Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence of chronic hepatitis was found on histological examination in nine out of 15 patients positive for hepatitis-B surface antigen (HBsAg) who had either chronic renal failure or a functioning renal transplant. Cirrhosis had already developed in three of the patients, who deteriorated rapidly and died. Liver biopsies from the remaining 12 patients showed the features of chronic aggressive hepatitis in two, chronic persistent hepatitis in four, and minor histological lesions in six. The persistence of HBsAg in patients with renal failure or in those receiving immunosuppressive drugs after a transplant must indicate some impairment of the normal immune response to hepatitis-B viral antigens. Nevertheless, cellular or humoral immunity to HBsAg was detected in all eight patients with chronic hepatitis tested compared with only one out of five with minimal liver lesions, which suggests that the severity of the liver damage may be directly related to the degree of immunocompetence.
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PMID:Immune response to HBsAg and the spectrum of liver lesions in HBsAg-positive patients with chronic renal disease. 77 35

Our knowledge of the cellular changes that lead to liver cell carcinoma in humans is limited by proper and necessary ethical restriction on clinical research. We know rather more about risk factors, the most important of which is cirrhosis, it seems that both the causative agent and the time of duration of the cirrhotic process are relevent to the magnitude of this risk. According to present knowledge, alpha1-antitrypsin deficiency, alcoholism, naturally occurring carcinogens, drugs, and the hepatitis B virus seem to carry the greatest risk of cancer developing in a cirrhotic patient. Cirrhosis, however, is not an essential prerequisite, and some or possibly all of these agents can also induce cancer without cirrhosis. Bile duct carcinoma commonly follows infestation with liver flukes. Cirrhosis is usually absent but duct epithelial hyperplasia is present prior to the development of cancer. Many cellular changes have been observed in patients and among populations considered to be at risk from liver cancer. Of these, liver cell dysplasia is the most striking and studies of its prevalence, natural history, and association with cirrhosis suggest that it is a precancerous change.
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PMID:Precursor lesions for liver cancer in humans. 77 94

Diabetes mellitus is more frequently found in pateints with hepatic cirrhosis (about 10%) than in subjects without liver disease. Cirrhosis has been the main subject of interest in this respect. Very few studies have been made in viral hepatitis or steatosis. In about 40% of cases, the diabetes is identified before the cirrhosis. More often (in about 60% of cases) the diabetes is discovered at the same time as or after the finding of cirrhosis. This "post-cirrhosis diabetes" shows no clinical peculiarity. In about 80% of patients with liver cirrhosis when fasting blood glucose is normal, abnormalities of carbohydrate metabolism are to be found by the oral glucose tolerance test. Approximately 50% show an abnormal response to intravenous glucose and 30% to intravenous tolbutamide. The "mechanism" of these metabolic abnormalities in liver cirrhosis is unknown. The following abnormalities are observed: 1) With similar glycaemic response to a glucose challenge, plasma insulin levels are higher than in patients without liver disease, suggesting insulin unresponsiveness. Resistance to exogenous insulin can be demonstrated. 2) Plasma free fatty acid levels are often elevated. 3) Plasma growth hormone levels are often raised. 4) Plasma glucagon levels are high when porto-caval shunting is present. 5) Potassium is often depleted. These metabolic abnormalities, in association with porto-caval shunting and hepatocyte insufficiency may explain the insulin resistance which characterises liver cirrhosis, and the diabetes which it may precipitate in predisposed persons.
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PMID:[Diabetes mellitus secondary to liver diseases. A review (author's transl)]. 79 27

Cirrhosis of the liver was provoked in adult rabbits by the administration of CCl4/0,3 ml subcutaneously two times a week during a period of six weeks. It was found that the infection by M. tuberculosis, M. avium and M. kansasii causes a considerably greater dissemination than in the case with the livers of rabbits unaffected by cirrhosis, and that even a non-pathogenic strain (M. intracellulare) is pathogenic, if the liver is affected. Our findings confirm the lowered resistance of a chemically damaged liver to the development of mycobacterial infection.
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PMID:[Pathogenesis of certain mycobacterioses in a chemically damaged liver of the rabbit (author's transl)]. 81 6

The surface features of single cells and of multicellular tissue units in cirrhotic rat livers have been studied by scanning electron microscopy (SEM). Cirrhosis of the liver was produced in rats by simultaneously treating them with carbon tetrachloride and sodium phenobarbital. Connective tissue septa consisted of a losse mesh-work of fibers in which fibroblasts were embedded. The arrangement and surface features of hepatocytes in cirrhotic nodules differed from those found in parenchyma of normal livers. Hepatocytes in cirrhotic nodules universally formed plates two cells thick. The portion of the hepatocyte surface covered by microvilli was greatly increased in cells from cirrhotic livers, and this was reflected in a corresponding reduction in the area occupied by the smooth-surfaced narrow intercellular space. Canaliculi between hepatocytes in cirrhotic livers were reduplicated and frequently branched. hepatocyte surfaces covered by microplicae and flattened microvilli, typical of connective tissue-facing surfaces in normal livers, were greatly increased in cirrhotic livers corresponding to the increase in connective tissue. Where hepatocytes directly contacted fibroblasts (and not fibers), their surfaces were entirely smooth. Sinusoidal endothelial cells in cirrhotic livers contained only isolated, relatively sparse pores, and they lacked both sieve plates (pore complexes) and large fenestrations.
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PMID:Surface features of cirrhotic liver. 82 92

The object of this study was to localize increased sodium resorption in rats with chronic hepatic cirrhosis. Cirrhosis was induced by the administration of phenobarbital and carbon tetrachloride. The animals retained salt and water after loading and showed edema and ascites. Salt and water balance, clearance, and micropuncture tests were performed. Five or six weeks after the start of procedures to induce injury, the rats were unable to excrete salt and water loads promptly. Urine flow and sodium concentration were significantly less in cirrhotic rats with edema and ascites than in the normal controls. The glomerular filtration rate was slightly lower in the right, nonmicropunctured kidney but was the same in the left. The nephron glomerular filtration rates of surface nephrons were equal in both the experimental and control rats. The fractional proximal resorption rate was notably greater in cirrhotic rats, as was the total proximal nephron resorption rate. That increased proximal resorption alone might account for diminished sodium and water excretion cannot be demonstrated from this study, although we believe that major evidence is provided of the importance of proximal resorption in this phenomenon.
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PMID:A micropuncture study of salt and water retention in chronic experimental cirrhosis. 85 Nov 88

In a follow-up study of 85 patients with chronic aggressive (active) hepatitis (CAH) repeated liver biopsies and/or autopsy liver sections were available in 74 cases. The median time of observation was 45 months. Cirrhosis was demonstrated in 38 patients, and cirrhosis was suspected in a further five cases. Fifteen patients showed convincing histological improvement; and the remaining 16 still had chronic hepatitis. Twenty-six patients died during the observation period, seven of these of liver failure after development of cirrhosis. The clinical follow-up of the 59 survivors (median observation time 69 months) showed biochemically active liver disease in 11 cases, all having cirrhosis or chronic aggressive hepatitis in the last biopsy. The clinical findings were correlated with the morphological follow-up diagnosis and the immunosuppressive treatment. Comparison of the initial histological, clinical, and serological variables was made in two well-defined follow-up groups. There were more females, and marked portal inflammation, abnormal bile duct epithelium, and circulating autoantibodies occurred more frequently in the group with later development of cirrhosis than among the patients with subsequent morphological improvement. The results thus suggest candidates for thorough follow-up and more intensive immunosupressive or other treatment.
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PMID:The prognosis of chronic aggressive hepatitis. A clinical and morphological follow-up study. 86 90

Hepatic dysfunction is a common finding in patients with sickle cell disease but viral hepatitis appears to be an unusual complication in the adult SS patient. Only five cases of viral hepatitis were recorded in 378 admissions for SS crisis. In contrast, hepatic crisis occurred as a distinct event in 9% of 88 patients with sickle cell anemia. This entity must be differentiated from acute cholecystitis or viral hepatitis. Transiently abnormal results of hepatitic function tests were observed in another 26 patients with extrahepatic crisis. Cirrhosis is relatively common and often the terminal event in SS disease. Choledocholithiasis and cholecystitis are infrequent complications despite the prevalence of gallstones in SS anemia.
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PMID:Sickle cell hepatopathy. 87 Sep 77

This study was designed to compare the clinical and immunological characteristics of the hepatitis B surface antigen (HBsAg)-positive and HBsAg-negative (cryptogenic) forms of chronic active hepatitis. The data of 48 patients with chronic active hepatitis, 24 with persistent HBs antigenemia and 24 without HBsAg, were analysed. HBsAg was detected by counter-immunoelectrophoresis and radioimmunoassay. The clinical features, biochemical liver function tests, immunoglobulins, complement C3, antoantibodies, and cell-mediated immunoreactivity of the two forms of the disease were compared. Cirrhosis was found to occur more frequently at the time of diagnosis in the HBsAg-negative group, and the serum alkaline phosphatase level was raised significantly compared to the HBsAg-positive form. The elevation of the IgG level was greater in the cryptogenic form, but the difference was not statistically significant compared to the HBsAg-positive patients. There was a marked difference in the frequency of the mitochondrial antibodies, but not of the antinuclear factor and other autoantibody-like serum factors. Lymphoblastic transformation revealed a similar diminution in response to phytohaemagglutinin stimulation in both groups of patients compared to the normal controls. An increase of the 3H-thymidine incorporation was seen after stimulation with human liver mitochondrial antigen, and leukocyte migration inhibition could be observed with this antigen in both forms of chronic active hepatitis.
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PMID:Chronic active hepatitis in patients with and without hepatitis B surface antigenemia. 91 64

To determine the usefulness of recognizing the different morphologic patterns of chronic active liver disease (CALD), we compared clinical and biochemical features as well as responses to treatment in 32 patients with chronic active hepatitis (CAH); 36 with subacute hepatitis and bridging necrosis (SHB); 30 with subacute hepatitis and multilobular necrosis (SHMN); and 30 with cirrhosis and active hepatitis (Cirrh). The morphological lesions did not correlate with clinical or etiologic features. Patients with CAH had less severe biochemical abnormalities, entered remission more often, and failed to respond to treatment less frequently than those with SHMN or Cirrh. SHB and SHMN resembled each other in many regards and showed greater functional changes than CAH. Cirrhosis developed more often after SHMN than CAH and was associated with a poorer prognosis than CAH. Serial liver biopsies revealed all possible histologic transitions, with reduction of inflammation usually occurring in patients treated with steroids and extension of inflammation being more frequent in those not receiving these drugs. CAH, SHB, SHMN, and Cirrh, therefore, reflect the degree and extent of disease activity at any given time in CALD, rather than representing different conditions. Identification of the initial morphologic lesion is helpful because of differences in prognosis.
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PMID:Severe chronic active liver disease. Prognostic significance of initial morphologic patterns. 92 Jul 8


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