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

This contribution presents data from the literature as well as our own results concerning the mechanisms of hepatic encephalopathy (HE). 1. Blood chemistry: In patients with liver cirrhosis, the plasma levels of ammonia, phenylalanine, tyrosine, phenolic acids, and octopamine correlated with the stages of HE. Methionine and free tryptophan concentrations were increased only in stages 2-4. Further, branched chain amino acids were below the normal range. Experimental findings in animals elucidated some mechanisms of these changes. 2. Effects of administered substances: With ammonia, methionine, methanethiol, tryptophan, phenolic substances, and fatty acids central nervous disturbances were observed. 3. Interactions: Anemia, methanethiol, and fatty acids favored ammonia toxicity. Alkalosis diminished cerebral symptoms. 4. Neurotransmitters: HE was accompanied by an enhanced turnover of serotonin and by increased amounts of false neurotransmitters (like octopamine) in the brain. 5. Oxydative brain metabolism: Disorders of cerebral oxygen and glucose utilization were mainly documented in cases of long term HE with EEG alterations. 6. Structural changes of the brain: Most of them are irreversible.
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PMID:[Pathogenesis of hepatic encephalopathy (author's transl)]. 1 66

36% of a total of chronic liver patients suffered from anaemia and 50.5% of patients affected with liver cirrhosis. In most cases the anaemias were normochrome and hypochrome or hyperchrome only in some cases. In analyzing possible single factors the reductions of vitamin B12 absorption could be made probable by means of the Schilling test and sometimes a folic acid deficiency in macrocyte anaemia with normal vitamin B12 absorption by determining the folic acid content in the serum and by successes of test treatment 82% of patients with liver cirrhosis showed a latent or manifest haemolysis. However, it was only in 1/3 of the patients with liver cirrhosis that the spleen turned out to be the place of an increased degradation of erythrocytes. In some cases an increased erythrocytoclasia into the liver could be identified. Predominantly, however, an increased degradation of erythrocytes in the total RHS had to be assumed. Twice an ineffective erythropoiesis could be found by ferrokinetic examinations. As a whole ferrokinetic examinations cannot be interpreted easily, because their static and dynamic values of iron transport in the plasma volume of liver patients will undergo considerable changes. Patients with disturbances of haematopoiesis and with haemolysis remaining in the latent stage may develop a manifest anaemia because of the influence of additional factors, such as increase of the plasma volume at lowered haematocrit value or microbleedings. The cause of anaemia cannot be concluded with sufficient probability from the type of anaemia; in a single case all pathogenetic factors will rather have to be analyzed. Therapeutic possibilities for hepatogenous anaemia of complex genesis are discussed.
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PMID:[Complex genesis of anemia in chronic liver diseases]. 8 89

An 11-year-old girl developed cholangiocellular carcinoma in association with biliary cirrhosis due to congenital biliary atresia. An exploratory laparotomy and an operative cholangiogram at 3 months of age had confirmed the diagnosis of extrahepatic biliary atresia. A liver biopsy specimen taken at 6 months of age showed biliary cirrhosis. The subsequent clinical course was characterized by persistent moderate jaundice, anemia, malnutrition, rickets, pathologic fractures, and recurrent gastrointestinal bleeding. The presence of cholangiocellular carcinoma of the liver with advanced biliary cirrhosis was established at an exploratory laparotomy a week before her death. We discuss here the pathogenesis of biliary cirrhosis and carcinoma of the liver; there may be a relation between the two in the childhood population.
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PMID:Cholangiocarcinoma associated with biliary cirrhosis due to congenital biliary atresia. 19 70

Three elderly females presenting with iron deficiency anaemia and faecal loss of blood were found to have a macronodular cirrhosis of the liver and an unusual red spotty appearence of the prepyloric antral mucosa. One patient underwent antral resection and the surgical specimen revealed abnormalities of the (sub)mucosal blood vessels. Anaemia and occult faecal blood loss disappeared after operation. It is suggested that this type of antral vascular abnormality is aetiologically related to hepatic cirrhosis and may represent a gastric equivalent of cutaneous spider angiomata.
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PMID:Abnormal blood vessels of the prepyloric antrum in cirrhosis of the liver as a cause of chronic gastrointestinal bleeding. 30 20

A study of 3451 cholesterol determinations in different diseases was carried out. The mean cholesterol levels for male and female adults and children with different diseases were compared with values for their healthy counterparts. Sickle cell anemia, leukemia, liver cirrhosis, hepatosplenomegaly, tuberculosis, and diabetic, nutritional, ataxic, and tropical neuropathies in male and female adults were associated with reduced cholesterol level while in children malnutrition and anemia were the main causes of low cholesterol levels. Obesity and hypertension caused an elevated level but the mean values were within the range for adult Nigerians in the high income group. Only nephrotic syndrome in both adult and children was associated with a markedly increased cholesterol level in Nigerians of low income status.
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PMID:Serum cholesterol and diseases in Nigerians. 50 76

The present study reported a group of 168 chronically alcoholic patients with a daily ingestion superior to 80 grams. Twenty of these patients (10 percent) did not have liver disease, and 148 (68.5 percent) had different forms of liver disease classified by histopathologic examination. Considering a 97 fi MCV as macrocytosis, we have found in the group of alcoholics without hepatopathy a 50 percent rate of macrocythemia with a mean value of 97.9 fl. In the group of chronic alcoholics with liver disease there was a 64.2 percent macrocytosis with a mean value of 100 fl. We have also studied 43 (21.5 percent) patients with cryptogenetic cirrhosis with a 32.6 percent macrocytosis and a mean value of 93.9 fl. With respect to the alcoholic hepatopathy subgroups, macrocytosis is more frequent in portal fibrosis and acute alcoholic hepatitis, the mean value being higher in the latter. We consider macrocytosis to be frequent among alcoholics, and a good persistence indicator of alcoholic ingestion, pathogenically linked to the now proven dyserythropoietic factor of the alcohol upon the bone marrow. There is no statistically significant correlation between anemia and reticulocytes. We consider macrocytosis to be a more precocious data, and believe that the positive correlation with certain intraerythrocitary enzymes in the juvenile population of red cells corroborates this fact. With respect to the rest of parameters studied there was a correlation with gammaglutamiltranspeptidase, glutamic-oxalacetic transaminase, and the value of prothrombin. The values of mean macrocytosis and elevations of gammaglutamiltranspeptidase and glutamic-oxalacetic transaminase are good persistence indicators of alcoholic ingestion.
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PMID:[Macrocytosis in chronic alcoholism (author's transl)]. 52 26

The influence of the spleen on the blood has been assessed in a series of 187 consecutive patients with chronic liver disease. Patients were described as having 'hypersplenism' if the white blood count and/or platelet count were below 4.0 X 10(9)/1 and 100 X 10(9)/1 respectively at the time of biopsy diagnosis and on at least one subsequent occasion. Using this definition 17 per cent of patients with alcoholic cirrhosis had hypersplenism, compared with 38 per cent with cryptogenic cirrhosis and 26 per cent with active chronic hepatitis. Studies with 51Cr labelled autogenous erythrocytes in 36 of the patients with different types of chronic liver disease showed that the spleen rarely caused anaemia either by excessive splenic pooling or splenic haemolysis. Further studies with 51Cr labelled platelets in 20 other patients showed that the splenic platelet pool was usually considerably increased and the platelet life span reduced. Some patients showed excessive destruction of platelets in the spleen but none of these features consistently related to thrombocytopenia. Splenic enlargement per se did not cause expansion of the plasma volume in chronic liver disease. Of a total of 17 patients who underwent surgical operations for reduction of portal pressure five had hypersplenism but in these the haematological state was not significantly improved at one month. However, none of the survivors of these operations subsequently developed hypersplenism. One patient with severe hypersplenism who underwent simple splenectomy was cured of leucopenia but not of thrombocytopenia.
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PMID:Splenic influences on the blood in chronic liver disease. 53 22

By observing a group of 20 patients with liver cirrhosis, we have clarified some features concerning the tissue hypoxia, which is often present in such a disease. By determining the levels of the haemoglobin and of the intraerythrocytic 2,3-DPG, and by evaluating the acid-base state of such patients, we have emphasized the increased output of the 2,3-DPG as mechanism of adaptation to hypoxia associated with hepatic cirrhosis, both in subjects with anemia and alkalosis and in subjects without anemia but with alkalosis.
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PMID:[Adaptation to hypoxia in liver cirrhosis: the role of 2,3-DPG (author's transl)]. 55 61

Serum zinc concentrations 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 disease states are indicative of true symptomatic or asymptomatic zinc deficiency or merely reflect a decrease in available zinc binding proteins. The low serum zinc concentrations and high urinary zinc excretions in patients with nephrotic syndrome do not appear to be due to loss of zinc bound to urinary proteins. Studies in dogs indicate increased serum and urine concentrations of certain amino acids(cysteine, histidine) greatly increase urinary zinc excretions. Studies are now underway to determine if the hyperzincuria and hypozincemia of cirrhosis, nephrotic syndrome and hyperalimentation can be explained by an increase in these urinary amino acids.
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PMID:Zinc metabolism in renal disease and renal control of zinc excretion. 60 38

Deferoxamine-chelatable iron was measured in 103 patients with known or suspected iron overload. All of 34 patients with untreated hemochromatosis had distinctly elevated values for deferoxamine-chelatable iron. The mean value in these cases was significantly greater than that in patients with cirrhosis, who had little or no stainable hepatic iron. In 15 patients with hemochromatosis who were tested sequentially during the course of phlebotomy therapy, deferoxamine-chelatable iron proved a reliable index of the degree of reduction of storage iron. In 22 additional patients with partially treated hemochromatosis and 14 with iron overload accompanying chronic anemia, this test correlated well with the magnitude of iron deposits in liver or bone marrow. In patients with unexplained elevations of serum iron, normal or only slightly elevated deferoxamine-chelatable iron correctly indicated that storage (hepatic) iron was not excessive. The test was more reliable than determination of serum iron or transferrin saturation as an indicator of increased storage iron. Elevated values could not be attributed to disturbed liver function. Determination of deferoxamine-chelatable iron is a safe, practical, and useful procedure for identifying persons with increased iron stores and for assessing the effect of phlebotomy therapy.
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PMID:Deferoxamine-chelatable iron in hemochromatosis and other disorders of iron overload. 62 26


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