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

Two sisters whose mother had pseudo-pseudohypoparathyroidism, simultaneously developed in infancy pseudohypoparathyroidism with severe liver damage leading to cirrhosis and characterised by "ectoplasmic vacuoles", as well as severe anaemia and thrombocytopenia. As any known metabolic or inflammatory liver disease could largely be excluded, a common genetic defect is assumed as the cause of the combined disorder in calcium and hepatic metabolism.
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PMID:[Familial liver cirrhosis in pseudohypoparathyroidism in young children (author's transl)]. 63 75

Alcohol-related disturbances are seen against the three blood cell systems. They appear after important alcohol consumption within few days and are independent from the existence of liver cirrhosis with splenomegaly. They are promptly and completely reversible after interruption of alcohol supply. Disturbances in erythropoiesis are manifested in bone marrow with megaloblasts, ring sideroblasts, and vacuoles in cytoplasma and nucleus of nucleated red cells. They are caused by folate deficiency and by perturbations of iron utilization, which is perhaps connected with impaired heme synthesis following pyridoxal phosphate deficiency. Serum iron generally increases during alcohol consumption and decreases in the following alcohol-free period. The anemia may be macrocytic and normochromic or dimorphic with hypochromic microcytes. Anemias of hard alcohol drinkers are observed also as consequence of bleeding or hemolysis of different causes. The lability against infections of drinkers is associated with changes in granulopoiesis. The most important findings are granulocytopenia, vacuoles in the immature marrow cells, perturbations in granulopoietic maturation, and decrease of marrow response. Frequently, alcohol drinkers demonstrate thrombocytopenia which is caused by ineffective thrombopoiesis and by shortened life span of platelets as direct effect of ethanol. Functional impairments of thrombocytes have been published, too.
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PMID:[Alcohol-related disturbances in haematopoiesis (author's transl)]. 64 97

Serum zinc conentrations are decreased in patients with a variety of clinical disorders including cirrhosis, nephrotic syndrome and renal insufficiency. Urinary zinc excretions are increased in the first two disease states. Symptoms of acute zinc deficiency (anorexia, dysfunction of smell and taste and mental and cerebellar disturbances) and chronic zinc deficiency (growth retardation, anemia, testicular atrophy and impaired wound healing) are common in these patients. It remains unresolved whether these low serum zinc concentrations in these disease states are indicative of true symptomatic or asymptomatic zinc deficiency, or merely reflect a decrease in available zinc-binding proteins, as well over 90% of serum zinc is bound to protein in normal subjects. The correlation between serum zinc and albumin concentrations, reportedly the major zinc-binding protein, is unimpressive. Studies of serum and urine binding of added radiozinc65 using Sephadex G-200 gel column chromatography and polyacrylamide gel electrophoresis suggest most of the radiozinc is bound to a protein with a molecular weight near albumin (68,000). Polyacrylamide gel electrophoresis suggests this might be a prealbumin. The low serum zinc concentration in the patient with nephrotic syndrome does not appear to be due to loss of zinc bound to urinary protein.
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PMID:Serum concentrations and urinary excretions of zinc in cirrhosis, nephrotic syndrome and renal insufficiency. 66 9

The morphology of red blood cells was studied in 30 patients with severe liver cirrhosis, in 10 patients with extrahepatic jaundice, and in 10 control subjects. In all the patients with extrahepatic jaundice more than 30% of red blood cells were target cells with increased resistance to osmotic lysis. In 12 patients with liver cirrhosis more than 30% of red blood cells were spur cells. The cholesterol: phospholipids (C/PL) molar ratio was 0.89 in target cells, 1.33 in spur cells, and 0.74 in normal red blood cells. The red blood cell membrane cholesterol and phospholipids exchanged with plasma lipoproteins, the lipid composition of which was studied in eight patients with spur cells; the free cholesterol: phospholipid (FC/PL) molar ratio was 0.33 (0.16 in the controls) in high density lipoproteins (HDL) and 1.40 (0.82 in the controls) in low density lipoproteins (LDL); in these patients the polyunsaturated fatty acid content was low in both phospholipids and cholesterol esters of lipoproteins. The irregular folds of the spur cells regressed when polyunsaturated lecithin was infused (2 g daily for five days) in eight patients with spur cell anaemia; the infusions decreased both C/PL ratio in RC to 0.88 and the concentration of unconjugated bilirubin (104.3 to 82.0 mumol/l (6.1 to 4.8 mg%)), whereas the activity of the plasma lecithin:cholesterol acyltransferase (LCAT) increased from 31.2 to 54.4 mumol/l/h. Polyunsaturated fatty acid content of RC lecithin increased after the infusion as it did in HDL, the FC/PL ratio of which decreased to 0.23.
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PMID:Membrane lipid composition of red blood cells in liver disease: regression of spur cell anaemia after infusion of polyunsaturated phosphatidylcholine. 71 Sep 73

The ammonia hypothesis is the most likely explanation for the pathogenesis of hepatic encephalopathy in cirrhosis patients. Reduction of hyperammonemia is therefore the most consistent therapy. From this point of view, the antibiotics have a central significance for the reduction of ammonia formation in the intestinal tract. Equally important is the correction of the hypopotassemia, which may lead to a renally induced hyperammonemia. At the same time, disorders which favor the cerebral toxicity of ammonia, especially anemia and hypoxias, must be compensated. These various measures have improved the prognosis for hepatic encephalopathy of the cirrhosis patient, but were without effect on the course of the coma in severe toxic hepatitis. During the last toxic hepatitis. During the last 10 years, many treatment methods have been reported whose efficacy, however, could not be proved.
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PMID:[Present-day therapy of hepatic encephalopathy (author's transl)]. 82 98

Evaluation of stored iron by means of DFOX-induced sideruria in 101 subjects with various degree of hyposideraemia with or without anaemia, is reported. Three groups were examined: 49 patients with chronic loss of blood and malabsorption and urinary iron values up to 1 mg/24hr; 43 with non-bleeding neoplasia, collagen disease, lymphoma, cirrhosis of the liver etc. and values of 1-2mg/24 hr; 9 with rheumatoid arthritis and cirrhosis of the liver and values over 2 mg/24 hr. The reasons why hyposideraemia may accompany incipient of frank tissue hypo-, normo- or hypersiderosis are discussed.
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PMID:[Desferrioxamine in the diagnosis of hypo-, normo-, and hypersiderotic hyposideremia]. 84 86

Hepatic dysfunction is a common finding in patients with sickle cell disease but viral hepatitis appears to be an unusual complication in the adult SS patient. Only five cases of viral hepatitis were recorded in 378 admissions for SS crisis. In contrast, hepatic crisis occurred as a distinct event in 9% of 88 patients with sickle cell anemia. This entity must be differentiated from acute cholecystitis or viral hepatitis. Transiently abnormal results of hepatitic function tests were observed in another 26 patients with extrahepatic crisis. Cirrhosis is relatively common and often the terminal event in SS disease. Choledocholithiasis and cholecystitis are infrequent complications despite the prevalence of gallstones in SS anemia.
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PMID:Sickle cell hepatopathy. 87 Sep 77

A high negative correlation (coefficient similar to 0.9) between increased 59Fe absorption from a diagnostic 0.56 mg 59Fe2+ dose and the depletion of available storage iron was observed in menstruating and pregnant women, fullterm and premature infants, blood donors, patients with infections, inflammations, tumors, hepatic cirrhosis, gastric surgery, increased urogenital or gastrointestinal blood loss. The increased diagnostic 59Fe2+ absorption is a reliable and sensitive indicator of at least depleted iron stores or prelatent iron deficiency as caused by iron malnutrition or maldigestion, increased iron requirement in pregnancy, infancy, urogenital or gastrointestinal blood loss. Although the messenger system which signalyzes the depletion of iron stores to the iron absorbing enterocytes of the duodenal and jejunal mucosa is not yet known available storage iron seems to control intestinal iron absorption under normal and the great majority o pathological condition in humans. Anemia per se or high erythropoietin levels in blood do not influence iron absorption since patients with even severe erythroblastic hypoplasia, aplastic anemia and megaloblastic anemia due to vitamin B12 deficiency absorb iron according to their iron stores. An only mild hyperplasia of the erythropoietic system in the bone marrow does also not effect iron absorption which was still under the control of available storage iron in patients with hereditary spherocytosis, nonspherocytic congenital hemolytic anemia due to glucose-6-phosphate dehydrogenase deficiency, acquired hemolytic anemia and vitamin B12 deficiency induced megaloblastic anemia..
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PMID:Intestinal iron absorption under the influence of available storage iron and erythroblastic hyperplasia. Comparative studies in children with hereditary spherocytosis, nonspherocytic enzymopenic hemolytic anemia, acquired hemolytic anemia, vitamin B12 deficiency induced megaloblastic anemia, erythroblastic hypoplasia and aplastic anemia. 113 Jan 21

Because of uncertainty as to the molecular weight of transferrin, a previous comparison [Von der Heul et al., Clin. Chim. Acta 38, 347 (1972)] between transferrin content of serum and total iron-binding capacity cannot be definitive. We found a conversion factor for expressing the maximum amount of iron bound by 1 mg of transferrin. We compared the resulting calculated value with values obtained by three other methods for measuring total iron-binding capacity. We agree with the previous observation that the latter, as measured radioisotopically, give higher results than would be judged from the transferrin content but the same as those for two chemical methods. The diffusion rate of transferrin in agar was the same irrespective of the degree of iron saturation. Serum transferrin concentrations were low in patients with anemia resulting from malignancy, chronic disorders, and cirrhosis of the liver, and high or normal in patients with iron deficiency anemia and in pregnant women or women who were taking birth-control pills. Measurement of transferrin concentration can be used to distinguish iron deficiency anemia from anemia resulting from chronic disorders, but offers no advantages over existing methods for estimating total iron-binding capacity.
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PMID:Immunological measurement of transferrin compared with chemical measurement of total iron-binding capacity. 113 10

The occurrence of hematologic changes has been studied in 256 patients with various liver diseases. Macrocytosis on smears and by MCV was found in 50% of acute and in over 70% of chronic liver diseases. MCV increased from 98 +/- 8 mu3 (acute hepatitis) up to 108 +/- 12 mu3 in alcoholic cirrhosis. Anemia, which occurred rarely in hepatitis but in 67% of cirrhosis, was always macrocytic, not correlating with reticulocyte counts. Target cells were found in 20% of acute hepatitis and 41% of cirrhosis. In patients with chronic liver disease target cells were associated with macrocytosis and increased bilirubin. Thrombocytopenia was found in 11% of acute, in 53% of chronic inflammatory and in over 60% of cirrhotic liver disease.
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PMID:[Changes in the blood picture in liver diseases]. 120 27


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