Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cirrhosis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Computerized morphometry of the cirrhotic liver: comparative analysis in primary biliary cirrhosis, alcoholic cirrhosis, and posthepatitic cirrhosis.

Fibrosis and nodular regeneration are the hallmarks of liver cirrhosis. To assess the degree of fibrosis and the severity of the structural changes affecting parenchymal and extraparenchymal components in liver cirrhosis, a computerized morphometric model has been applied to liver specimens from patients undergoing liver transplantation for primary biliary cirrhosis, posthepatitic and alcoholic cirrhosis. Fifty-eight hepatectomy specimens from patients undergoing liver transplantation for cirrhosis were analyzed: 17 alcoholic, 28 posthepatitic (HBV-related and HCV-related cirrhosis), and 13 primary biliary cirrhoses. Liver specimens were fixed in 10% neutral-buffered formalin and embedded in paraffin. Sections were stained with chromotrope-aniline blue method and monoclonal antibodies against cytokeratin 7 and CD31. Volume fractions of parenchymal compartment and fibrosis were stereologically determined on the specimens stained with chromotrope-aniline blue method. Volume fractions of portal bile ducts, proliferated bile ductules, and hepatocytes with biliary metaplasia were measured on cytokeratin 7 stains, while volume fractions of capillary units have been evaluated on CD31 staining. Volume fraction of fibrosis was higher in primary biliary cirrhosis than in the other disease-induced cirrhosis. The main differences were related to immunohistochemical staining. Volume fraction of hepatocytes with biliary metaplasia was higher in HCV-related cirrhosis, whereas volume fractions of biliary structures were more prominent in HBV-related cirrhosis. Primary biliary cirrhosis was characterized by a reduced number of bile ducts and by a wider expression of cytokeratin 7 into periportal hepatocytes. Capillary units were more prominent in primary biliary cirrhosis than alcoholic and posthepatitic cirrhosis. Our computerized morphometric model well describes and quantifies the morphological alterations of the liver and it could represent an adjunctive tool to evaluate the degree of dysplastic phenomena involving parenchymal and extraparenchymal compartments.

Adult↗

Regenerative pattern of liver cells in primary biliary cirrhosis, alcoholic cirrhosis, posthepatitic cirrhosis (HBV-related) and hepatocellular carcinoma: comparative analysis by computerized morphometry.

Computerized morphometrical measurements were made of liver cells and their nuclei taken from biopsy specimens of primary biliary cirrhosis (PBC), alcoholic cirrhosis, posthepatitic cirrhosis (HBV-related), and hepatocellular carcinoma (HCC). The specimens were stained with hematoxylin-eosin (HE), Mallory's stain for collagen fibers, orcein method, periodic acid Schiff (PAS) reaction, and silver impregnation. Light microscopic views were then selected and original liver cells were magnified x 1000. The size of liver cell nuclei, distance between corresponding liver cell nuclei and distribution pattern of hepatocytes were calculated by computer. Variation in regenerative activity among the four disease groups was noted. Regenerative features of liver cells were mild in degree in PBC. In alcoholic cirrhosis, regenerative features of liver cells were less prominent than in posthepatitic cirrhosis. In posthepatitic cirrhosis, regenerative liver cells were well developed, showing remarkable pleomorphism of liver cell nuclei and expansive arrangement of liver cell cords. This tendency towards regenerative activity suggests that the possibility of HCC occurring is greater in posthepatitic cirrhosis than in PBC or alcoholic cirrhosis. It was concluded that morphologically, there is a greater possibility of occurrence of HCC in posthepatitic cirrhosis than in any other type of cirrhosis, because of its high regenerative hepatocytic activity. Also etiological factors of liver diseases are more important in the development of liver cell regeneration. Furthermore, regenerative activity can be measured by computerized morphometry as an established methodology.

Adult↗

Portasystemic shunts in primary biliary cirrhosis: survival is the same as in patients with Laennec's cirrhosis and postnecrotic cirrhosis.

There is little information regarding survival of patients with primary biliary cirrhosis (PBC) who undergo portasystemic shunt operations. The few published reports suggest that survival may be better in this group than in patients with other types of cirrhosis who undergo this procedure. Therefore, we reviewed our experience with 17 patients with PBC who underwent portasystemic shunts and compared their survival with 100 patients with Laennec's and postnecrotic cirrhosis, using the life-table method. We find that survival rates are the same in patients with PBC, Laennec's cirrhosis, and postnecrotic cirrhosis following portasystemic anastomosis.

Adult↗

Clinicopathological studies and operative results of hepatocellular carcinoma with liver cirrhosis, comparing HB-associated cirrhosis to alcoholic and post-transfusion cirrhosis.

The present study was undertaken to elucidate clinicopathological findings and operative results of HCC with HB-associated cirrhosis, compared with those in HCC patients with alcoholic and post-transfusion cirrhosis. The number of the HBV group was 26 cases, consisting of 17 in sAg(+), 4 in eAg(+) and 5 in eAb(+) subgroups. The number of the post-transfusion group was 7 and that of alcoholic group was 12. A high incidence of hypersplenism and esophageal varix in the eAg(+) subgroup was found. ICG R15 was the highest, KICG and ICG Rmax were the lowest in the eAg(+) subgroup. The mean diameter of tumors was the largest, 6.6 +/- 3.9 cm, in the sAg(+) subgroup and was the smallest, 2.2 +/- 1.7 cm, in the eAg(+) subgroup. The incidence of postoperative jaundice, hyperammoninemia and live dysfunction were the highest in the sAg(+) and eAg(+) subgroup. One and three-year survival rate were 76.9% and 48.1% in the sAg(+) subgroup, 60.0% and 30.0% in the eAb(+) subgroup, and the one-year survival rate in the eAg(+) subgroup was 50.0%. The three-year survival rate could not be calculated because 3 years had not passed since the operation. The prognosis was the poorest in the HBV group among all groups. This study suggests that in HBV-associated cirrhosis, hepatectomy might induce "acute on chronic" changes (acute hepatitis and fulminant hepatitis). Therefore we should select operative procedures by considering surgical risk and the etiology of liver cirrhosis in hepatectomy.

Adult↗

Spontaneous regression of oesophageal varices after long-term conservative treatment. Retrospective study in 20 patients with alcoholic liver cirrhosis, posthepatitic cirrhosis and haemochromatosis with cirrhosis.

Spontaneous regression of oesophageal varices in liver cirrhotics without sclerotherapy or shunt operation has only been known in alcoholic cirrhosis after alcohol abstinence. Therefore, 20 liver cirrhotics of different aetiologies were controlled over 13 years (six alcohol, nine hepatitis, five haemochromatosis). Under strict alcohol abstinence, all underwent treatment with lactulose and ammonia-reducing amino acids to improve the urea synthesis in the liver. Since gastrointestinal bleeding was not observed, neither sclerotherapy nor shunt operation were performed. Initially, all patients had oesophageal varices (nine stage III, three stage II-III, eight stage II). Following conservative therapy, eight cirrhotics showed total regression and twelve showed stage I-II. Their Child-Pugh index, and urea synthesis rate improved significantly. Possible causes for the spontaneous regression of oesophageal varices are strict abstinence from alcohol, spontaneous seroconversion in six posthepatic B-cirrhoses and consequent phlebotomy in haemochromatosis.

Adult↗

Serum prealbumin, transferrin and immunoglobulins in fatty liver, alcoholic cirrhosis and primary biliary cirrhosis.

The serum concentrations of prealbumin, transferrin and immunoglobulins, as well as their concentration ratios, were determined in patients with fatty liver, alcoholic cirrhosis and primary biliary cirrhosis to evaluate the usefulness of these measurements in the differentiation between these diseases, and in the evaluation of the severity of the liver injury. Alcoholic cirrhosis was characterized by high IgA/prealbumin and IgG/prealbumin ratios, whereas in fatty liver these ratios remained normal or close to normal. The IgG concentration and the ratio of IgG/prealbumin were markedly higher in advanced than in early alcoholic cirrhosis, IgG/prealbumin being the most sensitive indicator. None of the assays reflected the degree of fatty degeneration. In primary biliary cirrhosis the mean IgG concentration was 93% higher than in alcoholic cirrhosis. One of ten patients with primary biliary cirrhosis had a normal IgM level, whereas 2 of 10 patients with alcoholic cirrhosis had a value above normal (greater than 2.9 g/l). IgM alone did not differentiate between alcoholic and primary biliary cirrhosis, while the ratio of IgA/IgM seems useful: a value over 2.0 was found in all patients with alcoholic cirrhosis but in none of those with primary biliary cirrhosis.

Adult↗

Pathology of the liver in Budd-Chiari syndrome: portal vein thrombosis and the histogenesis of veno-centric cirrhosis, veno-portal cirrhosis, and large regenerative nodules.

Hepatic vein (HV) thrombosis causes ascites, hepatomegaly, and severe congestion of the liver (Budd-Chiari syndrome [BCS]). Severe hepatic fibrosis develops in this syndrome with a variety of histological patterns. Some livers have a pattern of cirrhosis in which there is fibrous bridging between HVs and portal tracts (veno-portal cirrhosis). Other livers have a pattern of "reversed-lobulation cirrhosis" (veno-centric cirrhosis), in which fibrous bridging between HVs and portal tracts is minimal. The prevalence and pathogenesis of these forms of cirrhosis and the effect of portal vein (PV) thrombosis in this disease have not been studied. We examined 15 resected livers from patients with BCS to determine the distribution of vascular obstruction and the character of the parenchymal response. Six livers had veno-portal cirrhosis, and all of these had severe PV obliteration caused by thrombosis. Three livers had veno-centric cirrhosis and had normal medium and large PVs. The remaining six livers had mixed veno-centric/veno-portal cirrhosis and had moderate PV obliteration. The nodules in veno-centric cirrhosis had evidence of an unusual circulation with small arteries supplying a midzonal venous plexus that appeared to drain retrogradely into patent small PVs. Nine livers had large regenerative nodules histologically similar to focal nodular hyperplasia. PV thrombosis is a frequent occurrence in BCS. The correlation between PV thrombosis and the pattern of cirrhosis suggests a role for PV obliteration in the genesis of veno-portal bridging fibrosis in this disease and possibly in other diseases leading to cirrhosis.

Adult↗

Regression of human cirrhosis. Morphologic features and the genesis of incomplete septal cirrhosis.

CONTEXT: Cirrhosis is widely regarded as being irreversible. Recent studies have demonstrated that fibrosis may decrease with time in humans and experimental animals if the disease activity becomes quiescent. The histologic appearance of regressing cirrhosis in the human has not been described in detail. OBJECTIVES: To define histologic parameters that indicate regression of cirrhosis and to provide an interpretation of how regression occurs from a histologic point of view. DESIGN: A patient who underwent a series of biopsies that showed apparent regression of hepatitis B cirrhosis is presented. In addition, 52 livers removed at transplantation having cirrhosis or incomplete septal cirrhosis were graded for histologic parameters that suggest progression or regression of fibrosis. Progression parameters were steatohepatitis, inflammation, bridging necrosis, and piecemeal necrosis. The regression parameters (collectively called the hepatic repair complex) were delicate perforated septa, isolated thick collagen fibers, delicate periportal fibrous spikes, portal tract remnants, hepatic vein remnants with prolapsed hepatocytes, hepatocytes within portal tracts or splitting septa, minute regenerative nodules, and aberrant parenchymal veins. RESULTS AND CONCLUSIONS: Regression parameters were found in all livers and were prominent in the majority. Livers with micronodular cirrhosis, macronodular cirrhosis, and incomplete septal cirrhosis demonstrate a histologic continuum. A continuum of regressive changes was also seen within individual livers. These appearances allow one to understand visually how fibrous regions of hepatic parenchyma can be returned toward a normal appearance. Many examples of incomplete septal cirrhosis could be the product of regressed cirrhosis.

Adult↗

Characteristic differences according to the cirrhotic pattern of advanced primary biliary cirrhosis: Macronodular cirrhosis indicates slow progression.

It is important to evaluate advanced primary biliary cirrhosis (PBC) clinicopathologically to clarify its progressive mechanism. According to the cirrhotic pattern, 26 cases of explanted PBC were classified into non-cirrhotic (n=4), macronodular (n=4), mixed nodular (n=6), and micronodular cirrhosis (n=12), to compare their clinical and morphological features. In addition, the degree of preserved intrahepatic bile ducts and other histologic features were analyzed. Patients at living donor liver transplantation (LDLT) in the macronodular cirrhosis were significantly older than those in the micronodular cirrhosis. The mean duration between clinical presentation and LDLT in the macronodular cirrhosis was significantly longer than in the micronodular cirrhosis. The non-cirrhotic group showed a short duration between clinical presentation and LDLT. The ratio of explanted liver volume to standard liver volume (ELV/SLV) indicates that macronodular cirrhosis revealed more atrophic change than that in the other three types. The density of remnant intrahepatic bile ducts of less than 50mum per group in cases of macronodular cirrhosis was significantly higher than that in cases of micronodular cirrhosis. Therefore, different cirrhotic patterns of advanced PBC were correlated with the disease progression and the degree of bile duct disappearance. The macronodular cirrhotic patients were older, had a longer disease course, yet had less bile duct loss. We suggest that macronodular cirrhosis and micronodular cirrhosis of PBC are different type of PBC.

Journal Article↗

Survival in patients with postnecrotic cirrhosis and Laennec's cirrhosis undergoing therapeutic portacaval shunt.

Survival rates were compared in 82 patients who underwent therapeutic portacaval shunt. All patients were followed for at least 5 years after shunt or until death. Survival rates were calculated by Life Table methods. Based on a combination of currently accepted histological and clinical criteria, there were 45 patients with Laennec's cirrhosis, 29 patients with postnecrotic cirrhosis, 11 of whom had histological evidence of chronic active hepatitis, and 8 patients with primary biliary cirrhosis. Survival rates were similar in all three groups, alcoholic cirrhosis, postnecrotic cirrhosis, and primary biliary cirrhosis. Hepatic reserve, as defined by Child's classification, provided the best criteria for predicting survival. The type of shunt, end-to-side, side-to-side, or splenorenal, did not influence survival. Histological evidence of chronic active hepatitis adversely affected survival in patients with postnecrotic cirrhosis. However, histological evidence of ongoing alcoholic hepatitis in patients with Laennec's cirrhosis did not influence survival adversely. The data indicate that once a patient with cirrhosis has bled from esophageal varices, the etiology of the cirrhosis is not a major factor in determining survival after a therapeutic portacaval shunt.

Adult↗

Survival in hepatitis-B cirrhosis compared to alcoholic cirrhosis in patients with Child's C liver disease: a prospective study of endoscopic sclerotherapy for bleeding oesophageal varices.

A prospective comparative study was carried out on thirty-seven consecutive patients presenting with bleeding oesophageal varices at University Hospital, Kuala Lumpur. All patients received injection sclerotherapy if active bleeding was seen at the time of initial endoscopy, followed by repetitive courses of sclerotherapy to obliterate the varices. Predominant aetiological factors were hepatitis-B cirrhosis (43%) and alcoholic cirrhosis (30%). Chinese ethnic group accounted for 62.5% of hepatitis-B cirrhotics and Indian 73% of alcoholic cirrhotics. After excluding patients lost to follow-up, analysis of the remaining thirty-four patients showed reduced long-term survival in patients with Child's C disease. Log-rank analysis of survival curves between hepatitis-B cirrhosis and alcoholic cirrhosis in patients with Child's C liver disease showed no significant difference in long-term survival (p = 0.07). However, six deaths were seen in hepatitis-B cirrhosis compared to one death in alcoholic cirrhosis in the first eight months of follow-up. Most patients died from progressive liver failure. Median survival for Child's C hepatitis-B cirrhosis was 7.5 months whereas this had not been reached for Child's C alcoholic cirrhosis (median follow-up 11.6 months). We conclude that variceal haemorrhage in Child's C hepatitis-B cirrhosis is a bad prognostic sign and is associated with reduced survival with a median survival of 7.5 months despite control of the variceal bleed.

Adult↗

Distribution of constitutive (COX-1) and inducible (COX-2) cyclooxygenase in postviral human liver cirrhosis: a possible role for COX-2 in the pathogenesis of liver cirrhosis.

AIMS: Prostaglandins produced by the action of cyclooxygenases (COX) are important mediators of systemic vasodilatation and inflammation in liver cirrhosis. The aim of this study was to investigate the distribution of COX-1 and COX-2 in postviral cirrhosis. METHODS: The immunohistochemical expression of the constitutive (COX-1) and the inducible (COX-2) isoenzymes was investigated in 15 patients with cirrhosis after hepatitis B and C infection; three normal control livers were also analysed. RESULTS: COX-2 was absent from normal liver but was highly expressed in cirrhosis, mainly in the inflammatory, sinusoidal, vascular endothelial, and biliary epithelial cells. Low amounts of COX-1 were expressed in both normal and cirrhotic livers, exclusively in sinusoidal and vascular endothelial cells, with no differences seen between normal and cirrhotic livers. CONCLUSIONS: COX-2 is overexpressed in liver cirrhosis, and possibly contributes to prostaglandin overproduction, which may be a major component of the inflammation and hyperdynamic circulation associated with cirrhosis. Because COX-2 is thought to contribute to tumour development, high COX-2 production could be a contributor to hepatocellular carcinoma development in cirrhosis. The finding of COX-2 and not COX-1 upregulation in cirrhosis could provide a possible new role for selective COX-2 inhibitors in reducing inflammation and minimising the occurrence of hepatocellular carcinoma in patients with cirrhosis.

Adult↗

Clinical and biochemical features and therapy responses in primary biliary cirrhosis and primary biliary cirrhosis-autoimmune hepatitis overlap syndrome.

BACKGROUND/AIMS: Primary biliary cirrhosis and autoimmune hepatitis are two main immune-mediated liver diseases. Some patients display characteristics of both diseases, so called overlap syndrome. The aims of this study were to investigate and to compare the clinical and laboratory features and responses to therapy in primary biliary cirrhosis and overlap syndrome. METHODOLOGY: Twenty-three patients with primary biliary cirrhosis (21 females, 2 males; median age: 50 years) and 20 with primary biliary cirrhosis-autoimmune hepatitis overlap syndrome (18 females, 2 males; median age: 44 years) were included in the study. All patients with primary biliary cirrhosis were treated with ursodeoxycholic acid. Of patients with overlap syndrome, 16 were treated with ursodeoxycholic acid and 4 with ursodeoxycholic acid plus prednisolone. Histological findings laboratory and clinical data were compared at the baseline and at the 2nd year of treatment. RESULTS: Fatigue and pruritus were the most frequent and comparable symptoms in each group. Serum ALT, AST, gamma-glutamyl transpeptidase, total protein, globulin and gammaglobulin levels were higher in patients with overlap syndrome than those in patients with primary biliary cirrhosis. At the end of the 2nd year of the treatment, ALT normalization was achieved in 12 (52%), alkaline phosphatase in 7 (30%) patients with primary biliary cirrhosis. One of the non-responders to ursodeoxycholic acid therapy had the histological findings of overlap syndrome in her control biopsy. Fibrosis score deteriorated in 50% of the patients. Of ursodeoxycholic acid-treated overlap syndrome patients, 11 completed 2 years of treatment. Three patients were biochemically non-responsive and prednisolone was added to their regimen. Of the remaining 8 patients, 7 (64% of total patients) had normal ALT. Three patients had worse fibrosis score comparing the onset of the treatment. Six of 7 (86%) patients who were given ursodeoxycholic acid plus prednisolone including ursodeoxycholic acid-non-responsives had normal ALT and 2 of 6 biopsy-controlled patients display deterioration of their fibrosis score. CONCLUSIONS: Biochemical tests tended to be higher in patients with overlap syndrome comparing to those with primary biliary cirrhosis. Response to ursodeoxycholic acid treatment in patients with overlap syndrome was comparable with that obtained in primary biliary cirrhosis. Therefore it should be the first-line treatment. Non-responsive patients may benefit from the use of ursodeoxycholic acid plus prednisolone combination.

Adult↗