水通道蛋白2在梗阻性黄疸大鼠肾脏表达变化的实验研究

目的:明确水通道蛋白2(AQP2)在梗阻性黄疸大鼠肾脏表达变化及其与尿素氮(BUN)和肌酐(Cr)变化的关系。方法:采用手术结扎胆总管的方法造成实验大鼠梗阻性黄疸模型,于术后3、5、7、10、14 d处死大鼠取血和肾脏标本,检测血浆直接胆红素、尿素氮和肌酐值,光镜下观察肾脏病理形态学,免疫组化方法检测肾脏APQ2表达。结果:实验组3 d时光镜下见肾集合管上皮细胞排列不规则肿胀,5 d时可见细胞水样空泡变性、并且梗阻性黄疸组AQP2表达较对照组明显减少。7 d时见部分细胞脱落、间质有炎性细胞浸润,10和14 d时见局灶上皮细胞坏死、胞浆崩解、间质有大量炎性细胞浸润。水通道蛋白2表达在梗阻5 d后较对照组明显减少(P0.05),随着梗阻时间延长,其表达减少愈加明显。AQP2表达减少的同时,肾形态学损害在光镜下从肾集合管形态学改变得到证实。梗阻性黄疸组术后10 d Cr开始升高,梗阻14 d后BUN开始升高。结论:AQP2的减少表明肾功能发生损害,AQP2减少在前,CR和BUN增加在后,所以AQP2作为肾功能损害的早期检测指标是很有意义的。     

一氧化氮和内毒素在梗阻性黄疸致病机制方面的作用

梗阻性黄疸（obstructive jaundice）是临床常见的表现。梗阻性黄疸患者术后并发症和死亡率较高，常死于感染和败血症，提示机体术前的免疫功能受到了抑制。梗阻性黄疸可使网状内皮系统功能降低，细菌清除能力减弱。肠道来源的细菌和内毒素逃脱肝脏枯否细胞的监视，进入血液循环。有研究发现梗阻性黄疸常并发肠源性内毒素血症，内毒素激活枯否细胞，产生大量炎性介质，如一氧化氮（NO），肿瘤坏死因子α（TNFα）及氧自由基等。     

Predictor factors for choledocholithiasis

Background

The choledocolithiasis has an incidence of 8-20% in patients with cholecystolithiasis. The preoperative diagnosis guides the interventional treatment on the bile duct

Aim

To evaluate the sensitivity and specificity of the laboratory markers and imaging studies for choledocholithiasis preoperatively.

Methods

The study comprised 254 patients divided into two groups: the control group (207 patients), patients without choledocholithiasis intraoperatively and cases group (47 patients), that enrolled the patients with choledocholithiasis intra-operatively. Were evaluated the laboratory markers, image exams and intra-operative diagnostic aspects.

Results

The sample was homogeneous for age and gender. It was observed that 47% of the cases the patients did not show comorbidities. Hospitalization showes in cases group acute pancreatitis in12.8%, jaundice in 30%, fever in 30% and pain in the right hypochondrium in 95%. By comparing them, was observed that fever and jaundice were the signs and symptoms with statistical significance. Patients with choledocholithiasis had transaminases, alkaline phosphatase, gamma-glutamyl transferase and higher bilirubin with statistical significance (p<0.001). In regard to imaging studies, ultrasound was fairly accurate for cholelithiasis and choledocholithiasis (p<0.001).

Conclusion

Changes in canalicular and transaminase enzymes are suggestive for preoperative choledocholithiasis; GGT showed better sensitivity and alkaline phosphatase greater specificity; ultrasonography and nuclear magnetic resonance cholangiopancreatography showed high specificity.     

梗阻性黄疸患者实施经皮经肝胆道引流术后胆道感染的相关因素研究

目的探讨梗阻性黄疸患者接受经皮经肝胆道引流术(PTCD)并发胆道感染的相关因素。方法回顾性分析2012年2月至2014年7月期间在我院接受PTCD的170例梗阻性黄疸患者的临床资料,对PTCD术后的影响因素进行统计学分析。结果 170例梗阻性黄疸患者中,35例出现了术后感染,感染率为20.59%。单因素分析发现患者年龄、术前黄疸天数、术前KPS评分、术后每日引流量、术前ALT、ALP、TBIL是术后感染的危险因素,差异有统计学意义(P0.05)。对上述危险因素进行logistic回归分析发现,术前黄疸时间长、ALP水平过高是PTCD术后感染的危险因素,而术后引流良好是PTCD的保护因素。结论对于要实施PTCD手术的患者,加强术前的评估和术后管理对预防及控制感染有重大意义,早期的实施手术及良好的术后引流有助于降低术后感染,改善患者的预后。     

Infantile pyknocytosis,a rare cause of hemolytic anemia in newborns: report of two cases in twin girls and literature overview

Infantile pyknocytosis is a rare cause of neonatal jaundice and hemolytic anemia. We report on two cases in twin girls that were diagnosed on peripheral blood smear reading. Pyknocytosis should be considered in cases of early unexplained severe hemolytic anemia, and systematic peripheral smear review performed. Its management consists of phototherapy and RBC transfusion.     

肝细胞型胆汁淤积诊治进展

胆汁淤积是由于肝内外胆管阻塞或肝细胞功能障碍所致的胆汁不能到达十二指肠而在肝细胞和血液积聚的一种病理学状态。肝细胞是胆汁合成和分泌的主要场所。当肝细胞上的胆盐输出泵(bile salt export,BSEP)、ATP结合盒(ATP-binding cassette,ABC)转运蛋白、多耐药相关蛋白2(multidrug resistance-associated protein,MRP2)功能障碍或受抑制,则可导致胆汁酸或其结合胆盐在肝细胞和血清中聚积引起肝细胞型胆汁淤积[1]。引起肝细胞型胆汁淤积的常见病因包括细菌、病毒、真菌和寄生虫等感染、酒精或非酒精性脂肪性肝炎、自身免疫性或药物相关性肝损伤、全胃肠外营养、重症相关(缺血性)肝内胆汁淤积、良性复发性肝内胆汁淤积(benign recurrent intrahepatic cholestasis,BRIC)、进展性家族性肝内胆汁淤积(progressive familial intrahepatic cholestasis,PFIC)、ABCB4基因缺乏、妊娠期肝内胆汁淤积(intrahepatic cholestasis of pregnancy,ICP)、霍奇金病、转移性肿瘤、肉芽肿性肝炎和肉芽肿病、血管性疾病(如布加综合征和肝窦阻塞综合征)和各种原因的肝硬化等[2]。     

Preoperative biliary drainage of severely obstructive jaundiced patients decreases overall postoperative complications after pancreaticoduodenectomy: A retrospective and propensity score-matched analysis

ObjectivesThe influence of preoperative biliary drainage (PBD) for obstructive jaundiced patients before pancreaticoduodenectomy is debated in the past decades. The aim of this study is to assess the impact of preoperative biliary drainage on intraoperative and postoperative outcomes in patients with severely obstructive jaundice.MethodsData were collected retrospectively from severely obstructive jaundiced patients with serum total bilirubin level exceeding 250 μmol/L and undergoing pancreaticoduodenectomy from January 2012 to December 2017. The univariate and multivariate analyses were performed to assess independent risk factors for overall postoperative complications. A propensity score-matched (PSM) analysis was performed to adjust baseline characteristics between PBD and direct surgery (DS) groups. After PSM, intraoperative data and postoperative complications were compared between the two groups.ResultsA total of 200 patients were included. The rate of overall postoperative complication occurred in 119 (59.5%) patients, with prealbumin <150 mg/L (OR = 3.03; 95%CI = [1.63–5.62]; p < 0.001), ASA (American Society of Anesthesiology score) classification II-III (OR = 2.27; 95%CI = [1.21–4.27]; p = 0.011), and direct surgery (OR = 3.88; 95%CI = [1.67–8.99]; p = 0.002) identified as independent risk factors in multivariate analysis. After PSM, there was similar operative time and intraoperative transfusion between PBD and DS group. However, DS group had a higher incidence of overall postoperative complication (p = 0.005), grades B and C of post-pancreatectomy hemorrhage (PPH) (p = 0.032), and grades B and C of postoperative pancreatic fistula (POPF) (p = 0.045) compared to PBD group.ConclusionsIn this retrospective study, in order to reduce overall postoperative complications, PBD should be performed routinely for those patients with serum total bilirubin level exceeding 250 μmol/L and undergoing pancreaticoduodenectomy.     

Destruction of the hepatocyte junction by intercellular invasion of Leptospira causes jaundice in a hamster model of Weil's disease

Weil's disease, the most severe form of leptospirosis, is characterized by jaundice, haemorrhage and renal failure. The mechanisms of jaundice caused by pathogenic Leptospira remain unclear. We therefore aimed to elucidate the mechanisms by integrating histopathological changes with serum biochemical abnormalities during the development of jaundice in a hamster model of Weil's disease. In this work, we obtained three‐dimensional images of infected hamster livers using scanning electron microscope together with freeze‐cracking and cross‐cutting methods for sample preparation. The images displayed the corkscrew‐shaped bacteria, which infiltrated the Disse's space, migrated between hepatocytes, detached the intercellular junctions and disrupted the bile canaliculi. Destruction of bile canaliculi coincided with the elevation of conjugated bilirubin, aspartate transaminase and alkaline phosphatase levels in serum, whereas serum alanine transaminase and γ‐glutamyl transpeptidase levels increased slightly, but not significantly. We also found in ex vivo experiments that pathogenic, but not non‐pathogenic leptospires, tend to adhere to the perijunctional region of hepatocyte couplets isolated from hamsters and initiate invasion of the intercellular junction within 1 h after co‐incubation. Our results suggest that pathogenic leptospires invade the intercellular junctions of host hepatocytes, and this invasion contributes in the disruption of the junction. Subsequently, bile leaks from bile canaliculi and jaundice occurs immediately. Our findings revealed not only a novel pathogenicity of leptospires, but also a novel mechanism of jaundice induced by bacterial infection.