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Biomedical subjects

J De Groote

Publications and source records attributed to J De Groote.

At least 19 recordsLinked to original sources
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↗
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↗
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↗
PubMed1979

Hepatitis B core antigen immune complexes in the liver of hepatitis B patients.

Single liver biopsies from 102 clinically diagnosed hepatitis patients were examined by immunofluorescence for the presence of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg), complement and immunoglobulin deposition, and for their capacity to fix human complement in vitro. Of the sixty-five HBsAg positive livers, fifty-three were histologically diagnosed as chronic hepatitis, three as acute hepatitis, five as acute hepatitis with signs of transition to chronicity, and four as 'near normal liver'. In the group with chronic hepatitis, HGcAg was observed in thirty-nine livers, all of which also had HBsAg. Thirty-five of these thirty-nine cases also had the ability to fix complement in vitro in the hepatocyte nuclei and/or cytoplasm. Of these thirty-five cases, twenty-nine were positive for immunoglobulin deposition on the nuclei. All of these cases had antibody to HBcAg in the blood, but only five had anti-HBs. The frequency of in vitro complement fixation and immunoglobulin deposition was higher in active forms of the disease, such as chronic aggressive hepatitis and active cirrhosis, than in non-active disease such as chronic persistent hepatitis and mild cirrhosis. By the application of double fluorescent staining techniques, complement fixation was observed in some HBcAg-positive nuclei. In the 'near normal liver' cases there was no intrahepatic accumulation of HBcAg, and despite the presence of anti-HBc in the blood, in vitro complement fixation and immunoglobulin deposition were both absent. The group of three HBsAg ositive 'acute hepatitis with signs of transition to chronicity' cases behaved similarly to those with chronic aggressive hepatitis and had circulating anti-HBc, in vitro complement fixation and immunoglobulin deposition in the hepatocytes. None had circulating anti-HBs. In the group sith HBs-positive acute hepatitis, anti-HGc in the blood was the only other evidence of hepatitis B virus infection.

Antigen-Antibody Complex↗
PubMed1978

Long-term follow-up of chronic active hepatitis of moderate severity.

A group of patients with only moderately active chronic hepatitis has been studied. The follow-up was long (mean 87 months). All patients except one were treated with prednisone and/or azathioprine. Of the hepatitis B virus positive patients two-thirds developed cirrhosis between the second and fifth year of evolution, while in the hepatitis B negative group this occurred in less than one-third. The transition to cirrhosis was clinically silent. The patients were all allowed to do their normal work except in the terminal stages of cirrhosis. Five patients died of causes related to the disease: three patients with cirrhosis and hepatocellular carcinoma, one with gallbladder carcinoma, and one from bleeding varices. The high incidence of tumour, especially liver-cell carcinoma, may be due to a cumulative effect of the presence of hepatitis B virus, cirrhotic transformation, and immuno-suppression. The other patients are currently in apparently good health.

Adult↗
PubMed1976

Administration of human fibroblast interferon in chronic hepatitis-B infection.

One patient with hepatitis-B surface antigen (HBsAg)-positive chronic aggressive hepatitis, and two chimpanzee carriers of HBsAg, were each given seven doses of 10(7) I.U. of human fibroblast interferon over two weeks. The main differnce observed after treatment was a depression of the nucleocapsid hepatitis-0 core antigen in the liver, indicating that hepatitis-B virus infection is sensitive to interferon. Except for a short febrile reaction, no undesirable effects were seen after the administration of human fibroblast interferon which has not been previously given to man.

Adult↗
PubMed1976

Hepatitis B surface antigen (HBsAg) in the liver of patients with hepatitis; a comparison with serological detection.

Chronic hepatitis was diagnosed on liver biopsy of 76 patients; 52 (68%)had HBsAg. Of the 52 patients with HBsAg, 23% had HBsAg shown by immunofluorescence on the liver, while it could not be detected with radioimmunoassay on the serum; 77% had HBsAg detectable in liver and in serum, and none had HBsAg in serum only. HBsAg was detected more frequently in chronic aggressive hepatitis and active cirrhosis than in chronic persistent hepatitis and cirrhosis with little activity. No correlation was found in the different forms of chronic hepatitis between the HBsAg status on the one hand, and levels of transaminases, gammaglobulins, and auto-antibodies on the other. Acute hepatitis was diagnosed on liver biopsy of 24 patients; 50% had HBsAg. Liver tissue positivity was very low in the fully developed stage compared to serum positivity. In 146 patients with other liver ailments, both liver and serum were negative for HBsAg.

Acute Disease↗
PubMed1976

Distribution patterns of hepatitis B surface antigen (HBsAg) in the liver of hepatitis patients.

One hundred liver biopsies from 100 hepatitis patients were examined by the indirect immunofluorescent technique for the detection of HBsAg. Of the 60 positive specimens 52 were diagnosed as various types of chronic hepatitis and 8 were acute hepatitis. Four main distribution patterns of HBsAg were obtained: full cytoplasmic fluorescence with diffuse lobular distribution; cytoplasmic fluorescence with spotty distribution; peripheral fluorescence in the cell membrane and/or cell peripheries; and focal cytoplasmic positivity. There was an inverse relationship between the number of positive hepatocytes and the extent of liver cell necrosis. The distribution patterns of HBsAg were distinctive in each type of chronic hepatitis and in acute hepatitis. Homogeneous full cytoplasmic fluorescence, distributed diffusely in the whole liver lobule, was observed in chronic persistent hepatitis and in cirrhosis with little activity whereas peripheral liver cell membrane and/or peripheral cytoplasmic fluorescence associated with cytoplasmic positivity in a smaller number of hepatocytes was a characteristic finding in chronic aggressive hepatitis, active cirrhosis, and acute hepatitis with possible transition to chronicity. Focal cytoplasmic fluorescence was observed in acute hepatitis and a group of biopsies in chronic hepatitis in which HBsAg was detected in the liver but no antigen was detectable in the serum. The results show that the different patterns of distribution of HBsAg in the liver biopsy are helpful for the histological diagnosis of different types of HBAg positive viral hepatitis and are consistent with the hypothesis of the role of specific immune response in the pathogenesis of type B viral hepatitis.

Acute Disease↗
PubMed1976

Differential distribution of hepatitis B surface antigen and hepatitis B core antigen in the liver of hepatitis B patients.

One hundred liver biopsies from 100 patients with clinical presumptive diagnosis of hepatitis were examined by immunofluorescence for the presence of hepatitis B surface antigen (HBSAg) and hepatitis B core antigen (HBcAg). Of the 60 HBsAg-positive livers, 51 were diagnosed as chronic hepatitis on histological grounds, 6 as acute hepatitis, and 3 as "near-normal liver." From the 60 tissue-positive cases, 3 subjects were HBsAg seronegative. HBcAg was detected in 44 livers, all of which also had HBcAg in the localized in the cytoplasm and the membranes of the hepatocytes, and HBcAg in the nuclei and in 4 cases also in the cytoplasm. Predominant HBsAg expression in the cytoplasm was observed in near-normal liver, chronic persistent hepatitis, and cirrhosis with little activity. This correlated with the amount of ground glass hepatocytes in the biopsies. HBcAg and membrane-localized HBsAg were minimal in those conditions. HBcAg was most prevalent in patients with chronic aggressive hepatitis and active cirrhosis treated with immunosuppressive drugs, whereas the amounts of HBsAg and HBcAg in nontreated patients of those two groups and in acute hepatitis with signs of transition to chronicity were almost equal. HBsAg expression in liver cell membranes was most prominent in active forms of chronic hepatitis (chronic aggressive hepatitis and in active cirrhosis) and in acute hepatitis with signs of transition to chronicity. This observation correlated in the presence of HBcAg in the biopsies of those patients. In acute hepatitis both HBsAg and HBcAg were detected rarely and no membrane expression of HBsAg was observed. The over-all results show a significant relationship between the different degrees of accumulation of HBsAg and HBcAg in the liver and the various histological types of hepatitis and further suggest an interplay of both hepatitis B virus and host immune response in the development and pathogenesis of hepatitis B.

Acute Disease↗