翁舌汤灌肠治疗大肠湿热型溃疡性结肠炎临床研究

目的:观察翁舌汤灌肠治疗大肠湿热型溃疡性结肠炎的疗效及其对患者血清炎症因子水平的影响。方法:将80例大肠湿热型溃疡性结肠炎患者按随机数字表法分为观察组和对照组各40例。观察组给予翁舌汤灌肠治疗,对照组给予美沙拉嗪栓肛门塞入治疗,两组均连续治疗8周。比较两组患者的临床疗效、肠黏膜征象积分和血清炎症因子水平。结果:治疗后,观察组和对照组总有效率分别为95.00%、70.00%,两组疗效比较,差异有统计学意义(P<0.05)。治疗后,观察组患者炎症增生、黏膜溃疡、黏膜糜烂、黏膜水肿、黏膜充血积分均下降,与治疗前比较,差异有统计学意义(P<0.05);且观察组各项积分均低于对照组,差异有统计学意义(P<0.05)。治疗后,两组血清白细胞介素-8(IL-8)、肿瘤坏死因子-β(TNF-β)水平均降低,血清白细胞介素-10(IL-10)水平均升高,与治疗前比较,差异均有统计学意义(P<0.05);且观察组血清IL-8、TNF-β水平明显低于对照组,血清IL-10水平明显高于对照组,差异有统计学意义(P<0.05)。结论:翁舌汤灌肠治疗大肠湿热型溃疡性结肠炎疗效较好,可改善患者肠黏膜征象积分,调节血清炎症因子水平。     

Buried Bumper Syndrome: A common complication of levodopa intestinal infusion for Parkinson disease

BackgroundPercutaneous endoscopic gastrostomy (PEG) is required for Levodopa/Carbidopa Intestinal Gel (LCIG) delivery in patients with advanced Parkinson's disease (PD) as well as for enteral feeding in a variety of neurological disorders. Buried Bumper Syndrome (BBS) is a serious complication of PEG. The frequency of BBS in patients receiving LCIG treatment has never been reported.ObjectivesTo compare the frequency of BBS in patients on LCIG treatment or on enteral feeding over the past 12 years and identify possible risk factors.MethodsWe reviewed prospectively recorded data from 2009 to 2020 on two case-series: LCIG-treated PD patients and non-PD patients on enteral nutrition. We identified all BBS incidences. Patients’ characteristics, clinical manifestations, BBS management, possible risk factors and outcomes were analyzed.ResultsDuring the 12 years, 35 PD patients underwent PEG insertion for LCIG infusion, and 123 non-PD patients for nutritional support. There were eight cases of BBS in six PD patients (17.1%). Six of them were effectively managed without treatment discontinuation. Of the enteral feeding patients, only one developed BBS (0.8%) (p < 0.001). We identified inappropriate PEG site aftercare, weight gain, early onset PD, longer survival, treatment duration, dementia and PEG system design as potential risk factors for BBS development.ConclusionsBBS occurs more frequently in LCIG patients than in patients receiving enteral feeding. If detected early, it can be successfully managed, and serious sequalae or treatment discontinuation can be avoided. Regular endoscopic follow-up visits of LCIG-treated patients and increased awareness in patients and clinicians are recommended.     

Newly recruited intraepithelial Ly6A+CCR9+CD4+ T cells protect against enteric viral infection

1. Download : Download high-res image (215KB)
2. Download : Download full-size image

     

肠运动昼夜节律及其外科临床意义

肠运动存在昼夜节律，表现为白天活跃，夜间减弱或消失，这是一种内生性的、由时钟基因控制的生物节律。肠运动节律既可与中央节律保持高度一致，也可独立于中央节律而对外周环境刺激做出反馈。外科手术会破坏肠运动的昼夜节律，而围手术期合理使用褪黑素、五羟色胺（5-HT）受体激动剂和非甾体类解热镇痛药等药物则有助于促进此节律的恢复。外科医生了解肠运动节律的机制，有助于加深术后肠麻痹（POI）的认识，再基于时辰药理学，在合适的时机以适宜的剂量给药，或许能进一步缩短POI时间，促进肠运动功能尽早恢复。     

不同组织来源的生物补片修补腹壁肌部分层次缺损的研究

目的探讨不同组织来源的生物补片体内组织重塑的差异，并提供信息供临床选择生物补片时参考。 方法选取健康SD大鼠，随机分组，每组10处缺损，建腹壁肌部分层次缺损模型并以基底膜（basement membrane，BM）/小肠黏膜下层（small intestine submucosa，SIS）复合细胞外基质补片、SIS补片、真皮补片和心包补片修补，设立未修补组为空白对照。术后2、4、8、16周评价修复区血清肿发生、皱缩率、植入降解比例，取修复区组织做组织学切片分析补片内组织长入、新生血管化、周围组织包裹情况。 结果实验期内，BM/SIS复合细胞外基质补片未发生血清肿，基本维持植入面积，术后4周再生高度有序的新生胶原替代缺损区域，术后8周补片降解。术后2周，SIS补片的血清肿发生率为65%，修复区早期大量炎性细胞浸润，再生胶原组织有序性较差，术后8周补片降解，术后16周皱缩率为－52.0%±9.8%。50%的真皮补片细胞浸润补片中央，完全降解。其余真皮补片出现纤维囊包裹，细胞仅浸润交界区，修复区显著扩张，实验期内无降解。心包补片仅少量细胞浸润交界区，无组织长入，术后16周皱缩率为－29.5%±14.0%，出现致密纤维囊包裹，实验期内无降解。 结论与SIS补片、心包补片和真皮补片相比，BM/SIS复合细胞外基质补片具备优异的组织修补和再生疗效。     

Vasoactive intestinal peptide decreases inflammation and tight junction disruption in experimental necrotizing enterocolitis

Background and PurposeExcessive inflammatory cell infiltration and accumulation in the intestinal mucosa are pathological features of necrotizing enterocolitis (NEC) leading to intestinal barrier disruption. Vasoactive intestinal peptide (VIP) is a potent anti-inflammatory agent that regulates intestinal epithelial barrier homeostasis. We previously demonstrated that VIP-ergic neuron expression is decreased in experimental NEC ileum, and this may be associated with inflammation and barrier compromise. We hypothesize that exogenous VIP administration has a beneficial effect in NEC.MethodsNEC was induced in C57BL/6 mice by gavage feeding, hypoxia, and lipopolysaccharide administration between postnatal day (P) 5 and 9. There were four studied groups: Control (n = 6): Breast feeding without stress factors; Control + VIP (n = 5): Breast feeding + intraperitoneal VIP injection once a day from P5 to P9; NEC (n = 9): mice exposed to NEC induction; NEC + VIP (n = 9): NEC induction + intraperitoneal VIP injection. Terminal ileum was harvested on P9. NEC severity, intestinal inflammation, (IL-6 and TNFα), and Tight junctions (Claudin-3) were evaluated.ResultsNEC severity and intestinal inflammation were significantly decreased in NEC + VIP compared to NEC. Tight junction expression was significantly increased in NEC + VIP compared to NEC.ConclusionVIP administration has a beneficial therapeutic effect in NEC by reducing inflammation and tight junction disruption.     

Advances in the physiology of gastric emptying

There have been many recent advances in the understanding of various aspects of the physiology of gastric motility and gastric emptying. Earlier studies had discovered the remarkable ability of the stomach to regulate the timing and rate of emptying of ingested food constituents and the underlying motor activity. Recent studies have shown that two parallel neural circuits, the gastric inhibitory vagal motor circuit (GIVMC) and the gastric excitatory vagal motor circuit (GEVMC), mediate gastric inhibition and excitation and therefore the rate of gastric emptying. The GIVMC includes preganglionic cholinergic neurons in the DMV and the postganglionic inhibitory neurons in the myenteric plexus that act by releasing nitric oxide, ATP, and peptide VIP. The GEVMC includes distinct gastric excitatory preganglionic cholinergic neurons in the DMV and postganglionic excitatory cholinergic neurons in the myenteric plexus. Smooth muscle is the final target of these circuits. The role of the intramuscular interstitial cells of Cajal in neuromuscular transmission remains debatable. The two motor circuits are differentially regulated by different sets of neurons in the NTS and vagal afferents. In the digestive period, many hormones including cholecystokinin and GLP‐1 inhibit gastric emptying via the GIVMC, and in the inter‐digestive period, hormones ghrelin and motilin hasten gastric emptying by stimulating the GEVMC. The GIVMC and GEVMC are also connected to anorexigenic and orexigenic neural pathways, respectively. Identification of the control circuits of gastric emptying may provide better delineation of the pathophysiology of abnormal gastric emptying and its relationship to satiety signals and food intake.