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)

The type III procollagen aminopeptide (sPIIIP) serum levels were measured in 197 patients with liver disease and were correlated with morphological and serological alterations and with alcohol drinking habits. The sPIIIP levels resulted significantly increased in 51% of 43 patients with untreated chronic active hepatitis (CAH), in 61% of 36 patients with CAH plus cirrhosis, in 69% of 26 patients with inactive cirrhosis, in 4 out of 8 patients with alcoholic steatosis and fibrillogenesis, but remained unchanged in 38 cases of alcoholic steatosis plus siderosis and in 13 cases of chronic persistent hepatitis. A correlation between sPIIIP levels and the histological pattern of fibrosis could not be demonstrated in a single type of fibrotic liver disease and no differences were found between alcoholic and non-alcoholic patients. We agree upon the opinion that high sPIIIP levels may identify liver fibrogenic activity, but this test needs further technical improvements before it could be widely used in the clinical practice.
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PMID:Procollagen-type III peptide serum concentrations in alcoholic and non-alcoholic liver disease. 405 96

The development of siderosis of liver and spleen was investigated in rats subjected alternately to periods of starvation and periods of feeding of diets rich in iron (0.71% or 1.23% Fe) or of control diets, during periods ranging up to 245 days. With 0.71% iron in the diet, cyclic starvation-feeding markedly enhanced the accumulation of iron in rat livers by comparison to feeding ad libitum even though rats fed ad libitum ingested far greater total amounts of iron than cyclically fed rats. With 1.23% iron in the diet, the concentration of iron in livers reached more or less the same plateau in cyclically starved-fed rats and in rats fed ad libitum (betwen 4 and 5 mg Fe/g wet weight); but the mean rate of accumulation of iron in the livers of cyclically starved and fed rats was more than twice that in rats fed ad libitum, whereas mean ingestion of iron per feeding day was only 16% higher in the former group. Surgical removal of the spleen enhanced the accumulation of iron in the liver in cyclically starved-fed rats and in rats fed ad libitum. Histologically, siderosis of the liver was moderate in rats fed the diet with 0.71% iron but was severe in rats fed the diet with 1.23% iron and most severe in those without spleens. Stainable iron was deposited in hepatocytes and in Kupffer cells. None of the rats developed cirrhosis of the liver. The data suggest that in rats a barrier to the absorption of iron from the gut, or to its later utilization, is surmounted if the concentration of iron in the food exceeds a certain limit value, somewhere between 0.71 and 1.23%. With iron in the food below this value, cyclic starvation-feeding markedly potentiates accumulation of iron in the liver in the course of several months, but siderosis is moderate. With iron in the food above the limit value, cyclic starvation-feeding and feeding ad libitum can equally lead to massive siderosis of the liver.
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PMID:Effects of cyclic starvation-feeding and of splenectomy on the development of hemosiderosis in rat livers. 481 98

Starting in October 1966, 19 dogs have been subjected to massive parenteral iron loading using intravenous iron-dextran and intramuscular iron-sorbitol. Although 13 animals died, in many cases the deaths were attributable to fighting. The large doses of iron employed (up to 5.8 g/kg) were well tolerated by the surviving animals, and after 35 to 47 months five of the six survivors have developed hepatic cirrhosis with massive siderosis; the dog which has not yet developed cirrhosis received the smallest iron load. The liver pathology in many ways resembles that of human haemochromatosis, and may provide an experimental model for the study of chronic iron-induced liver injury.
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PMID:Experimental hepatic cirrhosis in dogs caused by chronic massive iron overload. 511 71

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

The chelating agent diethylenetriamine penta-acetic acid was used to measure iron stores in 83 patients with chronic liver disease. Iron chelation was normal in patients with chronic cholestasis. Chelation was increased above the control range in 14 out of 26 patients with alcoholic cirrhosis, in nine out of 28 patients with non-alcoholic cirrhosis, and in 11 out of 15 cirrhotics with a portacaval anastomosis. Iron stores in excess of 1.5 g were predicted from the results in 24 subjects; however, in only three were the values in the range found in propositi with untreated idiopathic haemochromatosis. Increased chelation did not correlate with hepatocellular impairment per se but was associated in 18 cases with surgical or large spontaneous portal systemic shunts. Exogenous factors for excess iron were present in three cases with alcoholic cirrhosis and portal systemic collaterals in one, but no special factor apart from alcoholism was apparent in the remainder. The correlation between chelatable iron and stainable liver iron content was not close and was better in haemochromatosis than in other forms of cirrhosis; in some cases considerable siderosis was present with normal or only slightly increased chelation values.
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PMID:Measurement of iron stores in cirrhosis using diethylenetriamine penta-acetic acid. 549 47

We report the findings in 53 biopsies from 45 patients with porphyria cutanea tarda (PCT). Red autofluorescence and birefringent acicular cytoplasmic inclusions were constant findings in all untreated cases. Autofluorescence occurs in other hepatic porphyrias, but acicular inclusions appear to be specific for PCT; we have seen them in subclinical porphyria and before development of cutaneous symptoms. They are probably uroporphyrins and they trend to disappear during rinsing by water during most staining procedures. We recommend unstained paraffin sections for their demonstration. Liver damage in PCT has features distinct from other liver diseases, including alcoholic liver disease. These include constant but mild periportal siderosis, focal lipofuscin deposition, focal lobular hepatocyte necrosis associated with groups of pigment-laden macrophages, focal steatosis, marked hepatocyte hyperplasia and the presence of periductal lymphocyte aggregates. The latter have not been previously described in PCT and were present in 43% of our cases. There is a direct relationship between increasing age and progressive distortion of liver architecture, with fibrosis present at a mean age of 48 years, cirrhosis at 57 and hepatocellular carcinoma at 66. The characteristic liver histology and the natural history of PCT are against this being the result of any non-specific liver damage and favour instead a specific liver disease whose pathogenesis may be mainly the result of the metabolic defect of PCT.
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PMID:The pathology of the liver in porphyria cutanea tarda. 625 81

Histochemical study of tissue iron in the various parts of the reticuloendothelial system in 15 subjects with cirrhosis was performed. Stainable iron in the liver and spleen sections, generally in large quantities, was found in 13 of 15 cases. Paradoxical association of hepatosplenic siderosis with depletion of marrow iron reserves was observed in seven subjects. In all seven, gross gastrointestinal blood loss had occurred during life and the source of bleeding from one or more anatomic lesions was identified at the time of autopsy. Depletion of marrow iron reserves in these seven subjects can be attributed to two factors: first, the available marrow iron stores were used for erythropoiesis; second, the ample hepatosplenic iron deposits could not be mobilized for transport to the bone marrow. Thus, hepatosplenic iron in cases of cirrhosis seems to be sequestered from its normal metabolic pathways.
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PMID:Dissociation between hepatosplenic and marrow iron in liver cirrhosis. 627 53

Over 14 years the authors have observed 6 adults with a special form of portal hypertension revealed by massive gastrointestinal hemorrhages due to rupture of voluminous esophageal varices. Though first suggested by huge enlargement of the spleen (5 out of 6 cases), cirrhosis was eventually discounted by laparoscopy and laparotomy. The liver was of normal volume, smooth (never nodular) and above all soft to the touch, to the biopsy needle and to the surgeon's hand. The histologic lesions of the liver were minimal and heterogeneous: fibrosis without cirrhosis (2 cases), isolated and mild steatosis (2 cases), one non-specific lymphohistiocytic granuloma (2 cases), moderate myeloid metaplasia (2 cases), hepatic siderosis without fibrosis (1 case), sinusoidal congestion (3 cases). Normality of the portal vein was evidenced by angiography (5 cases) or inferred from the elevated porta-caval gradient (1 case), and was confirmed once on autopsy. Sus-hepatic catheterization was performed in every case and provided the following information: right atrial pressure always normal, sus-hepatic veins normal, porta-caval gradient normal or slightly elevated in 4 patients (suggesting presinusoidal block) and obviously elevated in the other two (as in post-sinusoidal block). The minimal histologic lesions of the liver, the normality of the portal vein, the lack of sus-hepatic obstruction, and the variable porta-caval gradient make it impossible to localize the obstacle (if any) and thus say what is the mechanism of portal hypertension with soft liver. In the absence of elevated splenic inflow, this hypertension has to be classified as essential or idiopathic. Soft consistency of the liver has never been reported before in such cases.
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PMID:[Hemorrhagic portal hypertension with soft liver]. 660 45

Some parameters of iron metabolism in 26 patients with porphyria cutanea tarda (PCT) which is often associated with mild iron overload and hepatic siderosis, are studied. Serum iron, percent transferrin saturation and ferritin were pathologically increased. Statistical comparisons were performed between PCT patients and healthy controls, liver disease patients (cirrhosis, chronic active hepatitis) and patients with associated liver siderosis (alcoholic cirrhosis, cirrhosis and chronic active hepatitis in thalassemia). Ferritin levels are higher in patients with porphyria than in healthy controls (p less than 0,001) and in patients without liver siderosis (p less than 0,001). No statistical difference is observed between patients with porphyria and patients with siderosis. A significant decrease in ferritin levels is registered after venesection therapy. The conclusion is drawn that serum ferritin increase in PCT is related to hepatic iron store amounts rather than hepatic necrosis. It is assumed that ferritin follow-up during phlebotomy therapy and also during remission is useful to indicate the exhaustion or an early replenishment of hepatic iron stores.
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PMID:[Determination of serum ferritin in porphyria cutanea tarda. A reliable sign of hepatic siderosis]. 670 23

Problem areas in the necropsy diagnosis of alcoholic liver disease are reviewed, potential sources of confusion delineated, and diagnostic guidelines proposed. The entire spectrum of alcoholic liver disease, including alcoholic hepatitis, may be perfectly mimicked by severe obesity, diabetes, and perhexiline maleate toxicity. Focal fatty change in the liver introduces sampling errors in the assessment of steatosis. Nodular regenerative hyperplasia of the liver mimics a micronodular cirrhosis both clinically and macroscopically. Measurement of the liver iron concentration reliably differentiates between alcoholic liver disease with siderosis and idiopathic hemochromatosis. The evaluation of preexisting fibrosis or cirrhosis in cases of massive hepatic necrosis is aided by stains for elastic fibers. Alcohol abusers taking acetaminophen (paracetamol) in excessive, but not suicidal doses are at risk of developing fatal "late" acetaminophen hepatotoxicity. Fatal viral hepatitis may be overlooked in an alcoholic with preexisting liver disease.
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PMID:Problems in the necropsy diagnosis of alcoholic liver disease. 673 1


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