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

Iron and copper deposition were examined in patients with chronic active viral hepatitis (CAH) and posthepatitic liver cirrhosis (LC) by Berlin blue, rhodanine, or Victoria blue staining and X-ray microanalysis. Considerable iron or copper deposition was demonstrated in the peripheral zones of hepatic lobules in both CAH (53% of specimens) and LC (63% of specimens). Frozen sections taken from the 2 CAH surgical sections with iron depositions were examined by photoncounting image analysis, and superoxide liberation from the metal granules were demonstrated. In areas of metal deposition, vacuolation of liver cell nuclei, accumulation of lipofuscin, and induction of metallothionein (69% of rhodanine- or Victoria blue-positive specimens) were often demonstrated, whereas induction of ferritin was found only in 14% of Berlin blue-positive specimens. The PCNA index was significantly lower in areas of metal deposition than in the adjacent areas without metal deposition, indicating lowered proliferative capability in the former. These results indicate that cell-mediated immune mechanisms causing the disturbance of bile secretion and heavy metal deposition in the peripheral zones of hepatic lobules may be involved in the progression of viral hepatitis from its acute phase to CAH and finally to LC phase, resulting in piecemeal necrosis. However, cholangitis could not be demonstrated in the present study.
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PMID:Iron and copper deposition in chronic active hepatitis and liver cirrhosis; pathogenetic role in progressive liver cell damage. 863 Apr 40

Hemochromatosis is a disorder of iron metabolism that causes progressive damage to the liver, pancreas, heart and other organs. It is the most common autosomal recessive disorder among whites, and it occurs five times more frequently in males than in females. Manifestations include diabetes mellitus, hepatic dysfunction, congestive heart failure and other end-organ insufficiency. The presentation of hemochromatosis is often nonspecific, requiring the clinician to maintain a high index of suspicion. The diagnosis is suggested by abnormal iron studies, most notably an elevated serum ferritin level and/or transferrin saturation. Liver biopsy can confirm the diagnosis and document the presence of cirrhosis. The diagnosis is also supported by characteristic findings on a magnetic resonance imaging scan, and a diagnostic response to repeated phlebotomy (a hematocrit level that rapidly returns to normal). Phlebotomy treatments reduce the total body iron load, prevent continuing deposition of iron in the tissues, and prevent premature morbidity and mortality. Screening is recommended in affected families, and screening programs for wider populations are being evaluated.
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PMID:Hemochromatosis: diagnosis and management. 905 15

Ninety-four patients with portal hypertension (48 with cirrhosis of the liver and 46 with pathological changes of the portal vein trunk) were examined. The main parameters of iron metabolism were determined by the radioimmunoassay and the iron deports in the liver and spleen biopsy material were revealed. Tissue iron deficiency was found in all patients. The results of the tests were marked by essential peculiarities. In sharp reduction of the level of serum iron and ferritin the parameters of total and latent iron-binding capacity were decreased.
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PMID:[Iron metabolism in patients with portal hypertension]. 868 16

Tumor markers have been used for the evaluation of various malignancies though the existence of false positive results in some benign diseases is known. In this study, several established markers including carcinoembryonic antigen, alpha fetoprotein, beta human chorionic gonadotropin, ferritin, CA 19-9 and CA 125 were measured in 60 patients with chronic active hepatitis, 70 patients with cirrhosis and 40 normal subjects in order to evaluate the rate of false elevation of tumor markers in chronic liver disease. Prostate specific antigen and prostatic acid phosphatase levels were also measured in male patients and controls. Serum alpha fetoprotein levels were found elevated in 20% of patients with cirrhosis. The serum CA 19-9 level showed significant elevation in chronic active hepatitis (32%) and cirrhosis (44%). Increase in CA 125 concentration was also remarkable in chronic active hepatitis (23%) and especially in cirrhosis (74%). These results indicate that it is necessary to consider the presence of high false positivity rate of CA 19-9 and CA 125 during clinical interpretation of tumor markers in patients with chronic liver disease.
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PMID:Serum tumor markers in chronic liver disease. 884 54

The hepatitis C virus is a 9.4-kb single-stranded positive RNA virus. After infection, more than 80% of patients develop a chronic carrier state. The diagnosis is based on the detection of hepatitis C virus antibodies and of HCV RNA. Recently, methods have been established to quantify HCV RNA levels and determine HCV genotypes. Interferon treatment gives long-term response in 10-20% of individuals. Low transaminase levels, low levels of viremia and low histological activity are positive predictive parameters for treatment response. In contrast, cirrhosis, high ferritin levels and associated markers of autoimmunity are negative predictors of treatment response. At present, the combination of interferon with the nucleoside analogue ribavirin is being evaluated. Endstages of hepatitis-C-induced cirrhosis are treated with liver transplantation. Reinfection of the graft occurs regularly, the clinical implications of which are not yet clear. Our knowledge of the spontaneous course and treatment response of hepatitis C infection in hemodialysis patients is limited.
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PMID:Hepatitis C virus infection: diagnosis, natural course and therapy. 888 64

Genetic hemochromatosis is an autosomal recessive disease characterized by increased intestinal iron absorption and consequent tissue iron overload. The hemochromatosis gene has been localized on the short arm of chromosome 6, in close proximity to the HLA locus, but has yet to be identified. Neither the gene product nor the pathogenetic defect have been characterized. Clinical manifestations vary according to the degree of iron overload, ranging from the asymptomatic state to the features of cirrhosis and hepatocellular carcinoma. Early diagnosis remains essential, since the survival of patients without established cirrhosis is comparable to that of the general population. Transferrin saturation and ferritin levels are suggestive of the diagnosis, but measurement of the hepatic iron concentration still remains the gold standard, despite the utilization of computerized tomography and magnetic resonance imaging. Routine phlebotomies constitute the principal therapeutic option, despite the recent preliminary data on oral iron chelators.
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PMID:Genetic hemochromatosis: pathogenesis, diagnosis, and therapy. 890 16

The aim of this study was to investigate the relationship between iron overload, age, and clinical symptoms in genetic hemochromatosis. The relationship was studied between clinical symptoms and liver iron concentration, serum ferritin, and iron removed in a retrospective study of 410 homozygotes diagnosed using strict criteria. No significant relationship was found between liver iron concentration, iron removed by venesection, and serum ferritin level with age. The prevalence of cirrhosis, diabetes, cardiac disease, pigmentation, and fatigue increased as liver iron concentration increased. The most common presentations at diagnosis were fatigue or as an incidental finding in all age groups. Twenty-seven percent of patients (110 of 410) had no clinical symptoms of hemochromatosis. Iron accumulation is highly variable in patients with genetic hemochromatosis. The significant relationship between liver iron concentration and cirrhosis, diabetes, cardiac disease, pigmentation, and fatigue confirms the importance of iron toxicity in the pathogenesis of hepatic and extrahepatic disease. The nonspecific nature of the presenting features in patients and the presence of significant clinical symptoms in patients discovered through family investigations underscore the importance of family and population screening for hemochromatosis.
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PMID:The relationship between iron overload, clinical symptoms, and age in 410 patients with genetic hemochromatosis. 898 84

Hereditary hemochromatosis (HHC) is an inherited disease transmitted in an autosomal recessive pattern. With homozygosity occurring in up to 0.5% of the population, HHC is the most prevalent genetic disease among the white population worldwide and has the same prevalence as the sickle cell trait in the African-American population. An asymptomatic 50-year-old white man presented at the family practice clinic and stated that HHC had been diagnosed in his mother. Laboratory findings showed markedly elevated transferrin saturation and ferritin levels. The diagnosis of HHC was made on the basis of the laboratory results and family history, and therapy was begun. Clinical manifestations of HHC occur late and include diabetes mellitus, cirrhosis, and cardiomyopathy. As end-organ damage is preventable, optimal management involves early diagnosis and lifelong phlebotomy. Diagnosis is made by an elevated transferrin saturation level and an increased serum ferritin value. Hereditary hemochromatosis is a genetic disorder of iron metabolism that has an excellent prognosis if diagnosed early.
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PMID:Hereditary hemochromatosis. 907 Dec 52

Pruritus is a common symptom of chronic cholestatic liver diseases but is considered rare in chronic hepatitis. We observed pruritus to be an unusually common complaint in patients with advanced chronic hepatitis C. We reviewed the records of 175 chronic hepatitis C patients to identify patients with severe, diffuse, unexplained pruritus; 12 consecutive prospective patients undergoing liver biopsy for chronic hepatitis C served as controls. Assessment included laboratory biochemical tests and assessment of liver pathology by stage, grade, hepatic activity index, and a bile duct score. Pruritus was present in nine (5.1%) patients. Serum AST, ALT, alkaline phosphatase, GGTP, total bilirubin, and ferritin were similar in pruritics and controls. Pruritics had higher serum bile acids (2028.4 +/- 223.1 mmol/liter vs 423.1 +/- 194.3, P < 0.001), higher transferrin saturation (57.5 +/- 6.8% vs 33.2 +/- 3.3, P < 0.01), and lower HCV RNA by bDNA (24.5 +/- 12.7 x 10(5) vs 172.7 +/- 54.1 x 10(5), P < 0.05). Pathology revealed cirrhosis in 6/9 (66.6%) pruritics vs 1/12 (8.3%) controls (P < 0.01). Pruritics had higher pathologic stage (3.7 +/- 0.2 vs 2.2 +/- 0.4, P < 0.01), grade (4.4 +/- 0.2 vs 2.1 +/- 0.2, P < 0.001), activity index (14.3 +/- 1.9 vs 8.6 +/- 1.9, P < 0.025), and bile duct score (7.6 +/- 0.6 vs 4.7 +/- 0.4, P < 0.01). Of eight pruritics treated with IFN-alpha2b, two had complete ALT response and one relapsed. Pruritus followed a relapsing course and only three patients partially responded despite a variety of interventions. In conclusion, pruritus is a common complication of advanced CHC. Its presence is associated with high serum bile acids, advanced pathology and bile duct abnormalities. The clinical course of pruritus is relapsing and response to therapy is inconsistent. These features suggest that pruritus in CHC has a pathogenesis that may vary from that of chronic cholestatic diseases.
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PMID:Pruritus in chronic hepatitis C: association with high serum bile acids, advanced pathology, and bile duct abnormalities. 914 69

Discriminant function analysis has been used to investigate the relative value of six biochemical parameters (plasma ferritin, C-reactive-protein, bilirubin, alkaline phosphatase, glutamic oxaloacetic acid transaminase and albumin) in the diagnosis of liver disease. This was done among four groups totalling 70 subjects including healthy controls and patients with acute viral hepatitis, liver cirrhosis and primary hepatocellular carcinoma. Albumin had most value in distinguishing between groups, followed cumulatively by ferritin, alkaline phosphatase, C-reactive protein, bilirubin and glutamic oxaloacetic acid transaminase. However, if data on albumin, alkaline phosphatase, bilirubin and glutamic oxaloacetic acid transaminase had already been routinely collected, there would be no advantage in collecting data on ferritin and C-reactive protein. Any four of the six parameters would be of about equal value in distinguishing between diagnostic groups. When the data on all six biochemical parameters was combined in an optimum way, about 66% of all individuals could be correctly assigned to one of the four groups using biochemical markers alone. While the control subjects and patients with acute viral hepatitis formed a relatively well defined, tight cluster (apart from two patients with acute viral hepatitis), patients with liver cirrhosis and primary hepatocellular carcinoma were almost indistinguishable, using these biochemical parameters. If the latter two groups were pooled, then about 86% of subjects could be correctly classified.
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PMID:Discriminant analysis of biochemical parameters in liver disease. 919 66


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