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

Great importance has been given to nutritional evaluation concerning either diagnosis or prognosis, and also involving nutritional support as therapeutic approach. Nutritional evaluation of 32 cirrhotic patients was performed using anthropometric measures as triceps skinfold and arm muscular circumference, and laboratory data: creatinine/height index, serum albumin transferrin; and lymphocyte number in peripheral blood. Non-caloric stores, evaluated by triceps skinfold were extremely low in 81% of the cases studied, while muscular stores, evaluated by arm muscular circumference and creatinine/height index were depleted in respectively 37.5% and 43.7%. Visceral stores evaluated by serum levels of albumin and transferrin, as well as immunological state, measured by peripheral lymphocytes counts, showed severe depletion in 10 to 15% of the patients. The increasing importance of nutrition in hepatic cirrhosis is stressed and interpretation of the different methods used for nutritional evaluation in chronic liver disease is discussed.
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PMID:[Nutritional evaluation in cirrhotic patients]. 344 8

Primary hemochromatosis is a genetic disorder rarely recognized in childhood; its long-term consequences include cirrhosis and liver cancer. We report a family with primary hemochromatosis affecting three generations, including a 7-year-old child and a 29-month-old child; these are the youngest children with primary hemochromatosis yet reported. The pathophysiology, genetics, and clinical findings of this disorder are reviewed. Serum ferritin and transferrin saturation are useful screening tests; definitive diagnosis, however, depends on determination of hepatic iron content. A plan for evaluating and treating affected patients is proposed. Physicians caring for children must learn to recognize this potentially treatable disorder.
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PMID:Primary hemochromatosis in childhood. 365 74

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

The metabolism of transferrin was studied using purified 125I-labeled transferrin in 11 alcoholic patients; six with fatty liver and five with cirrhosis. Six healthy subjects whose alcohol intake was les than 40 gm daily were studied as a control group. There were no significant differences in the mean fractional catabolic rate and plasma volume in the alcoholic groups when compared with control subjects. A significantly decreased mean serum transferrin concentration was found in the alcoholic cirrhotic patients (1.8 +/- 0.3 gm per liter vs. 2.9 +/- 0.2; p less than 0.01), resulting from diminished total body synthesis (0.9 +/- 0.2 mg per kg per hr vs. 1.8 +/- 0.2; p less than 0.01). In contrast, in the patients with alcoholic fatty liver, the mean total body transferrin synthesis (2.4 +/- 0.3 mg per kg per hr) was significantly increased when compared with controls (p less than 0.05). For all the alcoholic patients, the serum transferrin correlated with transferrin synthesis (r = + 0.70; p less than 0.01) but the serum iron did not. These results suggest that, in alcoholic cirrhosis, transferrin synthesis is decreased, probably reflecting diminished synthetic capacity by the liver. In contrast, in patients with alcoholic fatty liver, transferrin turnover is accelerated.
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PMID:Transferrin metabolism in alcoholic liver disease. 402 86

In order to assess the specificity of transferrin molecular changes, we compared concentrations of subfractions and total transferrin in cirrhotic patients, in patients having non-alcoholic hepatitis, in patients with liver cancer, and in controls. The study was carried out in 79 patients divided into four groups: 20 patients with biopsy-proven cirrhosis of alcoholic origin, 20 patients with non-alcoholic hepatitis, 19 patients with liver cancer and 20 controls. Subfractions of serum transferrin were separated by isoelectric focusing followed by direct immunofixation. Fractions pI 5.7 percentages (expressed as percentages of one fraction over total transferrin) were significantly higher in the cirrhotic group than in the control group (p less than 0.01). Fraction pI 5.9 percentages were significantly higher in the cirrhotic group than in the hepatitis or control groups (p less than 0.05), or liver cancer group (p less than 0.01). A quantitative increase of fraction pI 5.7 was found in the cirrhotic patients. However, in this study, this parameter did not discriminate between patients with parenchymal liver diseases of alcoholic or other origin. Therefore, the value of determining fraction pI 5.7 as a marker of chronic alcohol consumption seems questionable. The elevation of fraction pI 5.9 constantly found in the cirrhotic patients could not be explained and needs further investigations.
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PMID:A study of the microheterogeneity of transferrin in cirrhotic patients. 405 85

Agarose-gel electrophoresis of serum of a 72-year-old woman with liver cirrhosis showed virtually no beta-globulins two weeks before the patient's death. There was marked decrease in the concentrations of transferrin, beta-lipoproteins, hemopexin, complement component C3, beta-glycoprotein I, and cholesterol in serum. Absence of a beta-globulin band appears to signify an ominous prognosis.
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PMID:Absence of beta-globulin band in the serum protein electropherogram of a patient with liver disease. 616 19

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

The excessive storage of iron in idiopathic haemochromatosis leads to severe organic lesion up to life-threatening conditions (cardiac insufficiency, portal decompensation). The symptoms melanodermia , diabetes mellitus and other endocrine failures, liver cirrhosis, cardiac insufficiency and arthropathy appear together or in various combinations. The diagnosis is ascertained by the proof of iron storage, the multiple organic affection and by familial accumulation of the various laboratory diagnostic possibilities are particularly to be emphasized the serum iron value together with the percetal transferrin saturation (as search test), serum ferritin, the desferrioxamine test, simple ferrokinetic investigations and the quantitative determination of iron in the liver in the bioptate . For family examinations, apart from the search test, a HLA typisation is reasonable, in order to estimate the risk of the disease (particularly of brothers and sisters). The therapy of choice are blood- lettings (0.5 l once to twice a week) up to obtaining a permanent easy iron deficiency anaemia. The maintenance therapy should be performed with monthly to quarterly blood- lettings . Only in cases exception a desferal treatment is indicated. Endocrine failures and cardiac disturbances need a particular therapy.
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PMID:[Idiopathic hemochromatosis--diagnosis and therapy]. 673 May 91

The reliability of serum iron, transferrin saturation, and serum ferritin in the detection of early iron overload in hemochromatosis was determined in 120 young (less than 35 yr old) relatives whose genetic susceptibility for the disease was determined by HLA typing of families. Serum ferritin and transferrin saturation demonstrated high levels of sensitivity and specificity, whereas serum iron concentration was an unreliable test in the detection of hemochromatosis. In hemochromatosis homozygotes there was an excellent correlation between serum ferritin and mobilized body iron (r = 0.92), 1 microgram/L of serum ferritin corresponding to approximately 7.5 mg of body iron stores. For a given age, serum ferritin values were higher in homozygotes compared with heterozygotes or homozygous-normal subjects and increased by approximately 65 micrograms/L X yr, reflecting the progressive accumulation of iron in hemochromatosis homozygotes. All hemochromatosis subjects with either hepatic fibrosis or cirrhosis had serum ferritin concentrations greater than 700 micrograms/L. We conclude that the combination of serum ferritin and transferrin saturation is a reliable screening regimen for the detection of hemochromatosis and for predicting the level of body iron stores in young hemochromatosis subjects.
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PMID:Diagnosis of hemochromatosis in young subjects: predictive accuracy of biochemical screening tests. 674 16

1. In 37 patients with cirrhosis of the liver of different severity (11 in class A, 18 in class B, and 8 in class C, according to Child's criteria modified by Hobbs), inulin and p-aminohippurate clearances, total fractional protein excretion and the fractional clearances of alpha 1-acid glycoprotein, albumin, transferrin, alpha 2-macroglobulin and beta 2-microglobulin (in 20 patients) were determined. 2. Insulin clearance was lower than 70 ml/min in 19 patients had p-aminohippurate clearance was lower than 300 ml/min in 20 patients. Total fractional protein excretion was above normal in 19 patients; alpha 1-acid glycoprotein fractional clearance was above normal in 11, albumin fractional clearance in 10, transferrin fractional clearance in five, alpha 2-macroglobulin fractional clearance in three, and beta 2-microglobulin fractional clearance in 10. 3. The increases in protein excretion were independent of any impairment of renal tubular function. An inverse relationship between protein excretion and the clearances of inulin and p-aminohippurate was found. No difference in protein excretion was found between the three groups of patients with different degrees of liver damage. 4. The results suggest that in cirrhosis an increase in glomerular permeability is frequent, though generally slight; it is correlated with an impairment of kidney function and is independent of the severity of the liver damage.
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PMID:Proteinuria in patients with cirrhosis: relationship between renal and hepatic function. 710 34


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