Peripheral helper T cells represent a recently characterized subset of CD4+ T cells present in inflammatory bowel disease (IBD) patients. Bile acids act as signaling molecules in immune regulation. However, the role of bile acids in Tph cell differentiation remains unclear. Immunofluorescence staining was used to detect the presence of Tph cells in intestinal tissue samples; Wild-type (WT) and Fxr−/− mice were treated with or without the FXR agonist obeticholic acid (OCA) in dextran sulfate sodium (DSS)-induced acute colitis. The proportions of Tph cells and innate immune cells were analyzed by FACS. Bone marrow-derived dendritic cells (BMDCs) and naïve T cells of WT and Fxr−/− mice were sorted, differentiated and cultured in vitro to observe the regulatory effects of FXR on BMDCs function and Tph cell differentiation. Tph proportion was significantly elevated in inflamed intestinal tissues. OCA treatment increased the Tph cell proportion in the intestinal LP of WT mice. The proportion of dendritic cells (DCs) in the LP of Fxr−/− mice was significantly lower than WT mice after DSS-mediated colitis induction. FXR deficiency impaired the ability of BMDCs to induce Tph cell differentiation in vitro. CD11c and MHC-II expression levels were reduced in BMDCs from Fxr−/− mice upon stimulation with LPS. FXR deficiency activated the PPAR-γ signaling pathway and decreased IL-12 expression in BMDCs. Tph cell levels were elevated in inflamed intestinal tissues. FXR suppression in BMDCs was associated with activated PPAR-γ signaling; and with reduced DC maturation, IL-12 secretion, and Tph cell differentiation.

The selection of optimal first-line biologic therapy for treatment-naïve Crohn’s disease (CD) patients continues to present a clinical dilemma. Existing evidence remains limited by its predominant focus on anti-TNF-exposed populations or reliance on clinical endpoints alone. Our investigation provides a comprehensive comparative effectiveness analysis of ustekinumab (UST) versus infliximab (IFX) as first-line therapies in biologic-naïve CD, incorporating advanced cross-sectional imaging characteristics and specifically evaluating differential rates of endoscopic mucosal healing (MH) across longitudinal follow-up. This retrospective cohort study enrolled 210 biologic-naïve CD patients. Primary outcome was MH at 1, 1.5, and 2 years. Subgroup analyses were performed to explore potential treatment heterogeneity among different patient subgroups. Furthermore, logistic regression analyses were conducted to identify MH-related factors. While 1-year and 1.5-year MH rates were comparable (27.8

BACKGROUND:Ulcerative colitis (UC) is a chronic relapsing inflammatory bowel disease with a globally increasing incidence. Faecalibacterium prausnitzii (F. prausnitzii) is known for its anti-inflammatory and immunomodulatory properties. However, the mechanisms by which gut microbiota and bile acid metabolism contribute to the therapeutic effects of F. prausnitzii in colitis remain unclear. AIMS:This study aims to investigate the effects of F. prausnitzii on colitis and elucidate its potential mechanism through modulation of gut microbiota and bile acid metabolism. METHODS:Mice were treated with dextran sulfate sodium (DSS), followed by administration of F. prausnitzii and its supernatant. Colitis symptoms, inflammatory responses, and intestinal barrier integrity were then evaluated. 16S rRNA sequencing and targeted bile acid metabolomics analysis were performed. RESULTS:F. prausnitzii and its supernatant reshaped dysbiotic gut microbiota in DSS-induced colitis mouse models, increasing the ratio of unconjugated to conjugated bile acids and secondary to primary bile acids, thereby activating the farnesoid X receptor (FXR) signaling pathway. Experiments in FXR-/- mice confirmed that FXR is a critical target for the protective effects of F. prausnitzii, promoting intestinal mucosal repair and inhibiting NLRP3 inflammasome activation, which in turn alleviates colitis. Additionally, the differential bile acid isoLCA, enriched by F. prausnitzii and its supernatant, effectively suppressed inflammation and enhanced intestinal barrier function. CONCLUSION:This study demonstrates that F. prausnitzii alleviates colitis by modulating bile acid composition and regulating FXR signaling, suggesting that targeting the microbiota-bile acid-FXR pathway may represent a promising therapeutic strategy for inflammatory bowel disease.

Background:Autoimmune enteropathy (AIE) is a rare autoimmune disorder characterized primarily by villous atrophy of the small intestinal mucosa. This article presents a case of adult-onset AIE featuring intractable diarrhea and severe malnutrition, along with a review of the existing literature to summarize its clinical characteristics, aiming to provide insights for the diagnosis and management of AIE. Case Description:A 60-year-old male was admitted due to intermittent abdominal pain, diarrhea, and weight loss. Laboratory tests revealed gliadin immunoglobulin A (IgA) (+) and immunoglobulin G (IgG) (+), but tissue transglutaminase IgA (-) and IgG (-). Endoscopy revealed that the mucous membrane of the small intestine was congested and edematous, the villi were atrophied and prone to bleeding after biopsy, and some of the villi exhibited a white mossy appearance. Pathologically, the villi of many segments of the small intestine presented diffuse and obvious atrophy, and there was lymphocytic infiltration in the intestinal glands. After exclusionary diagnosis, the patient was considered to have AIE. After effective initial treatment with corticosteroid, the patient exhibited recurrent symptoms and poor nutritional status, and eventually died of sepsis. Conclusions:For patients with refractory diarrhea and intestinal villous atrophy, a comprehensive diagnosis should be made based on medication history, epidemiological factors, gluten dietary response, serological markers, and histopathological findings. Early intervention with corticosteroids combined with nutritional support is critical, while vigilance against severe adverse events such as life-threatening infections is essential.

An increasing number of patients with oesophageal or gastric cancer are being diagnosed with colorectal lesions. This single-centre, retrospective study assessed the risk of colorectal lesions in patients with early oesophagogastric cancer. 170 patients were enrolled in the early oesophagogastric cancer group, of whom 113 (66.47%) had colorectal lesions. 238 individuals were included in the control group, among whom 38 (15.97%) were diagnosed with colorectal lesions. The incidence of colorectal lesions between the two groups was statistically significant (P < 0.05), and patients with early oesophagogastric cancer had a risk of colorectal lesions (odds ratio = 10.434, 95% confidence interval = 6.516–16.708). Multivariate analysis identified three independent risk factors: faecal occult blood test positivity, oesophagogastric lesion diameter >2 cm, and the presence of multiple oesophagogastric lesions. These findings suggest that the early oesophagogastric cancer increased the risk of colorectal lesions, particularly among individuals with the identified risk factors.

AIM:Endoscopic submucosal dissection (ESD) for colonic neoplasms is a technically intricate procedure. Internal traction using a single clip has emerged as a promising supportive technique for colonic ESD. Therefore, this study aimed to comprehensively evaluate and compare the efficacy and safety of ESD with and without the aid of single-clip traction. METHODS:This retrospective study encompassed 36 patients who underwent single clip traction-assisted colonic ESD and 66 who underwent the traditional method of colonic ESD at Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University. We employed the propensity score-matching method to mitigate disparities in resected specimen size and tumor location. Post-matching, we comprehensively assessed treatment outcomes and incidence of adverse events between the two treatment groups (single clip traction-assisted ESD (scESD) and conventional ESD (cESD)). RESULTS:After propensity score matching, we observed 34 matched pairs. There were no significant differences between the two treatment groups regarding the en bloc resection rate, complete resection rate, and curative rate. However, the procedure duration was significantly shorter in the single clip traction-assisted ESD group compared to the conventional ESD group (20.00 [Interquatile Range (IQR)] (16.00-32.50) minutes vs 31.50 [IQR] (17.00-54.00) minutes, p = 0.0474). Furthermore, there was a significant increase in dissection speed in the single clip traction-assisted ESD group compared to the conventional ESD group (0.29 [IQR] (0.20-0.45) mm2/min vs 0.19 [IQR] (0.11-0.35) mm2/min, p = 0.0015). All lesions were resected in a single piece. Among the propensity-score-matched patients, only those treated with single clip traction-assisted ESD exhibited faster dissection speeds (p = 0.015). Furthermore, there were no substantial differences in adverse events such as intraoperative perforation, delayed perforation, or delayed bleeding. CONCLUSIONS:Our findings suggest that single clip traction-assisted colonic ESD is preferable to traditional colonic ESD, owing to its shorter procedure duration and faster dissection speed.

The gut has been a focal point in the research of digestive system disorders. The internal microbiota generates metabolites that function as signaling molecules and substrates, interacting with the intestinal wall and influencing host physiology and pathology. Besides, the gut microbiota and metabolites owe highly diverse types and quantities, posing challenges for quantitative analysis, and monitoring frequent interactions between digestive tract metabolites and the intestinal wall remains a challenge. However, research targeting gut microbiota metabolites has elucidated their relevance to digestive diseases. By modulating metabolites such as short-chain fatty acids, bile acids, and lipopolysaccharides, it is possible to intervene in the progression of diseases such as inflammatory bowel disease and non-alcoholic fatty liver disease. Currently, research on gut microbiota is advancing, and more work is required to explore the interactions between host, microbes and underlying mechanisms. In this review, we have revisited the generation of gut microbiota-related metabolites, their impact on diseases, and modes of interaction, emphasizing the significant role of metabolites in digestive system disorders. It is believed that the linkage between gut microbiota and diseases in current research can be established through metabolites, providing a framework and foundation for research in the field of metabolomics and fundamental mechanisms.

Abstract Background Colorectal signet-ring cell carcinoma (SRCC) is a rare cancer with a bleak prognosis. The relationship between its clinicopathological features and survival remains incompletely elucidated. Tumor deposits (TD) have been utilized to guide the N staging in the 8th edition of American Joint Committee on Cancer (AJCC) staging manual, but their prognostic significance remains to be established in colorectal SRCC. Patients and methods The subjects of this study were patients with stage III/IV colorectal SRCC who underwent surgical treatment. The research comprised two cohorts: a training cohort and a validation cohort. The training cohort consisted of 631 qualified patients from the SEER database, while the validation cohort included 135 eligible patients from four independent hospitals in China. The study assessed the impact of TD on Cancer-Specific Survival (CSS) and Overall Survival (OS) using Kaplan-Meier survival curves and Cox regression models. Additionally, a prognostic nomogram model was constructed for further evaluation. Results In both cohorts, TD-positive patients were typically in the stage IV and exhibited the presence of perineural invasion (PNI) (P < 0.05). Compared to the TD-negative group, the TD-positive group showed significantly poorer CSS (the training cohort: HR, 1.87; 95% CI, 1.52–2.31; the validation cohort: HR, 2.43; 95% CI, 1.55–3.81; all P values < 0.001). This association was significant in stage III but not in stage IV. In the multivariate model, after adjusting for covariates, TD maintained an independent prognostic value (P < 0.05). A nomogram model including TD, N stage, T stage, TNM stage, CEA, and chemotherapy was constructed. Through internal and external validation, the model demonstrated good calibration and accuracy. Further survival curve analysis based on individual scores from the model showed good discrimination. Conclusion TD positivity is an independent factor of poor prognosis in colorectal SRCC patients, and it is more effective to predict the prognosis of colorectal SRCC by building a model with TD and other clinically related variables.

Although endoscopic necrosectomy (EN) is more frequently used to manage walled-off necrosis (WON), there is still debate over how much time should pass between the initial stent placement and the first necrosectomy. This study aims to determine the effect of performing EN within different timings after placing the initial stent on clinical outcomes for WON. A retrospective study on infected WON patients compared an early necrosectomy within one week after the initial stent placement with a necrosectomy that was postponed after a week. The primary outcomes compared the rate of clinical success and the need for additional intervention after EN to achieve WON resolution. 77 patients were divided into early and postponed necrosectomy groups. The complete resolution of WON within six months of follow-up was attained in 73.7% and 74.3% of patients in both the early and postponed groups. The early group tended to a greater need for additional intervention after EN (26.8% early necrosectomy vs. 8.3% postponed necrosectomy, P = 0.036). Our study does not demonstrate that early necrosectomy is superior to postponed necrosectomy in terms of clinical success rate, total count of necrosectomy procedures, procedure-related complications, length of hospitalization and prognosis. Conversely, patients in the postponed group received fewer additional interventions.

State Key Laboratory of Oncogenes and Related Genes, Center for Single-Cell Omics, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China, Division of Digestive Diseases, Department of Medicine, Emory University School of Medicine, Atlanta, GA, United States, Center for IBD Research, Department of Gastroenterology, The Shanghai 10th People’s Hospital, Tongji University, Shanghai, China, Department of Gastroenterology, The Shanghai 10th People’s Hospital, Department of Bioinformatics, School of Life Sciences and Technology, Tongji University, Shanghai, China, Department of Gastroenterology, First Affiliated Hospital of Kunming Medical University, Yunnan Institute of Digestive Diseases, Kunming, China, Department of Gastroenterology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, China, Guangdong Institute of Gastroenterology, Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, Department of Colorectal Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China

Astract Background Honokiol (HKL), a natural extract of the bark of the magnolia tree and an activator of the mitochondrial protein sirtuin-3 (SIRT3), has been proposed to possess anti-inflammatory effects. This study investigated the inhibitory effects of HKL on T helper (Th) 17 cell differentiation in colitis. Methods Serum and biopsies from 20 participants with ulcerative colitis (UC) and 18 healthy volunteers were collected for the test of serum cytokines, flow cytometry analysis (FACS), and relative messenger RNA (mRNA) levels of T cell subsets, as well as the expression of SIRT3 and phosphorylated signal transducer and activator of transcription/retinoic acid-related orphan nuclear receptor gamma t (p-STAT3/ROR gamma t) signal pathway in colon tissues. In vitro, naive clusters of differentiation (CD) 4 + T cells isolated from the mouse spleen differentiated to subsets including Th1, Th2, Th17, and regulatory T (Treg) cells. Peripheral blood monocytes (PBMCs) from healthy volunteers were induced to the polarization of Th17 cells. After HKL treatment, changes in T cell subsets, related cytokines, and transcription factors were measured. The dextran sulfate sodium (DSS)-induced colitis and interleukin (IL)-10-deficient mice were intraperitoneally injected with HKL. These experiments were conducted to study the effect of HKL on the development, cytokines, and expression of signaling pathway proteins in colitis. Results Patients with UC had higher serum IL-17 and a higher proportion of Th17 differentiation in blood compared with healthy participants; while IL-10 level and the proportion of Treg cells were lower. Higher relative mRNA levels of ROR gamma t and a lower SIRT3 expression in colon tissues were observed. In vitro, HKL had little effect on the differentiation of naive CD4(+) T cells to Th1, Th2, or Treg cells, but it downregulated IL-17 levels and the Th17 cell ratio in CD4(+) T cells from the mouse spleen and human PBMCs under Th17 polarization. Even with a STAT3 activator, HKL still significantly inhibited IL-17 levels. In DSS-induced colitis mice and IL-10 deficient mice treated with HKL, the length of the colon, weight loss, disease activity index, and histopathological scores were improved, IL-17 and IL-21 levels, and the proportion of Th17 cells were decreased. Sirtuin-3 expression was increased, whereas STAT3 phosphorylation and ROR gamma t expression were inhibited in the colon tissue of mice after HKL treatment. Conclusions Our study demonstrated that HKL could partially protect against colitis by regulating Th17 differentiation through activating SIRT3, leading to inhibition of the STAT3/ROR gamma t signaling pathway. These results provide new insights into the protective effects of HKL against colitis and may facilitate the research of new drugs for inflammatory bowel disease. An imbalance in Th17/Treg cells is one of the leading causes of inflammatory bowel disease. In this introductory study, honokiol (HKL), an activator of mitochondrial protein SIRT3, has been shown to inhibit Th17 cell differentiation and alleviate colitis through the activation of SIRT3 and inhibition of the STAT3/ROR gamma t signaling pathway. Honokiol has been poorly studied in IBD; therefore, this study provides new directions for treating IBD.

Inflammatory bowel disease (IBD) is a group of chronic non-specific intestinal inflammatory diseases mediated by multiple factors such as immune disorders, mainly including ulcerative colitis (UC) and Crohn′s disease (CD) . Malignant tumors are the second leading cause of death in IBD patients, including intestinal tumors and extraintestinal tumors. At present, the risk and related mechanism of extraintestinal tumors in IBD patients are still unknown. The study has found that the difference in the risk of extraintestinal tumors between UC and CD is also statistically significant. This article will outline the overall risk of extraintestinal tumors in IBD, and describe the risk, pathogenesis, and monitoring program of multi-system extraintestinal solid tumors in IBD, UC and CD, providing a theoretical basis for the prevention, surveillance and early diagnosis of extraintestinal tumors in IBD patients.

安宁疗护是对疾病终末期患者通过控制痛苦和不适症状,提供身体、心理、社会、精神等方面的照护和人文关怀等服务,来提高生命质量,帮助患者舒适、安详、有尊严地离世.2017年国家卫生健康委员会连发两文:《安宁疗护实践指南(试行)》[1]和《安宁疗护中心基本标准和管理规范(试行)》[2] ,并在北京、上海、洛阳等地区开展第一批安宁疗护试点工作.在第一批安宁疗护试点工作取得突破性进展后,2019年10月国家卫健委等部门联合印发的"两个《意见》"中均指出要加强安宁疗护服务发展,安宁疗护进入全面推进新局面,并开展了全国第二批安宁疗护试点工作,其中南京市作为第二批安宁疗护试点城市.本规范拟针对安宁疗护的服务模式、服务内容、质量评价制定标准,借鉴国内外各指南标准和实验研究,结合实践经验,归纳总结出符合南京市的安宁疗护标准,以提供更科学、同质化的安宁疗护服务,更好地发挥安宁疗护作用.

目的:回顾近几年来,医院在单病种质量控制工作中的措施、效果等,了解改进成效,形成管理经验.方法:回顾近几年医院采取的单病种管理措施,实施的成效、意义,对当前的管理现状提出思考和建议.结果:该院加强单病种质量控制管理,多措并举,取得了显著成效.结论:这些针对单病种质量控制的管理措施有效,经验值得推广.

Background The etiology of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is not completely clear, but its pathogenesis is closely related to T helper 17 (Th17) cells. Several histone deacetylase (HDAC) inhibitors have been shown to exert potent anti-inflammatory effects and modulate Th17 cell polarization. Owing to the large variety and broad expression of HDACs, finding specific therapeutic targets for IBD is of clinical importance. Methods The proportions of Th17 cells and interleukin (IL)-17A produced between patients with UC and healthy volunteers were compared. The differentiation of human peripheral blood mononuclear cells (PBMCs) into Th17 cells was induced in vitro. Differentiated Th17 cells were treated with RGFP109 (RG), a selective inhibitor of HDAC1 and 3, to observe its effects on these cells. Subsequently, colitis was induced in mice and treated with RG. The proportion of Th17 cells, the severity of colitis in mice, and colon histopathology and immunohistochemistry were evaluated respectively. Results The proportion of Th17 cells and IL-17A production was significantly increased in patients with UC than in healthy individuals. RG inhibited the differentiation of human PBMCs into Th17 cells and reduced IL-17A secretion in vitro. RG-treated colitis mice had a lower Th17 ratio, mild colon inflammation, and decreased expression of HDAC1 and 3 in the colon. Conclusions HDAC1 and 3 inhibitors can modulate the differentiation of inflammatory Th17 cells, downregulate IL-17A levels, and exert anti-inflammatory effects in experimental colitis mice, indicating that HDAC1 and 3 may be potential therapeutic targets for patients with IBD.

The natural protoberberine jatrorrhizine (JA) is reported to have several medicinal properties and a significant effect on the gut microbiota of mice. The regulation of gut microbiota is generally known to play an important role in the intestinal mucosal immune response to ulcerative colitis (UC). However, whether JA can be used in the treatment of UC is still unclear. Our study aimed to investigate the underlying therapeutic effects and mechanisms of JA in treating colitis. Compared with the DSS-induced colitis model group, the JA + DSS treated group had more significant improvements in weight loss, disease activity index score, colon length shortening, and pathological inflammation. 16s rRNA sequencing analysis showed that JA treatment protected colitis mice against DSS-induced disturbance of gut microbiota. At the phylum level, reductions in Deferribacteres and Proteobacteria were observed in the JA-treated group; At the genus level, the JA-treated group showed an increased relative abundance of Akkermansia and decreased abundance of Escherichia-Shigella, Desulfovibrio, Mucispirillum, etc. Network pharmacology was then used to screen out five drug-disease target genes (NOS2, ESR1, CALM1, CALM2, CALM3). Transcriptomics analysis further validated that the NOS2 expression was significantly reduced in colon tissue of JA-administered mice compared with DSS control mice. Additionally, analysis of correlation suggested that NOS2 expression was negatively correlated with the relative abundance of AKKermansia and positively correlated with Desulfovibrio, Rikenella. JA alleviates ulcerative colitis via regulating gut microbiota and NOS2 expression.

目的 探讨胃蛋白酶原(PG)、人类白细胞抗原-G(HLA-G)对诊断早期胃癌及癌前病变的临床意义.方法 以病理检查诊断的20例早期胃癌患者(胃癌组),30例癌前病变患者(上皮内瘤变组),50例慢性浅表性胃炎患者(对照组)、50例慢性萎缩性胃炎患者(萎缩性胃炎组)为研究对象.比较4组患者血清PGⅠ、PGⅡ、PGⅠ/PGⅡ(PGR)、HLA-G水平,采用受试者工作特征(ROC)曲线分析PGⅠ、PGⅡ、PGR、HLA-G对早期胃癌及癌前病变的诊断价值.结果 与对照组比较,萎缩性胃炎组、上皮内瘤变组、胃癌组的PGⅠ、PGR水平明显降低,PGⅡ水平明显升高,差异均有统计学意义(P<0.05);胃癌组HLA-G水平明显高于其他3组,差异均有统计学意义(P<0.05).PGR、PGⅠ+PGR、PGⅡ+PGR、PGR+HLA-G诊断上皮内瘤变的曲线下面积(AUC)分别为0.705、0.728、0.713、0.721(P<0.05);4项指标联合检测(PGⅠ+PGⅡ+PGR+HLA-G)诊断上皮内瘤变的AUC为0.734(P<0.05).PGⅡ、PGR、HLA-G诊断胃癌的AUC分别为0.719、0.730、0.674(P<0.05);PGⅡ+PG R、PGⅡ+HLA-G、PG R+HLA-G诊断胃癌的AUC分别为0.740、0.723、0.742(P<0.05),明显高于HLA-G诊断胃癌的AUC(P<0.05);4项指标联合检测(PGⅠ+PGⅡ+PGR+HLA-G)对诊断胃癌有一定价值(P<0.05),其AUC均高于上述指标单独及两项联合检测.结论 PGⅠ、PGⅡ、PGR、HLA-G对早期胃癌及癌前病变具有良好的诊断价值,4项指标联合检测有助于提高临床诊断价值.

目的 探讨扶正养胃方对胃癌术后患者胃肠功能的调节作用.方法 将南京江北人民医院收治的90例胃癌根治术的患者按照随机数字表法分为研究组和对照组,每组各有45例患者.对照组采用西医常规治疗.研究组在对照组基础上,联合扶正养胃方治疗.两组在治疗2周后统计疗效.对比两组的临床疗效.比较患者的肠鸣音恢复时间、首次排便时间、首次进食时间.在治疗前与治疗后(2周),检测患者血清中C反应蛋白(CRP)、肿瘤坏死因子α(TNF-α)、白介素6(IL-6)、胃动素(MTL)、胃泌素(GAS)、血管活性肠肽(VIP)的水平.结果 研究组在治疗后的总有效率为93.3％,对照组为77.8％,组间比较有明显差异(P<0.05).研究组的肠鸣音恢复时间、首次排便时间、首次进食时间均比对照组少(P<0.05).两组治疗后的CRP、TNF-α、IL-6明显降低,以研究组降低更多,差异有统计学意义(P<0.05).两组治疗后的MTL、GAS、VIP明显升高,以研究组升高更多,差异有统计学意义(P<0.05).结论 扶正养胃方能有效改善胃癌术后患者的胃肠功能,可能与降低炎症因子和调节胃肠激素分泌有关.

To review the clinical data of 13 patients with benign stenosis in deep small intestine treated by balloon-assisted enteroscopy from September 2017 to December 2019, and to evaluate the stenosis characteristics, endoscopic treatment effects and its safety in different lesions. The results showed that there were 6 cases of Crohn disease (CD), 4 cases of cryptogenic multifocal ulcerative stenosing enteritis (CMUSE) and 3 cases of small bowel stenosis with unknown etiology. A total of 38 stenoses were found after 17 enteroscopic treatments, including 35 web-like stenoses and 3 columnar stenoses. Thirteen stenoses were found in 6 patients with CD, including 4 single stenosis, 1 case of 3 stenoses and 1 case of 6 stenoses. Twenty-one stenoses were found in 4 patients with CMUSE and they were all web-like stenosis. A total of 18 times of balloon dilatation and 10 times of IT knife incision were performed. The technical success rate was 88.2% (15/17), and the clinical effective rate was 76.9% (10/13). The follow-up time was 3-28 months, and one patient underwent surgical treatment. There was 1 case of delayed hemorrhage and 3 cases of delayed perforation after operation. They were all improved by medical treatment. These results indicated that treatment of benign stenosis in deep small intestine by enteroscopy is technically feasible and can improve the symptoms of patients in a short time.