Navigating Long-Term Management Challenges in Short Bowel Syndrome: A Case Report of Chronic Intestinal Failure Complicated by Kidney Dysfunction

The most common cause of intestinal failure is short bowel syndrome (SBS), occurring as a result of a small functional intestine length, usually less than 200 cm, leading to intestinal malabsorption. A 59-year-old female with a past medical history of Crohns disease status post total colectomy with ileostomy over 20 years ago came to the hospital due to progressive weakness. Despite medical management, the patient had high ileostomy output, leading to electrolyte disbalance, metabolic acidosis, dehydration, and progressive kidney decline. Due to the high dependence on continuous fluid supplementation, it was decided to place a port for parenteral hydration to maintain fluid replacements and homeostasis after discharge. Prompt initiation of parenteral fluid replacement and close follow-up on patients with ileostomy and intestinal failure is strongly recommended to avoid complications and prevent intestinal, liver, or kidney transplants.

Ethyl pyruvate prevents inflammatory factors release and decreases intestinal permeability in rats with D-galactosamine-induced acute liver failure

BACKGROUND: The pathogenesis and progression of acute liver failure (ALF) are closely associated with intestinal endotoxemia because of the high permeability of the intestinal wall. Treatment with ethyl pyruvate (EP) has been shown to protect liver failure effectively. The current study aimed to explore the relationship between proinflammatory cytokines and intestinal permeability, and to investigate whether EP administration might prevent the release of multiple proinflammatory cytokines and decrease intestinal permeability and therefore, protect the liver from injury. METHODS: The ALF model was induced by D-galactosamine in rats. The rats were randomly divided into control (saline i.p.), model (D-galactosamine, 1.2 g/kg, i.p.), prevention [EP injection (40 mg/kg) 2 hours ahead of D-galactosamine] and treatment groups (EP injection 2 hours after D-galactosamine) Samples were obtained at 12 and 24 hours after ALF induction respectively. The histology of liver and intestinal tissue was accessed. Serum alanine aminotransferase, endotoxin, D(-) lactate, diamine oxidase (DAO), tumor necrosis factor-alpha (TNF-α), interferon-γ (IFN-γ) and high mobility group box-1 (HMGB1) were evaluated. The survival of rats was also recorded. RESULTS: The rats in model group showed severe damage to liver tissue and intestinal mucosa 12 and 24 hours after ALF induction. EP significantly improved liver or intestinal injury In addition, serum endotoxin, D(-)-lactate, DAO, TNF-α IFN-γ and HMGB1 levels were significantly increased in the model group compared with the control group. There was a positive correlation between intestinal permeability andproinflammatory cytokines. EP significantly reduced serum endotoxin, D(-)-lactate, DAO, TNF-α, IFN-γ and HMGB1 levels. The median survival time was significantly prolonged in both prevention and treatment groups (126 and 120 hours compared with 54 hours in the model group). CONCLUSIONS: EP has protective and therapeutic effects on intestinal mucosa. EP decreases intestinal permeability, and inhibits the release of multiple proinflammatory cytokines in rats with ALF.

Protective effect of heme oxygenase-1 on Wistar rats with heart failure through the inhibition of inflammation and amelioration of intestinal micro- circulation

Background Myocardial infarction （MI） has likely contributed to the increased prevalence of heart failure （HF）. As a result of re- duced cardiac function, splanchnic blood flow decreases, causing ischemia in villi and damage to the intestinal barrier. The induction of heme oxygenase-1 （HO-1） could prevent, or lessen the effects of stress and inflammation. Thus, the effect and mechanism thereof of HO-1 on the intestines of rats with HF was investigated. Methods Male Wistar rats with heart failure through ligation of the left coronary artery were identified with an left ventricular ejection fraction of 〈 45% through echocardiography and then divided into various experimental groups based on the type of peritoneal injection they received [MI： saline; MI ＋ Cobalt protoporphyrin （CoPP）： CoPP solution; and MI ＋ Tin mesoporphyrin IX dichloride （SnMP）： SnMP solution]. The control group was comprised of rats without coronary ligation. Echocardiogra- phy was performed before ligation for a baseline and eight weeks after ligation in order to evaluate the cardiac function of the rats. The bac- terial translocation （BT） incidence, mesenteric microcirculation, amount of endotoxins in the vein serum, ileum levels of HO- 1, carbon oxide （CO）, nitric oxide （NO）, intedeuldn （IL）-10, turnour necrosis factor-et （TNF-ct）, and the ileum morphology were determined eight weeks after the operation. Results The rats receiving MI ＋ CoPP injections exhibited a recovery in cardiac function, an amelioration of mesenteric microcirculation and change in morphology, a lower BT incidence, a reduction in serum and ileac NO and TNF-ct levels, and an elevation in ileac HO-1, CO, and interleukin-10 （[L-10） levels compared to the MI group （P 〈 0.05）. The rats that received the MI ＋ SnMP injections exhibited results inverse to the MI （P 〈 0.05） group. Conclusions HO-1 exerted a protective effect on the intestines of rats with HF by inhibiting the inflammation and amelioration of microcirculation through the CO pathway. This protective effect could be independent from the recovery of cardiac function.

Intestinal failure in obstructive jaundice

TO THE EDITORWe read with great interest the article by Ding LA and LiJS, which aimed to review the current knowledge on the physiology of normal intestinal barrier function and highlight the role of intestinal failure after various injurious insults in the development of septic complications or multiple organ failure with subsequent rapid clinical deterioration or even death.

Chronic intestinal failure and short bowel syndrome in Crohn’s disease

Chronic intestinal failure(CIF)is a rare but feared complication of Crohn’s disease.Depending on the remaining length of the small intestine,the affected intestinal segment,and the residual bowel function,CIF can result in a wide spectrum of symptoms,from single micronutrient malabsorption to complete intestinal failure.Management of CIF has improved significantly in recent years.Advances in home-based parenteral nutrition,in particular,have translated into increased survival and improved quality of life.Nevertheless,60%of patients are permanently reliant on parenteral nutrition.Encouraging results with new drugs such as teduglutide have added a new dimension to CIF therapy.The outcomes of patients with CIF could be greatly improved by more effective prevention,understanding,and treatment.In complex cases,the care of patients with CIF requires a multidisciplinary approach involving not only physicians but also dietitians and nurses to provide optimal intestinal rehabilitation,nutritional support,and an improved quality of life.Here,we summarize current literature on CIF and short bowel syndrome,encompassing epidemiology,pathophysiology,and advances in surgical and medical management,and elucidate advances in the understanding and therapy of CIF-related complications such as catheter-related bloodstream infections and intestinal failure-associated liver disease.

Intestinal dendritic cells change in number in fulminant hepatic failure

AIM:To investigate the change in intestinal dendritic cell(DC)number in fulminant hepatic failure(FHF).METHODS:An animal model of FHF was created.Intestinal CD11b/c was detected by immunohistochemistry and Western blot.Quantitative real-time polymerase chain reaction(PCR)was used to detect intestinal integrin-αm RNA expression.Intestinal CD83,CD86,CD74,CD3 and AKT were detected by immunohistochemistry,Western blot and PCR.Phosphorylated-AKT(p-AKT)was detected by immunohistochemistry and Western blot.RESULTS:In the FHF group[D-galactosamine(D-Galn)+lipopolysaccharide(LPS)group],the mice began to die after 6 h;conversely,in the D-Galn and LPS groups,the activity of mice was poor,but there were no deaths.Immunohistochemistry results showed that in FHF,the expression of CD11b/c(7988400±385941vs 1102400±132273,P<0.05),CD83(13875000±467493 vs 9257600±400364,P<0.05),CD86(7988400±385941 vs 1102400±13227,P<0.05)and CD74(11056000±431427 vs 4633400±267903,P<0.05)was significantly increased compared with the normal saline(NS)group.Compared with the NS group,the protein expression of CD11b/c(5.4817±0.77 vs 1.4073±0.37,P<0.05)and CD86(4.2673±0.69 vs 1.1379±0.42,P<0.05)was significantly increased.Itg-α(1.1224±0.3 vs 0.4907±0.19,P<0.05),CD83(3.6986±0.40 vs 1.0762±0.22,P<0.05)and CD86(1.5801±0.32 vs 0.8846±0.10,P<0.05)m RNA expression was increased significantly in the FHF group.At the protein level,expression of CD74in the FHF group(2.3513±0.52)was significantly increased compared with the NS group(1.1298±0.33),whereas in the LPS group(2.3891±0.47),the level of CD74 was the highest(P<0.05).At the gene level,the relative expression of CD74 m RNA in the FHF group(1.5383±0.26)was also significantly increased in comparison to the NS group(0.7648±0.22;P<0.05).CD3 expression was the highest in the FHF group(P<0.05).In the FHF,LPS and D-Galn groups,the expression of AKT at the protein and m RNA levels was elevated compared with the NS group,but there wasno statistical significance(P>0.05).The p-AKT protein expression in the FHF(1.54±0.06),LPS(1.56±0.05)and D-Galn(1.29±0.03)groups was higher than that in the NS group(1.07±0.03)(P<0.05).CONCLUSION:In FHF,a large number of DCs mature,express CD86,and activate MHC classⅡmolecular pathways to induce a T cell response,and the AKT pathway is activated.

Tumor necrosis factor alpha increases intestinal permeability in mice with fulminant hepatic failure

AIM:To determine the effect of tumor necrosis factor alpha(TNF-α) on intestinal permeability(IP) in mice with fulminant hepatic failure(FHF),and the expression of tight junction proteins.METHODS:We selected D-lactate as an index of IP,induced FHF using D-galactosamine/lipopolysaccharide and D-galactosamine/TNF-α,assessed the results using an enzymatic-spectrophotometric method,transmission electron microscopy,immunohistochemistry,Western blotting and real-time quantitative polymerase chain reaction.The effect of the administration of antiTNF-α immunoglobulin G(IgG) antibody,before the administration of D-galactosamine/lipopolysaccharide,on TNF-α was also assessed.RESULTS:IP was significantly increased in the mouse model of FHF 6 h after injection(13.57 ± 1.70 mg/L,13.02 ± 1.97 mg/L vs 3.76 ± 0.67 mg/L,P = 0.001).Electron microscopic analysis revealed tight junction(TJ) disruptions,epithelial cell swelling,and atrophy of intestinal villi.Expression of occludin and claudin-1 mRNA was significantly decreased in both FHF models(occludin:0.57 ± 0.159 fold vs baseline,P = 0.000;claudin-1:0.3067 ± 0.1291 fold vs baseline,P = 0.003),as were the distribution density of proteins in the intestinal mucosa and the levels of occludin and claudin-1 protein(occludin:0.61 ± 0.0473 fold vs baseline,P = 0.000;claudin-1:0.6633 ± 0.0328 fold vs baseline,P = 0.000).Prophylactic treatment with antiTNF-α IgG antibody prevented changes in IP(4.50 ± 0.97 mg/L vs 3.76 ± 0.67 mg/L,P = 0.791),intestinal tissue ultrastructure,and the mRNA levels of occludin and claudin-1 expression(occludin:0.8865 ± 0.0274 fold vs baseline,P = 0.505;claudin-1:0.85 ± 0.1437 fold vs baseline,P = 0.1),and in the protein levels(occludin:0.9467 ± 0.0285 fold vs baseline,P > 0.05;claudin-1:0.9533 ± 0.0186 fold vs baseline,P = 0.148).CONCLUSION:Increased in IP stemmed from the downregulation of the TJ proteins occludin and claudin-1,and destruction of the TJ in the colon,which were induced by TNF-α in FHF mice.

Intestinal expressions of eNOSmRNA and iNOSmRNA in rats with acute liver failure

AIM: To observe the gene expression change of eNOSmRNA and iNOSmRNA in the small and large intestines with acute liver failure (ALF), and to reveal the biological function of NO on the pathogenesis of ALF and multiple organs dysfunction at the molecular level. METHODS: Sixty male Wistar rats were selected, weighing from 250g to 350g, and divided into 5 groups randomly: SO, ALF (6h, 12h), L-Arg, L-NAME, L-Arg and L-NAME, each group with 10 rats. The dose of L-Arg was 300mg.kg(-1), and L-NAME was 30mg.kg(-1), the reagents diluted by normal saline were injected through tail vein 30 minutes pre and post operation. The rats in the ALF group were respectively sacrificed postoperatively at 6h, 12h, and the rats in the other groups were sacrificed postoperatively at 6h. The tissues of small and large intestines were harvested in 4% paraforaldehyde containing the reagent of DEPC and fixed at 6h, embedded in paraffin, and 4 microm section was cut. The expression of eNOSmRNA and iNOSmRNA in these tissues was determined with in situ hybridization, and analyzed with the imaging analysis system of CMM-3 and SPSS statistical software. RESULTS: The expression of eNOSmRNA in the large intestine and iNOSmRNA in the small and large intestines increased significantly at 6h after ALF, but the expression of iNOSmRNA in the small and large intestines reduced notably at 12h after ALF (P【0.05); the expression of eNOSmRNA in the large intestine and iNOSmRNA in the small and large intestines decreased significantly with the reagents of L-Arg at 6h ALF, but the expression of eNOSmRNA and iNOSmRNA in the small and large intestines decreased totally with the reagents of L-NAME or association with L-Arg 6h ALF. CONCLUSION: The expression of eNOSmRNA in the large intestine increased notably at the early stage of ALF, NO induced by the enzyme of eNOS from the transplantation of eNOSmRNA can protect the function of the large intestine, the high expression of iNOSmRNA is involved in the damaged function of the small and large intestines. NO precursor can reduce the expression of iNOSmRNA in the small and large intestines and the damage to intestines; NOS inhibitor or association with NO pre-cursor can totally lower the expression of eNOSmRNA and iNOSmRNA in the small and large intestines, it cannot notably influence the NOS inhibitor in the gene expression of eNOSmRNA and iNOSmRNA to supply the additional NO precursor.

Glucagon-like peptide-2 analogues for Crohn’s disease patients with short bowel syndrome and intestinal failure

Short bowel syndrome(SBS)with intestinal failure(IF)is a rare but severe complication of Crohn’s disease(CD),which is the most frequent benign condition that leads to SBS after repeated surgical resections,even in the era of biologics and small molecules.Glucagon-like peptide-2 analogues have been deeply studied recently for the treatment of SBS-IF.These drugs have a significant intestinotrophic effect and the potential to reduce the chronic dependence of SBSIF patients on parenteral support or nutrition.Teduglutide has been approved for the treatment of SBS-IF,and apraglutide is currently in clinical development.The use of these drugs was examined with a focus on their use in CD patients.

To explore the effects of probiotics on patients with chronic heart failure based on intestinal flora

Objective:To investigate the effects of probiotics on trimethylamine oxide,serum inflammatory markers,cardiac function and daily life in patients with chronic heart failure.Methods:Randomly selected from Mianyang Central Hospital in January 2019-December 2019,by using random Numbers table is divided into control group and treatment group,control group with conventional western medicine therapy(strong heart,diuresis and expand blood vessels),treatment group using group(conventional western medicine treatment+probiotics),12 weeks after treatment of chronic heart failure(CHF)in patients with cardiac function in left ventricular ejection fraction(LVEF)and cardiac volume index(LVEDVI),left ventricular end systolic volume index(LVESVI);Intestinal flora metabolite TMAO;Serum inflammatory markers were tumor necrosis factor-(TNF-)and c-reactive protein(CRP).Quality of life score(ADL),indexes of 6min walking experiment and changes before treatment.Results:After treatment,cardiac function(LVEDVI,LVESVI,LVEF)in both groups was higher than that before treatment.Plasma TMAO,serum inflammatory indicators TNF--,CRP,daily life quality score,and 6min walking test were significantly improved(p<0.05).The expression levels of TMAO,TNF-,and CRP in the treatment group were significantly lower than those in the control group,with statistically significant differences(p<0.05),while the ADL score and 6MWT were significantly higher than those in the control group,with statistically significant differences(p<0.05).There was no significant difference between the treatment group and the control group in improving cardiac function(LVEDVI,LVESVI,LVEF)(p>0..05).Conclusion:Probiotics can correct intestinal flora disorder,control TMAO secretion,inhibit inflammatory response,and effectively improve the quality of life of patients.But it cannot repair damaged cardiomyocytes and heart function.

Management of intestinal failure in inflammatory bowel disease:Small intestinal transplantation or home parenteral nutrition?

Inflammatory bowel disease and Crohn&#x02019;s disease in particular, is a common cause of intestinal failure. Current therapeutic options include home parenteral nutrition and intestinal transplantation. For most patients, home intravenous therapy including parenteral nutrition, with a good probability of long-term survival, is the favoured choice. However, in selected patients, with specific features that may shorten survival or complicate home parenteral nutrition, intestinal transplantation presents a viable alternative. We present survival, complications, quality of life and economic considerations that currently influence individualised decision-making between home parenteral nutrition and intestinal transplantation.

Role of nutritional status and nutritional support in outcome of hepatitis B virus-associated acute-on-chronic liver failure

BACKGROUNDHepatitis B virus-associated acute-on-chronic liver failure (HBV-ACLF) is animportant type of liver failure in Asia. There is a direct relationship between HBVACLFand gastrointestinal barrier function. However, the nutritional status ofHBV-ACLF patients has been poorly studied.AIMTo investigate the nutritional risk and nutritional status of HBV-ACLF patientsand evaluated the impact of nutritional support on the gastrointestinal barrier and28-d mortality.METHODSNutritional risk screening assessment and gastrointestinal barrier biomarkers ofpatients with HBV-ACLF (n = 234) and patients in the compensatory period ofliver cirrhosis (the control group) (n = 234) were compared during the periodbetween 2016 and 2018. Changes were analyzed after nutritional support in HBVACLFpatients. Valuable biomarkers have been explored to predict 28-d death.The 28-d survival between HBV-ACLF patients with nutritional support (n = 234)or no nutritional support (2014-2016) (n = 207) was compared.RESULTSThe nutritional risk of the HBV-ACLF patients was significantly higher than thatof the control group. The nutritional intake of the patients with HBV-ACLF waslower than that of the control group. The decrease in skeletal muscle and fatcontent and the deficiency of fat intake were more obvious (P < 0.001). Thecoccus-bacillus ratio, secretory immunoglobulin A, and serum D-lactate weresignificantly increased in HBV-ACLF patients. The survival group had a lowernutritional risk, lower D-lactate, and cytokine levels (endotoxin, tumor necrosisfactor alpha, interleukin-10, and interleukin-1). Interleukin-10 may be a potentialpredictor of death in HBV-ACLF patients. The 28-d survival of the nutritionalsupport group was better than that of the non-nutritional support group (P =0.016).CONCLUSIONPatients with HBV-ACLF have insufficient nutritional intake and high nutritionalrisk, and their intestinal barrier function is impaired. Individualized and dynamicnutritional support is associated with a better prognosis of 28-d mortality in HBVACLFpatients.

Measurement of the intestinal permeability in chronic kidney disease

AIM： To evaluate methods measuring the intestinal permeability in chronic kidney disease （CKD） and clarify whether there is an increased intestinal permeability in CKD.METHODS： We reviewed the literature in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-analysis （PRISMA） protocol and performed a systematic literature search through MEDline and EMBASE. All controlled trials and cohort studies using non-invasive methods to assess intestinal permeability in CKD patients were included. Excluded were： Conference abstracts and studies including patients younger than 18 years or animals. From the included studies we summarized the used methods and their advantages and disadvantages. For the comparison of their results we divided the included studies in two categories based on their included patient population, either assessing the intestinal permeability in mild to moderate CKD patients or in end stage renal disease （ESRD） patients. Results were graphically displayed in two plots, one comparing the intestinal permeability in mild to moderate CKD patients to healthy controls and one comparing the intestinal permeability in ESRD patients to healthy controls. RESULTS： From the 480 identifed reports, 15 met our inclusion criteria. Methods that were used to assess the intestinal permeability varied from markers measured in plasma to methods based on calculating the urinary excretion of an orally administered test substance. None of the applied methods has been validated in CKD patients and the infuence of decreased renal function on the different methods remains unclear to a certain extent. Methods that seem the least likely to be influenced by decreased renal function are the quantitative PCR （qPCR） for bacterial DNA in blood and D-lactate. Considering the results published by the included studies; the studiesincluding patients with mild to moderate CKD conductedconflicting results. Some studies did report an increasein intestinal permeability whilst other did not find asignificant increased permeability. However, despite thevariety in used methods among the different studies, allstudies measuring the intestinal permeability in ESRDpoint out a significant increased intestinal permeability.Results should nevertheless be interpreted with cautiondue to the possible infuence of a decreased glomerularfltration rate on test results.CONCLUSION： The intestinal permeability in CKD： （1） could be measured by qPCR for bacterial DNA in blood and D-lactate; and （2） seems to be increased in ESRD.

Extra-intestinal and long term consequences of Giardia duodenalis infections

Giardiasis is the most common waterborne parasitic infection of the human intestine worldwide.The etiological agent,Giardia duodenalis(syn.G.intestinalis,G.lamblia),is a flagellated,binucleated protozoan parasite which infects a wide array of mammalian hosts.Human giardiasis is a true cosmopolitan pathogen,with highest prevalence in developing countries.Giardiasis can present with a broad range of clinical manifestations from asymptomatic,to acute or chronic diarrheal disease associated with abdominal pain and nausea.Most infections are self-limiting,although re-infection and chronic infection can occur.Recent evidence indicating that Giardia may cause chronic post-infectious gastrointestinal complications have made it a topic of intense research.The causes of the post-infectious clinical manifestations due to Giardia,even after complete elimination of the parasite,remain obscure.This review offers a state-of-the-art discussion on the long-term consequences of Giardia infections,from extra-intestinal manifestations,growth and cognitive deficiencies,to post-infectious irritable bowel syndrome.The discussion also sheds light on some of the novel mechanisms recently implicated in the production of these postinfectious manifestations.

六味地黄丸调节肠道微生物组平衡抑制卵巢早衰小鼠的氧化应激

背景:研究表明,卵巢早衰患者肠道菌群结构发生变化,肠道菌群失调可能是卵巢早衰发生的重要机制之一。目的:探讨六味地黄丸对环磷酰胺诱导卵巢早衰小鼠氧化应激和肠道微生物群的影响。方法:45只雌性ICR小鼠随机分为3组:空白组(正常小鼠)、模型组(卵巢早衰小鼠)、六味地黄丸组,后2组小鼠一次性腹腔注射环磷酰胺(120 mg/kg)制备卵巢早衰小鼠模型,造模成功后六味地黄丸组小鼠连续灌胃六味地黄丸(1.56 g/kg)28 d,其余2组灌胃等量生理盐水28 d,灌胃结束后取材。每周记录小鼠体质量,计算卵巢指数,苏木精-伊红染色观察小鼠卵泡的发育情况,ELISA法检测血清抗苗勒管激素、雌二醇、促卵泡激素、超氧化物歧化酶、谷胱甘肽过氧化物酶和丙二醛水平,并通过16S rDNA测序检测所有小鼠的肠道微生物组。结果与结论:(1)模型组小鼠的毛发疏松,活力及抓力下降,体质量几乎无增长,卵巢指数下降;六味地黄丸治疗后小鼠的体质量高于模型组,卵巢指数也随之升高(P<0.05)。(2)模型组小鼠动情周期紊乱;六味地黄丸能恢复卵巢早衰小鼠的发情周期,减少闭锁卵泡数量。(3)模型组小鼠血清中促卵泡激素、丙二醛水平显著升高(P<0.01),血清雌二醇、抗苗勒管激素、超氧化物歧化酶和谷胱甘肽过氧化物酶水平显著下降(P<0.01);六味地黄丸组小鼠血清促卵泡激素、丙二醛水平显著降低(P<0.01),雌二醇、抗苗勒管激素、超氧化物歧化酶、谷胱甘肽过氧化物酶水平升高。(4)根据16S rDNA测序结果,六味地黄丸可调控肠道微生物群的丰度和多样性,可增加有益菌的相对丰度,KEGG通路分析显示,肠道微生物群与代谢途径、次生代谢产物的生物合成、不同环境中的微生物代谢、氨基酸的生物合成等通路受六味地黄丸的调控。(5)结论:肠道微生物组的改变可能是六味地黄丸治疗卵巢早衰的潜在机制之一。六味地黄丸能调节肠道微生物组结构,增加有益菌数量,减少有害菌数量,从而改善肠道微生态平衡。这种调节作用有助于降低氧化应激水平,进一步抑制卵巢早衰小鼠卵巢氧化应激。

Effects of Buyang Huanwu Decoction on Intestinal Barrier, Intestinal Flora, and Trimethylamine Oxide in Rats with Heart Failure

Objective: To explore the mechanisms of Buyang Huanwu Decoction(BYHWD) modulating the gut microbiome and trimethylamine oxide(TAMO) to exert cardioprotective effects. Methods: Ligation of the left anterior descending coronary artery was performed in rats to induce heart failure(HF). Except for the shamoperation group(n=10), 36 operation-induced models were randomized into 3 groups using a random number table(n=12 in each group): the model group, the BYHWD group(15.02 g/kg BYHWD), and the positive group(4.99 g/kg metoprolol succinate). After 4-week treatment(once daily by gavage), echocardiography was applied to evaluate the cardiac function and the Tei index(the ratio of ventricular isovolumic contraction time(IVCT)and isovolumic diastolic time(IVRT) to ejection time(ET)) was calculated;hematoxylin-eosin(HE) staining was observed to characterize the pathology of the myocardium and small intestinal villi. D-lactic acid was detected by an enzyme-linked immunosorbent assay(ELISA). Expressions of occludin, claudin-1, and zonula occludens(ZO-1) were detected by Western blot. 16S ribosomal ribonucleic acid(16S rRNA) sequencing was used to explore the changes in the intestinal flora. TMAO was detected via liquid chromatography-tandem mass spectrometry(LC-MS/MS). Results: In the echocardiography, the Tei index was considerably lower in the positive and BYHWD groups compared with the model group(P<0.05). Besides, BYHWD improved the pathology of myocardium and small intestine of HF rats and lowered the D-lactic acid content in the serum, when compared with the model group(P<0.05). BYHWD also improved the expression of occludin and claudin-1(P<0.05);in the gut microbiota analysis, BYHWD slowed down modifications in the structure distribution of gut microbiota and regulated the diversity of intestinal flora in HF rats. The content of TMAO in the serum was significantly lowered by BYWHT compared with the model group(P<0.05). Conclusion: BYHWD may delay progression of HF by enhancing the intestinal barrier structure, and regulating intestinal flora and TAMO.

肠道菌群与心力衰竭关系的研究进展

慢性心力衰竭患者肠道菌群的构成、功能及代谢产物发生了明显的变化。心力衰竭患者肠道菌群中大肠杆菌/志贺菌属、韦荣球菌属、肠杆菌属丰度升高。色胺酸代谢、脂质代谢和脂多糖合成等微生物功能增加,且与生成有益代谢产物丁酸盐相关的细菌基因减少,有害代谢产物氧化三甲胺相关的细菌基因明显增加。肠道菌群的代谢产物,如氧化三甲胺、短链脂肪酸、氨基酸衍生物、胆汁酸,是肠道菌群与宿主相互作用的主要途径之一。这些代谢产物可以直接吸收进入宿主循环系统,然后迁移至不同的器官;或者被宿主酶代谢,产生信号分子,从而发挥作用。

超声评估心力衰竭患者胃肠壁淤血程度的应用价值

目的探讨超声评估心力衰竭患者胃肠壁淤血程度的应用价值。方法招募2023年8月至10月首都医科大学附属北京安贞医院收治的心力衰竭患者32例作为心衰组,另选择同期无心脏疾病的健康人群33名作为对照组。通过胃肠超声及腹部超声测量两组的胃壁、胃壁黏膜下层、肠壁厚度,以及下腔静脉内径、肝静脉内径、门静脉内径、肠系膜上静脉内径。对心衰组进行超声心动图检查,测量左心室射血分数(LVEF)、右室三尖瓣环收缩期位移(TAPSE)及肺动脉收缩压。比较两组临床资料,分析心衰组患者胃肠壁厚度与腹部静脉内径、心脏功能指标间的相关性。结果心衰组患者胃壁厚度、胃壁黏膜下层厚度、肠壁厚度较对照组增厚,下腔静脉内径、肝静脉内径、门静脉内径、肠系膜上静脉内径较对照组增宽,差异有统计学意义(P<0.05)。心衰组患者LVEF为45.5(25.0,57.7)%,TAPSE为16.0(11.0,18.0)mm,肺动脉收缩压为43.5(28.5,59.0)mmHg。心衰组患者胃壁厚度与TAPSE呈负相关(P<0.05),与门静脉内径呈正相关(P<0.05);胃壁黏膜下层厚度与TAPSE呈负相关(P<0.05),与肺动脉收缩压、下腔静脉内径、肝静脉内径、门静脉内径呈正相关(P<0.05);肠壁厚度与TAPSE呈负相关(P<0.05),与下腔静脉内径、肝静脉内径、门静脉内径呈正相关(P<0.05)。心衰组患者胃壁厚度、胃壁黏膜下层厚度、肠壁厚度与LVEF相关性不显著(P>0.05)。结论超声可以实时监测心衰患者胃肠壁及胃壁黏膜下层厚度指标,可作为评估心衰患者胃肠壁淤血程度的影像学方法。

基于“脾为之卫”理论探讨肠道微生态的失衡与心力衰竭的关系

心力衰竭是心血管疾病终末期的致命阶段,因其死亡率和再住院率一直居高不下,故给社会带来了巨大的医疗负担。肠道微生态(IM)是人体最大、最复杂的微生态系统,它是由数以万计的微生物寄居在人体的胃肠道内,这些微生物被统称为肠道菌群(GM)。近些年来随着对肠道菌群研究的不断深入,越来越多的研究发现肠道菌群的失衡会改变心力衰竭患者体内基础代谢,促进全身炎症级联反应,是心力衰竭发生发展的关键诱因之一,因此以肠道微生物稳态作为治疗心力衰竭的新切入点将是医学研究的热点。然而中医理论“脾为之卫”涵盖了脾主运化、脾主升清、藏意主思等生理功能,肠道菌群与“脾为之卫”的职能有一定的相似性。文章从整体观念出发,以中医“脾为之卫”理论为切入,就肠道微生态失衡与心力衰竭发病机制进行阐述,为心力衰竭中医治疗或药物研究提供参考。

2023版《ESPEN实践指南:家庭肠外营养》解读

2023年1月,欧洲临床营养与代谢协会(ESPEN)发布最新家庭肠外营养指南——《ESPEN实践指南:家庭肠外营养》,为临床实践中提供适当和安全的建议。该指南基于先前发表的指南,提供最新证据和意见,并将建议及声明转换为流程图形式,内容更具逻辑性。该指南从家庭肠外营养适应证、中心静脉通路装置与输液泵、输液导管与中心静脉通路装置部位的护理、营养混合液、程序监测和管理6个方面提出71条建议、5项声明,现对该指南的主要内容进行解读,希望为我国家庭肠外营养的开展及应用提供有益参考。