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)

Serum ferritin is often elevated in patients with hepatocellular carcinoma (HCC). Its use as a disease marker has been proposed. We have measured serum ferritin levels in 85 patients with HCC and in 62 comparable subjects with cirrhosis. Abnormal values (greater than or equal to 300 ng/ml) were found in 54% of the patients with HCC and in 35% of those with cirrhosis (median 323 and 204 ng/ml, respectively). The overlap of the range of concentration in HCC and cirrhosis was so great that no discriminant level could be chosen. No relationship was found between alpha-fetoprotein and ferritin concentrations. Among 61 patients who received Adriamycin treatment, no discernible fall in ferritin levels was observed, while alpha-fetoprotein increased progressively during the follow-up. Serum ferritin has no role in diagnosing and/or monitoring the response to treatment of patients with HCC.
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PMID:The clinical value of serum ferritin in hepatocellular carcinoma. 241 33

Total serum ferritin concentrations were serially estimated in 24 patients with primary hepatocellular carcinoma (HCC) for 4 to 8 weeks after resection of the tumor. The patients were divided into four groups according to the tumor size and the result of ferritin was compared with that of serum alpha-fetoprotein (AFP) levels. All patients had underlying parenchymal diseases of the liver (liver cirrhosis in 19 and chronic hepatitis in 5 cases). The serum ferritin levels did not reflect the therapeutic result of hepatic resection in most of the patients of all groups. Serum AFP levels, which were measured simultaneously with ferritin levels, were much superior to the ferritin estimation. The current study may indicate that ferritin cannot be used as a tumor marker in the follow-up of Japanese patients with HCC and associated liver disease. Acidic isoferritin, which is known to be produced in and secreted from HCC, should be measured for this purpose.
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PMID:Serum ferritin level after resection of hepatocellular carcinoma. Correlation with alpha-fetoprotein level. 242 Apr 38

Forty-two male patients with alcoholic liver disease were studied for iron status by indirect hematological assays, including red cell ferritin (RCF), and histochemical estimations. Serum iron and ferritin, total iron-binding capacity levels were unrelated to iron deposits, whereas RCF concentration was a good index of iron stores as detected by direct assessment on bone marrow and liver biopsy specimens. A relatively high proportion of alcoholics (19%) were iron-deficient. Alcoholic patients with cirrhosis exhibited higher RCF values than patients with alcoholic hepatitis. However, this increase was apparently unrelated to cirrhosis per se. In alcoholics we found that RCF was mainly related to levels of bone marrow iron. The increased RCF values observed in patients with hepatic siderosis was mediated by marrow iron stores. RCF can therefore be regarded as a useful test to distinguish patients with liver siderosis and normal values of bone marrow iron.
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PMID:Evaluation of iron stores in patients with alcoholic liver disease: role of red cell ferritin. 245 66

Endomyocardial biopsy was performed in 13 patients with primary or secondary iron overload. Prussian blue staining showed visible iron in the biopsy fragments of 8 out of 13 patients. Because of the inhomogeneity of iron deposition in the biopsy fragments, a semi-quantitative myocardial iron grading system was used in which the percentage of Perls' positive cells on 4 to 6 biopsy fragments was averaged from each case. The presence of stainable iron in the myofibrils was not predictable from serum iron, transferrin saturation, serum ferritin or liver iron grading, nor from evidence of endocrine dysfunction. In patients with Perls' positive material in the myocardium, there was a significant correlation between the endomyocardial iron grade and serum iron and transferrin saturation. These results suggest that other factors besides the body iron load determine cardiac iron deposition. The fact that myocardial siderosis was documented only in patients with hepatic cirrhosis, irrespective of the hepatic iron load, suggests that severe liver damage may be a prerequisite for the accumulation of iron in the heart.
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PMID:Myocardial iron grading by endomyocardial biopsy. A clinico-pathologic study on iron overloaded patients. 247 Jun 15

This study was undertaken in order to compare the usefulness of three indices of tumour proliferation in detecting primary hepatocellular carcinoma (HCC) and in differentiating this neoplasm from liver cirrhosis. In 10 patients with HCC and in 63 with liver cirrhosis serum alpha-fetoprotein (AFP), tissue polypeptide antigen (TPA) and ferritin were assayed. Increased levels of AFP but not of TPA and ferritin were observed in HCC as compared to liver/cirrhosis. The receiver-operating characteristic curves demonstrated that AFP is more discriminating between HCC and liver cirrhosis than the other two markers. Correlations between liver function tests and serum markers were observed in liver cirrhosis but no in HCC. We can conclude that AFP is more useful than TPA and ferritin in detecting HCC in patients with liver cirrhosis, owing to the high frequency of false positive results of the latter two indices in liver cirrhosis. Liver dysfunction is probably involved in increasing all these markers of malignancy, thus reducing the specificity of these tests.
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PMID:Alpha-fetoprotein, tissue polypeptide antigen and ferritin in diagnosing primary hepatocellular carcinoma in patients with liver cirrhosis. 247 90

Several inherited forms of iron overload have been described. It is now accepted that HC, usually regarded as a disease of adult life, is an inherited disorder, hence all first degree relatives must be presumed to be at increased risk of developing iron overload and the diagnosis is now frequently made in young relatives. The combination of serum iron, transferrin saturation and serum ferritin determination will detect iron overload in an early, precirrhotic stage. Liver biopsy and the determination of hepatic iron concentration provide the definitive proof. Where HC is recognized sufficiently early to permit adequate removal of iron before cirrhosis has developed, the prognosis is excellent. Thus haemochromatosis as a clinical disease should be preventable in a large proportion of patients. Severe iron overload has been described in juveniles and also in neonates. These conditions are familial but whether they are HLA-related has not been determined. Cardiac and endocrine disorders are frequently the presenting manifestations of parenchymal iron overload in the young and, at least in neonates, the condition is usually fatal in early infancy. It is not possible at present, to say whether these rare juvenile and neonatal forms of haemochromatosis are related to the much more common adult form. Identification of the gene for HC may assist in answering this question.
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PMID:Inherited iron overload. 248 90

Primary or genetic haemochromatosis is an inherited disease characterized by an inappropriate degree of iron absorption with accumulation of excessive amounts of tissue iron. Parenchymal iron accumulation results in the typical clinical features of the disease including hepatic cirrhosis, diabetes, testicular atrophy and skin pigmentation. The disease is inherited in an autosomal recessive manner. The gene for the disease has not been identified but is tightly linked to the A locus of the histocompatibility complex on chromosome 6. The approximate homozygote frequency in Caucasians is 0.3% with an equal sex ratio. Excessive body iron stores have been described in a number of other conditions, particularly alcoholic liver disease. There is increasing evidence that many of these individuals are in fact also suffering from genetic haemochromatosis. Diagnostic tests including serum iron, transferrin saturation, serum ferritin and liver iron concentration make it possible to detect sufferers of the disease. Screening relatives of affected individuals with these tests allows a diagnosis to be made before permanent tissue damage has occurred. Removal of excess iron stores by repeated phlebotomy is the primary treatment. If iron is removed before significant tissue damage has occurred, the complications and natural course of the disease will be prevented provided reaccumulation of iron does not occur. Excessive iron accumulation with resultant organ damage also occurs in anaemias associated with ineffective erythropoiesis and after excessive parenteral iron administration or repeated blood transfusions. Similar clinical features may be seen. Chelation therapy is the mainstay of treatment in these cases where long-term venesection is not possible.
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PMID:The clinical manifestations of chronic iron overload. 266 Sep 35

Iron-chelating treatment is indicated in all children on prolonged transfusion therapy (i.e., chiefly patients with thalassemia and Blackfan-Diamond anemia). The purpose of iron-chelating treatment is to prevent the development of manifestations of iron overload including cardiac hemosiderosis and insulin-dependent diabetes mellitus (which are two potentially fatal complications), hepatic cirrhosis, hypoparathyroidism, hypothyroidism, and delayed puberty. Deferoxamine is the only effective iron-chelating agent and should be given in a daily dose of 40 mg/kg at initiation of the transfusion program. Administration is by subcutaneous infusions from 8 to 10 hours per day. The goal of iron-chelating treatment is to maintain serum ferritin levels between 500 and 1,000 ng/ml. This long-term treatment is a significant burden for patients and it can be hoped that non-toxic iron-chelating agents, active by mouth, will become available.
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PMID:[Iron chelation in children]. 268 51

Results are presented from the determination of tissue iron and ferritin in 15 pathological livers (6 with steatosis, 8 with fibrosis/cirrhosis and 1 with haemochromatosis). The histological assessment according to the Rowe system, after Perls' staining, was compared with the measurement of the iron content in liver homogenate by flameless atomic absorption spectrophotometry. The results of the flameless atomic absorption spectrophotometry were less accurate than in normal livers, but the method can still be considered reliable with satisfactory precision. As in normal livers, the range of chemically determined values in the histological staining grades was considerable and there was quite an overlap between consecutive grades. The chemical determination of liver iron content is to be preferred. The levels of ferritin protein and ferritin iron follow the same pattern as the total iron content.
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PMID:Determination of tissue iron and ferritin in liver pathology comparison of histochemical and biochemical results. 275 94

Rats fed a carbonyl iron-supplemented diet for 4-15 months were studied for iron content and morphologic changes in the liver, spleen, intestinal mucosa, pancreas and heart. All organs had an increased iron content measured by atomic absorption, with the highest concentrations in the liver and spleen. The periportal distribution of stored iron in the liver was similar to that in human hemochromatosis. In animals treated beyond 6 months Kupffer cells and sinusoidal lining cells also showed cytosiderosis. Electron microscopy provided information on ferritin and hemosiderin content and distribution within parenchymal and sinusoidal cells of the liver but no excessive fibrosis was found. Except for the spleen, the other organs showed less iron deposition. Iron-filled lysosomes (siderosomes) were found in macrophages in the intestinal lamina propria and pancreas, as well as in enterocytes, pancreatic acinar cells and heart muscle cells. Heavily iron-laden siderosomes had increased membrane instability which was demonstrated both morphologically and by measurements of latent lysosomal enzyme activities. Even though cirrhosis was not found, the distribution pattern of accumulated storage iron and lysosomal lability indicated that the carbonyl iron-fed rat is a suitable experimental model for human hemochromatosis.
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PMID:Ultrastructural observations in the carbonyl iron-fed rat, an animal model for hemochromatosis. 289 Feb 33


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