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)

1. In 13 dogs used repeatedly as donors for plasmapheresis and plasma injection experiments and fed a kennel diet that for a period of over a year consisted chiefly of bones with much adherent fat, cirrhosis of the liver occurred in 10. Marked fatty change without definite fibrosis occurred in 2 of the dogs. 2. In control dogs fed the same kennel diet during the same period but not subjected to repeated bleedings, no instance of cirrhosis was observed. 3. In previous plasmapheresis and plasma injection experiments "donor dogs" subjected to similar bleedings over comparable periods but maintained on a different kennel diet did not develop cirrhosis. 4. This series of events suggests that in dogs maintained on a relatively high fat diet repeated bleedings predispose them to cirrhosis of the liver. No data are available to decide the more fundamental question: Do the repeated bleedings remove something (other than hemoglobin) necessary for continued integrity of the liver, or is the cirrhosis the result of relative anoxia or increased lipemia occasioned by the repeated bleedings or perhaps of both combined?
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PMID:CIRRHOSIS OF THE LIVER IN "DONOR" DOGS FED A HIGH FAT DIET AND SUBJECTED TO REPEATED BLEEDINGS. 1987 65

Patients with thalassemia have disturbances in hemoglobin chain production which leads to anemia requiring long-term and multiple transfusions, increasing the risk for transfusion-related viruses, including hepatitis B and C viruses. Although this transfusion-related risk has been virtually eliminated with optimal blood screening practices, a significant number of patients transfused prior to 1990 are infected with hepatitis C virus. Treatment of hepatitis B and hepatitis C has improved rapidly leading to viral eradication - or control of viral replication - with the aim of stopping the progression to liver cirrhosis and its complications. Treatment of chronic hepatitis B in patients with thalassemia does not differ from that of other patients. However, current treatment of hepatitis C necessitates the use of ribavirin, which is associated with dose-dependent hemolysis, requiring adjustment of the transfusion protocol for thalassemia patients during the treatment period. Several measures should be taken in thalassemia patients to prevent viral infection including vaccination for hepatitis B and adequate screening of blood and blood products.
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PMID:Treatment and prevention of hepatitis B and C in thalassemia. 2000 18

Beta-thalassemias are a group of hereditary blood disorders characterized by anomalies in the synthesis of the beta chains of hemoglobin resulting in variable phenotypes ranging from severe anemia to clinically asymptomatic individuals. The total annual incidence of symptomatic individuals is estimated at 1 in 100,000 throughout the world and 1 in 10,000 people in the European Union. Three main forms have been described: thalassemia major, thalassemia intermedia and thalassemia minor. Individuals with thalassemia major usually present within the first two years of life with severe anemia, requiring regular red blood cell (RBC) transfusions. Findings in untreated or poorly transfused individuals with thalassemia major, as seen in some developing countries, are growth retardation, pallor, jaundice, poor musculature, hepatosplenomegaly, leg ulcers, development of masses from extramedullary hematopoiesis, and skeletal changes that result from expansion of the bone marrow. Regular transfusion therapy leads to iron overload-related complications including endocrine complication (growth retardation, failure of sexual maturation, diabetes mellitus, and insufficiency of the parathyroid, thyroid, pituitary, and less commonly, adrenal glands), dilated myocardiopathy, liver fibrosis and cirrhosis). Patients with thalassemia intermedia present later in life with moderate anemia and do not require regular transfusions. Main clinical features in these patients are hypertrophy of erythroid marrow with medullary and extramedullary hematopoiesis and its complications (osteoporosis, masses of erythropoietic tissue that primarily affect the spleen, liver, lymph nodes, chest and spine, and bone deformities and typical facial changes), gallstones, painful leg ulcers and increased predisposition to thrombosis. Thalassemia minor is clinically asymptomatic but some subjects may have moderate anemia. Beta-thalassemias are caused by point mutations or, more rarely, deletions in the beta globin gene on chromosome 11, leading to reduced (beta+) or absent (beta0) synthesis of the beta chains of hemoglobin (Hb). Transmission is autosomal recessive; however, dominant mutations have also been reported. Diagnosis of thalassemia is based on hematologic and molecular genetic testing. Differential diagnosis is usually straightforward but may include genetic sideroblastic anemias, congenital dyserythropoietic anemias, and other conditions with high levels of HbF (such as juvenile myelomonocytic leukemia and aplastic anemia). Genetic counseling is recommended and prenatal diagnosis may be offered. Treatment of thalassemia major includes regular RBC transfusions, iron chelation and management of secondary complications of iron overload. In some circumstances, spleen removal may be required. Bone marrow transplantation remains the only definitive cure currently available. Individuals with thalassemia intermedia may require splenectomy, folic acid supplementation, treatment of extramedullary erythropoietic masses and leg ulcers, prevention and therapy of thromboembolic events. Prognosis for individuals with beta-thalassemia has improved substantially in the last 20 years following recent medical advances in transfusion, iron chelation and bone marrow transplantation therapy. However, cardiac disease remains the main cause of death in patients with iron overload.
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PMID:Beta-thalassemia. 2049 8

Several clinical trials of bone marrow cell infusion in patients with liver cirrhosis (LC) have shown clinical improvement, despite conflicting results from animal models. We investigated serial pathological features and the clinical impact after autologous bone marrow infusion (ABMI) in patients with advanced LC. Ten patients with advanced LC due to chronic hepatitis B virus infection underwent ABMI. Serological tests, MRI, and liver biopsies were performed, and quality of life was assessed by a questionnaire. Median serum albumin and hemoglobin levels increased significantly after ABMI. All patients showed an improvement in quality of life, with no serious adverse events. Liver volume, measured by MRI, increased in 80% of the patients, and ascites decreased after ABMI. Child-Pugh scores were also significantly improved at 6 months after ABMI. In the serially biopsied livers, a gradually increasing activation of the hepatic progenitor cell (HPC) compartment, including HPC activation (ductular reaction) and HPC differentiation (intermediate hepatocyte), reached a peak after 3 months, with continued proliferation of hepatocytes, and returned to baseline levels after 6 months. There was no significant change in grade or stage of liver fibrosis or stellate cell activation after ABMI. ABMI is suggested to improve liver function and to activate the progenitor cell compartment. Although clinical improvement was sustained for more than 6 months, histological changes in the liver returned to baseline 6 months after ABMI. Further comparative studies are warranted.
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PMID:Autologous bone marrow infusion activates the progenitor cell compartment in patients with advanced liver cirrhosis. 2052 30

The hemoglobin vesicle (HbV) is an artificial oxygen carrier in which a concentrated Hb solution is encapsulated in lipid vesicles. Our previous studies demonstrated that HbV is metabolized by the mononuclear phagocyte system, and the lipid components are excreted from the liver. It is well-known that many hepatically-metabolized and -excreted drugs show altered pharmaceutics under conditions of liver impairment, which results in adverse effects. The aim of this study was to determine whether the administration of HbV causes toxicity in rats with carbon tetrachloride induced liver cirrhosis. Changes in plasma biochemical parameters, histological staining and the pharmacokinetic distribution of HbV were evaluated after an HbV injection of the above model rats at a putative clinical dose (1400 mgHb/kg). Plasma biochemical parameters were not significantly affected, except for a transient elevation of lipase, lipid components and bilirubin, which recovered within 14 days after an HbV infusion. Negligible morphological changes were observed in the kidney, liver, spleen, lung and heart. Hemosiderin, a marker of iron accumulation in organs, was observed in the liver and spleen up to 14 days after HbV treatment, but no evidence of oxidative stress in the plasma and liver were observed. HbV is mainly distributed in the liver and spleen, and the lipid components are excreted into feces within 7 days. In conclusion, even under conditions of hepatic cirrhosis, HbV and its components exhibit the favorable metabolic and excretion profile at the putative clinical dose. These findings provide further support for the safety and effectiveness of HbV in clinical settings.
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PMID:Hepatically-metabolized and -excreted artificial oxygen carrier, hemoglobin vesicles, can be safely used under conditions of hepatic impairment. 2070 91

It is known that glycation among various proteins is increased in diabetic patients compared with non-diabetic subjects. Currently, among these glycated proteins, glycated hemoglobin (HbA(1C)) is used as the gold standard index of glycemic control in clinical practice for diabetes treatment. However, HbA(1C) does not accurately reflect the actual status of glycemic control in some conditions where plasma glucose changes during short term, and in patients who have diseases such as anemia and variant hemoglobin. In comparison, another index of glycemic control, glycated albumin (GA), more accurately reflects changes in plasma glucose during short term and also postprandial plasma glucose. Although GA is not influenced by disorders of hemoglobin metabolism, it is affected by disorders of albumin metabolism. This review summarizes diseases and pathological conditions where GA measurement is useful. These include the status of glycemic control changes during short term, diseases which cause postprandial hyperglycemia, iron deficiency anemia, pregnancy, chronic liver disease (liver cirrhosis), chronic renal failure (diabetic nephropathy), and variant hemoglobin.
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PMID:Clinical impact of glycated albumin as another glycemic control marker. 2072 96

The hemoglobin-vesicle (HbV) is a cellular, hemoglobin-based oxygen carrier. Our previous pharmacokinetic studies demonstrated that the liver is strongly associated with the metabolism and excretion of HbV. The aim of this study was to evaluate the pharmacokinetics of HbV in a chronic cirrhosis rat (CCR) model induced by carbon tetrachloride (CCl(4) ) and explore whether liver functional parameters and Kupffer cell (KC) phagocyte activity are related to the pharmacokinetics of HbV. The CCRs were induced three times weekly by intraperitoneal administration of CCl(4) for 8 weeks and categorized as Child-Pugh grade B. To analyze the pharmacokinetics, the CCRs were given a single intravenous injection of (3) H-HbV (1400 mg of Hb/kg). The total clearance and hepatic distribution of HbV were negatively correlated with plasma aspartate aminotransferase (AST) levels (p = 0.007). In addition, the phagocyte index was negatively correlated with plasma AST levels (p = 0.047). The excretion of lipid components in feces was also negatively correlated with plasma AST levels (p = 0.049). In conclusion, alteration in the pharmacokinetics of HbV in CCRs can be attributed to a decrease in KC phagocyte activity and the extent of damage to parenchymal cells. This represents the first demonstration of the pharmacokinetics of a liposome preparation in chronic liverimpairment.
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PMID:Alteration in the pharmacokinetics of hemoglobin-vesicles in a rat model of chronic liver cirrhosis is associated with Kupffer cell phagocyte activity. 2079 62

We developed a high-sensitivity C-reactive protein quantifiable chemiluminescent immunoassay (hs-CRP CLIA). The high-purity native CRP was purified from hepatic cirrhosis patient ascetic fluid by affinity and ion exchange chromatography and used as an immunogen to develop the monoclonal antibodies (mAbs) against CRP. Twenty-two mAbs were identified reactive with CRP in ELISA and 13 of them were reactive in the phosphorycholine ligand capture ELISA. The mAbs 10C5 and 10C11 were selected to develop the hs-CRP CLIA. The linearity and performance of the hs-CRP CLIA was characterized. It was showed not reactive when testing against other serum materials (IgG, hemoglobin and triglyceride). The reliable correlation (R2 > 0.993) was obtained between testing value (RLU/S) and the concentration of human serum CRP calibrator. The linearity fell in the range of 0.04-20.38 mg/L. The assay has good accuracy and reproducibility, the mean recovery was 99% and the precision of the intra- and inter assay was CVs (4.2%-5.8%) and (9.0%-11.5%), respectively. In testing of 90 human sera, this assay performed well and correlated comparably with a commercial hs-CRP ELISA kit. Thus, hs-CRP CLIA is an accurate, reliable, quantifiable assay for detection of high-sensitive C-reactive protein in serum, it may be useful to improve the risk assessment of cardiovascular disease and the prognosis of inflammatory bowel disease.
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PMID:[Chemiluminescent immunoassay for high-sensitivity C-reactive protein]. 2109 Jan 22

Sickle cell disease (SCD) frequently affects the liver; if acute liver failure (ALF) develops, the only potentially effective therapeutic option is liver transplantation (LT). Only 12 patients for whom LT was performed for SCD-related ALF have been described so far. We report a retrospective series of 6 adult patients with SCD (3 men and 3 women, median age = 40.1 years) who underwent emergency LT. The indication for LT was ALF complicating cirrhosis in 5 patients (hepatitis C/iron overload-induced cirrhosis in 3 and iron overload-induced cirrhosis in 2); one patient had autoimmune hepatitis. The median follow-up was 52.7 months (0.5-123 months). The 1-, 3-, 5-, and 10-year survival rates were 83.3%, 66.7%, 44.4%, and 44.4%, respectively. One patient died of hepatocellular failure precipitated by hyperacute allograft rejection on post-LT day 10. Soon after LT, 2 patients developed seizures; in 1 case, the seizures were a complication of early calcineurin inhibitor-induced leukoencephalopathy. Four long-term survivors benefited from specific management of SCD; specifically, the hemoglobin S fraction was maintained below 30% and the total hemoglobin level was maintained between 8 and 10 g/dL. Two patients had mild vaso-occlusive crises. Three patients experienced a recurrence of hepatitis C virus (HCV) infection; 2 of these patients experienced reversible neurological complications while they were receiving antiviral treatment. Carefully selected patients with SCD may benefit from emergency LT. However, such patients seem to be particularly susceptible to neurological complications after LT. In contrast, severe SCD-related crises do not seem to recur if specific management is provided. Outcomes may be improved if the neurological complications can be minimized; for example, the administration of a calcineurin inhibitor can be delayed, and the management of HCV infection recurrence can be improved.
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PMID:Transplantation for liver failure in patients with sickle cell disease: challenging but feasible. 2144 21

Liver cancer patients are confronted with the additional risk of malnutrition because the disease is often associated with hepatitis, liver cirrhosis, and metabolic disturbances. Nutritional intervention can improve treatment outcome, but early detection is important. This study aimed to determine whether the Mini Nutritional Assessment (MNA) could effectively rate the nutritional status of patients with liver cancer in Taiwan. A total of 300 patients were evaluated for nutritional status with two modified versions of the MNA in short and long forms. MNA-Taiwan Version 1 adopted population-specific anthropometric cutpoints, whereas Version 2 replaced mid-arm and calf circumferences in place of body mass index. Predicted statuses were compared to results predicted by the Council on Nutrition Appetite Questionnaire (CNAQ) and analyzed for correlations with biochemical or cancer status parameters. Results showed that both versions of the MNA were effective in predicting nutritional status, and predictions by the short forms agreed well with those by the long forms. The nutritional scores correlated well with hemoglobin, serum albumin, C-reactive protein, r-glutamyl transpeptidase, TNM (tumor, node, metastasis) staging, and severity of cirrhosis. These results suggest that the MNA can be an effective tool for assessing the nutritional status of patients with liver cancer.
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PMID:Usefulness of the mini nutritional assessment in predicting the nutritional status of patients with liver cancer in Taiwan. 2146 83


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