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

We analyzed the clinical data and liver histology for iron overload in 74 renal allograft recipients. Twenty of the 74 patients had histological evidence of hemosiderosis. Four patients had hemochromatosis. Of the 2 noninvasive diagnostic tests the serum ferritin level was more reliable than percent saturation of transferrin in predicting the histological diagnosis of hemosiderosis. Of the 20 patients with hemosiderosis 14 died either from liver failure or concomitant sepsis. Female patients and those who received long-term dialysis had higher susceptibility for developing hemosiderosis. Of the 6 patients treated with phlebotomies, the response was good in 4 and incomplete in 2. Hemosiderosis and hemochromatosis should be considered in the differential diagnosis of posttransplant liver disease. Intermittent phlebotomies if carried out early may prevent the progression of hemosiderosis to micronodular cirrhosis.
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PMID:Hemosiderosis and hemochromatosis in renal transplant recipients. Clinical and pathological features, diagnostic correlations, predisposing factors, and treatment. 390 17

Serum ferritin, an index of iron stores, was studied in 60 patients with porphyria cutanea tarda (PCT), in 21 patients who had other liver diseases without siderosis (cirrhosis [LC] and chronic active hepatitis [CAH]), and in 32 patients with associated liver siderosis (alcoholic LC, LC and CAH in minor thalassemia). Ferritin levels were higher in patients with porphyria than in healthy controls and patients without liver siderosis (P less than 0.001), whereas no statistical difference was observed between patients with porphyria and those with liver siderosis. Because iron removal is considered the treatment of choice for PCT, some patients with PCT underwent phlebotomy and others received chelating therapy with subcutaneous infusion of deferoxamine. Follow-up of the patients showed a correlation between serum ferritin level and urinary porphyrin excretion; when the clinical and biochemical syndrome became normal, serum iron and ferritin had fallen to normal values (t test pair data analysis before and after: P less than 0.001 in each group). No appreciable difference was found between controls and patients with PCT whose conditions had been normalized, irrespective of the chronic liver damage always present in PCT. Our results suggest that serum ferritin increase in PCT is related more to liver iron overload than to liver damage, and ferritin follow-up is recommended to indicate the exhaustion of hepatic iron stores during iron depletion therapy, as well as to detect an early replenishment after remission.
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PMID:Serum ferritin in the assessment of liver iron overload and iron removal therapy in porphyria cutanea tarda. 394 Dec 93

This case emphasizes that absence of ascites does not rule out cirrhosis as the cause of a massive pleural effusion. Consideration of hemochromatosis as a cause of cirrhosis is worthwhile both for the patient and his family, as the course of the cirrhosis may be benefited by periodic phlebotomy to reduce the iron overload, and disease may be prevented in asymptomatic relatives.
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PMID:Massive hydrothorax complicating occult cirrhosis. 397 22

To assess the value of type III procollagen peptide (sPIIIP) as a marker of hepatic fibrosis, sera from 73 patients with alcohol-related liver disease and 30 patients with idiopathic hemochromatosis (IHC) were studied by a specific radioimmunoassay. sPIIIP was increased in 87% of 30 patients with cirrhosis, in 16% of 32 with steatofibrosis but in none of 11 with steatosis. There was a significant correlation with histologic hepatocellular necroinflammation (r = 0.42, p less than 0.01), but not with hepatic fibrosis. sPIIP was increased in 33% of 30 patients with IHC, whether or not they had cirrhosis or fibrosis, and whatever the level of iron overload or the extent of the hepatic deterioration. IHC patients with increased levels of sPIIIP had a higher prevalence of superimposed hepatic damage than did those with normal procollagen levels (p less than 0.05). Our findings, therefore, weaken the diagnostic value of sPIIIP as an index of connective tissue deposition in the liver, and suggest that, at least in alcohol-related liver disease and IHC, hepatocellular necroinflammation influences the results.
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PMID:Serum type III procollagen peptide in alcoholic liver disease and idiopathic hemochromatosis: its relationship to hepatic fibrosis, activity of the disease and iron overload. 399 75

Biliary obstruction is an important complication of chronic calcifying pancreatitis. In this study, liver biopsies were examined to determine the nature and severity of hepatic complications in 23 such cases. The most striking changes were portal tract expansion due to oedema and fibrosis, with proliferation of bile ducts. Although common, these changes were not severe, and no patient had developed secondary biliary cirrhosis. Other features of note were intrahepatic cholestasis, iron overload (56.5%), copper-associated protein stained with the orcein technique (34.7%) and mild fatty change or perivenular sclerosis in 13%. It is concluded that no serious, irreversible pathological changes occurred in the liver despite clinically marked biliary obstruction.
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PMID:The liver in biliary obstruction due to chronic pancreatitis. 405 70

Liver biopsies from 4 baboons taken during 15 months of iron-polymaltose injections, were compared with specimens from 2 controls. A morphometric method was used to assess ferritin concentration in various cells. Initially, ferritin and siderosomes were conspicuous in reticuloendothelial cells but rare in hepatocytes. Unusual findings included intranuclear ferritin and coalesced ferritin within bile canaliculi. With advancing overload, ferritin and hemosiderin increased not only in sinusoidal cells, but also in hepatocytes, with concomitant elevation of transaminases. The hepatocytes now showed evidence of damage and excessive collagen was present mainly around portal spaces. A year after cessation of iron injections, hepatocyte ultrastructure was near normal while sinusoidal cells were still heavily overloaded. The baboon appeared to be a useful model for the study of iron overload. Although in this study most of the damage was reversible, it is suspected that more prolonged overload, a different route of administration or other, more toxic iron compounds, may lead to cirrhosis similar to that of the iron-loading anemias.
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PMID:Iron overload of the liver in the baboon. An ultrastructural study. 406 58

In the present study, cirrhosis of the liver was found in one of six cases of transfusional siderosis. The relationship between iron overload and cirrhosis is discussed and the suggestion is made that factors other than iron deposition may have been responsible for the hepatic fibrosis. Three patients with a greater degree of iron overload, and for a longer period, did not develop fibrosis or cirrhosis. The possibility remains that iron absorbed from the gut and stored in excess without having passed through the haemoglobin molecule or the reticuloendothelial system may be toxic, as cases have been reported in which cirrhosis of the liver was attributed to prolonged iron medication. The cirrhosis in idiopathic haemochromatosis may be due to lack of an unknown hepatic cell enzyme, as in galactosaemia, and the increased iron absorption may be a concomitant finding. Transfusional or secondary haemochromatosis is not a definite entity, and the liver cirrhosis is probably due to causes other than the excess deposition of haemosiderin.
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PMID:Transfusional siderosis and liver cirrhosis. 536 42

Iron absorption is under delicate control and the level of absorption is adjusted to comply with the body's need for iron. To measure the intestinal setting for iron absorption, and thereby indirectly assess body iron requirements, cobaltous chloride labelled with (57)Co or (60)Co was given by mouth and the percentage of the test dose excreted in the urine in 24 hours was measured in a gamma counter. Seventeen control subjects with normal iron stores excreted 18% (9-23%) of the dose. Increased excretion, 31% (23-42%), was found in 10 patients with iron deficiency anemia and in 15 patients with depleted iron stores in the absence of anemia. In contrast, 12 patients with anemia due to causes other than iron deficiency excreted amounts of radiocobalt within the normal control range. In patients with iron deficiency, replenishment of iron stores by either oral or parenteral iron caused the previously high results to return to normal.Excretion of the test dose was normal in portal cirrhosis with normal iron stores but it was markedly increased in patients with cirrhosis complicated by either iron deficiency or endogenous iron overload. It was also raised in primary hemochromatosis. Excretion of the dose was reduced in gluten-sensitive enteropathy. Gastrointestinal surgery and inflammatory disease of the lower small intestine had no effect on the results except that some patients with steatorrhea had diminished excretion.The cobalt excretion test provides the clinician with a tool for the assessment of iron absorption, the detection of a reduction in body iron stores below the level that is normal for the subject in question, the differentiation of iron deficiency anemia from anemia due to other causes, and the investigation of patients with iron-loading disorders.
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PMID:Cobalt excretion test for the assessment of body iron stores. 557 25

The differential ferrioxamine test measures the amount of body iron as ferrioxamine (Fv) chelated by a standard dose of desferrioxamine.Five patients with untreated, uncomplicated idiopathic haemochromatosis and one with transfusion haemosiderosis gave Fv in the range 1,948 to 2,462 mug./kg. (normal 110 to 500). One case of transfusion haemochromatosis with haemolytic anaemia and renal failure gave an Fv value of 8,019 mug./kg. Four patients with idiopathic haemochromatosis after therapeutic venesection gave Fv values of 212 to 885 mug./kg. One relative with a value for Fv of 776 mug./kg. was shown to have early cirrhosis by liver biopsy. Serial Fv measurement after venesection in this patient provided a preliminary assessment of the relationship between Fv values and available iron stores up to about 2,000 mg. iron. This relationship applies only when red cell survival is normal. Approximate figures for the range of available storage iron in 31 healthy men are deduced, namely, 200 mg. to 1,000 mg. (3 to 14 mg./kg.). The test should prove useful in the diagnosis of iron overload, in the screening of relatives for early haemochromatosis, and in the management of iron storage diseases.
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PMID:Differential ferrioxamine test in idiopathic haemochromatosis and transfusional haemosiderosis. 590 97

Various abnormalities of the renal tract can be detected from the renal images seen on 99Tcm methylene diphosphonate (MDP) bone scintigrams. Diffusely increased renal parenchymal activity has been associated with cytotoxic and other drug therapy, radiation nephritis, iron overload and cirrhosis. A further association--with hypercalcaemia--is reported here. In a retrospective study, 1950 bone scintigrams were reviewed and a significant relationship between high renal activity and hypercalcaemia was found. This was subsequently confirmed by a small prospective study. None of the patients whose bone scintigrams showed this association had evidence of nephrocalcinosis on X rays. It is postulated that in these hypercalcaemic patients there may be high tissue calcium in the kidneys which results in the high uptake of MDP, and it is suggested that serum calcium be measured in patients with previously unsuspected hypercalcaemia whose bone scintigrams exhibit the finding of high parenchymal renal activity.
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PMID:High renal activity on bone scintigrams. A sign of hypercalcaemia? 622 81


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