甲亢性肝损害116例临床分析

目的探讨甲状腺功能亢进症（甲亢）肝损害的临床特点。方法收集228例甲亢患者的临床资料,分为肝损害组及无肝损害组,对两组患者的年龄、性别、甲亢病程、肝功能及甲状腺功能等指标进行分析比较。结果 228例甲亢患者中发生肝损害116例,发生率为50.72%。甲亢患者的性别与甲亢性肝损害的发生率无相关性;而年龄越大甲亢性肝损害发生率越高,病程越长甲亢性肝损害发生率也越高。甲亢性肝损害患者甲状腺功能指标TT4、FT3明显高于甲亢肝功能正常的患者,差异有统计学意义（P〈0.05）;肝功能测定以ALT、ALP升高多见。结论甲亢性肝损害的发病率较高,病情的严重程度与年龄、病程、甲状腺激素水平有密切关系;建议临床医生对初诊及复诊甲亢患者进行肝功能常规测定,以便合理选用治疗方案,使甲亢性肝损害得以及早治疗。     

急性肾功能衰竭对肝损害的实验研究

探讨急性肾功能衰竭 (以下简称为 ARF)时尿毒症毒素对肝的损害情况 ,为临床防治提供形态学依据。Wistar大白鼠 32只 ,随机分成正常对照组 ,14只 ;双输尿管结扎结扎组 ,18只。模型建成后 2 3- 37小时内将动物处死 ,取肝组织作NOS、 MAO、 SDH、 L DH、 Ch E、 ATPase、 ACP等项酶组织化学显色及超微结构观察。结果显示 :实验组 SDH、 Mg2 + -ATPase 的活性均由正常的强阳性 ( )下降为阳性 (+) ;MAO、 Ch E的活性均由正常的中等阳性 ( )下降为阳性(+) ;ACP、 L DH的活性均由阳性 (+)增强到中等阳性 ( ) ;NOS活性由正常的弱阳性 (± )增强为阳性 (+) ;肝细胞器结构受损。结果表明 :ARF的尿毒素的大量淤积通过影响肝脏酶的活性来干扰和抑制糖代谢、三羧酸循环、蛋白质合成及解毒等功能 ,并导致肝损害发生。 2用改良的 NADPH-黄递酶法可显示肝组织 NOS的存在 ,该法操作简便 ,经济 ,特别适用于同时需要留取活组织做其它检查者。当输尿管结扎时 ,NOS的确切作用有待于进一步探讨     

脂类介质与肝损害

脂类介质是一类具有广泛生物学活性的花生四烯酸代谢物和血小板活化因子,在肝脏的病理生理过程中起着重要的介质作用。本文介绍了脂类介质的代谢,生物学作用及其与肝损害和肝病的关系。     

16例妊娠合并急性胰腺炎的护理体会

急性胰腺炎诱发因素多为暴饮暴食、感染等,但妊娠发生的急性胰腺炎其两者的关系尚未十分清楚,一般认为妊娠期急性胰腺炎的病因为多样性,往往由于一个以上的因素协同作用。我院于1992-2002年共收治妊娠合并急性胰腺炎16例,现将护理体会总结如下。     

肝硬化合并肝肺综合征23例临床分析

目的探讨肝肺综合征（HPS）的临床特点及常见影响因素。方法回顾性分析我院确诊为乙肝肝硬化的患者临床数据,应用血气分析仪测定其动脉血氧分压。结果乙肝肝硬化患者89例,其中23例合并HPS,发生率25．84％。肝硬化患者并发HIS与杵状指、发绀、黄疸、肝掌、蜘蛛痣、肝性脑病、腹水、门静脉增宽和消化道出血等无关（P〉0．05）;与并发肝肾综合症（x2=7．432,P=0．006）、发绀（r=3．543,P=0．06）和Child．pugll分级有关（x2=0．914,P=0．010）。结论临床上Child—pughB级和C级肝硬化中并发肝肾综合征、发绀的患者须注意HPS的发生,应及时并采取相应的治疗措施。     

76例急性胰腺炎护理体会

急性胰腺炎(acute pancreatitis,AP)是由各种致病因素所导致的胰酶在胰腺内被激活,从而引起胰腺自身组织和周围组织的消化、水肿、出血甚至坏死的炎性反应。临床上表现为急性上腹部的疼痛、恶心、呕吐、发热等症状,实验室检查发现血尿中的胰酶增高,B超及CT可见胰腺组织溶解改变等。     

重症急性胰腺炎合并真菌感染的分布情况及防治

目的 探讨重症急性胰腺炎(severe acute pancreatitis,SAP)合并深部真菌感染(deep funsal infection,DFI)的特点和防治方法.方法 回顾性分析新疆维吾尔自治区人民医院2011年3月至2013年3月收治的97例SAP合并DFI患者的临床资料.结果 97例SAP合并DFI的患者中,常规治疗组和预防治疗组的死亡率分别为43.24％和21.56％,未治疗组患者全部死亡,组间两两比较差异有统计学意义(P＜0.05);其中以真菌引起的呼吸系统感染和泌尿系统感染为主,分别为35例(36.08％)和21例(21.64％);并且所感染的真菌中,以白色念珠菌和克柔假丝酵母菌居多,分别为49例(50.51％)和17例(17.52％).结论 DFI是重症急性胰腺炎的常见并发症,病死率较高,临床中应早期诊断,及时合理的抗真菌治疗.氟康唑可作为首选的抗真菌药物.     

1例急性马拉硫磷中毒并发急性胰腺炎的护理

马拉硫磷属低毒类有机磷农药,中毒后常并发心肌炎、肝脏损害、肾脏损害、肺水肿、脑水肿、胰腺炎、上消化道出血、中间型综合征、迟发性多发性神经病等．其中,并发急性胰腺炎少见,如不及时治疗,后果严重。我科近期收治1例急性马拉硫磷中毒并发急性胰腺炎患者．经过有效的治疗、精心的护理．效果满意,现将护理报告如下。     

益生菌与重症急性胰腺炎

重症急性胰腺炎（SAP）病情危重,病死率高,发病机制复杂,至今未完全阐明。在病程的第1周,由于全身炎症反应综合征引起多器官功能障碍,在病程的第1—3周,由于感染和菌血症引起第2个死亡高峰,占病死率的80％。目前认为细胞因子的过度生成和肠屏障功能损伤导致肠内细菌移位,是发生胰腺坏死感染的主要原因。针对此类感染的早期抗生素预防治疗一直存在争议,而且大量长期的抗生素应用易导致细菌的抗药性及真菌的过度生长。     

重症急性胰腺炎合并腹腔感染的感染特点和相关因素分析

目的 探讨重症急性胰腺炎（SAP）合并腹腔感染的感染特点及其相关因素分析。方法 回顾性分析2008年1月至2015年6月我院收治的125例SAP患者的临床资料,分析腹腔感染细菌菌谱的特点及影响腹腔感染发生的危险因素。结果 125例患者中48例（38.40%）合并腹腔感染,死亡12例（9.60%）。共培养出病原菌92株,其中革兰阴性菌61株（66.30%）,革兰阳性菌25株（27.17%）和真菌6株（6.52%）。单因素分析显示病因、APACHEⅡ评分、合并多器官功能障碍综合征（MODS）、外科干预及全肠外营养时间与SAP发生腹腔感染有关（P0.05）。多因素分析结果显示,APACHE Ⅱ评分≥11、合并MODS、全肠外营养时间≥1周是SAP发生腹腔感染的独立危险因素（P<0.05）。结论 SAP合并腹腔感染多为多重感染,以革兰阴性菌感染为主。APACHE Ⅱ评分≥11、合并MODS、全肠外营养时间≥1周的SAP患者,易并发腹腔感染。     

ERCP治疗急性胆源性胰腺炎86例胆汁细菌培养及药敏分析

目的了解急性胆源性胰腺炎（ABP）患者胆汁中主要致病菌的分布及其耐药情况,为临床治疗提供理论依据和治疗指导。方法选取2008年6月至2013年2月平顶山市第一人民医院消化内科收治的经内镜逆行胰胆管造影（EndoscopicRetrogradeCholangio—Pancreatography,ERCP）治疗的ABP患者86例,对术中抽取的胆汁标本行细菌培养和药敏试验,回顾性分析其临床结果。结果86例送检标本中,共检出76株病原菌,检出率为88．4％,胆汁感染的革兰阴性菌以大肠埃希菌为最多,革兰阳性菌以粪肠球菌最多;厌氧菌以感染脆弱类杆菌、产气荚膜梭菌等为主。结论ABP胆汁感染检出率高,致病菌种类与肠道细菌的种类基本一致,在胆汁细菌培养和药敏结果明确之前应尽量选用广谱的抗生素联合、足量用药;如药敏结果明确,则可根据治疗效果或药敏结果调整抗生素继续治疗,以提高疗效,避免浪费。     

Protective effect of colchiceine against acute liver damage

Pretreatment of rats with colchiceine (10 micrograms/day/rat) for seven days protected against CCl4-induced liver damage. CCl4 intoxication was demonstrated histologically and by increased serum activities of alanine amino transferase (ALT), alkaline phosphatase (Alk. Phosph.) gamma glutamyl transpeptidase (GGTP), bilirubins and decreased activity of glucose-6-phosphatase (G-6Pase). Furthermore, an increase in liver lipid peroxidation and a decrease in plasma membrane GGTP and Alk. Phosph. activities were found. Colchiceine increased 1.5-fold the LD50 of CCl4 and prevented the release of intracellular enzymes as well as the decrease in GGTP and Alk. Phosph. activities in plasma membranes. It also completely prevented the lipid peroxidation induced by CCl4 and limited the extent of the histological changes.     

柴芩承气汤对重症急性胰腺炎并发肝损伤大鼠的治疗作用及其机制

目的：研究柴芩承气汤（CQCQD）对重症急性胰腺炎（SAP）并发肝损伤大鼠的治疗作用及其机制。方法：72只SD大鼠随机分为3组（n=24）：假手术（sham）组,重症急性胰腺炎模型（SAP）组和柴芩承气汤治疗（CQCQD）组。去氧胆酸钠胰胆管逆行注射建立SAP大鼠模型,CQCQD组给予柴芩承气汤治疗,于造模后1 h、5 h、10 h观察各组不同时间点的胰腺、肝脏组织病理学变化,检测血清中淀粉酶（AMS）、丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）活性、白介素-6（IL-6）水平及胰腺、肝脏组织单核细胞趋化蛋白-1（MCP-1）和IL-6 mRNA的表达情况。结果：与sham组比较,SAP组血清AMS、ALT、AST活性及IL-6水平明显升高,胰腺、肝脏组织MCP-1及IL-6 mRNA表达升高（P<0.05）;与SAP组比较,CQCQD组血清AMS、ALT、AST活性及IL-6水平明显降低;胰腺和肝脏组织病理损伤减轻,胰腺、肝脏组织MCP-1及IL-6 mRNA表达明显减弱（P<0.05）。结论：MCP-1参与了SAP并发肝损伤的进展;柴芩承气汤能显著抑制胰腺、肝脏组织MCP-1的表达,减轻SAP时胰腺、肝脏组织病理损伤,对SAP并发肝损伤起到治疗作用。     

Vasoactive intestinal peptide promotes gut barrier function against severe acute pancreatitis

To explore the influence of vasoactive intestinal peptide (VIP) on the gut barrier function in severe acute pancreatitis (SAP). Fifty four SD rats were randomly divided into three groups: sham operated (SO) group, SAP group and VIP intervention group. Each group was further divided into three time points: 1, 6 and 12 h after operation with 6 rats for each treatment point. SAP models were induced by retrograde injection of 4% sodium taurocholate into the bili-pancreatic duct. VIP intervention group was made by 5 nmol VIP intraperitoneal injection within 5 min after SAP model successfully obtained. The VIP in plasma and intestinal homogenate were detected with ELISA. The endotoxin in plasma of all groups was also tested. The expression levels of TLR4, TNF-α, IL-6, and IL-10 in gut mucosa were measured by RT-PCR. Meanwhile intestinal samples were harvested for pathological examination. Compared to SO group, the VIP in plasma and intestinal homogenate of SAP group were significantly decreased at 1 h after induction, and then gradually increased to beyond the level of SO group at 12 h. The endotoxin of SAP group was continually increased. The mRNA levels of TLR4, TNF-α, IL-6, and IL-10 were also increased with obvious pathological injuries in the intestine. In the VIP group, endotoxin in plasma was obviously decreased compared to SAP group. The expressions of TNF-α, IL-6 mRNA were suppressed while IL-10mRNA was increased. The intestinal pathological injuries were also markedly alleviated. These results suggested that VIP had protective effects on SAP gut barrier function through inhibiting intestinal mucosal inflammatory responses.     

益生菌联合大豆卵磷脂保健食品对亚急性酒精性肝损伤的辅助保护功能评价

目的研究益生菌联合大豆卵磷脂保健食品对亚急性酒精性肝损伤的辅助保护作用。方法实验动物选用50只180~220g SPF级SD雄性大鼠,按体重随机分成5个组,分别为0.355g/(kg BW·d)、0.710g/(kg BW·d)、2.130g/(kg BW·d)、正常对照组和模型对照组。各剂量组经口灌胃给予受试物,正常对照组和模型对照组给予蒸馏水。17d后,模型对照组和3个剂量组每天在给予样品4h后给予30%乙醇,按10mL/kg BW给予染毒,正常对照组给予等量蒸馏水,连续14d。实验结束后,将各组动物称重,摘眼球取血,分离血清,测定TBIL、LDL-C、TC,同时处死动物,取肝脏进行组织病理学检查。结果模型对照组大鼠的血清TC、TBIL和LDL-C含量均高于正常对照组,差异有统计学意义(P0.05);样品各剂量组的血清TC、TBIL和LDL-C含量均低于模型对照组,差异有统计学意义(P0.05)。肝脏组织病理学检查,3个剂量组与模型组比较,肝细胞损伤程度均有明显降低。结论益生菌联合大豆卵磷脂保健食品对亚急性酒精性肝损伤有辅助保护功能。     

Ultrastructural changes in rat liver in early stages of experimental acute pancreatitis]

Morphologic disorders in the liver during the acute pancreatitis are an important aspect of multiorgan disturbances seen in this disease. The study aimed at evaluating ultrastructural disorders in the of the experimental pancreatitis. The study involved 24 male Wistar rats. The acute experimental pancreatitis has been produced by the injection of a 5% sodium taurocholate during sterile laparotomy. Samples for examination have been taken after 1, 3, 6, and 12 hours. Collected samples have been examined systematically. Mitochondrial pleomorphism, partial RER degranulation, decrease in glycogen content, and autophagocytosis have been noted already within 1 and 3 hours. The degree of these disorders has increased within 6 hours, reaching its peak after 12 hours. Marked degeneration of mitochondria, high autophagocytosis, nearly complete disappearance of glycogen, impaired sinusal endothelium, and Kupffer's cells stimulation, in which increased phagocytic activity has been noted made a complete picture of the ultrastructural disorders. Such morphologic changes in the liver have indicated its damage in the early stages of the acute pancreatitis. It may be of importance for the development of multiorgan complications of this disease.