2016 IAP国际共识：自身免疫性胰腺炎的治疗 CQ-1. What are the indications for treatment of AIP? Consensus statements A. “Symptomatic patients as follows are indication for treatment”: (level B). Pancreatic involvement: e.g., obstructive jaundice, abdominal pain, back pain. Other organ involvement (OOI): e.g., Jaundice due to bile duct stricture. B. “Asymptomatic patients as follows are indication for treatment”: (level B). Pancreatic: Persistent pancreatic mass on imaging. OOI: Persistent liver test abnormalities in a patient with associated IgG4-related sclerosing cholangitis (IgG4-SC). CQ-2. What is the best approach to inducton of remission? Consensus statements “For induction of remission, steroid is the first-line agent in all patients with active untreated AIP, unless if there are contraindications to steroid use.” (level A). “In those with contraindications to steroid treatment, rituximab can induce remission as single agent. ” (level B). “Except for rituximab, other steroid-sparing such as thiopurines are poorly effective as single agents for induction of remission. ”(level C). CQ-3. Is biliary drainage needed in obstructive jaundice before treatment? Consensus statements “Biliary drainage is useful to prevent biliary infection and use of brushing and cytology can differentiate IgG4-SC from biliary malignancy. ” (level B). “In some cases of mild jaundice without signs of infection, steroid treatment alone can be performed safely without biliary stenting. ” (level B). CQ-4. What should be the minimum starting dose steroids for induction of remission? Consensus statements “ Prednisone with the initial dose of 0.6-1.0 mg/kg/day should be started. ” (level A). “ A minimum of 20 mg/day is generally necessary to induce remission. ” (level B). CQ-5. How to taper steroids? Consensus statements “Usually tapered by 5-10 mg/day every 1-2 weeks until a daily dosage of 20 mg, followed by tapering with 5 mg every 2 weeks.” (level B). “Another acceptable regimen is 40 mg/day for 4 weeks followed by taper by 5 mg/week until off. ” (level B). “Duration of total remission treatment should generally last 12 weeks. ” (level A). “Very short duration (4 weeks) of steroid induction treatment with a high dose of steroid 20 mg is not recommended. ” (level C). CQ-6. Is maintenance treatment useful to prevent relapse of AIP? Consensus statements “The patients with type 1 AIP having low disease activity before treatment and those with type 2 do not need maintenance treatment. ” (level C). “After successful induction of remission, maintenance therapy with low-dose glucocorticoids or steroid-sparing agents may be useful in some patients with type 1 AIP”. (level B). CQ-7. Can we predict who will relapse? Consensus statements “Risk factors for relapsing remain poorly understood.” “Some predictors of relapse include. Remarkably high serum IgG4 levels (such as x4 UNL) before treatment. Persistently high serum IgG4 levels after steroid treatment. Diffuse enlargement of the pancreas. Proximal type of IgG4-SC. Extensive multi-organ involvement (2xOOI) ” (level B). CQ-8. How should relapse be treated ? Consensus statements “Although there is no “gold standard” for treatment in relapse cases, steroid and steroid-sparing agents such as immunemodulators or rituximab are useful. ” (level B) CQ-9. Is surgical treatment useful? Consensus statements “Although steroid or alternative medications should be initially performed, surgical treatment may be useful in some refractory cases. ” (level B) 指南目录 “腰椎间盘突出症的康复治疗”中国专家共识 2017急性深静脉血栓形成诊断和治疗指南 2017年GOLD慢性阻塞性肺疾病定义和诊断的全球策略解读 2017年最新克罗恩病治疗指南 2017年最新溃疡性结肠炎治疗指南 2017 ADA糖尿病视神经病变最新指南推荐 儿童及成人惊厥性癫痫持续状态(CSE)的治疗 中国急/慢性非特异性腰背痛诊疗专家共识 中国帕金森病的诊断标准(2016版) 中国血管性认知障碍诊疗指导规范 2016年中国偏头痛防治指南 阿尔茨海默病诊疗指南 关于肥厚型心肌病诊断和猝死防治建议 心房颤动诊疗指南 2016 ESC 和 AHA/AHA/HFSA慢性心力衰竭新指南解读
急性胰腺炎 急性胰腺炎是多种病因导致胰酶在胰腺内被激活后引起胰腺组织自身消化、水肿、出血甚至坏死的炎症反应。临床以急性上腹痛、恶心、呕吐、发热和血胰酶增高等为特点。病变程度轻重不等，轻者以胰腺水肿为主，临床多见，病情常呈自限性，预后良好，又称为轻症急性胰腺炎。少数重者的胰腺出血坏死，常继发感染、腹膜炎和休克等，病死率高，称为重症急性胰腺炎。临床病理常把急性胰腺炎分为水肿型和出血坏死型两种。 氧化应激是各种炎症性疾病共同的机制，在急性胰腺炎也必然十分重要。过去曾经有大量研究证明氢气对各类炎症和氧化应激损伤相关疾病具有理想的治疗作用，也有学者曾经报道氢气对精氨酸诱导的急性胰腺炎的治疗作用，但没有人观察和探讨过对牛磺酸胆酸诱导的急性胰腺炎的治疗效果。最近来自四川大学华西医院的学者开展了这方面的研究，文章发表在 Evidence-BasedComplementary and Alternative Medicine 。 研究通过血清炎症因子、胰腺组织病理学分析、组织炎症因子基因表达和氧化应激相关指标，证明氢气生理盐水对这种疾病具有保护作用。研究提示氢气对急性胰腺炎具有潜在的治疗价值。 731932(2).pdf http://www.hindawi.com/journals/ecam/2013/731932/ Oxidativestress plays an important role in the pathogenesis of acute pancreatitis (AP).As an ideal exterminator of poisonous free radicals, hydrogen can clearlyreduce the degree of oxidative damage caused by severe acute pancreatitis (SAP)and lessen the presence of inflammatory cytokines. The aim of this study was toinvestigate the effects and mechanism of hydrogen-rich saline on SAP in rats.Serum TNF-α, IL-6, and IL-18 and histopathological score in the pancreas werereduced after hydrogen-rich saline treatment. Malondialdehyde (MDA) andmyeloperoxidase (MPO) contents were obviously reduced, while superoxidedismutase (SOD) and glutathione (GSH) contents were increased afterhydrogen-rich saline treatment. The expression of mRNA of tumor necrosisfactor-α (TNF-α) and intercellular adhesion molecule-1 (ICAM-1) in the pancreaswas reduced in hydrogen-rich saline treated group. In conclusion, intravenoushydrogen-rich saline injections could attenuate the severity of AP, probablyvia inhibiting the oxidative stress and reducing the presence of inflammatorymediators.
Hydrogen-rich saline reduces the oxidative stress and relieves the severity of t.pdf 胰腺炎是胰腺因胰蛋白酶的自身消化作用而引起的疾病。常见类型有急性胆源性胰腺炎、蛔虫性急性胰腺炎、胆源性急性胰腺炎、急性出血坏死型胰腺炎等急性胰腺炎，自身免疫性胰腺炎、胆源性慢性胰腺炎等慢性胰腺炎。治疗原则是手术和对症支持治疗。 胰腺是人体第二大消化腺体，是消化作用最强的器官。胰腺分泌的胰液是人体最重要的消化液。正常情况下，胰液在其腺体组织中含有不活动即无活性的胰酶原。胰液沿胰腺管道不断地经胆总管奥狄氏括约肌流入十二指肠，由于十二指肠内有胆汁存在，加上十二指肠壁粘膜分泌一种肠激酶，在二者的作用下，胰酶原开始转变成活性很强的消化酶。一般情况下，胰管和胆管虽然都经过一条通道流入十二指肠，但由于胰管内的压力高于胆管内的压力，胆汁不会反流入胰管内。只有当奥狄氏括约肌痉挛或胆管内压力升高，如结石，肿瘤阻塞，胆汁才会反流入胰管并进入胰腺组织，此时，胆汁内所含的卵磷脂被胰液内所含的卵磷脂酶 A 分解为溶血卵磷脂，可对胰腺产生毒害作用。或者胆道感染时，细菌可释放出激酶将胰酶激活，同样可变成能损害和溶解胰腺组织的活性物质。这些物质将胰液中所含的胰酶原转化成胰蛋白酶，此酶消化活性强，渗透入胰腺组织引起自身消化，亦可引起胰腺炎。 胰腺炎发病原因有胆道系统疾病、酒精或药物引起、传染病并发胰腺炎，家族性高脂血症患者、动脉粥样硬化及结节性动脉周围炎、十二指肠克罗恩病波及胰腺容易发生胰腺炎，胰管阻塞，胰管结石、狭窄、肿瘤等可引起胰液分泌旺盛，胰管内压增高，胰管小分支和胰腺腺泡破裂，胰液与消化酶渗入间质，引起急性胰腺炎。低蛋白饮食可导致慢性胰腺炎，多见于东南亚、非洲及拉丁美洲各国。遗传性胰腺炎 (hereditary pancreatitis) 较少见，属染色体显性遗传。 外伤与手术是急性胰腺炎的常见原因，只有在创伤严重或损伤主胰管后方可能引起慢性胰腺炎。 胰腺炎该病主要由胰腺组织受胰蛋白酶的自身消化作用。胰腺炎时因某些因素（下述）激活了胰蛋白酶，后者又激活了其它酶反应，如弹性硬蛋白酶（ elastase ）及磷脂酶 A （ phospholipaseA ），对胰腺发生自身消化作用，促进了其坏死溶解。另外，胰蛋白酶对由脂蛋白构成的细胞膜及线粒体膜并无作用，而胰液中的磷脂酶 A 被脱氧胆酸激活后，作用于细胞膜和线粒体膜的甘油磷脂，使之分解变为脱脂酸卵磷脂，亦称溶血卵磷脂（ lysolecithin ），后者对细胞膜有强烈的溶解作用，可溶解、破坏胰腺细胞膜和线粒体膜的脂蛋白结构，致细胞坏死。脂肪坏死也同样先由胰液中的脱脂酸卵磷脂溶解、破坏了脂肪细胞膜后，胰脂酶才能发挥作用。 急性胰腺炎是胰酶消化胰腺及其周围组织所引起的急性炎症，主要表现为胰腺呈炎性水肿、出血及坏死，故又称急性出血性胰腺坏死（ acutehemorrhagicnecrosisofpancreas ），好发于中年男性，发作前多有暴饮暴食或胆道疾病史。临床表现为突然发作的上腹部剧烈疼痛并可出现休克。按病变表现不同，可将本病分为急性水肿性（或间质性）胰腺炎及急性出血性胰腺炎二型。坏死出血型较少见，但病情严重，死亡率高。 急性胰腺炎非手术治疗除常规支持疗法，如禁食鼻胃管减压、补充体液防治休克、解痉止痛、抗生素、中药和腹腔渗出液的处理外，比较特异的方法是抑制胰腺外分泌及胰酶抑制剂，胃管减压、 H2 受体阻滞剂 { 如西咪替丁 ) 、抗胆碱能药 ( 如山莨菪碱、阿托品 ) 、生长抑素等，但后者价格昂贵，一般用于病情比较严重的病人。胰蛋白酶抑制剂如抑肽酶、加贝酯等具有 — 定的抑制胰蛋白酶的作用。 曾经有报道氢气生理盐水可以治疗精氨酸诱导的急性胰腺炎，最近 J Trauma Acute Care Surg. 发表来自成都军区总医院的文章，证明氢气生理盐水注射可以治疗创伤性急性胰腺炎，研究发现氢气生理盐水注射后，尽管创伤性急性胰腺炎血浆中淀粉酶、脂酶活性未见明显改变，但治疗组动物死亡率明显下降，血浆炎症因子、胰腺组织 丙二醛显著下降， 胰腺组织谷胱甘肽和超氧化物歧化酶（ SOD ）显著增高。研究结果表明，氢气对创伤性急性胰腺炎后全身炎症反应、局部组织抗氧化能力和氧化应激等均有改善作用。提示氢气对创伤性急性胰腺炎具有治疗价值。 Ren J, Luo Z, Tian F, Wang Q, Li K, Wang C. Hydrogen-rich saline reduces the oxidative stress and relieves the severity of trauma-induced acute pancreatitis in rats. J Trauma Acute Care Surg. 2012 Jun;72(6):1555-61. Currently, little evidence exists to support whether the therapeutic approaches for treating ordinary acute pancreatitis (AP) are effective in trauma-induced pancreatitis. Hydrogen-rich (H2) saline is an antioxidant treatment capable of ameliorating the severity of L-arginine-induced AP. In this study, we attempted to validate its protective role against traumatic pancreatitis (TP). A previously established experimental rat model of TP was generated by controlled delivery of high pressure air impact. The protective effects of H2 saline against TP were evaluated in this model system by measuring survival rate and determining changes in histopathology, plasma enzymes, cytokines, and oxidative stress-associated molecules. Intraperitoneal administration of H2-rich saline produced a pronounced protection against TP in rats. Significant improvements were observed in survival rate and histopathological findings. In addition, plasma cytokines concentrations were reduced in H2 saline-treated TP rats. Although no marked inhibitory effect on plasma amylase and lipase activities was observed, H2 saline caused considerable suppression of pancreatic malondialdehyde level and recruitment of endogenous pancreatic antioxidants, such as glutathione and superoxide dismutase. H2-rich saline has beneficial effects on TP, presumably because of its detoxification activities against excessive reactive oxygen species. Our findings highlight the potential of H2-rich saline as a therapeutic agent of trauma-induced AP.
标签: 胰腺炎
