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Biomedical subjects

J Fevery

Publications and source records attributed to J Fevery.

At least 127 records · Page 7Linked to original sources
PubMed1988

Endoscopic sclerotherapy of esophageal varices. Long-term follow-up, recurrence, and survival.

One hundred thirty-three patients (34.5% Child's C class) with at least one severe variceal hemorrhage and treated with repeated endoscopic sclerotherapy had a follow-up of 1-6 years (mean 20 months). The risk of rebleeding decreased significantly from 2 months after onset of sclerotherapy. Sixty-four patients (or 48%) rebled, within 2 months in 45 (70%). The incidence of rebleeding correlated with Child's category and with the size of the varices. The 2-month mortality rate was 28.6%; two-thirds died of severe rebleeding. Thirteen patients underwent emergency surgery for bleeding uncontrolled by sclerotherapy; nine of them died. Of the 120 treated only by sclerotherapy 93% ultimately died, 90% from variceal rebleeding. Mortality related to the liver disease was thus determined by rebleeding mainly within 2 months and by hepatic failure but not by etiology of the disease or number of previous hemorrhages. The more pronounced mortality in Child C versus B or A patients is thus due to early rebleeding and to more pronounced liver insufficiency in the early and later period. Varices could not be eradicated within 1 year by sclerotherapy in 9 patients; 68 of the 72 patients alive had total eradication, but recurrence of varices was observed in 19 (or 28%) within 1 year, independent of the etiology and severity of liver disease and varices. Only four patients rebled within 1 year, with no mortality. After 1-4 years, another five recurrences were noted, with two nonfatal bleeding episodes. This study argues for continuation of sclerotherapy until total eradication of varices as well as for regular follow-up to avoid recurrences.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Incomplete septal cirrhosis: histopathological aspects.

We have reviewed 60 liver specimens from 47 patients with the diagnosis of incomplete septal cirrhosis observed between 1968 and 1987. In reaching this diagnosis evaluation of the following histological features appeared to be helpful: parenchymal nodularity, thin incomplete septa, hypoplastic portal tracts, increased number of venous channels, abnormal spacing between portal tracts and veins, crowding of reticulin fibres between adjacent zones of hyperplastic parenchyma, hyperplasia of hepatocytes and dilated sinusoids. These histological features were not specific for incomplete septal cirrhosis as they were also present--although less evident and less frequent--in a series of 87 non-cirrhotic liver specimens. Reticulin stains were an essential adjunct to assess the architectural disturbance, which was often inconspicuous in needle biopsies. Histological features indicating a specific aetiology were lacking in the great majority of cases. On histological and clinical grounds, incomplete septal cirrhosis resembles idiopathic portal hypertension, nodular regenerative hyperplasia and partial nodular transformation; in these entities an obliterative portal venopathy with non-uniformity of portal blood supply to the parenchyma has been suggested as a pathogenic mechanism. In the present study phlebosclerotic lesions of the portal vein were found in only two cases. This might be explained by sampling error or, alternatively, the hypoplastic portal tracts observed might be a functional equivalent of obliterative portal venopathy resulting in a deficient portal blood supply. Non-uniformity of blood supply to the parenchyma may explain the similarities between incomplete septal cirrhosis and the diseases mentioned.

Humans↗
PubMed1988

Separate transport systems for biliary secretion of sulfated and unsulfated bile acids in the rat.

Biliary secretion of 3 alpha-sulfated bile acids has been studied in Wistar rats with an autosomal recessive defect in the hepatic transport of bilirubin. Liver function, established by measurement of various enzymes in plasma, by enzyme histochemical methods, and by electron microscopy, appeared to be normal in these rats. Serum levels of unconjugated, monoglucuronidated, and diglucuronidated bilirubin were 0.62, 1.62, and 6.16 mumol/liter, respectively, compared with 0.17, 0.08, and 0.02 mumol/liter in control rats. Biliary bilirubin secretion was strongly reduced in the mutant animals: 0.21 +/- 0.03 vs. 0.39 +/- 0.03 nmol/min per 100 g body wt in control rats. Despite normal biliary bile acid output, bile flow was markedly impaired in the mutant animals, due to a 53% reduction of the bile acid-independent fraction of bile flow. The transport maximum for biliary secretion of dibromosulphthalein (DBSP) was also drastically reduced (-53%). Biliary secretion of intravenously administered trace amounts of the 3 alpha-sulfate esters of 14C-labeled taurocholic acid (-14%), taurochenodeoxycholic acid (-39%), taurolithocholic acid (-73%), and glycolithocholic acid (-91%) was impaired in the jaundiced rats compared with controls, in contrast to the biliary secretion of the unsulfated parent compounds. Hepatic uptake of sulfated glycolithocholic acid was not affected in the jaundiced animals. Preadministration of DBSP (15 mumol/100 g body wt) to normal Wistar rats significantly impaired the biliary secretion of sulfated glycolithocholic acid, but did not affect taurocholic acid secretion. We conclude that separate transport systems in the rat liver exist for biliary secretion of sulfated and unsulfated bile acids; the sulfates probably share secretory pathways with the organic anions bilirubin and DBSP. The described genetic defect in hepatic transport function is associated with a reduced capacity to secrete sulfated bile acids into bile; this becomes more pronounced with a decreasing number of hydroxyl groups on the sulfated bile acid's molecule.

Animals↗
PubMed1987

Relationships between serum bilirubins and production and conjugation of bilirubin. Studies in Gilbert's syndrome, Crigler-Najjar disease, hemolytic disorders, and rat models.

The pattern of serum bilirubins was determined in serum of humans and rats with unconjugated hyperbilirubinemia due to increased pigment load or defective hepatic conjugation. Bilirubin ester conjugates were present in all serum samples tested and were identified as bilirubin 1-O-acyl glucuronides. In Gilbert's syndrome, the concentration of total conjugates was comparable to the values in healthy control subjects. Because the concentration of unconjugated pigment was increased, the fraction of conjugated relative to total bilirubins was markedly decreased. Sera from patients with Crigler-Najjar disease differed from those with Gilbert's syndrome by the higher unconjugated bilirubin levels and the undetectability of diconjugated bilirubins. A striking finding was that in hemolytic disease, the concentration of both monoconjugates and diconjugates was enhanced in parallel with the increase of unconjugated pigment. Therefore, the fraction of conjugated relative to total bilirubins remained within the normal range. As in Gilbert's syndrome, heterozygote R/APfd-j/+ rats with impaired hepatic bilirubin conjugation exhibit an increased unconjugated bilirubin level in serum, whereas the concentration of total conjugates was comparable to the values in normal rats. In serum of normal rats loaded intraperitoneally with unconjugated bilirubin, both unconjugated and mono- and diconjugated bilirubins were increased in parallel so that the ratio of unconjugated to esterified pigment remained unaffected. Decreased hepatic conjugation or increased bilirubin load was associated with a lower percentage of diconjugates relative to total conjugates both in human and rat serum. The present results are consistent with a compartmental model in which there is bidirectional transfer across the sinusoidal membrane for unconjugated bilirubin as well as for the bilirubin glucuronides. Because typical patterns of serum bilirubins are found in Gilbert's syndrome and patients with hemolytic hyperbilirubinemia, determination of esterified bilirubins in serum is of value to study the pathophysiology and the differential diagnosis of unconjugated hyperbilirubinemia.

Anemia, Hemolytic↗
PubMed1987

Hepatic echinococcosis ruptured into the biliary tract. Clinical, radiological and therapeutic features during five episodes of spontaneous biliary rupture in three patients with hepatic hydatidosis.

Three patients are described with hepatic involvement by Echinococcus granulosus, complicated by spontaneous rupture into the biliary tract. Clinical features consisted of upper abdominal pain, jaundice, fever, anorexia, and vomiting. Hepatomegaly and marked epigastric tenderness were consistently observed. Laboratory findings included obstructive liver function tests, leucocytosis, eosinophilia, and hyperamylasemia. Abdominal computed tomography, showing the cystic wall, the presence of wall calcifications, daughter cysts and wall enhancement, provided a correct diagnosis of hepatic hydatidosis in all patients. Dilatation of the bile ducts with the presence of intraluminal material was clearly shown by sonography and endoscopic retrograde cholangiography. These abnormalities were most frequently found in the common bile duct and in the left hepatic duct. On sonography, the intraluminal material appeared as amorphous, sludge-like hydatid sand, and as daughter cysts. On ERCP, the intrabiliary parasitic material appeared as non-homogeneous, irregularly shaped and mobile filling defects. Other findings at ERCP were displacement and distortion of intrahepatic bile ducts by the hepatic cysts and a mild dilatation of the pancreatic duct. In one occasion, evacuation of a daughter cyst through the papilla was observed. The therapeutic value of mebendazole and endoscopic sphincterotomy in our patients is discussed.

Adult↗
PubMed1987

Postoperative biliocutaneous fistula: successful treatment by insertion of an endoprosthesis.

An elderly patient with a postoperative biliocutaneous fistula, the persistence of which was due to an unrecognized fibro-malignant stricture of the distal common bile duct, was treated by the insertion of an endoscopic biliary endoprosthesis. Immediately after the procedure, bile discharge through the fistula ceased completely, and the fistula closed in three days. Endoscopic treatment methods are worth trying before surgical revision of a biliocutaneous fistula is performed.

Aged↗
PubMed1987

Subtotal resection of the head of the pancreas combined with ductal obliteration of the distal pancreas in chronic pancreatitis.

Subtotal resection of the head of the pancreas combined with duct obliteration of the distal pancreas by prolamine was performed in 12 selected patients who had chronic alcohol-induced pancreatitis with most destruction in the proximal pancreas. The main indication for operation was intractable pain. There was no postoperative mortality but morbidity was high when no pancreaticojejunostomy was constructed. After a follow-up period of 32 months, lasting pain relief was obtained in 10 patients; pseudocyst formation occurred in three patients; calcification of the distal pancreas, absent before operation, was demonstrated in four of six patients; six of 11 nondiabetic patients became hyperglycemic either abruptly (1 patient) or progressively (5 patients); quality of life improved in most patients. This procedure preserves the stomach, duodenum, spleen, distal pancreas and common bile duct if possible. However, pancreatic ductal obliteration with prolamine does not prevent relapses of chronic pancreatitis.

Adult↗
PubMed1987

Ulcerative colitis, primary sclerosing cholangitis, bile duct carcinoma, and generalized sarcoidosis. Report of a unique association.

We describe a young man with a hitherto unreported association of chronic ulcerative colitis, primary sclerosing cholangitis (PSC), bile duct carcinoma, and generalized sarcoidosis with features of high-intensity alveolitis. This finding suggests that common immunological mechanisms may be involved in the pathogenesis of these diseases.

Adenocarcinoma, Scirrhous↗
PubMed1986

Biliary lipid composition in patients with nonoperated Crohn's disease.

Lipid composition of fasting duodenal bile was studied in 56 patients with nonoperated Crohn's disease, 21 normals matched for age and sex, 13 patients with cholesterol cholelithiasis, and 9 patients with ileal resections. Crohn's patients had a significantly higher mean saturation index, calculated according to Thomas (0.84 +/- 0.51) when compared to normal (0.63 +/- 0.25). Patients with ileocolonic Crohn's disease and patients with severe bile acid malabsorption, particularly, showed an increased incidence of cholesterol saturated bile. Saturation in patients with nonoperated Crohn's disease was not increased to the levels found in patients with ileal resection or cholesterol gallstones. Bile acid composition of gallbladder bile was characterized by a significant decrease of the deoxycholate fractions in patients with Crohn's ileocolitis and colitis as well as in ileal resected patients. These qualitative changes of bile acid composition may influence cholesterol solubility. It is concluded that patients with nonoperated Crohn's disease may have an increased risk of developing cholesterol gallstones.

Adult↗
PubMed1986

Detection of Pi Z phenotype individuals by alpha-1-antitrypsin (AAT) immunohistochemistry in paraffin-embedded liver tissue specimens.

Immunostaining for alpha-1-antitrypsin (AAT) was applied on paraffin-embedded liver specimens from 38 Pi Z phenotype (27 Pi MZ; 9 Pi ZZ; 2 Pi SZ) individuals (33 adults, 5 newborns). Histological diagnoses included normal liver, various forms of chronic hepatitis, cirrhosis. A positive hepatocytic staining for AAT was revealed in all cases, whereas on PAS-D staining 5 cases were negative. Immunostaining revealed different patterns: type I: fine solid granules or coarse laminated globules filling the whole liver cell cytoplasm; type II: positive granules marginated towards the cell's periphery; type III: positive granules restricted to focal areas in the cytoplasm. Type I and III patterns were observed in all specimens. Association of type I and III with type II was seen in all Pi MZ and Pi SZ cases, but only in 3 of the 9 Pi ZZ specimens. To check the specificity of these staining patterns for the Z allele of AAT in adults and newborns, 180 further cases were investigated blindly by immunohistochemistry. Recognition of hepatocytic staining patterns type I, II and III allowed to reliably diagnose the Pi Z phenotype in 6 cases, whose heterozygous state was confirmed by independent serum phenotyping (5 Pi MZ, 1 Pi SZ). These results allow to conclude that: (1) immunohistochemistry is a reliable technique (superior to PAS-D staining) to identify Pi Z individuals (homo- and heterozygotes) on paraffin-embedded liver sections; (2) heterozygotes Pi MZ and Pi SZ cannot be differentiated without serum phenotyping; (3) immunohistochemistry is helpful in distinguishing between Z homozygotes from heterozygotes, but determination of AAT serum concentration is required to allow confident distinction without phenotyping. AAT immunohistochemistry thus allows to diagnose the Z allele of AAT when phenotyping procedures are not available or in retrospective studies on biopsy and autopsy material.

Adult↗
PubMed1986

'Lupus' anticoagulant and thrombosis of the hepatic veins (Budd-Chiari syndrome). Report of three patients and review of the literature.

Three patients with Budd-Chiari syndrome in association with the 'lupus' anticoagulant are described. This anticoagulant was looked for in our patients with an otherwise idiopathic hepatic venous thrombosis because of the presence of a pronounced thrombocytopenia, a prolonged activated partial thromboplastin time or a history of repeated abortions and deep leg vein thrombosis, respectively. An active search for the 'lupus' anticoagulant should be performed to lower the percentage of apparently idiopathic cases of Budd-Chiari syndrome.

Adult↗
PubMed1986

Unconjugated and conjugated bilirubin pigments during perinatal development. I. Studies on rat serum and intestine.

Unconjugated, mono- and diconjugated bilirubin was measured in rat plasma and intestine during perinatal development. Bilirubin monoconjugates were present in the intestines of 18-day-old fetuses, while diconjugates appeared on the 20th day. The concentration of conjugates increased rapidly, reaching 312 mumol/g of intestinal tissue 1 day after birth. The absolute concentration of unconjugated bilirubin increased in parallel. On the 18th day of fetal life, about 80% of the pigment in the intestine was unconjugated, while conjugates largely predominated from the 20th day onwards. Conjugation and/or excretion of bilirubin in the intestine seems therefore to develop rapidly during the last days of life. The plasma concentration of total bilirubin in 18-day-old fetuses was about 2-3 times higher than in adult serum, and it increased slightly during the following days. 2-7% of the pigment was conjugated. Transplacental clearance of bilirubin seems therefore to be deficient in this species. On the 1st day of extrauterine life, bilirubin concentration increased sharply in plasma, reaching 14.76 mumol/l, 38% in the conjugated form. This finding suggests that, unlike humans, an excretory defect is predominant in the neonatal rat.

Animals↗