ML EGD spared 75 (58.1%) EGDs with a missed HRV rate of 1.4%. To externally test the performance of ML EGD, 966 patients from 14 university hospitals in China (test cohort 1) and 545 from 2 hospitals in Singapore and India (test cohort 2) comprised the 2 test cohorts. In test cohort 1, ML EGD spared 506 (52.4%) EGDs with a missed HRV rate of 2.8%. In test cohort 2, ML EGD spared 224 (41.1%) EGDs with a missed HRV rate of 3.1%. When compared with the Baveno VI criteria, ML EGD spared more screening EGDs in all cohorts (training cohort, 52.6% vs 29.4%; validation cohort, 58.1% vs 44.2%; test cohort 1, 52.4% vs 26.5%; test cohort 2, 41.1% vs 21.1%, respectively; P <.001). Conclusions: We identified a novel model based on liver stiffness, platelet count, and total bilirubin, named ML EGD, as a free web-based calculator. ML EGD could efficiently help rule out HRV and avoid unnecessary EGDs in patients with compensated cirrhosis. (Clinical trial registration number: NCT04307264.) [GRAPHICS] .

通过1例少见的乙型病毒性肝炎肝硬化食管静脉曲张TIPS术后消化道出血病例的诊疗,加以文献复习,分析出血原因,以探讨乙型病毒性肝炎肝硬化患者通过治疗最大获益的治疗方案.

The mechanism of hepatitis B virus (HBV) immune tolerance remains unclear. Our previous studies showed that ATOH8 plays an important role in the liver tumor immune microenvironment; however, the specific immune regulatory mechanism requires further studies. Studies have shown that the hepatitis C virus (HCV) can cause hepatocyte pyroptosis; however, the relationship between HBV and pyroptosis is contested. Therefore, this study aimed to determine whether ATOH8 interfered with HBV activity through pyroptosis to further study the mechanism of ATOH8 on immune regulation and enrich our understanding of HBV‑induced invasion. The expression levels of pyroptosis‑related molecules (GSDMD and Caspase‑1) in liver cancer tissues and peripheral blood mononuclear cells (PBMCs) of patients with HBV were assessed using qPCR and western blotting. HepG2.2.15 and Huh7 cells were used to overexpress ATOH8 using a recombinant lentiviral vector. The HBV DNA expression levels in HepG2.2.15 cells were detected using absolute quantitative (q)PCR, and the hepatitis B surface antigen expression levels in the HepG2.2.15 cell culture supernatant were measured using ELISA. The expression of pyroptosis‑related molecules in Huh7 and HepG2.2.15 cells was detected using western blotting and qPCR. Additionally, the expression levels of inflammatory factors including TNF‑α, INF‑α, IL‑18, and IL‑1β were detected using qPCR and ELISA. The liver cancer tissues and PBMCs of patients with HBV showed higher expressions of pyroptosis‑related molecules than those of normal samples. ATOH8‑overexpressed HepG2.2.15 cells had higher HBV expression levels but lower levels of pyroptosis‑related molecules, such as GSDMD and Caspase‑1, than those in the control group. Similarly, the expression levels of pyroptosis‑related molecules in Huh7 cells overexpressing ATOH8 were lower than that in Huh7‑GFP cells. Further detection of the expression of INF‑α and TNF‑α in HepG2.2.15 cells overexpressing ATOH8 showed that ATOH8 overexpression increased the expression of these inflammatory factors, including those associated with pyroptosis (IL‑18 and IL‑1β). In conclusion, ATOH8 promoted HBV immune escape by inhibiting hepatocyte pyroptosis.

Background and Aims: The Baveno VI and expanded-Baveno VI criteria has been validated as single-use screening for varices needing treatment (VNT) in patients enriched with hepatitis C virus and alcoholic-related compensated cirrhosis. Here, we aimed to develop and validate novel CHESS model for single-use screening and dynamic monitoring of VNT in patients with predominantly hepatitis B virus (HBV)-related compensated cirrhosis. Methods: A total of 3,470 patients with compensated cirrhosis from China, Singapore and India were included in the international multicenter study with six cohorts as follows: real-world cohort; multicenter validation cohort; international validation cohort; multicenter HBV cohort; dynamic monitoring longitudinal cohort; multicenter, clinical practice cohort. Primary outcomes were the rates of VNT missed and spared esophagogastroduodenoscopy (EGD).Results: In the real-world cohort (65%HBV), implementing Baveno VI criteria would have spared 30% of EGDs and missed 3·6% of VNT. Expanded-Baveno VI criteria had an unacceptable VNT missed rate of 6·2%. Using the new CHESS model (platelets>110×109/L and liver stiffness<19kPa) would have spared 46% of EGDs (p<0.001 vs. Baveno VI criteria) and missed 4·9% of VNT. In the multicenter cohort (75%HBV), international cohort (14%HBV) and HBV cohort, CHESS model would also have spared more EGDs (all p<0·001) than Baveno VI criteria. Notably, employing CHESS model in dynamic monitoring cohort would have safely spared 41% and 54% of EGDs for primary and secondary monitoring, respectively. In the prospective clinical practice cohort, 75% of EGDs were spared according to CHESS model, with a VNT rate of 36% in patients dissatisfied CHESS model who underwent EGD.Conclusion: CHESS model were superior to Baveno VI criteria and expanded-Baveno VI criteria for the screening and monitoring of varices in patients with HBV-dominated compensated cirrhosis.Funding Information: None. Declaration of Interests: None.Ethics Approval Statement: All procedures were performed in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1975, as revised in 2008. The study was approved by the Ethics Committees of all the involved centers. The committees waived the need for written informed consent from subjects in two retrospective cohorts because de-identified secondary data were analyzed. Written informed consent was obtained from all patients prior to inclusion in the prospective cohorts.

目的 总结分析艾滋病合并肝脓肿患者的临床表现、诊断、治疗和预后,为临床诊治提供参考.方法 收集上海市公共卫生临床中心2015年1月至2020年12月收治的艾滋病合并肝脓肿患者的临床资料,回顾性分析其临床特征、治疗情况及预后等.结果 41例患者均确诊艾滋病合并肝脓肿,男40例,女1例,其中经治艾滋病肝脓肿患者17例,年龄(39.2±11.6)岁,未治疗艾滋病肝脓肿患者24例,年龄(35.7±9.5)岁.主要表现为发热(85.4％)和肝区不适(34.1％).41例患者均出现CRP升高,CD4降低34例(82.9％),中性粒细胞百分比升高27例(65.9％),GGT升高35例(85.4％),ALB降低39例(95.1％).肝脓肿病灶主要位于肝右叶26例(63.4％),肝左叶7例(17.1％),双叶8例(19.5％),多发脓肿13例(31.7％).治疗上以联合抗感染为主,32例(78.0％)患者联合穿刺引流,40例(97.6％)患者痊愈或好转出院.结论 艾滋病合并肝脓肿患者临床特征无特异性,病情复杂多变.早期经验性治疗推荐碳青霉烯类或第三代头孢菌素联合硝基咪唑类抗生素,注意特殊病原体感染.脓肿穿刺引流安全有效,未治疗艾滋病肝脓肿患者建议尽早HAART治疗,可减少机会菌感染,可能减少肝脓肿复发.

Objectives: Hepatitis E virus (HEV) infection causes high mortality in pregnant women of developing regions during large outbreaks. The aim of this study was to investigate the clinical features of HEV-infected pregnant women in Shanghai, China where the epidemiology of HEV has shifted from large outbreaks to the sporadic form. Methods: Clinical data of 516 pregnant and nonpregnant child-bearing age women diagnosed with HEV infection during 2009-2020 was collected at the Shanghai Public Health Clinical center. Patients' data were analysed for clinical features and laboratory parameters accordingly. Results: Most of the hospitalized HEV-infected pregnant women (85.23%, 127/149) showed no obvious clinical symptoms and the disease outcome was generally benign with no liver failure or maternal mortality observed in the patients. By comparison, fewer (37.21%, 32/86) of the HEV-infected nonpregnant women were asymptomatic, and five cases (5.81%, 5/86) of liver failure were observed among them. The levels of serum alanine aminotransferase, aspartate aminotransferase, total bilirubin (TBiL), direct bilirubin (DBiL) and total bile acids (TBA) were significantly higher ( P < 0.05) in nonpregnant women than those of the pregnant women. We found 42.99% (46/107) births had adverse foetal/neonatal outcome. Mothers who presented with adverse foetal/neonatal outcome showed higher ( P < 0.05) serum TBiL, DBiL and TBA levels than those without. Conclusion: We found that the clinical features of sporadic HEV infection in pregnant women in Shanghai, China are generally mild and no maternal mortality occurred. However foetal/neonatal adverse outcomes including preterm births and stillbirths were observed in HEV-infected pregnant women. (c) 2021 The British Infection Association. Published by Elsevier Ltd. All rights reserved.

目的 探讨钾离子竞争性酸阻滞剂(potassium-competitive acid blocker,P-CAB)富马酸伏诺拉生替代质子泵抑制剂(proton pump inhibitor,PPI)治疗持续难治性幽门螺杆菌(Helicobacter pylori,H.pylori)感染的临床疗效.方法 12例H.pylori感染慢性胃炎患者,男7例,女5例,年龄41～70岁,均给予PPI+铋剂+阿莫西林+克拉霉素或左氧氟沙星+呋喃唑酮等治疗2～3个疗程,H.pylori仍持续阳性2年以上.均给予富马酸伏诺拉生20 mg,1次/d,枸橼酸铋钾胶囊2粒,3次/d,左氧氟沙星0.5 g,2次/d,阿莫西林1.0 g,2次/d,用药2周.停药后1个月行13C尿素呼气试验.结果 12例患者13C尿素呼气试验均呈阴性.结论 富马酸伏诺拉生联合铋剂及抗生素有助于根治难治性H.pylori持续感染.

肝衰竭患者出现精神障碍时除了考虑肝性脑病之外,还需鉴别低血糖症、代谢性疾病、水电解质紊乱、脑血管疾病及感染等.现报道1例肝衰竭合并有低血糖症、Wernicke脑病患者,旨在提高临床医师对本病的认识,减少漏诊.

Bioinformatics analysis showed that Serine/threonine kinase 39 (STK39), which was testified to play an important role in human cancers, may be a hub gene in diagnosing hepatocellular carcinoma (HCC). This study aimed to explore whether STK39 could be regulated by specificity protein 1 (SP1) to affect HCC cells malignant processes. Firstly, STK39 expression in tissues of HCC patients and several cell lines was analyzed. After STK39 silencing, cell proliferation was evaluated by methyl thiazolyl tetrazolium and colony formation assay. Tunel staining was used to detect cell apoptosis. Then, the abilities of cell migration and invasion were determined with wound healing and transwell assays. The expression of epithelial–mesenchymal transition (EMT)-related proteins and transforming growth factor-β1 (TGF-β1)/Smad2/3 pathway proteins was tested by western blot analysis. Thereafter, cells were overexpressed with SP1 under the circumstance of STK39 knockdown, and then the above cellular processes were under observation. Results revealed that the increased expression of STK39, which was found in both HHC patients and HCC cell lines, exhibited poor HCC prognosis. STK39 silencing inhibited Hep3b cell proliferation, migration, invasion, EMT and TGF-β1/Smad2/3 expression but promoted cell apoptosis. Additionally, SP1 could bind to the STK39 promoter and facilitate STK39 expression. Further studies revealed that the effects of STK39 silencing on Hep3b cells were blocked by SP1 overexpression. In conclusion, SP1-mediated STK39 up-regulation leads to the increased proliferation, migration, invasion and EMT of HCC cells via activating TGF-β1/Smad2/3 pathway. Therapies that target SP1 to knockdown STK39 expression may contribute to the inhibition of HCC progression.

Antiviral therapy is effective in decreasing disease progression in HBV cirrhosis. However, the long-term effect of antiviral therapy on health-related quality of life (HRQoL) in patients with compensated HBV cirrhosis is unknown. The patients with compensated HBV cirrhosis enrolled in a randomized controlled trial of entecavir-based therapy were recruited in the present study, if they had HRQoL score at 5-year follow-up or who developed liver-related events (LRE) during follow-up were included. HRQoL was measured with 36-Item Short-Form Health Survey (SF-36) and EuroQol-5D (EQ-5D) at baseline and yearly during follow-up. LRE was defined as the development of decompensation, HCC, or death. A total of 161 patients were included in the present study, with a median age of 48.0 (41.0, 53.0) years, 77.6% being male and 37.2% being HBeAg-positive. During 5 years, 45 patients developed LRE. All eight dimensions of SF-36 were significantly improved after 5 years of antiviral therapy (all p < 0.001), with all dimensions improved more than five points except for physical functioning. Proportion of patients reporting no problems in all five dimensions in EQ-5D increased from 57.8 to 72.0%; visual analogue scale (VAS) and utility index (UI) increased significantly (VAS 79.8 ± 16.4 to 84.4 ± 13.2, UI 0.91 ± 0.13 to 0.95 ± 0.10, both p < 0.001). HRQoL improved or kept stable in the majority of patients who had LRE during follow-up, even stratified by Baveno VI criteria for clinically significant portal hypertension. After 5 years of ETV treatment, HRQoL significantly improved in patients with compensated HBV cirrhosis. (NCT01943617, NCT02849132)

The early recognition and treatment of ectopic varicose vein hemorrhage caused by portal hypertension in hepatic cirrhosis is a difficult problem in clinical work because of its difficulty in diagnosis, large amount of bleeding, difficulty in hemostasis, poor prognosis and high mortality. In this paper, the recognition and treatment of ectopic varicose vein hemorrhage in hepatic portal hypertension are summarized by referring to relevant literature.

Aims Patients with COVID-19 can also have enteric symptoms. Here we analyzed the histopathology of intestinal detachment tissue from a patient with COVID-19. Methods The enteric tissue was examined by hematoxylin & eosin stain, PAS (Periodic acid–Schiff) staining, Gram staining, Ziehl–Neelsen stain and Grocott’s Methenamine Silver (GMS) Stain. The distribution of CD3, CD4, CK20 and CD68, cytomegalovirus (CMV) and Herpes Simplex Virus (HSV) antigen were determined by immunohistochemistry. In situ hybridization (ISH) of SARS-CoV-2 and Epstein-Barr virus-encoded small RNA (EBER) were also performed. Results We observed mucosal epithelium shedding, intestinal mucosal erosion, focal inflammatory necrosis with hemorrhage, massive neutrophil infiltration, macrophage proliferation accompanied by minor lymphocyte infiltration. Fungal spores and gram positive cocci but not mycobacteria tuberculosis were identified. Immunohistochemistry staining showed abundant CD68 + macrophages but few lymphocytes infiltration. HSV, CMV and EBV were negative. ISH of SARS-CoV-2 RNA showed positive signal which mostly overlapped with CD68 positivity. Conclusions The in situ detection of SARS-CoV-2 RNA in intestinal macrophages implicates a possible route for gastrointestinal infection. Further study is needed to further characterize the susceptibility of enteric cells to SARS-CoV-2 infection.

Many models have been developed to predict liver-related events (LRE) in chronic hepatitis B, few focused on compensated HBV-induced cirrhosis. We aimed to describe the incidence of LRE and to determine independent risk predictors of LRE in compensated HBV-induced cirrhosis patients receiving antiviral therapy using routinely available parameters. Prospective cohorts of treatment-naïve adults with compensated HBV-induced cirrhosis were enrolled. Patients were treated with entecavir (ETV) or ETV + thymosin-alpha1 (Thy-α1) or lamivudine (LAM) + adefovir (ADV). Data were collected at baseline and every 6 months. LRE was defined as development of decompensation, HCC or death. Totally 937 patients were included, 608 patients treated with ETV, 252 with ETV + Thy-α1, and 77 with LAM + ADV. After a median follow-up of 4.5 years, 88 patients developed LRE including 48 with HCC. The cumulative incidence of LRE at year 1, 3, and 5 was 2.1%, 7.0%, and 12.7%, respectively, and was similar for three treatment groups. All models using variables at month 6 or 12 had better fit than models using baseline values. The best model for prediction of LRE used PLT, GGT, and AFP at month 6 [AUC: 0.762 (0.678–0.814)], for hepatic decompensation—PLT, LSM and GGT at month 12 (AUC: 0.834 (0.675–0.919)), and for HCC—AFP and GGT at month 6 [AUC 0.763 (0.691–0.828)]. All models had negative predictive values of 94.0–98.8%. Models using on-treatment variables are more accurate than models using baseline variables in predicting LRE in patient with compensated HBV-induced cirrhosis receiving antiviral therapy. ClincialTrials.gov number NCT01943617, NCT01720238, NCT03366571, NCT02849132.

目前病毒性肝炎是一个全球关注的公共卫生问题,当病毒性肝炎患者合并有炎症性肠病时,其接受免疫抑制剂或生物制剂治疗后可能会导致肝炎病毒复制活跃、肝功能异常,甚至有肝功能衰竭的风险.但也有研究表明,抗病毒治疗可诱发或加重炎症性肠病的发生,且不少学者对病毒性肝炎的抗病毒治疗对炎症性肠病影响的观点不一.因此,本文就病毒性肝炎的抗病毒治疗对炎症性肠病的影响进行综述.