小儿胆汁性腹膜炎27例诊断与治疗

目的　探讨小儿胆汁性腹膜炎的病因 ,提高小儿胆汁性腹膜炎的诊治水平。方法　对 2 7例小儿胆汁性腹膜炎的病因与诊治进行回顾分析。结果　 2 7例中 17例手术中发现穿孔灶 ,行胆总管引流和腹腔引流 ,合并胆道扩张症作二期根治术 ;未明确穿孔灶 10例 ,作腹腔引流 ,合并胆道扩张症作一期根治术。无手术死亡及严重并发症 ,疗效满意。其中婴幼儿 6例 (2 2 .2 % ) ,儿童 2 1例 (77.8% )。病因多与胆总管囊肿 (6 2 .9% )、胆道结石与蛔虫 (7.4% )、经皮肝穿刺胆道造影 (PTC)损伤 (3 .7% )等有关 ,部分原因不明 (2 2 .2 % )。结论　小儿胆汁性腹膜炎容易误诊 ,掌握其临床特点、提高诊断意识及选择合适的手术方法 ,是提高早期诊断率和减少并发症的关键。     

术中胆道造影在小切口胆囊切除术中的应用价值

目的 探讨术中胆道造影在小切口胆囊切除术中的应用价值。方法 小切口胆囊切除术中经胆囊管和胆总管穿刺行胆道造影５００例。结果 术中造影发现胆道结石４２例。结论术中胆道造影安全方便,胆道系统解剖清晰,对预防术后残余结石,避免胆道损伤,降低术后并发症,提高胆囊手术质量有较好的应用价值。     

重型胆源性胰腺炎术后死亡原因分析

目的：分析重型胆源性胰腺炎的死亡原因,方法：对我院自１９８８年４月至１９９８年１２月间行早期手术的重型胆源性胰腺炎６３例,术后死亡２６例作回顾性分析,结果：术后３ｄ内死亡１２例,其余术后２４ｄ死亡,死亡主要原因为休克、ＡＲＤＳ等。结论早期手术仍有较高的病死亡率。     

Serological markers of rheumatoid arthritis in patients with primary biliary cholangitis and the vice versa: A Tunisian study

BackgroundPrimary biliary cholangitis (PBC) is an autoimmune disease of the liver characterized by destructive lymphocytic cholangitis and anti-mitochondrial antibodies (AMA). Anti-gp210 and anti-Sp100, are used for the diagnosis of PBC in AMA-negative PBC patients. Patients with PBC have a propensity to have an extrahepatic manifestation which is especially autoimmune.ObjectiveWe aimed to determine the frequency of serological markers of rheumatoid arthritis (RA) (CCP-Ab or RF) in PBC patients and to do the vice versa.MethodsOur PBC study included 70 patients with PBC and 80 healthy blood donors (HBD) and our RA study included 75 patients with RA and 75 HBD. Anti-cyclic citrullinated peptide antibodies (CCP-Ab) and rheumatoid factor (RF) were performed by indirect ELISA. AMA, anti-Sp100 and anti-gp210 were determined by indirect immunofluorescence.ResultsRA autoantibodies (CCP-Ab or RF) were more frequent in PBC patients than in HBD (65.7% vs. 8.7% p 〈1 0 ⁻⁶). CCP-Ab were significantly more frequent in patients than in controls (15.7% vs. 2.5%; p = 0.004). Nine patients had both CCP-Ab and RF vs. none of controls (12.8% vs. 0%; p = 0.001). RF were detected in 45 patients with PBC and in 5 HBD (64.3% vs. 6.2%; p 〈1 0 ⁻⁶). In PBC patients, RF were more frequent than CCP-Ab (64.3% vs. 15.7%; p 〈1 0 ⁻⁶). RF-IgG were present in 18.5% of patients; RF-immunoglobulin (Ig) A in 34.3% and RF-IgM in 54.3%. These frequencies were significantly higher than those found in control group (1.2% for RF-IgG (p 〈1 0 ⁻³); 0% for RF-IgA (p 〈1 0 ⁻⁶); and 6.2% for RF-IgM (p 〈1 0 ⁻⁶)). In our PBC patients, RF-IgA were more frequent than RF-IgG (34.3% vs. 18.5%; p = 0.03) and than CCP-Ab (34.3% vs. 15.7%; p = 0.01). Six patients had only RF-IgA versus none of the control group (8.6% vs. 0%; p = 0.01). AMA, anti-Sp100 and anti-gp 210 were absent in all RA patients.ConclusionsSerological markers of RA were more frequent in PBC patients than in HBD and the vice versa was not true.     

Extensive Biliary Excretion of the Model Opioid Peptide [D-PEN2,5] Enkephalin in Rats

Purpose. This study was designed to test the hypothesis that the enzymatically stable opioid peptide, [D-pen^2,5] enkephalin (DPDPE), is excreted extensively into bile. Methods. Following an i.v. bolus dose of DPDPE (10 mg/kg) to rats, concentrations of DPDPE in serum, bile, liver homogenate and urine were measured by a novel capillary zone electrophoresis method. Data were analyzed to recover the fundamental pharmacokinetic parameters (volumes of distribution; distribution and elimination rate constants governing DPDPE systemic and biliary disposition). Parallel in vitro experiments were performed to evaluate the partitioning of DPDPE between erythrocytes and plasma, as well as to assess the degree of binding of DPDPE to serum proteins. Results. The majority of the administered dose (~80%) was recovered from bile as intact peptide. DPDPE disposition was best described by a two-compartment model with Michaelis-Menten elimination (K_m: 37.5 ± 11 g/ml; V_max: 1143 ± 368 g/min/kg) from the central compartment into bile, suggestive of an active hepatic transport system. DPDPE was associated with a distributional space of 486 ± 62 ml/kg. In vitro incubation of DPDPE with whole blood showed that ~65% of the peptide was associated with erythrocytes. The difference between concentrations of DPDPE in erythrocytes and plasma was statistically significant (29.2 ± 4.9 vs. 18.1 ± 3.1 g/ml, p < 0.05), but not between whole blood and plasma (21.3 ± 2.8 vs. 18.1 ± 3.1 g/ml, p > 0.05). Concentration-independent binding of DPDPE to serum proteins was evidenced between 10 and 100 (g/ml, with an unbound fraction of 0.517 ± 0.182. Conclusions. DPDPE undergoes extensive biliary excretion after i.v administration in rats. The apparent nonlinearity in the biliary excretion of DPDPE revealed by the pharmacokinetic modeling strongly suggests the existence of an active transport system(s) in hepatocytes which may mediate the rapid disappearance of DPDPE from the systemic circulation.     

New hepatocellular diffusion model for analysis of hepatobiliary transport processes of drugs

A new hepatocellular diffusion model was developed to kinetically evaluate the hepatobiliary transport processes of drugs in the perfusion system, based on the physiological structure of the liver. Since the equations describing the hepatocellular diffusion phenomena were derived as image forms in the Laplace domain, the fast inverse Laplace transform (FILT) was adopted to manipulate the image equations. Cefixime and cefpiramide were selected as model drugs. The concentrations in the perfusate and the excreted amounts into the bile were simultaneously measured at appropriate intervals after the rapid administration of each drug into the portal vein. The hepatocellular diffusion model was fitted to the biliary excretion profiles from rat livers, by means of a nonlinear least squares program, MULTI(FILT). According to this model, the hepatobiliary transport process of drug is kinetically separated into three steps, that is, the diffusion into and through the hepatocytes, the transfer from the hepatocytes into the bile canaliculi, and the movement through the bile canaliculi to the outlet of bile duct. These steps are characterized by the diffusion rate constant through hepatocytes (k_dif), the permeability rate constant into the bile canaliculi (k_bmc) and the transit time through the bile canaliculi to the outlet of bile duct ( ), respectively. It was demonstrated that k_dif of cefixime (0.023min¹) was significantly smaller than that of cefpiramide (0.044 min¹), while the differences in k_bmc and were not obvious between cefixime and cefpiramide. k_bmc and of both drugs were about 1.2 min¹ and about 1.0 min, respectively. These parameters were correlated to the excretion ratio into the bile (F_bile) and the mean transit time from the sinusoid through the hepatocytes to the outlet of bile duct ( ).     

金石散胶囊溶解胆石的临床研究

自１９８７年迄今,用金石散（４－６胶囊／次,２－３次／天）治疗胆结石患者１７７例,３月为一疗程,共２－４疗程。治疗前后均经Ｂ超检查以判断疗效。结果显示：１．服药一月,９０％病人的发热、腹胀、疼痛等临床症状消失。２、６２例胆囊结石经服药平均８．１８＋７．１４月后,３例结石完全消失（４．８４％）,３７例结石减少变小,总有效率６４．５２％;而临床类型型相似的另外２３例,用ＵＤＣＡ治疗作为对照组,总有效率     

Metastatic seeding of bile duct carcinoma in the transhepatic catheter tract: Report of a case

We describe herein the case of a 51-year-old woman in whom metastatic tumor seeding of the percutaneous transhepatic biliary drainage tract occurred following a pancreatoduodenectomy for carcinoma of the distal common bile, duct. An abdominal computed tomography scan done 6 months after the initial operation detected a hepatic lesion located at the site of the previous percutaneous transhepatic biliary drainage tract. Implantation of bile duct carcinoma in the drainage tract was diagnosed, and the recurrent tumor was successfully resected by performing a subsegmentectomy of segment 3 and removal of the adjacent abdominal wall. At present, 5 years and 4 months after the second resection, the patient is in good health without any signs of recurrence. This case report demonstrates that an aggressive surgical approach should be performed for tumor seeding of a transhepatic biliary catheter tract.     

Definition and pathology of primary sclerosing cholangitis

Although primary sclerosing cholangitis (PSC) is not a common disease, it is important in the differential diagnosis of hepatobiliary tract diseases in clinical practice. A diagnosis of PSC should be made only after the exclusion of similar diseases with well known etiologies or pathogeneses. In this review, the pathology of classical PSC and its variants or related diseases is highlighted. PSC is histologically characterized by progressive periductal fibrosis with luminal stenosis or obliteration, along with the formation of a fibrous core, as well as dilatation (cholangiectasis). Its etiology is unknown. Bacterial ascending cholangitis is superimposed on its long clinical course. Such a heterogeneous distribution of biliary lesions with biliary obliteration and cholangiectasis is responsible for the radiological demonstration of biliary abnormalities, particularly the beaded appearance. Sampling variability is common in needle or wedge biopsied specimens. As a result of biliary damage, the liver shows progressive cholestatic change followed by biliary fibrosis and cirrhosis, and this hepatic progression is divisible into four stages. There are several variants of PSC or related diseases, such as localized biliary sclerosis and stenosis, sclerosing cholangitis associated with inflammatory pseudotumor, and PSC-autoimmune hepatitis overlapping syndrome. Cholelithiasis, including secondary hepatolithiasis and, to a lesser degree, biliary carcinoma and dysplasia, are also known to develop at the perihilar bile ducts as a late complication of PSC. Received for publication on March 8, 1999; accepted on April 30, 1999     

Clinicopathologic findings of recurrent primary sclerosing cholangitis after orthotopic liver transplantation

Whether primary sclerosing cholangitis (PSC) occurs after orthotopic liver transplantation is controversial, largely because the pre-transplant diagnosis of PSC is based on nonspecific radiological and histological findings. We reviewed clinical, radiological, and histological records of 53 patients who underwent liver transplantation for PSC between 1985 and 1998. Three patients with patent hepatic arteries and no evidence of chronic rejection had radiological and histological findings that may have been due to recurrent PSC. Bile duct stricturing in these patients proved permanent and progressive and affected both the quality of life and graft survival. The first patient, who is 110 months after transplantation, has had repeated episodes of cholangitis for the last year. The second patient underwent excision of a strictured hepatic duct 45 months after transplantation and was ultimately retransplanted 95 months after initial transplantation. The third patient underwent left hemihepatectomy of an atrophied lobe 50 months after transplantation. Although the patient population assessed in this study is limited, putative recurrent PSC in the allografts has led either to graft loss or to clinically significant hepatobiliary complications of the graft. Received for publication on March 8, 1999; accepted on April 30, 1999