The action of VIP on bile secretion and bile acid output in the non-anaesthetized rat.
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Animals↗
Biomedical subjects
J Fevery
Publications and source records attributed to J Fevery.
Gastric leiomyoblastoma with metastases to the liver. A 36-year follow-up study.
A patient presented with large intrahepatic tumoral masses 36 yr after the initial detection of multiple liver metastases during a gastrectomy. The operation had been performed to remove four ulcerated polypoid gastric lesions. Reexamination of the previous liver and gastric biopsy specimens revealed a gastric leiomyoblastoma with metastases to the liver. The smooth muscle origin of this tumor was confirmed by positive staining for desmin intermediate filaments. This very long survival is extremely unusual in cases of metastatic gastric leiomyoblastoma.
Adolescent↗
The maximal biliary excretory rate (Tm) of ioglycamide in the rat. Effect of taurocholate.
Biliary excretion of ioglycamide was studied in Wistar and Gunn rats. A hepatic transport-maximum (Tm) was observed. Higher Tm-values were found in Gunn rats, which have a greater bile flow compared to the parent Wistar rats, in spite of having a similar bile acid output. This suggests that the Tm is related to the bile acid-independent bile flow. In bile acid-depleted Wistar rats, bile acid output was 30% of control values whereas bile flow and ioglycamide-Tm had only decreased by approximately 15%. Ioglycamide excretion could not be increased by taurocholate infusion. An additional 22.0 ml of bile was excreted per mmol of biliary ioglycamide. Loads of the contrast agent markedly exceeding the Tm resulted in a decrease of its own biliary excretion and its choleretic properties. These presumed 'toxic' effects were counteracted by near-physiological amounts of taurocholate. Thus, the effect of taurocholate varies greatly depending upon the amounts of the contrast agent and the taurocholate administered.
Animals↗
An unusual case of Crigler-Najjar disease in the adult. Classification into types I and II revisited.
We present the case of a 25-year-old man with Crigler-Najjar disease who had since birth a marked unconjugated hyperbilirubinemia without bilirubin overproduction, without any neurological involvement and in whom phenobarbital administration failed to produce any effect. Analysis of his biliary bile pigments on two occasions showed (i) a decrease excretion of bilirubin, as indirectly suggested by a high ratio of biliary bile acids over total bilirubin; (ii) an increase in unconjugated bilirubin IX alpha quantitated by thin-layer chromatography (TLC) following alkaline methanolysis and by direct extraction and TLC of the tetrapyrroles; (iii) a high proportion of bilirubin monoconjugates whereas the excretion of diconjugates was very low. Classification of the present patient into Crigler-Najjar disease type I or II was not possible. The most striking and practical difference among the various cases of Crigler-Najjar disease remains the response to phenobarbital. Among cases of Crigler-Najjar disease which respond to enzyme induction and Gilbert's syndrome, the continuous spectrum suggests a common defect.
Adult↗
Cimetidine-induced liver injury. Report of three cases.
Cimetidine-induced liver injury has only very rarely been reported. Three patients are described who developed signs of hepatic damage after the institution of cimetidine therapy. Transient signs of acute liver failure were noticed in one patient. Histologically, a cytotoxic type of injury with centrilobular confluent and bridging portal-central necrosis, accompanied by a mixed mono- and polymorphonuclear infiltrate with signs of cholangiolitis in the portal tracts was observed in two patients, whereas a hepatocanalicular type of cholestatic hepatitis was noticed in another patient. It is proposed that the mechanism of cimetidine-induced liver injury may vary in different patients: it may be due either to a 'metabolic idiosyncrasy' because of the production of hitherto unknown toxic metabolites or to a hypersensitivity reaction.
Aged↗
The bilirubin diglucuronide controversy.
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Animals↗
Storage of alpha-1-antitrypsin in intrahepatic bile duct cells in alpha-1-antitrypsin deficiency (Pi Z phenotype).
Storage of alpha-1-antitrypsin (AAT) has been found in a small number of bile duct cells in liver tissue specimens from patients with Pi MZ, Pi SZ and Pi ZZ phenotypes. The storage appeared in the form of intracellular AAT immunoreactive inclusions. On EM investigation, AAT-like material was detected within cisternae of the RER and SER. Such AAT inclusions were found in proliferating bile ductules in conditions such as cirrhosis, focal nodular hyperplasia and extrahepatic obstruction. They were also observed in normal biliary structures at the level of the canals of Hering, bile ductules and interlobular ducts in 13 out of 47 cases. These findings are interpreted as indicating that the intrahepatic bile duct cells are a further source of AAT, and that in case of defective export of AAT from the cell, as is the case for the Z protein, the protein accumulates not only in hepatocytes but in biliary cells as well.
Bile Ducts, Intrahepatic↗
Dilatation of the cystic veins in portal hypertension: sonographic demonstration.
High-resolution real-time ultrasound (6 MHz) demonstrated vascular dilatation in the adventitial layer of the gallbladder in 7 patients with portal hypertension. The hypertension was due to long-standing cirrhosis in 4 patients; the other 3 patients had prehepatic hypertension due to thrombosis involving the portal vein in 1 and the splenoportal confluence in 2. In one of the cirrhotic patients, postmortem correlation of sonographic, angiographic, and pathological findings showed that the dilated vessels seen on sonography were cystic veins draining normally into the portal vein rather than portosystemic anastomoses. This indicates that varicosity of the cystic vein can be associated with portal hypertension, taking the form of either passive dilatation or hepatopetal portal collateral circulation.
Dilatation, Pathologic↗
The sonographic aspects of haemobilia. Clinical and experimental study.
The sonographic aspect of the gallbladder in seven cases of haemobilia is analysed. The changes include a diffuse echogenic gallbladder content during the initial stage. Later, irregular shaped inhomogeneous non shadowing masses are seen in the dependent parts of the lumen. This variable aspect was studied in an experimental model by percutaneous injection of blood in the gallbladder of Guinea pigs. The hyperechoic gallbladder content, seen early after injection is a transitory phenomenon which seems related to red cell aggregation before coagulation occurs. During the later stage the intraluminal masses were shown by histology to represent bloodclots. In a patient the observation of such a rapid evolution from diffuse hyper-reflectivity to less reflective masses is strongly suggestive of haemobilia.
Animals↗
Intramural hematoma of the esophagus: unusual complication of variceal sclerotherapy.
A patient is described who developed severe retrosternal pain and dysphagia immediately after sclerotherapy of esophageal varices. Extensive submucosal bleeding of the esophageal wall was demonstrated radiologically and endoscopically. This lesion resolved within 2 weeks of conservative treatment.
Adult↗
Sonographic diagnosis of intraluminal bile duct neoplasm: a report of 3 cases.
Intraluminal growing tumors of the bile duct are uncommon causes of jaundice. The sonographic appearance of 2 hilar cholangiocarcinomas or Klatskin tumors and a benign extrahepatic biliary cystadenoma is described. Compared to contrast studies of the bile ducts, sonography better defined the intraductal character of the neoplasms. However, the ultrasound appearance did not allow differentiation between the adenocarcinomas and the benign cystadenoma.
Adenocarcinoma↗
Simultaneous alpha-1-antitrypsin accumulation in liver and pancreas.
Inclusions positive for periodic acid-Schiff, resistant to diastase, and immunoreactive to alpha-1-antitrypsin (AAT) were found in hepatocytes and pancreatic islet cells of a patient with clinical and pathologic features of AAT deficiency. Alpha-1-antitrypsin was detected in all pancreatic islets, and AAT-positive cells were observed in the excretory pancreatic ducts. These findings suggest that the pancreas synthesizes AAT and possibly serves as a "storage" place in AAT deficiency. Intercalated cells in the excretory pancreatic ducts may be an additional source of AAT.
Carcinoma, Hepatocellular↗
Effect of clofibrate on the metabolism of bilirubin, bromosulphophthalein and indocyanine green and on the biliary lipid composition in Gilbert's syndrome.
Clofibrate (20 mg day-1 kg-1 body weight) given orally for 2 weeks to 18 subjects with Gilbert's syndrome reduced the total serum bilirubin concentration from 44.4 (22.1-71.7) mumol/l (median, range) to 15.0 (7.9-28.9) mumol/l, mainly by decreasing the 'indirect' fraction to 34.5% of pretreatment values. In contrast to treatment with phenobarbitone, clofibrate did not change the ratio of bilirubin mono- to di-conjugates in bile. The initial plasma disappearance rate of indocyanine green and of bromosulphophthalein did not show consistent changes during clofibrate treatment but the 'apparent' maximal biliary secretion capacity of bromosulphophthalein (Tm) decreased in most of the patients studied, whereas the relative storage capacity (S) tended to increase. As expected, the cholesterol saturation of bile increased in all subjects. These results suggest that clofibrate increases mainly the glucuronidation of bilirubin, promoting as such the overall hepatic transport in Gilbert's syndrome. However, it decreases the maximal biliary secretion of bromosulphophthalein, possibly by an increased hepatic retention. These phenomena might be linked to the augmented content of Z protein in the liver.
Adult↗
Sclerotherapy of oesophageal varices after variceal haemorrhage.
Fifty-six patients with recent variceal haemorrhage were studied in a trial of repeated injection sclerotherapy through the flexible oesophagoscope, with a mean follow-up of 15.2 months (1-39). Twenty-five patients (45%) did not suffer further bleedings. The risk of bleeding per patient-month of follow-up decreased significantly (p less than 0.05) after starting therapy, in all groups of cirrhosis, classified according to Child's criteria. Mortality during the study period was 39% (19.6% due to recurrence of variceal bleeding). The main complications of the procedure were the development of oesophageal wall ulcerations and oesophageal stricture.
Adolescent↗
Non-A, non-B hepatitis-like nuclear particles in nonparenchymal cells of the liver.
Nuclear particles, morphologically similar to those seen in hepatocytes during non-A, non-B (NANB) hepatitis, were detected in several types of nonparenchymal cells in 10 human liver-biopsy specimens, including cases of hepatitis A and B and nonviral hepatic disease. They were also found in nonparenchymal cells of the liver in two of four normal chimpanzees and in two of four chimpanzees during experimental NANB viral hepatitis. In nonparenchymal cells the particles formed loose-to-intermediate aggregates, similar to those first described in hepatocytes during NANB hepatitis. Tightly packed aggregates, the predominant pattern in hepatocytes, were generally missing. The high prevalence of morphologically identical particles in various liver diseases and their presence in healthy livers, both in hepatocytes and in nonparenchymal cells not presumed to support the growth of hepatitis viruses, speak against their specificity for NANB hepatitis viruses. It is proposed that the particles represent a newly recognized and widespread cellular feature, of as yet unknown function.
Animals↗
Immunohistochemical characterization of inflammatory infiltrates in primary biliary cirrhosis.
Ten liver biopsy specimens from nine patients with PBC stages II to IV were studied immunohistochemically with a broad panel of monoclonal antibodies. In areas of bile-duct proliferation, many BA1+ B-lymphocytes and OKT4+/Leu3a+ helper/inducer T-cells were observed, admixed with some C3b-receptor positive, mono- and polymorphonuclear OKM1+ cells. Numerous IgM-containing plasma cells were seen in portal tracts showing bile-duct proliferation. In contrast, areas of piecemeal necrosis and intralobular spotty necrosis consisted mainly of OKT4+/Leu3a+ helper/inducer, and OKT8+ suppressor/cytotoxic T-cells, admixed with some OKM1+ polymorphonuclear granulocytes. Almost no BA1+ B-lymphocytes or Ig-containing plasma cells were observed in areas of piecemeal necrosis and spotty necrosis. Major histocompatibility complex (MHC)-class I antigens (i.e. HLA-A,B,C) were demonstrated either on the liver cell membrane, or on sinusoidal lining cells. The latter also expressed MHC-class II antigens (i.e. HLA-DR). In two liver biopsies, an increased expression of HLA antigens was observed near areas of piecemeal and spotty necrosis. Our results indicate that several immune mechanisms each with a particular topographical distribution, are operative in PBC. Inflammatory cells, involved in humoral immunity, are present mainly in areas of bile duct proliferation. In contrast, the effector cells of antigen-specific cellular cytotoxicity are present in areas of piecemeal necrosis and spotty necrosis. In the latter areas, a pronounced expression of MHC products representing the afferent limb of the cell-mediated immune response, may permit an optimal T-cell-mediated immune effect or, eventually, result in adverse effects.
Antibodies, Monoclonal↗
Serum vitamin D metabolites and their binding protein in patients with liver cirrhosis.
Serum parameters of calcium metabolism were measured in 32 consecutive patients with biopsy-proven cirrhosis due to either hepatitis (n = 13), alcohol abuse (n = 11), Wilson's disease (n = 3), or primary or secondary biliary cirrhosis (n = 5). All measurements were normal in the small group of patients with Wilson's disease. The serum concentrations of albumin, vitamin D-binding protein, total calcium, phosphorus, and 1,25-dihydroxyvitamin D3 (1,25-(OH2)D3) were decreased in the other patients with cirrhosis, but their mean serum concentrations of ionized calcium, 25-hydroxyvitamin D3 (25-OHD3) and free 1,25-(OH2)D3 index were normal. A slight but significant increase in the serum PTH measured using a carboxyl-terminal antiserum was found. A significant correlation was found between the serum concentration of either albumin or vitamin D-binding protein and the serum concentrations of total calcium, 25-OHD3, 1,25-(OH2)D3, and PTH but not with ionized calcium or free 1,25-(OH2)D3 index. The observed abnormalities of calcium metabolism in unselected patients with cirrhosis were mainly due to decreased protein synthesis. Only the patients with severe cirrhosis had decreased concentrations of 25-OHD3 but they were nevertheless able to maintain a normal ionized serum calcium and free 1,25-(OH2)D3 level, possibly by means of compensatory hyperparathyroidism.
Adolescent↗