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

It is well-known that cirrhosis is a predisposing factor to Yersinia septicemia. This study includes 73 cirrhotics and shows a high number of positive serologic tests (47/73 : 64.4%). However, there is no correlation with clinical features or bacteriological findings. The most frequent serotypes, i.e. pseudotuberculosis IV and enterocolitica 0:9, differ from those which are usually found in Yersinia septicemias. Iron overload in cirrhosis, increased intestinal load of gram-negative bacilli and possible latent bacteremia may partly explain these results. However, the role probably played by as yet poorly known cross-reactions between Yersinia and other pathogens (Shigella, E. Coli...) must be underscored. The authors conclude that slightly positive, stable, serodiagnostic tests have little meaning in cirrhotics.
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PMID:[Serodiagnosis of Yersinia infections in cirrhotic patients. Study apropos of 73 patients]. 631 24

Hepatic tumors unassociated with cirrhosis were encountered in seven patients aged 10 to 19 years. Four patients had received androgens for aplastic anemia. Two patients had transfusional hemosiderosis. One patient had had a renal transplant 2 1/2 years ago. Two patients are alive at 2 3/4 and 2 1/2 years after surgical resections. Nodules were found at autopsy in the others. The tumors were well differentiated and, in the androgen-related cases, differed from the others in the following features: canalicular bile retention, mild nuclear atypia, and acinar formation. No mitoses, vascular invasion, or metastatic tumor were evident. The clinical setting was variable; different factors, including iron overload and androgen therapy, played a role in the development of tumor. Although the androgen-related cases showed mild cellular atypia, biologic evidence of malignancy was lacking as in most previous reports.
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PMID:Benign hepatocellular tumors in the young. A clinicopathologic spectrum. 632 Jul 60

Serum ferritin concentrations are elevated in 35% to 100% of patients with hepatocellular carcinoma (HCC). With an immunoperoxidase technique, ferritin was demonstrated in tumor tissue from 32 of 74 (43%) black southern African patients, and from 12 of 19 (63%) American patients with HCC (P greater than 0.1). Ferritin was present in nonneoplastic liver in 82% of African and 100% of American patients (P greater than 0.1). Moderate to large amounts of stainable hepatic storage iron (hemosiderin) were present in 76% of African and 67% of American patients (P greater than 0.1). Fifty-two (70%) African patients had macronodular cirrhosis. In the literature, 80% to 90% of American patients with HCC have cirrhosis. High serum ferritin levels in patients with HCC may be due to ferritin production by the tumor, or related to the associated iron overload and/or cirrhosis.
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PMID:Immunohistochemical ferritin in hepatocellular carcinoma. 632 63

Hemochromatosis is a syndrome which, when fully expressed, is manifested by melanoderma , diabetes mellitus, and liver cirrhosis, with iron overload involving parenchymal and reticuloendothelial cells in many organ systems. This clinical presentation may arise as a consequence of either hereditary or acquired abnormalities of iron overload, although the mechanisms are quite different. In hereditary hemochromatosis (also known as primary, or idiopathic, hemochromatosis), increased intestinal iron absorption leads to excessive accumulations of iron, throughout the body, particularly in parenchymal cells. In secondary forms of iron overload including transfusional hemosiderosis, alcoholic cirrhosis, thalassemia, sideroblastic anemia, and porphyria cutanea tarda, iron accumulates in the reticuloendothelial system initially, but with increasing amounts of total body iron, excessive iron deposits eventually accumulate in parenchymal cells throughout the body producing a picture indistinguishable from hereditary hemochromatosis. In this article, the course, prognosis, and therapy of iron overload will be reviewed in detail. Clinical and experimental data concerning the pathogenesis of the different forms of iron overload will be examined critically. In particular, information relating to possible abnormalities of reticuloendothelial function, intestinal mucosal iron transport, and alterations in serum and tissue isoferritin patterns in hereditary hemochromatosis will be analyzed, and possible directions for future research will be suggested. The mode of inheritance and linkage with the major histocompatibility (HLA) complex will be discussed. Theories on the pathogenesis of tissue damage by excess iron will be evaluated. Methods for measuring the extent of iron overload in clinical practice will be described, including measurements of serum iron, serum ferritin, iron absorption, cobalt excretion, desferrioxamine excretion, liver biopsy and tissue iron determinations, and HLA typing. Finally, unresolved problems in the understanding of the disease process, diagnosis, and therapy will be delineated.
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PMID:Iron overload disorders: natural history, pathogenesis, diagnosis, and therapy. 637 41

Severe congestive cardiac failure developed in a few weeks in a 44 year old man who had undergone porto-caval anastamosis for post-hepatitis cirrhosis one year previously and then treated for anaemia by repeated blood transfusion and chronic daily oral iron therapy. Infiltrative, congestive and restrictive cardiomyopathy was diagnosed in the presence of global cardiomegaly, electrocardiographic changes (microvoltage, diffuse ST-T wave changes), echocardiographic appearances (dilatation of the left ventricle, with hypertrophic and hypokinetic walls), and hemodynamic signs of adiastole with equalisation of filling pressures at 15 mmHg and a cardiac index of 1,88 l/min/m2. Cardiac haemochromatosis was confirmed by the laboratory (serum iron: 35 mumol/l; siderophilin saturation: 100 p. 100; serum ferritin: 1854 ng/ml; induced siderouria: 51 mg/24 hours) and histological findings (endomyocardial biopsy showing pigment overload). The absence of a family history, of homozygote A3 antigen, of diabetes, of iron overload on hepatic biopsy one year previously, excluded the diagnosis of familial idiopathic haemochromatosis. A secondary form of the disease was diagnosed on a possible genetic predisposition (heterozygote A3 antigen) and on environmental factors (blood transfusions, iron therapy, cirrhosis, alcoholism and perhaps the porto-caval anastamosis. Cardiac haemochromatosis was cured in this case by iron chelating therapy comprising daily subcutaneous infusions of 2 g of desferrioxamine for 2 months. The cure was confirmed by regression of the signs of clinical cardiac failure and of cardiomegaly, the increase in QRS voltages and the near normalisation of the hemodynamic and laboratory findings.
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PMID:[Adiastole caused by a secondary cardiac hemochromatosis. Successful treatment with an iron chelating agent]. 641 3

Patients with diffusely increased uptake in both kidneys (often referred to as "host kidneys") on Tc-99m-MDP bone imaging were evaluated. Among 2056 patients reviewed, this finding was seen in 13 patients (0.63%): four with liver cirrhosis, two with lung cancer, one each with primary hepatoma, Hodgkin's disease, malignant lymphoma, thyroid cancer, leukemia, sideroblastic anemia and diabetes mellitus. Renal vascular disease and iron overload are considered to be the major causes of this finding.
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PMID:Diffusely increased Tc-99m-MDP uptake in both kidneys. 645 33

A patient with coexistent hemochromatosis and alpha-1-antitrypsin deficiency which led to cirrhosis and death despite adequate therapy for hemochromatosis is reported. Evaluation of the family revealed first degree relatives with iron overload and others with alpha-1-antitrypsin deficiency but none with both conditions. The role of family studies in the early recognition and possible prevention of overt clinical disease in individuals with either of these two genetic diseases is discussed.
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PMID:Idiopathic hemochromotosis and alpha-1-antitrypsin deficiency: coexistence in a family with progressive liver disease in the proband. 660 88

A further case of sporadic congenital sideroblastic anaemia is reported. Despite no contributing factors such as blood transfusion, oral ingestion of iron or alcoholic beverages, were present excessive iron stores occurred with consecutive tissue damage resulting in cirrhosis of the liver, portal hypertension and diabetes mellitus. HLA phenotype was A3 B7 as in primary hemochromatosis. Correction of anemia was obtained by vitamin B6 administration. Improvement of iron overload was achieved through the use of daily subcutaneous infusions of the iron chelating drug desferrioxamine with a portable infusion pump.
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PMID:[Hemochromatotic cirrhosis complicating pyridoxine-sensitive hereditary sideroblastic anemia. Case report]. 661 12

A radioimmunoassay for serum procollagen III aminopeptide (sPIIIP) was proposed recently for monitoring hepatic fibroplasia in patients with various inflammatory hepatic lesions. To determine whether sPIIIP also can detect fibroplasia in noninflammatory liver disorders, we measured this index in 16 patients with idiopathic hemochromatosis (IHC) at various stages of the disease and iron overload. Interestingly, we found normal levels of sPIIIP in 12 out of 16 patients examined (75%), despite clear histologic features of fibrosis or cirrhosis. The levels of sPIIIP exhibited no relationship to any of the clinical, laboratory, or histologic parameters of the disease. Thus, unlike other types of cirrhosis, in which sPIIIP is increased, the liver disease in IHC may be a fibrotic process unrelated to type III collagen stimulation. Accordingly, the determination of sPIIIP in these patients is of no value for monitoring the fibrosis associated with the liver disease.
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PMID:Serum marker of type III procollagen in patients with idiopathic hemochromatosis and its relationship to hepatic fibrosis. 662 14

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


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