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J De Groote

Publications and source records attributed to J De Groote.

At least 19 recordsLinked to original sources
PubMed1994

Clinical aspects of incomplete septal cirrhosis in comparison with macronodular cirrhosis.

BACKGROUND/AIMS: Incomplete septal cirrhosis (ISC) is a form of macronodular cirrhosis characterized by slender, incomplete septa that demarcate inconspicuous nodules. Its clinical features have not been investigated in a large series. The aims of this study were to review the clinical symptoms and evolution of ISC in 42 patients. METHODS: Forty-two patients with at least one liver biopsy strongly suggestive of ISC were selected for the study covering a period between 1968 and 1987. Data for these patients were compared with the evolution of 49 patients with classical macronodular cirrhosis after chronic active hepatitis type B or C. RESULTS: Possible etiological factors for ISC were alcohol abuse, arsenic treatment, and hepatitis B infection. In three cases, a genetic factor could not be excluded. Patients with ISC had significantly lower serum concentrations of transaminases and bilirubin at diagnosis. Compared with macronodular cirrhosis, bleeding varices were more frequent (57% vs. 22%) in ISC. Ten-year survivals in the ISC and the macronodular cirrhosis groups were 54% and 57%, respectively. CONCLUSIONS: ISC represents a relatively stable burnt-out form of macronodular cirrhosis with an unusually high incidence of variceal bleeding. This could be explained by a superimposed insufficiency of the portal vascular supply.

Adolescent↗
PubMed1991

Light chain deposition disease of the liver associated with AL-type amyloidosis and severe cholestasis.

A 67-year-old man with a 3-month history of jaundice presented with hepatomegaly. Laboratory studies revealed abnormal liver tests with raised bilirubin. Renal function was normal. Endoscopic retrograde cholangiopancreatography revealed normal extrahepatic bile ducts. Liver biopsy showed severe bilirubinostasis and a typical bile infarct. Laminar and globular deposits of PAS-positive diastase-resistant non-congophilic material were observed in the sinusoidal walls. In addition, congophilic material was detected in the portal tracts. Immunohistochemistry revealed the presence of lambda-light chain deposits both in the sinusoids and in the portal tracts. Collagens type I and IV and fibronectin appeared markedly increased in the perisinusoidal space. On electron microscopy, the deposited material in the Disse spaces was mainly composed of fibrils indistinguishable from amyloid, admixed with small amounts of granular electron-dense material. The similarities of light chain deposition disease and AL amyloidosis are discussed.

Aged↗
PubMed1990

Increase in the relative amount of bilirubin diconjugates in rat bile and serum under infusion of phthaleins and indocyanine green.

The effect of organic anions on bilirubin metabolism and excretion was investigated in rats. Biliary excretion of bromosulfophthalein, bromcresol green and indocyanine green led to a significant decrease in excretion of bilirubin pigments and to an increase of their concentration in serum. This was concomitant with a marked increase in the ratio of bilirubin diconjugates to monoconjugates in bile and serum. These changes were unrelated to either bile flow, biliary lipid output, or hepatic activity of bilirubin UDP-glucuronyl transferase. Following bolus injection of [14C]bilirubin, peak excretory rate of radioactivity was markedly delayed in rats infused with bromosulfophthalein, as compared to controls. It is concluded that administration of the organic anions increased the ratio of bilirubin diconjugates to monoconjugates in bile and serum, by slowing down the intrahepatic transit of bilirubin pigments. This, in turn, allowed more efficient enzyme-catalyzed formation of bilirubin diconjugates from the intermediate bilirubin monoconjugates.

Animals↗
PubMed1990

Reversal of hepatorenal syndrome in four patients by peroral misoprostol (prostaglandin E1 analogue) and albumin administration.

Four consecutive patients with alcoholic cirrhosis and hepatorenal syndrome were treated with misoprostol, a synthetic methylester prostaglandin E1 analogue at twice the dosage advocated for anti-ulcer therapy (i.e., 0.4 mg four times per day orally) and albumin infusions. The mean urinary output obtained over the 3 days preceding misoprostol administration was 250, 315, 550 and 195 ml per 24 h, respectively, in the four patients, despite adequate volume expansion by plasma albumin to reach normal or high central venous pressure. Diuresis increased to 1450, 2440, 925 and 1300 ml, respectively, on days 2-4 after onset of therapy. Serum creatinine levels were 71, 51, 33 and 35 mg/l before and dropped to 26, 21, 13 and 17 mg/l during treatment. All patients had hyponatraemia (117-128 mequiv/l) which normalized, although they were continued on a low sodium intake of less than 10 mequiv per 24 h. Urinary sodium excretion increased from 0.4-3 mmol per 24 h, to 15-40 in the first two cases and only slightly to 3-5 in the last two patients. Three patients died after 10, 30 and 40 days due to oesophageal bleeding, encephalopathy or pulmonary infection, whereas one patient underwent an orthotopic liver transplantation when her serum creatinine attained a level of 13 mg/l. In the first patient, hepatorenal syndrome recurred 10 days after stopping the misoprostol treatment. High doses of misoprostol in the presence of adequate volume expansion thus seem to produce marked diuresis and creatininuria as well as mild natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

Arsenic and non-cirrhotic portal hypertension. A report of eight cases.

It was discovered that eight patients with complications of non-cirrhotic portal hypertension had received an arsenical preparation for psoriasis as Fowler's solution some years age. Seven of them were admitted for bleeding oesophageal varices. Upon admission, splenomegaly and hypersplenism were present. Liver tests were normal and palmar skin keratosis and melanosis were noted. Liver biopsy of six patients showed features of incomplete septal cirrhosis. Malignant skin lesions were present in half of the patients. One patient died from lung carcinoma and another from an ovarium neoplasm. Chronic arsenic intake should be actively looked for in all patients with psoriasis and non-cirrhotic portal hypertension. They should be followed up for many years for development of malignant lesions in skin, lung and liver. Liver abnormalities present in the biopsies are often minor and may escape detection.

Adult↗
PubMed1990

Percutaneous transhepatic cholecystostomy for acute complicated cholecystitis in elderly patients.

We report our experience with percutaneous transhepatic cholecystostomy in 10 elderly patients with acute cholecystitis, complicated by empyema formation. Most of these patients has severe underlying disease, rendering them at high risk for surgical intervention. In all patients, the percutaneous procedure was followed by a rapid regression of clinical symptoms and of radiologic abnormalities. Six were considered inoperable. Three of these remain free of biliary symptoms, respectively 22, 10, and 7 months after percutaneous cholecystostomy. Three others died of nonbiliary disease 1-4 months after cholecystostomy. Three patients underwent successful elective cholecystostomy 1-5 wk after percutaneous cholecystostomy. In one patient, cholecystectomy had to be performed because of recurrence of hydrops, 1 wk after catheter removal. In our opinion, percutaneous transhepatic cholecystostomy is a safe and effective procedure in the treatment of elderly patients with acute complicated cholecystitis. It can be followed by elective cholecystectomy in good surgical candidates, or by an expectant conservative management in high surgical risk patients.

Acute Disease↗
PubMed1989

Thyroid hormones and the hepatic handling of bilirubin. I. Effects of hypothyroidism and hyperthyroidism on the hepatic transport of bilirubin mono- and diconjugates in the Wistar rat.

The effects of thyroidectomy and of thyroid hormone administration on the hepatic transport of endogenous bilirubin were investigated in the Wistar R/APfd rat. Hypothyroidism resulted in an enhanced hepatic bilirubin UDP-glucuronosyltransferase activity and in a decreased p-nitrophenol transferase activity. It caused a cholestatic condition with a 50% decrease in bile flow and bile salt excretion, and an increased proportion of conjugated bilirubin in serum. The biliary output of unconjugated and monoconjugated bilirubins decreased in parallel by about 65%, whereas the excretion rate of the diconjugate dropped by only 47%, resulting in an increased di- to monoconjugate ratio in bile. Hyperthyroidism was characterized by a decreased bilirubin and an increased p-nitrophenol transferase activity, and by an augmented bilirubin output in bile. The output of unconjugated and monoconjugated bilirubins increased in parallel by about 50 or 100%, whereas the excretion of the diconjugate increased by only 20 to 50%, depending on the dose of thyroxine administered; this resulted in a decreased di- to monoconjugate ratio in bile. A linear positive relationship was found between bilirubin UDP-glucuronosyltransferase activity and the ratio of bilirubin di- to monoconjugates present in bile or formed by in vitro incubation of liver homogenates at low concentration of bilirubin (10 to 15 microM), indicating that bile pigment composition is mainly determined by the conjugation activity in the liver. The inverse relationship observed between hepatic beta-glucuronidase activity and the ratio of di- to monoconjugates in bile warrants further investigation to analyze whether this enzyme activity also plays a possible role in the changes in bile pigment composition in hypo- and hyperthyroid rats.

4-Nitrophenylphosphatase↗
PubMed1989

Taurocholate increases the biliary output of bilirubin pigments in the rat, due to haemolysis.

In order to investigate the effect of bile salts on the biliary transport of bilirubin, we infused rats with taurocholate at 1-3 mumol/min/kg body weight. When administered in saline, taurocholate induced haemolysis, and a dose-dependent increase in biliary excretion and serum concentration of all bilirubin pigments. The addition of human or rat serum albumin to the infusate, at an albumin:taurocholate molar ratio equal to or above 200, completely prevented haemolysis and the above-mentioned alterations in bilirubin transport, without any change in the bile acid output. In order to mimic a haemolytic condition, an erythrocyte haemolysate was further added to the taurocholate-albumin solution. This again resulted in an increased bilirubin output. We suggest that taurocholate treatment increases bilirubin output due to the increased load of the pigment on the liver, as a result of the bile acid-induced haemolysis.

Animals↗
PubMed1988

Thyroid hormones and the hepatic handling of bilirubin. II. Effects of hypothyroidism and hyperthyroidism on the apparent maximal biliary secretion of bilirubin in the Wistar rat.

This study was undertaken in the Wistar R/A Pfd rat to investigate the effects of hypothyroidism and of hyperthyroidism on the maximal biliary excretion (Tm) of bilirubin and on the concentration and composition of bilirubin in liver and plasma at the end of a bilirubin load. Hypothyroidism caused a cholestatic condition with a 50% decrease in bile flow and in bilirubin Tm, and with an increased proportion of conjugated bilirubin in liver and plasma. This was associated with an increased ratio of bilirubin diconjugates to monoconjugates in bile, liver, and plasma, which can be ascribed to the increased hepatic conjugation activity towards bilirubin and/or to the prolonged retention of bile pigments in the hepatocytes with increased conversion of monoconjugates to diconjugates. Cholestasis induced by hypothyroidism was further characterized by a decreased biliary output of unconjugated bilirubin. The latter phenomenon might represent an indirect effect related to a decreased output of bilirubin monoconjugates with impaired hydrolysis to unconjugated bilirubin; it might also reflect the cholestatic condition with decreased excretion of the unesterified bile pigment as such. Hyperthyroidism resulted in a 1.3-1.4-fold increase in bile flow. The maximal bilirubin concentration in bile decreased 1.3-1.4-fold, so that the apparent maximal bilirubin excretion rate remained unchanged at 115 nmol.min-1.100 g-1, as observed in untreated rats. Hyperthyroidism lowered the bilirubin UDP-glucuronosyltransferase activity, produced a decreased ratio of bilirubin di- to monoconjugates in bile and plasma, and a decreased ratio of conjugated to total bile pigment concentration in liver and in plasma. Similar findings are present in the heterozygous Gunn rat strain and in patients with hepatic bilirubin UDP-glucuronosyltransferase deficiency. We therefore propose the hyperthyroid rat as an experimental animal model of Gilbert's syndrome.

Animals↗
PubMed1988

The diagnostic significance of periportal hepatic necrosis and inflammation.

In this review the several types of cell damage and cell death which may be found in liver biopsy specimens are defined. We describe the different processes which occur at the portal/parenchymal or septal/parenchymal interface, viz. periportal spillover, periportal hepatitis, classic or lymphocytic piecemeal necrosis and biliary piecemeal necrosis. The diagnostic implications of these lesions in relation to the clinicopathological diagnosis and prognosis in various liver diseases are discussed.

Diagnosis, Differential↗
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↗
PubMed1987

Transection of the pancreas demonstrated by ultrasound and computed tomography.

The early occurrence of peritoneal signs and hyperamylasemia in a 14-year-old boy, who had fallen off his horse, urged us to perform a sonographic and computed tomographic study of the upper abdomen. Both examinations showed a complete pancreatic rupture. Distal pancreatectomy led to a rapid and uneventful recovery.

Adolescent↗
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↗