Intestinal failure-associated liver disease (IFALD) is a serious complication of long-term parenteral nutrition in patients with short bowel syndrome (SBS), and is the main cause of death in SBS patients. Prevention of IFALD is one of the major challenges in the treatment of SBS. Impairment of intestinal barrier function is a key factor in triggering IFALD, therefore promoting intestinal repair is particularly important. Intestinal repair mainly relies on the function of intestinal stem cells (ISC), which require robust mitochondrial fatty acid oxidation (FAO) for self-renewal. Herein, we report that aberrant LGR5+ ISC function in IFALD may be attributed to impaired farnesoid X receptor (FXR) signaling, a transcriptional factor activated by steroids and bile acids. In both surgical biopsies and patient-derived organoids (PDOs), SBS patients with IFALD represented lower population of LGR5+ cells and decreased FXR expression. Moreover, treatment with T-βMCA in PDOs (an antagonist for FXR) dose-dependently reduced the population of LGR5+ cells and the proliferation rate of enterocytes, concomitant with decreased key genes involved in FAO including CPT1a. Interestingly, however, treatment with Tropifexor in PDOs (an agonist for FXR) only enhanced FAO capacity, without improvement in ISC function and enterocyte proliferation. In conclusion, these findings suggested that impaired FXR may accelerate the depletion of LGR5 + ISC population through disrupted FAO processes, which may serve as a new potential target of preventive interventions against IFALD for SBS patients.

UNASSIGNED: Understanding the quality of life and the factors that influence it for patients with short bowel syndrome (SBS) and their caregivers is of utmost importance in order to enhance their well-being. Therefore, This study aimed to provide a comprehensive understanding of the impact of SBS on patients and their caregivers, as well as its associated factors, by synthesizing the available evidence.
UNASSIGNED: A systematic review of the literature was done using PubMed, Embase databases, CNKI, and ISPOR conference papers. Included articles were manually searched to identify any other relevant studies. Quality was assessed using appropriate Joanna Briggs Institute critical appraisal tools.
UNASSIGNED: This review included 16 studies, comprising 15 observational studies and 1 randomized controlled trial. The findings revealed that the QoL of patients with SBS was lower than that of the general population regarding physical functioning and psychological domain. Meanwhile, caregivers experienced challenges in maintaining their QoL. The QoL of SBS patients was found to be influenced by various factors such as treatment, age, sex, stoma, and small intestine length. Among them, the treatment is the most noteworthy factor that can be effectively improved through external interventions.
UNASSIGNED: While numerous studies have provided insights into the compromised QoL experienced by individuals with SBS and their caregivers, there remains a scarcity of large-sample quantitative investigations examining the determinants of QoL. The existing body of literature on caregivers is also notably deficient.

Short bowel syndrome (SBS) features nutrients malabsorption and impaired intestinal barrier. Patients with SBS are prone to sepsis, intestinal flora dysbiosis and intestinal failure associated liver disease. Protecting intestinal barrier and preventing complications are potential strategies for SBS treatment. This study aims to investigate the effects of farnesoid X receptor (FXR) agonist, obeticholic acid (OCA), have on intestinal barrier and ecological environment in SBS.
Through testing the small intestine and serum samples of patients with SBS, impaired intestinal barrier was verified, as evidenced by reduced expressions of intestinal tight junction proteins (TJPs), increased levels of apoptosis and epithelial cell damage. The intestinal expressions of FXR and related downstream molecules were decreased in SBS patients. Then, global FXR activator OCA was used to further dissect the potential role of the FXR in a rat model of SBS. Low expressions of FXR-related molecules were observed on the small intestine of SBS rats, along with increased proinflammatory factors and damaged barrier function. Furthermore, SBS rats possessed significantly decreased body weight and elevated death rate. Supplementation with OCA mitigated the damaged intestinal barrier and increased proinflammatory factors in SBS rats, accompanied by activated FXR-related molecules. Using 16S rDNA sequencing, the regulatory role of OCA on gut microbiota in SBS rats was witnessed. LPS stimulation to Caco-2 cells induced apoptosis and overexpression of proinflammatory factors in vitro. OCA incubation of LPS-pretreated Caco-2 cells activated FXR-related molecules, increased the expressions of TJPs, ameliorated apoptosis and inhibited overexpression of proinflammatory factors.
OCA supplementation could effectively ameliorate the intestinal barrier disruption and inhibit overexpression of proinflammatory factors in a rat model of SBS and LPS-pretreated Caco-2 cells. As a selective activator of FXR, OCA might realize its protective function through FXR activation.

Intestinal failure is a syndrome characterized by a diminished intestinal function that is inadequate to maintain normal digestion and absorption, leading to systemic metabolic disorder and requiring long-term nutritional supplementation to sustain health and growth. Short bowel syndrome (SBS) is one of the primary causes of intestinal failure. Given the significant differences among SBS patients, nutritional treatment strategies should emphasize individualization. This review focuses on SBS, combining its anatomical and pathological characteristics, to introduce nutritional support treatment plans and experiences for patients with intestinal failure.
肠衰竭是指由于肠道功能降低而不能维持正常的消化吸收功能，导致全身代谢紊乱并需要长期补充营养以维持健康及生长的综合征。短肠综合征（SBS）是肠衰竭的主要原因之一，SBS患者存在巨大差异，其营养治疗策略应强调个体化。本文以SBS为主线，结合其解剖和病程特点，介绍肠衰竭患者营养支持治疗的方案及经验。.

Objective: To investigate the efficacy of strategies for minimizing small bowel resection during surgery for pelvic radiation-induced terminal small intestinal stenosis in preventing postoperative complications such as anastomotic leakage and short bowel syndrome. Methods: This was a retrospective cohort study. There are two subtypes of chronic radiation enteritis (CRE) with combined intestinal stenosis and intestinal obstruction: (1) Type I: terminal ileal lesions with a normal ileal segment of 2-20 cm between the ileal lesion and ileocecal junction; and (2) Type II: the lesion is located in the small bowel at a distance from the ileocecal region, usually accompanied by extensive damage to the bowel segments outside the lesion. The indications for minimal bowel resection are as follows: (1) diagnosis of Type I small bowel CRE; (2) absence of radiological evidence of rectosigmoid damage; and (3) absence of colonic obstruction. The contraindications are: (1) stenotic, penetrating lesions of the distal cecum; (2) emergency surgery; (3) recurrence of malignant tumor or history of radiotherapy for recurrent malignant tumor; (4) interval between radiotherapy and surgery <6 months; and (5) history of preoperative small bowel resection or abdominal chemotherapy. Case data of 40 patients with Type I CRE who met the above criteria and had undergone minimal bowel resection between April 2017 and December 2019 were retrospectively analyzed (minimal bowel resection group; including 13 patients from Jinling Hospital, 16 from the Ninth People\'s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, and 11 from the Affiliated Hospital of Xuzhou Medical University). Forty patients with Type I CRE who had undergone resection of intestinal stenosis lesions and the ileocecal region between October 2015 and March 2017 were included as historical controls (conventional resection group; all from Jinling Hospital). The specific strategy for minimal bowel resection was one-stage partial ileal resection+ileo anastomosis+protective small bowel stoma. In contrast, conventional resection comprised ileocecal resection+ileocecal-ascending colon anastomosis. Postoperative complications, intraoperative and postoperative recovery, and changes in postoperative quality of life were analyzed in both groups. The severity of postoperative complications was assessed by Clavien-Dindo and the Comprehensive Complication Index (CCI). Karnofsky performance scores (KPS) were used to evaluate the quality of life of patients in the two groups preoperatively and postoperatively. The higher the KPS score, the better the quality of life. Results: Baseline patient characteristics did not differ significantly between the two groups (P>0.05). Compared with the conventional resection group, the length of small bowel resected in the minimal bowel resection group (51 [20-200] cm vs. 91 [60-200] cm, Z=5.653, P<0.001), duration of postoperative total enteral nutrition [9 (3-18) days vs. 12 (4-50) days, Z=2.172, P=0.030], and duration of postoperative hospital stay [17 (9-24) days vs 29 (13-57) days, Z=6.424, P<0.001] were shorter; all of these differences are statistically significant. The overall incidence of postoperative complications was lower in the minimal bowel resection group than in the conventional resection group [20.0% (8/40) vs. 70.0% (28/40), χ2=19.967, P<0.001], These comprised short bowel syndrome [5.0% (2/40) vs. 25.0% (10/40), χ2=6.274, P=0.012], anastomotic leakage or fistula [2.5% (1/40) vs. 22.5% (9/40), χ2=7.314, P=0.014], and pleural effusion [7.5% (3/40) vs. 25.0% (10/40), χ2=4.500, P=0.034], all of which occurred less often in the minimal bowel resection than conventional resection group. The CCI index was also lower in the minimal bowel resection group than in the conventional resection group [CCI>40: 2.5% (1/40) vs. 12.5% (5/40), Z=18.451, P<0.001]. KPS scores were higher in the minimal bowel resection group 1 and 3 months postoperatively than they had been 1 day preoperatively (79.9±4.7 vs. 75.3±4.1, 86.2±4.8 vs. 75.3±4.1, both P<0.05). In the minimal bowel resection group, seven patients were satisfied with their current quality of life and refused to undergo stoma reduction at follow-up and one deferred stoma reduction because of rectal bleeding. The remaining 32 patients underwent stoma reduction 3 to 12 months after surgery, 26 of whom underwent ileo-cecal anastomosis. The remaining six underwent resection of the stoma and anastomosis of the ileum to the ascending colon. Conclusions: The strategy of minimal small bowel resection in patients with radiation-induced bowel injuries reduces the length of resected small bowel, decreases the risk and severity of postoperative complications, and is associated with a better prognosis and quality of life than conventional resection.
目的： 探讨小肠最小化切除策略对预防慢性放射性肠损伤（CRE）术后吻合口漏和短肠综合征等并发症的效果。 方法： 采用回顾性队列研究方法。合并肠狭窄和肠梗阻的小肠CRE可分为以下两种分型：（1）Ⅰ型：回肠末端病变，但在回肠病变与回盲部之间始终存在2~20 cm的正常回肠段；（2）Ⅱ型：病灶位于距离回盲部较远的小肠，病灶外的肠段通常广泛受损。最小化肠切除术适应证：Ⅰ型小肠CRE、直肠乙状结肠无放射性损伤、无结肠梗阻。禁忌证包括各种原因导致的盲肠远端狭窄性或穿透性病变、急诊手术、恶性肿瘤复发或复发性恶性肿瘤的放疗史、放疗与手术时间间隔<6个月、术前小肠切除史或腹腔化疗史。根据上述指征，回顾性分析2017年4月至2019年12月期间，接受最小化肠切除术策略治疗的40例Ⅰ型CRE患者病例资料（最小化肠切除组，其中东部战区总医院13例，上海交通大学医学院附属第九人民医院16例，徐州医科大学附属医院11例）；同时纳入2015年10月至2017年3月期间，40例接受切除肠狭窄病变及回盲部的Ⅰ型CRE患者作为历史对照（传统肠切除组，均来自东部战区总医院）。最小化肠切除组采用小肠最小化切除策略，即一期回肠部分切除+回肠-回肠吻合术+保护性小肠造口术。传统肠切除组采用回盲部切除+回肠升结肠吻合术。观察两组手术情况、术后并发症的发生情况、术后恢复情况和手术前后生活质量变化。术后并发症严重程度采用Clavien-Dindo和综合并发症指数（CCI）评估。采用卡氏评分（KPS）对两组患者术前和术后的生活质量进行评价，得分越高，表示生活质量越好。 结果： 两组基线资料比较，差异无统计学意义（均P>0.05）。与传统肠切除组相比，最小化肠切除组的小肠切除长度［51（20~200）cm比91（60~200）cm，Z=5.653，P<0.001］、术后全肠内营养时间［9（3~18）d比12（4~50）d，Z=2.172，P=0.030］和术后住院时间［17（9~24）d比29（13~57）d，Z=6.424，P<0.001］均更短，差异有统计学意义。最小化肠切除组术后并发症发生率低于传统肠切除组［20.0%（8/40）比28/40（70.0%），χ2=19.967，P<0.001］，其中短肠综合征［5.0%（2/40）比25.0%（10/40），χ2=6.274，P=0.012］、吻合口漏或瘘［2.5%（1/40）比22.5%（9/40），χ2=7.314，P=0.014］和胸腔积液的发生率［7.5%（3/40）比25.0%（10/40），χ2=4.500，P=0.034］均低于传统肠切除组。最小化肠切除组CCI指数也低于传统肠切除组［CCI>40：2.5%（1/40）比12.5%（5/40），Z=18.451，P<0.001］。最小化肠切除组术后1个月和3个月的KPS评分均高于术前1 d［（79.9±4.7）分比（75.3±4.1）分，（86.2±4.8）分比（75.3±4.1）分，均P<0.05］。在最小化肠切除组中，7例患者对目前的生活质量满意，随访时拒绝接受肠造口还纳手术；1例患者由于直肠出血暂缓造口还纳；其余32例于术后3~12个月行造口还纳术，其中26例行回肠-回肠吻合术，余6例切除造口至回盲部肠段，行回肠-升结肠吻合术。 结论： 小肠最小化切除策略可以减少切除小肠的长度，降低术后并发症的风险和严重程度，对改善放射性肠损伤患者的预后和生活质量具有积极意义。.

UNASSIGNED: Short bowel syndrome (SBS) is featured by impaired nutrients and fluids absorption due to massive small intestine resection. Gut dysbiosis has been implicated in SBS, this study aimed to characterize the metagenomic and metabolomic profiles of SBS and identify potential therapeutic targets.
UNASSIGNED: Fecal samples from SBS and Sham rats (n = 8 per group) were collected for high-throughput metagenomic sequencing. Fecal metabolomics was measured by untargeted liquid chromatography-mass spectrometry.
UNASSIGNED: We found that the species-level α-diversity significantly decreased in SBS rats, accompanied by altered microbiome compositions. The beneficial anaerobes from Firmicutes and Bacteroidetes were depleted while microorganisms from Lactobacillus, Escherichia, Enterococcus, and Streptococcus were enriched in faces from SBS rats. LEfSe analysis identified 17 microbial species and 38 KEGG modules that were remarkably distinct between SBS and Sham rats. In total, 1,577 metabolites with known chemical identity were detected from all samples, among them, 276 metabolites were down-regulated and 224 metabolites were up-regulated in SBS group. The typical signatures of SBS fecal metabolome comprised reduced short-chain fatty acids and products of amino acid metabolism (indole derivatives and p-cresol), as well as altered bile acid spectrum. We revealed 215 robust associations between representative differentially abundant microbial species and metabolites, the species with the same changing trend tended to have a similar correlation with some certain metabolites.
UNASSIGNED: The fecal microbiome and metabolome significantly altered in SBS. Our findings may lay the foundation for developing new strategies to facilitate intestinal adaptation in SBS patients.

BACKGROUND: Infection due to multidrug-resistant Klebsiella pneumoniae is a common cause of graft resection after small bowel transplantation. We report a failed case in which the intestinal graft was resected 18 days after the operation due to postoperative infection with multidrug-resistant K pneumoniae and a literature review of other common causes of small bowel transplantation failure have been reported.
METHODS: A female, 29 years of age, underwent partial living small bowel transplantation for short bowel syndrome. After the operation, the patient was infected with multidrug-resistant K pneumoniae, even though various anti-infective regimens were employed. It further developed into sepsis and disseminated into intravascular coagulation, leading to exfoliation and necrosis of the intestinal mucosa. Finally, the intestinal graft had to be resected to save the patient\'s life.
RESULTS: Multidrug-resistant K pneumoniae infection often affects the biological function of intestinal grafts and can even lead to necrosis. Other common causes of failure, including postoperative infection, rejection, post-transplantation lymphoproliferative disorder, graft-vs-host disease, surgical complications, and other related diseases, were also discussed throughout the literature review.
CONCLUSIONS: Pathogenesis due to diverse and interrelated factors makes the survival of intestinal allografts a great challenge. Therefore, only by fully understanding and mastering the common causes of surgical failure can the success rate of small bowel transplantation be effectively improved.

UNASSIGNED: Short bowel syndrome (SBS) has high morbidity and mortality rates, and promoting intestinal adaptation of the residual intestine is a critical treatment. Dietary inositol hexaphosphate (IP6) plays an important role in maintaining intestinal homeostasis, but its effect on SBS remains unclear. This study aimed at investigating the effect of IP6 on SBS and clarified its underlying mechanism.
UNASSIGNED: Forty male Sprague-Dawley rats (3-week-old) were randomly assigned into four groups (Sham, Sham + IP6, SBS, and SBS + IP6 groups). Rats were fed standard pelleted rat chow and underwent resection of 75% of the small intestine after 1 week of acclimation. They received 1 mL IP6 treatment (2 mg/g) or sterile water daily for 13 days by gavage. Intestinal length, levels of inositol 1,4,5-trisphosphate (IP3), histone deacetylase 3 (HDAC3) activity, and proliferation of intestinal epithelial cell-6 (IEC-6) were detected.
UNASSIGNED: IP6 treatment increased the length of the residual intestine in rats with SBS. Furthermore, IP6 treatment caused an increase in body weight, intestinal mucosal weight, and IEC proliferation, and a decrease in intestinal permeability. IP6 treatment led to higher levels of IP3 in feces and serum, and higher HDAC3 activity of the intestine. Interestingly, HDAC3 activity was positively correlated with the levels of IP3 in feces (r = 0.49, P = 0.01) and serum (r = 0.44, P = 0.03). Consistently, IP3 treatment promoted the proliferation of IEC-6 cells by increasing HDAC3 activity in vitro. IP3 regulated the Forkhead box O3 (FOXO3)/Cyclin D1 (CCND1) signaling pathway.
UNASSIGNED: IP6 treatment promotes intestinal adaptation in rats with SBS. IP6 is metabolized to IP3 to increase HDAC3 activity to regulate the FOXO3/CCND1 signaling pathway and may represent a potential therapeutic approach for patients with SBS.

Intestinal adaptation is a spontaneous compensation of the remanent bowel after extensive enterectomy, which improves the absorption capacity of the remanent bowel to energy, fluid and other nutrients. Intestinal adaptation mainly occurs within 2 years after enterectomy, including morphological changes, hyperfunction and hyperphagia. Intestinal adaptation is the key factor for patients with short bowel syndrome to weaning off parenteral nutrition dependence and mainly influenced by length of remanent bowel, type of surgery and colon continuity. In addition, multiple factors including enteral feeding, glucagon-like peptide 2 (GLP-2), growth hormone, gut microbiota and its metabolites regulate intestinal adaptation via multi-biological pathways, such as proliferation and differentiation of stem cell, apoptosis, angiogenesis, nutrients transport related protein expression, gut endocrine etc. Phase III clinical trials have verified the safety and efficacy of teduglutide (long-acting GLP-2) and somatropin (recombinant human growth hormone) in improving intestinal adaptation, and both have been approved for clinical use. We aim to review the current knowledge about characteristics, mechanism, evaluation methods, key factors, clinical strategies of intestinal adaptation.
广泛肠切除术后，残余肠道出现自发性代偿性改变，以此来增加能量、液体和营养要素的吸收能力被称为“肠道适应”现象。这主要发生在肠切除术后2年内，表现为残余肠道的形态改变、功能亢进及患者的行为学变化。肠道适应的程度是短肠综合征患者能否摆脱肠外营养依赖的关键，这主要与残余肠道长度、手术解剖类型和是否保留结肠连续性有关。此外，肠腔内营养物质刺激、胰高血糖素样肽-2（GLP-2）、生长激素、肠道菌群及其代谢产物等因素可通过多种途径调控肠道适应，如干细胞增殖与分化、细胞凋亡、血管生成、营养物质转运相关蛋白表达和肠道内分泌功能等。三期临床试验已经验证了Teduglutide（长效GLP-2）和Somatropin（重组人生长激素）用于改善肠道适应的安全性和有效性，并获批应用于临床。本文旨在梳理肠道适应特征、发生机制、评估方法、影响因素和临床策略等方面的研究进展。.

Parenteral nutrition (PN)-induced villus atrophy is a major cause of intestinal failure (IF) for children suffering from short bowel syndrome (SBS), but the precise mechanism remains unclear. Herein, we report a pivotal role of farnesoid X receptor (FXR) signaling and fatty acid oxidation (FAO) in PN-induced villus atrophy. A total of 14 pediatric SBS patients receiving PN were enrolled in this study. Those patients with IF showed longer PN duration and significant intestinal villus atrophy, characterized by remarkably increased enterocyte apoptosis concomitant with impaired FXR signaling and decreased FAO genes including carnitine palmitoyltransferase 1a (CPT1a). Likewise, similar changes were found in an in vivo model of neonatal Bama piglets receiving 14-day PN, including villus atrophy and particularly disturbed FAO process responding to impaired FXR signaling. Finally, in order to consolidate the role of the FXR-CPT1a axis in modulating enterocyte apoptosis, patient-derived organoids (PDOs) were used as a mini-gut model in vitro. Consequently, pharmacological inhibition of FXR by tauro-β-muricholic acid (T-βMCA) evidently suppressed CPT1a expression leading to reduced mitochondrial FAO function and inducible apoptosis. In conclusion, impaired FXR/CPT1a axis and disturbed FAO may play a pivotal role in PN-induced villus atrophy, contributing to intestinal failure in SBS patients.