原位肝移植术后胆管狭窄的诊断和治疗

目的探讨原位肝移植术后胆管狭窄的诊断和治疗方法。方法利用胆道内镜技术，对14例原位肝移植术后发生的胆管狭窄进行了诊断和分析；采取球囊扩张后支撑管支撑狭窄的方法进行治疗。结果经胆道造影和内镜综合诊断胆管吻合口狭窄13例（92．86％，其中1例是结石导致的狭窄假象）；非吻合口狭窄1例（进行了2次肝移植）。通过胆道造影明确诊断的4例吻合口狭窄中，1例采取球囊扩张1次治愈，2例行经内镜十二指肠乳头括约肌切开术＋网篮取石＋鼻胆引流术后仍然发生胆系感染和黄疸而行手术以及纤维胆道镜治疗，1例2次肝移植术后发生急性排斥反应而死亡。通过T型管造影，1例发现条状负影，无狭窄，纤维胆道镜观察胆管吻合口愈合佳，黏膜移行良好；2例肝内显影差或不显影而呈胆管消失改变，纤维胆道镜取净结石后，扩张吻合口的狭窄后用支撑管分别支撑3、4个月时狭窄消失，黏膜移行良好，拔管治愈；8例肝内外胆管显影模糊，肝外和肝内Ⅰ、Ⅱ级胆管有条索状、柱状、树枝状负影和非吻合性狭窄征象，纤维胆道镜观察取净结石后观察吻合口处均有不同程度的狭窄、充血水肿，扩张支撑平均2．5个月后，镜下观察狭窄消失，黏膜移行佳；1例造影提示吻合口狭窄，经扩张后，内镜观察未发现结石，支撑2个月后拔管治愈。结论应用胆道内镜诊断胆管狭窄直观可靠。胆道狭窄扩张支撑后拔管的标准为：T型管造影通畅无狭窄，内镜观察狭窄环消失，吻合口处黏膜移行。通过内镜技术治疗胆管狭窄具有微创、安全、有效和方便等优点。     

Acute renal failure due to xanthine stones

A 9-month-old child with the skeletal abnormalities of Fuhrmann's syndrome presented with acute renal failure secondary to bilateral renal calculi. Hereditary xanthinuria was shown to be the underlying metabolic defect. Treatment with allopurinol was unsuccessful at reducing the xanthine excretion.     

Management of malignant biliary stricture with self-expanding metallic stent

Background: Self-expanding metallic mesh stents are designed to remain patent longer than polyethylene (PE) stents, which generally clog in 3 to 4 months. Though more expensive, metal stents may therefore be a better choice for malignant strictures. Methods: From January 1991 to October 1995, we performed ERCP in 212 patients with malignant or benign strictures, and 34 ultimately had insertion of a metallic stent. These stents were placed by the percutaneous transhepatic route in 17 patients and endoscopically in 17. Results: Metallic stent insertion was successful in each case and relieved the preoperative jaundice and cholangitis. There were no procedure-related deaths; complications were pancreatitis (one) and hemorrhage (one). Overall stent patency was 6.2 months. Three of 34 stents occluded due to tumor ingrowth at 3, 4.5, and 8 months and were treated by placing a new PE stent through the blocked metal stent. The remaining 31 stents remained patent until patient death (n= 15, mean survival = 4.9 months) or are still open (n= 16, mean patency = 12.2 months). Conclusions: Self-expanding metal stents provide effective palliation of malignant biliary strictures and should be considered an alternative to open surgery. Metal stents remain patent much longer than PE stents and usually a single session of metal stenting can palliate biliary obstruction for life. Received: 20 March 1996/Accepted: 9 May 1996     

美国2021版《妊娠期肾结石诊治-单中心多学科指南》解读——提高临床诊断能力，加强多学科协作管理

妊娠期肾结石是妊娠期患者非产科因素住院的常见病因,容易出现疼痛、恶心、呕吐、肾功能下降、泌尿道感染等并发症,处理不当会导致流产、早产等不良妊娠结局。美国医学中心多学科联合发布《妊娠期肾结石诊治-单中心多学科指南》,以规范妊娠期肾结石的诊治。本指南共形成10个指南推荐意见,其中4个用于指导诊断和影像学检查,6个用于指导临床治疗。值得关注的是,与国内指南相比,该指南提供了循证依据,证实了妊娠期使用低剂量CT平扫的安全性、有效性,并可以在患者病情变化且诊断不明确时优先使用,本文就以上内容对该指南展开深度解读。     

肾盂加肾后唇实质段间线切开治疗巨大鹿角形肾结石(附24例报告)

目的：探讨。肾内型。肾盂并发巨大鹿角型。肾结石的手术疗效。方法：采用。肾盂加。肾后唇实质段间线切开取石术治疗24例25侧巨大鹿角型。肾结石。结果：本组手术顺利取尽结石者22例23侧。肾，术后。肾内残留小结石（直径〈5mm）2例，经ESWL治愈。随访3个月，25侧术。肾功能良好。结论：该术式不阻断。肾蒂，操作简单，出血少，取石干净，对肾功能影响小，是治疗巨大鹿角型。肾结石较理想的手术方法之一。     

34例鹿角形肾结石手术取石的疗效观察

目的探讨肾下极肾盂肾盏联合切开术治疗复杂性鹿角形肾结石的疗效。方法回顾性分析采用肾下极肾盂肾盏联合切开术式治疗复杂性鹿角形肾结石34例临床资料。手术方法:分离肾窦内肾盂后,用1-0肠线在肾后唇中下1/3连接处紧贴肾盂肾盏表面缝合肾实质2针,中间尖刀切开肾实质,然后弧形切开肾盂及肾下盏,用神经剥离子将结石与肾盂肾盏粘膜粘连分离后,取石钳夹住结石轻轻撬出。盏颈狭窄者必要时先用气压弹道碎石器将其在分支处击断。4-0肠线缝合肾盂及肾下盏,再用2-0肠线间断全层缝合肾实质切口数针,包膜层用4-0肠线缝合。结果34例均一次性取净结石。术中平均出血量约90ml。术后无大出血病例。结论肾下极背侧肾实质与肾盂联合切开取石术具有术中出血少,无须阻断肾蒂,肾功能受损轻,便于一次取尽结石等优点。适合于肾窦内肾盂特别是肾下盏盏颈相对狭窄的复杂性鹿角形肾结石的治疗。     

Fine-needle aspiration biopsy of hepatic papillary cystadenocarcinoma in Caroli's disease.

A case of papillary adenocarcinoma arising in Caroli's disease (CD) in a 25-yr-old woman is reported. The diagnosis of malignancy was made by ultrasound-guided, fine-needle aspiration biopsy (FNAB). As there were no metastasis, a liver transplant was performed and the diagnosis was histologically confirmed. Only 22 cases of malignant transformation of CD have been reported to date, all among middle-aged subjects (mean age: 52 yr) of both sexes. Most of these reported cases (83%) were found to be bile duct adenocarcinomas with occasional reports of hepatocellular and undifferentiated carcinomas. Our case is the youngest reported to date and the first to be diagnosed cytologically.     

Analysis of proliferating biliary epithelial cells in human liver disease using a monoclonal antibody against DNA polymeraseα

The proliferative activity and ultrastructural characteristics of proliferating biliary epithelial cells were analysed immunohistocytochemically in 39 biopsied liver specimens from patients with acute viral hepatitis, chronic hepatitis and liver cirrhosis using a monoclonal antibody against DNA polymerase (DNA-PA). In acute viral hepatitis with perivenular confluent necrosis, proliferation of typical bile ducts was found frequently in portal areas. In chronic aggressive hepatitis and cirrhosis, ductular proliferation of both typical and atypical forms was found in enlarged portal and periportal areas and in confluent necrotic areas. The number of proliferating biliary epithelial cells that stained positive for DNA-PA was small. There were very few positively stained cells in atypical bile ducts in confluent necrotic areas of cirrhosis. Atypical bile ducts seen in chronic aggressive hepatitis, cirrhosis and acute hepatitis with confluent necrosis were positively stained for both cytokeratins 8 and 19. In cirrhosis, the number of stained biliary epithelial cells in typical bile ducts was larger than the number of such cells in atypical bile ducts (P< 0.01). By electron microscopy, the cells positively stained for DNA-PA were mostly so-called clear cells with irregular nuclei containing coarse nucleoplasm, and a few small cells with scanty cytoplasm and few organelles.     

Gemfibrozil absorption and elimination in kidney and liver disease

Summary The disposition of the lipid-lowering drug gemfibrozil was studied in patients with either renal (n= 8) or hepatic disease (n= 8) and compared to those of healthy volunteers (n= 6). Gemfibrozil was determined in plasma and urine by means of a HPLC method. Urine was also analyzed for gemfibrozil conjugates.Following oral administration of 900 mg gemfibrozil, maximal plasma levels of the parent drug were 46.1±15.8 g/ml, attained after 2.2±1.1 h. In chronic renal failure and in liver cirrhosis the plasma concentrations of gemfibrozil did not significantly differ from that of controls except in those patients who were comedicated with antacids. These patients had significantly lower C_max and AUC values. The elimination half-life of the drug was 1.5 h in controls, 2.4 h in renal failure, and 2.1 h in liver disease. In healthy volunteers, only 0.02 to 0.15% of the given dose was recovered in the urine as parent gemfibrozil, while conjugates made up 7–14%. In patients with renal failure also, only traces of parent gemfibrozil could be detected, and conjugates accounted for 0.5–9.8%. In those with liver disease, however, about 0.1–0.2% were recovered in urine as parent gemfibrozil and up to 50% as conjugates. Strikingly, the amount of excreted conjugates in the urine was positively correlated to the direct bilirubin plasma concentration. It can be concluded that the elimination of gemfibrozil is not significantly influenced by renal failure. However, comedication with antacids markedly reduced plasma disposition of the drug. Patients with severe liver disease excreted more conjugated gemfibrozil via the kidney than did healthy controls. Thus, transfer across the canalicular cell membrane to the bile duct, rather than drug metabolization, is primarily disturbed in liver disease. Gemfibrozil accumulation is unlikely to occur in either kidney or liver disease.Abbreviations Cl_r creatinine clearance (ml/min) - HPLC high pressure liquid chromatography - C_max maximal plasma concentration (g/ml) - t_max time (h) after which C_max is attained - k_e elimination rate constant (h^–1) - t_1/2 elimination half-life (h) - A_e amount of drug excreted into the urine (% of given dose) - MRT mean residence time (h) - AUMC area under the first moment curve (g h²/ml) - AUC area under the plasma level time curve (g·h/ml) - ANOVA analysis of variance The paper is gratefully dedicated to G.W. Löhr     

Differences in gallstone structure in primary common bile duct lithiasis and gallbladder lithiasis

Summary Some differences between gallbladder lithiasis and primary common bile duct lithiasis are described. Microbiological cultures and biochemical analyses were carried out on the bile of two groups of patients: 27 suffering from gallbladder and 5 from primary common duct lithiasis. The microstructure and composition of gallstones were also examined by polarized light microscopy and X-ray diffraction. Women predominated in gallbladder lithiasis but not in primary common duct lithiasis group (P<0.05) and body weight was higher in the former group (P<0.02). Primary common duct lithiasis patients had a higher, although not significant, incidence of duodenal diverticulosis (P=0.15), and a higher incidence ofE. coli-positive cultures in bile (P<0.001). No significant difference in the biochemical composition of the bile was found between the groups. Brown pigment stones predominated in primary common duct lithiasis, while cholesterol stones did in gallbladder and secondary common duct lithiasis (P<0.0001). Stones formed in the gallbladder generally show linear, radial growths of cholesterol crystals, while those from the common duct present a polystratified, concentric deposition of microgranules composed mainly of pigmentary salts.These differences should be taken into account as additional criteria in the differential diagnosis between primary and secondary common duct lithiasis, as the classical criteria for diagnosing of the former greatly underestimate its actual incidence. The distinction between primary and secondary common duct lithiasis is of practical significance, since each entity requires different treatment.Abbreviations CBD common bile duct - CBDL common bile duct lithiasis - ERCP endoscopic retrograde cholangiopancreatography - GBL gallbladder lithiasis - HDL high density lipoproteins - PCBDL primary common bile duct lithiasis - SCBDL secondary common bile duct lithiasis - SGOT serum glutamic-oxalacetic transaminase - SGPT serum glutamic-pyruvic transaminase