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 purpose of the investigation was to study the metabolism of erythropoietin (EPO) in patients with liver disease. Twelve patients with liver cirrhosis and 10 healthy volunteers were studied. The patients were moderately anemic with a hematocrit of 33 vs 42% (medians) in the volunteers. The pharmacokinetic parameters were calculated after an intravenous (i.v.) injection of 100 U/kg of recombinant human EPO. The serum EPO was measured by radioimmunoassay at regular intervals until 48 h. The median terminal elimination half life in the cirrhosis patients was 5.15 h vs 5.37 h in the control subjects. The clearance was 7.78 vs 7.52 ml/min/1.73 m2 (ns). The steady-state volume of distribution was 3.69 vs 3.09 1/1.73 m2 (ns). The estimated endogenous EPO production was significantly higher in liver cirrhosis (486 vs 290 U/d/1.73m2, p < 0.01). The basal serum EPO was significantly higher in the cirrhosis patients (43.5 vs 26.3 U/l, p < 0.01). The hematocrit correlated inversely with the basal serum EPO level in the cirrhosis patients (r = -0.63, p < 0.04). The EPO-clearance was not related to the presence of ascites, esophageal varices, or to abnormal blood chemistry. It was concluded that normal metabolism of EPO was maintained in liver cirrhosis and that the cirrhotic patients had a moderate compensatory increase of EPO production in response to anemia.
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PMID:The metabolism of erythropoietin in liver cirrhosis patients compared with healthy volunteers. 769 93

Although full blood counts (FBC) are among the most commonly performed laboratory tests, the contribution of routine FBCs to the diagnosis of new problems is controversial. This study represents a unique linkage of a consultant haematology team, reviewing all abnormal blood counts, to an organization providing ambulatory health care to 350,000 patients. The objective was to establish the underlying clinical disorders responsible for all abnormal FBCs during a 2-month period, and to estimate the impact of the haematology team on the diagnostic work-up and management of newly identified problems. 572 (2.55%) of the 22,454 FBCs were abnormal. Of these, 357 showed microcytosis, caused by iron deficiency (58%), thalassaemia minor (35%), inflammation (6%) or chronic renal failure (1%). The most common causes of normocytic anaemia (25 patients) were disseminated malignancy and acute blood loss; of macrocytosis (27 patients), chronic liver disease and cancer; of erythrocytosis (16 patients), chronic hypoxia; of thrombocytopaenia (48 patients), chronic liver disease and ITP; of thrombocytosis (47 patients), iron deficiency and inflammation; of leukopaenia or pancytopaenia (20 patients), cirrhosis and disseminated malignancy; and of leukocytosis (26 patients), chronic leukaemias in the elderly and infection in children. Major new haematological abnormalities were encountered in 0.24% of all blood counts, representing about one new diagnosis per day. Routine blood counts do contribute to the health care of a population. Screening for haematological disease through a central clinical laboratory covering a large high-risk ambulatory population offers a cost-effective way of searching for serious clinical problems, alerting the primary physicians of their existence, and offering advice in continued evaluation and problem management.
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PMID:The haematologist as watchdog of community health by full blood count. 779 88

Hemochromatosis, an iron storage disease, was diagnosed in 3 horses with hepatic cirrhosis. Each horse had bridging portal fibrosis and abundant iron deposits in the cytoplasm of hepatocytes. Serum concentrations of liver-derived enzymes and total bile acids were high. However, serum iron concentration was not high, and iron binding capacity was only 46% saturated in the 1 horse in which it was measured. However, the concentration of iron in the liver of this horse was 20 times the reference limits. Hemochromatosis is common in mynah birds and human beings. There are several types of this iron storage disease. In human beings, there is a familial disease with iron absorption inappropriate for the level of stored iron. Hemochromatosis also occurs secondary to cirrhosis of the liver, and in certain anemia diseases. Another type of hemochromatosis is seen in association with dietary iron overload. These horses were not related, and there was not any evidence of high dietary iron intake.
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PMID:Hepatic cirrhosis and hemochromatosis in three horses. 804 6

The authors describe a case of antral Watermelon Stomach (WS) in a seventy-eight year old woman with severe iron-deficient chronic anemia, liver cirrhosis and diabetes mellitus. Endoscopy was diagnostic on the 3rd-4th examination because of the disease's rarity and the concomitance of systemic pathologies, such as portal hypertension, in which often a congestive gastropathy with similar aspects is associated. Whether out of clinical evolution, or capillary thrombosis, or vertical fibromuscular hyperplasia of the lamina propria were considered distinctive elements. By means of literature review it wasn't possible to establish the portal hypertension's prevalence out of the WS cases, but it could be a chance factor. In this way some polycentric prospective trials could be useful. The endoscopic practice is important not only for diagnosis but also for therapeutical means, even if in our case surgery was the chosen treatment.
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PMID:[A case of watermelon stomach]. 805 94

Hypersplenism is defined as the association of anemia, leukopenia, or thrombocytopenia with bone marrow hyperplasia and splenomegaly. Hypersplenism is common in liver cirrhosis and frequent in patients with portal hypertension. The effects of portacaval shunt are variable; hypersplenism hardly ever improves but rarely develops after surgery. Since the spleen is a major component of the mononuclear phagocyte system, splenectomy reduces antibody synthesis. Although splenectomy abolishes hypersplenism, it may lead to sepsis. Recently, partial splenic embolization, using gelform injected directly into the splenic artery, has been performed in patients with cirrhosis. Partial splenic embolization induces an increase in the number of circulating blood cells. In addition, the levels of albumin, hepaplastintest, cholesterol and cholinesterase are increased significantly after treatment. Partial splenic embolization rarely causes problems and may actually be beneficial.
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PMID:[Hypersplenism in liver cirrhosis]. 811 16

Lysinuric protein intolerance is an autosomal recessive disease caused by defective transport of cationic amino acids. Of the 38 lysinuric protein intolerance patients diagnosed in Finland since 1965, four pediatric patients have died. We describe the clinical courses and autopsy findings for these patients. All patients developed acute respiratory insufficiency. In addition to pulmonary hemorrhages, three of the patients had pulmonary alveolar proteinosis and one had cholesterol granulomas. Three patients had a clinically obvious renal insufficiency, but all four showed histologic signs of immune complex-mediated glomerulonephritis. The patients also developed hepatic insufficiency with fatty degeneration or cirrhosis. All patients showed anemia, thrombocytopenia, and a severe bleeding tendency. The bone marrow of three patients was hypercellular, but the amount of megakaryocytes was decreased in two cases. Amyloid was present in the lymph nodes and the spleen. Bone specimens showed osteoporosis. We conclude that pediatric patients with lysinuric protein intolerance are predisposed to develop pulmonary alveolar proteinosis and glomerulonephritis. They are also at risk of protein malnutrition in the active growth phase, probably due to higher requirements for total nitrogen and amino acids.
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PMID:Pulmonary alveolar proteinosis and glomerulonephritis in lysinuric protein intolerance: case reports and autopsy findings of four pediatric patients. 816 73

Regularities in the development of anemia in patients with chronic hepatitis or hepato-cirrhosis were studied with regard to the pattern and stage of the affection of the liver. The impact of inefficient erythropoiesis on anemia development in patients with chronic diffuse diseases of the liver was demonstrated. Reasons of the red cells imperfection that caused their rapid hemolysis were indicated. In the bone marrow of chronically ill patients there were lower levels of early precursors of erythropoiesis with their proliferative activity reduced. On the basis of the data obtained the authors gave practical recommendations for anemia treatment.
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PMID:[Anemic syndrome in chronic hepatitis and liver cirrhosis]. 830 86

We measured serum erythropoietin (EPO) immunoenzymatically in 245 subjects (151 male, 94 female) to investigate the pathophysiology of its liberation in patients with liver disease. Twelve patients had acute hepatitis, 60 mild chronic liver disease (CLD), 50 cirrhosis (CIR), 43 hepatocellular carcinoma (HCC), 16 malignant extrahepatic disease, 32 benign extrahepatic disease (BEN); 32 subjects served as healthy controls. Higher EPO levels were found in all groups of patients as compared with controls (Bonferroni's test, P < 0.01); CIR and HCC had higher values than CLD and BEN (P < 0.01). By multiple regression analysis, EPO correlated with haematocrit, cholinesterase and C-reactive protein (F = 18.63, P < 0.0001). Thus, circulating EPO increases in patients with liver disease, particularly in its more advanced forms. Besides anaemia, both impairment of liver function (possibly via decreased EPO metabolism) and inflammation seem to play contributory roles in elevating serum EPO.
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PMID:Evidence for a multifactorial control of serum erythropoietin concentration in liver disease. 755 88

Anorexia, weight loss, fatigue, symptoms of alcohol withdrawal and hepatomegaly are common early presenting signs and symptoms of alcohol abuse. The clinical diagnosis of alcoholic hepatitis can be made in alcoholics with associated fever, leukocytosis, jaundice and tender hepatomegaly. Associated laboratory abnormalities may include leukocytosis or leukopenia, anemia, a prolonged prothrombin time and elevated liver enzymes, including aspartate amino-transferase (AST), alanine aminotransferase (ALT), alkaline phosphatase and bilirubin. An AST-to-ALT ratio greater than 2 is common in patients with alcoholic hepatitis. Liver biopsy may be required to establish the diagnosis and to identify other pathology, such as cirrhosis. Histologic diagnosis of alcoholic hepatitis requires the presence of liver cell damage, an inflammatory infiltrate and fibrosis. Biopsy-proven cirrhosis with alcoholic hepatitis or a significantly elevated total bilirubin level and prolonged prothrombin time are associated with a worse prognosis. Abstinence from alcohol, nutritional supplementation and corticosteroids are the mainstays of treatment for severe alcoholic hepatitis.
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PMID:Alcoholic hepatitis. 846 12

A 78-year-old man was admitted to our hospital with anemia and jaundice. Hematological studies revealed hyperchromic macrocytic anemia, and biochemical studies revealed findings of hemolysis. The folic acid level was low and megaloblasts were observed in the bone marrow. From these findings, the patient was diagnosed as having megaloblastic anemia due to folic acid deficiency. This patient had been a heavy alcohol drinker in the habit of drinking alcohol without meals. He began to eat regular meals in the hospital, and the anemia and jaundice improved gradually. Since liver cirrhosis was suspected, amino acid analysis of the urine was performed, and abnormal excretion of beta-amino-isobutyric acid (BAIB) was found. According to the amount of BAIB excreted, the Japanese population can be divided into low and high BAIB excretors comprising 65% and 36%, respectively. BAIB is also considered to reflect dissimilation of thymine. The present patient was included in the high excretion group because of the abnormally high urine level of BAIB, which was considered to be caused by ineffective hematopoiesis in the bone marrow as a result of his megaloblastic anemia. For this reason, dissimilation of thymine was considered to have been active in this patient.
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PMID:[A case of megaloblastic anemia with abnormally high urine level of beta-aminoisobutyric acid]. 847 30


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