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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatic fibrosis may result from collapse after hepatocellular necrosis or from new formation of connective tissue. Fibroplasia, particularly within the lobular parenchyma, is a dynamic process. Newer cellular and biochemical investigations clarified its various steps. The process begins with stimulation of cells to connective tissue formation and can be divided into (1) intracellular synthesis, (2) extracellular maturation, and (3) collagen breakdown. The turnover of the connective tissue in the liver is conspicuously increased in chronic hepatitis of any type, as indicated by an elevation of several cellular and metabolic parameters. They are particularly raised in chronic hepatitis and in alcoholic liver injury. Further development of these parameters in the future should facilitate the analysis of the dynamics of fibroplasia. The strongest stimuli for hepatic fibroplasia are hepatocellular necrosis and inflammation, but ethyl alcohol and steatosis are also stimulating, though to a lesser degree. This explains the particular elevation of the fibroplastic parameters in alcoholic hepatitis. It points, however, also to the possibility that cirrhosis might develop without significant hepatocellular necrosis and inflammation. Perihepatocellular, periductular, and septal fibrosis are the functionally most important localizations leading to additional hepatic injury. The initiation of these types of fibrosis by liver injury points to a vicious circle. Specific anti-fibroplastic therapy is still in infancy.
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PMID:[Hepatic fibrosis--mechanism, dynamics and clinical consequences (author's transl)]. 20 39

Collagen in bulk was isolated in about 30% yield from the livers of normal human beings and from livers of persons with alcholic cirrhosis. Analyzed chemically and examined by electron microscopy, the collagen in each case was shown to consist of two types identical with, or resembling closely, type I and type III collagens of skin. The collagen from normal liver was predominantly type I, whereas, that from cirrhotic livers consisted or approximately equal amounts of the two types. By chromatography on carboxymethyl-cellulose, the type I collagen from the cirrhotic livers showed one alpha2chain and two alpha1 chains. The alpha1 chains were separable from one another, but gel electrophoretic patterns of peptides obtained from them after treatment with CNBr were almost identical, and resembled the pattern obtained with CNBr peptides of the alpha1 chain of rat skin type I collagen. The increased collagen of both types was responsible in part for the observed distortion of the architecture of the cirrhotic livers associated with increased rigidity of the stroma. The predominance of type III collagen in the areas of collapse of architecture where, as shown by others, few fibroblasts are present, suggests that hepatocytes might have an important function in fibrogenesis during the course of liver cirrhosis.
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PMID:Increase in type I and type III collagens in human alcoholic liver cirrhosis. 106 Nov 56

Two sisters had erythropoietic protoporphyria and a spectrum of liver disease. One (F.B.) died in hepatic failure within 3 months after the development of jaundice. Only 10 months before she died, she had exhibited only bromsulfalein retention and a borderline increase in serum transaminase. Surgical exploration because of the jaundice revealed patency of the bile ducts which was confirmed at autopsy. Wedge biopsy and autopsy specimens of liver showed an active cirrhosis with massive amounts of protoporphyrin in Kupffer cells, portal histiocytes, bile canaliculi and parenchymal cytoplasm. The other sister (L.R.) had never had symptomatic liver disease and only a slight increase in serum transaminase and bromsulfalein retention. On needle biopsy, the liver specimen showed portal inflammation with erosion of limiting plates, occasional bridging between triads and central areas of cell dropout. Protoporphyrin pigment was present in portal histiocytes, areas of central collapse and, more rarely, in parenchymal cytoplasm. These studies demonstrate that significant, progressive hepatic disease may occur insidiously in erythropoietic protoporphyria, and that once jaundice appears it may be followed rapidly by fatal hepatic failure.
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PMID:Hepatic disease in erythropoietic protoporphyria. 113 41

Twenty-two patients with hepatocellular carcinoma were treated by a new method of transcatheter arterial chemoembolization using an autologous blood clot as an embolizing agent. All had underlying advanced cirrhosis (14 Child's class B and 8 Child's class C patients). The median follow-up interval was 11 mo (range = 2 to 30 mo). The results of the treatment were compared with those of conventional chemoembolization using gelatin sponge particles for 19 Child's class B patients as historical controls. The survival rate for Child's class B patients treated by the new procedure estimated by the Kaplan-Meier method was 100% at 2 yr, whereas the survival rate for Child's class B patients treated by conventional chemoembolization was 89% at 1 yr and 72% at 2 yr. The survival rate for Child's class C patients was 75% at 1 yr and 50% at 2 yr. Side effects such as pyrexia of more than 38 degrees C or an elevation of the serum bilirubin level of more than 1.5-fold were less common in patients treated by the new method than in those treated by conventional chemoembolization, and thus the new procedure could be performed even for Child's class C patients. The autologous blood clot did not collapse the hepatic arteries even when the embolization was performed repeatedly, and thus fine collateral vessels feeding recurrent hepatocellular carcinoma did not develop. The results suggest that the new chemoembolization using an autologous blood clot is a promising therapeutic procedure in the management of hepatocellular carcinoma associated with advanced cirrhosis.
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PMID:Treatment of hepatocellular carcinoma associated with advanced cirrhosis by transcatheter arterial chemoembolization using autologous blood clot: a preliminary report. 131 Apr 76

Before the availability of serological markers for hepatitis C, the morphological features of this diagnosis, which represents most non-A, non-B hepatitis, could not be confirmed. We examined biopsy specimens from 50 patients with chronic hepatitis C and 21 patients with autoimmune chronic hepatitis. Each biopsy specimen was graded on 19 different histological features. The results indicated that at the time of biopsy, the average age of patients with chronic hepatitis C was 46 yr vs. 36 yr for autoimmune chronic hepatitis. Cirrhosis was seen more frequently in autoimmune chronic hepatitis (90%) than in hepatitis C (58%). Features more commonly observed in chronic hepatitis C were bile duct damage (91% vs. 40%), bile duct loss (91% vs. 20%), steatosis (72% vs. 19%) and lymphoid cell aggregation (follicles) within portal tracts (49% vs. 10%). Severe lobular necrosis and inflammation (76% vs. 38%), piecemeal necrosis (81% vs. 10%), multinucleated hepatocytes (29% vs. 6%) and broad areas of parenchymal collapse (76% vs. 6%) were seen more often in autoimmune chronic hepatitis. Exclusion of five patients with autoimmune chronic hepatitis who received immunosuppression before biopsy accentuated these differences. In conclusion, morphological criteria, in addition to serological data, may be useful for differentiating chronic hepatitis C from autoimmune chronic hepatitis, which histologically is a more aggressive disease.
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PMID:The histological features of chronic hepatitis C and autoimmune chronic hepatitis: a comparative analysis. 155 32

In order to see if the term of "plasma cell hepatitis", dating back to the early sixties, is still valid as a morphological diagnosis for autoimmune chronic hepatitis (AICH), and to find out if the existence of several subgroups is reflected by histopathology, we investigated 26 patients with chronic hepatitis, who met the criteria of autoimmune hepatitis based on tests for antinuclear, anti-smooth muscle antibodies (SMA) and on immunoassays for liver-kidney-microsomal (LKM) antigen, liver membrane antigen (LMA), and soluble liver antigen (SLA). In our material autoimmune hepatitis represent the entire spectrum of chronic hepatitis with variable inflammatory activity ranging from chronic persistent hepatitis to severe inflammatory lesions in chronic active hepatitis with transition to cirrhosis. When compared to viral chronic hepatitis A and non-A, non-B, however, characteristic features can be evaluated consisting in broad hypocellular areas of collapse and microacinar transformation of hepatocytes with hydropic swelling being the predominant type of cell lesion. Eosinophilic clumping and acidophilic necrosis were insignificant. Plasma cells were not a constituent feature of AICH. From this histopathologic pattern it may be concluded that the disease seems to run a sluggish course in most patients, however, in few cases a dramatic development may determine the disease with fatal acute episodes which are terminated by death or fade into slow progression. The different subgroups could not be distinguished by histopathology.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histologic features in autoimmune hepatitis. 250 55

Eleven cases of Wilson's disease presenting as fulminant hepatic failure were analysed retrospectively to determine the specificity or otherwise of the histological findings. All cases were cirrhotic, eight with a micronodular pattern. There was marked parenchymal collapse with ductular proliferation and mild inflammation. Other features included cholestasis, hepatocyte necrosis, microvesicular fat and nuclear vacuolation. Orcein staining demonstrated copper-associated protein in the periphery of cirrhotic nodules in all cases and also variably within nodules in eight cases. Copper was demonstrable by the rhodanine method in similar locations but the staining reaction was qualitatively weaker in all cases. Characteristically, there was staining of both parenchymal and mononuclear phagocytic cells. This triad of cirrhosis, strong copper-associated protein deposition and copper positivity was not present in a control group of 20 cases of fulminant hepatic failure of other aetiology and with a similar clinical presentation. It is concluded that in the clinical context of fulminant hepatitis the presence of cirrhosis should raise the suspicion of Wilson's disease and that, with routinely processed and stained tissue, including autopsy tissue, the diagnosis can be made histologically.
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PMID:Hepatic morphology and histochemistry of Wilson's disease presenting as fulminant hepatic failure: a study of 11 cases. 280 95

Ninety five cases of HBV marker-negative cirrhosis with excess alcohol intake were examined clinicopathologically to obtain some clues and insights into the pathogenesis of hepatocellular carcinoma (HCC). The following data were obtained: cases were divided morphologically into 37 cases of macronodular cirrhosis (MacCir), 16 mixed cirrhosis (MixCir), and 42 micronodular cirrhosis (MicCir), the mean age at death was the oldest in MacCir (61 yrs), the youngest in MicCir (51 yrs), and intermediate in MixCir (59 yrs), association of HCC was common both in MacCir and MixCir (78 and 63%, respectively) but infrequent in MicCir (17%), all livers of MicCir with HCC had broad collapse and a small number of macronodules in non-cancerous areas and the mean age of them was older than that of MicCir without both the collapse and macronodules (56 vs 48 yrs), in total cases, the mean age at death of patients with HCC was 7 years older than that without HCC (60 vs 53 yrs), the mean liver weight was the largest in MicCir (1,211 g), the smallest in MacCir (829 g), and intermediate in MixCir (1,022 g), the incidence of MacCir was significantly higher in patients who had given up alcohol for more than one year before death than those without abstinence, and neither the subtypes of cirrhosis nor the incidence of HCC was significantly related to the total amount of alcohol intake. These data indicate that the development of HCC in HBV-negative alcoholics with cirrhosis occurs in relation to the development of macronodules and loss of liver weight, most likely along with the prolongation of the life span.
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PMID:Studies on the pathogenesis of hepatocellular carcinoma in HBV-negative alcoholic cirrhotics. 302 47

An association of alcoholic cirrhosis of the liver, hepatoma, extensive aortic thrombosis, and chronic bleeding peptic ulcer of the duodenal bulbus in a patient who survived only three days after hospitalisation is reported. An explanation of each disease is given and the fact that a basically hypocoagulative situation (cirrhosis) can give rise to thrombosis of the aorta is stressed. Production and release into the circulation of thromboplastins by the hepatoma (paraneoplastic syndrome), leading aortic atherosclerosis and slow circulation due to haemorrhagic cardiocirculatory collapse was the most likely explanation.
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PMID:[Association of liver cirrhosis, hepatoma, extensive aortic thrombosis and chronic duodenal peptic ulcer in the same patient]. 626 18

We report immunohistological findings in liver, spleen, brain, and skeletal muscle of a 23-year-old woman with hepatitis nonA/nonB caused by contaminated anti-D-globulin. She died in a liver coma. At autopsy, a chronic liver dystrophy with cirrhosis was diagnosed. The necrotic areas of the liver showed a collapse of the reticulin framework, newly formed collagen fibres, and diffuse inflammation with immunohistological evidence of IgG, CIq, C9, and fibrinogen. C4 and C9 could be localised in bile thrombi and in the cytoplasm of pseudotubular transformed hepatocytes. In addition, C9 was found in blood vessel walls. A local distribution of HBsAg was found in the cytoplasm and/or the periphery of liver cells. HBcAg could not be detected in any of 5 different regions of the liver. A serum with antibodies to acute phase antigen of nonA/nonB hepatitis stained the cytoplasm and nuclei of (mostly intact) liver cells focally and their cell membranes diffusely. Patchy deposits of IgA and IgM were demonstrated in liver, brain und spleen. Circulating antibodies to cell nuclei and smooth muscle reacted with the patient's own liver and brain but not with spleen and skeletal muscle.--It is suggested that the manifold immunohistological findings in this patient are an expression of the vain attempt of the organism to clear away antigenic material, probably induced by different hepatitis viruses.
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PMID:[Immunohistologic findings in the liver, spleen, brain and skeletal muscles in fatal cholestatic viral hepatitis (following double infection with hepatitis B and non-A/non-B?)]. 641 98


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