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

Gastric intramucosal bleeding in portal hypertensive gastropathy was investigated in terms of gastric mucosal microcirculation, coagulation-fibrinolysis factors, and local fibrinolysis in patients with liver cirrhosis. The gastric mucosa was examined by endoscopy, and the patients were classified into two groups with or without bleeding. Gastric mucosal blood flow was measured simultaneously with coagulation-fibrinolysis factors or local fibrinolysis in both groups. As gastric mucosal blood flow, the gastric mucosal blood volume (IHb) and the oxygenated hemoglobin concentration (ISO2) were determined by the organ reflection spectrum method. Coagulation-fibrinolysis factors were measured in the blood. For evaluation of local fibrinolysis, gastric biopsy specimens were placed on a standard fibrin plate, and the fibrinolysis area was measured. Compared with the non-bleeding group, the bleeding group showed increased IHb and decreased ISO2 (p < 0.05), suggesting marked congestion of blood flow. Gastric intramucosal bleeding was frequently observed in patients with marked congestion of blood flow and markedly abnormal values of coagulation-fibrinolysis factors. Gastric local fibrinolysis was also significantly enhanced in the bleeding group (p < 0.05). In addition, local fibrinolysis was correlated positively with the gastric mucosal blood volume (r = 0.68, p < 0.05) and negatively with the oxygenated hemoglobin concentration (r = -0.58, p < 0.05). These results suggest the following mechanism of gastric mucosal bleeding in liver cirrhosis and portal hypertension. Congestion of gastric mucosal blood flow is present in liver cirrhosis and portal hypertension. An increase in the microvascular pressure and hypoxia cause release of tissue plasminogen activators from gastric mucosal cells and vascular endothelial cells. As a result, gastric local fibrinolysis is enhanced, causing gastric mucosal bleeding.
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PMID:Bleeding in portal hypertensive gastropathy evaluated in terms of gastric mucosal microcirculation and coagulation-fibrinolysis system. 947 67

We developed a new, highly sensitive enzymatic method for quantifying creatine in erythrocytes, which comprises creatine amidinohydrolase, sarcosine oxidase, and peroxidase. In the present method, an N-methylcarbamoyl derivative of methylene blue, 10-N-methylcarbamoyl-3,7-bis(dimethylamino)phenothiazine (MCDP), was used as a sensitive chromogenic compound. Potassium ferrocyanide was used to prevent nonspecific oxidation of MCDP. The enzymatic method exhibited good analytical performance: precision, within-run CVs <1.0% and between-day CVs <2.0%; average analytical recovery, 99.3% +/- 1.8%; detection limit, 1.0 micromol/L in hemolysate; and linearity, at least up to 500 micromol/L as creatine concentration in hemolysate. Excellent agreement was observed between the present method (y) and HPLC (x), y = 1.029x - 0.002 micromol/g hemoglobin, r = 0.9998, S(y/x) = 0.053 micromol/g hemoglobin (n = 110). No significant interference was produced by various compounds, including guanidino compounds, amino acids, and reducing materials. The reference intervals (mean +/- 2 SD) for erythrocyte creatine obtained from 60 males and 60 females were (in micromol/g hemoglobin) 1.18 +/- 0.52 (0.66-1.70) for males and 1.35 +/- 0.49 (0.86-1.84) for females. Using this method, we documented changes in erythrocyte creatine in patients with various hemolytic conditions, including hemolytic anemia, liver cirrhosis, renal insufficiency, and chronic renal failure treated with hemodialysis with or without the administration of erythropoietin. We conclude that the use of MCDP allows sensitive measurement of erythrocyte creatine and that MCDP with potassium ferrocyanide can improve the sensitivity of assays that use peroxidase for detection of H2O2.
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PMID:Sensitive enzymatic assay for erythrocyte creatine with production of methylene blue. 966 28

We have shown that administration of inorganic potassium phosphates (Pi) to patients with severe diabetic ketoacidosis was able to increase the P50 (the PO2 necessary to achieve a hemoglobin saturation of 50%) by a non diphosphoglycerate (DPG) mediated effect. This suggests that the oxyhemoglobin dissociation curve (ODC) may be determined not only by pH, temperature, CO2 content and DPG but also by plasmatic ions. In order to test this hypothesis we have determined the ODC on whole blood in two groups of subjects, 49 control subjects with matching age and sex and 49 patients suffering from liver cirrhosis, acute pancreatitis, septic shock and acute respiratory distress syndrome. The patients had many ionic disorders induced either by their diseases or by the applied treatment. The mean ODC of the patients did not differ from the normal values. In contrast, the dispersion of PO2 around the saturations values was increased from 5 to 80% saturation. A forward regression analysis showed that the DPG level and the levels of inorganic phosphates and natrium (Na+) played a significant role in determining the position of the ODC according to the following equation: P50 (mmHg) = 34.5 + 0.225 DPG + 0.62 Pi-0.09 Na+, where DPG is in micromol.gHb-1 and Pi and Na+ in mEq.l-1. In separate experiments we showed that the Bohr effect as expressed in d (log PO2)/dpH amounted to -0.53, -0.46 and -0.42 for SO2 equal to 5%, 50% and 95%, respectively. The corresponding values for the temperature effect was expressed in d (log PO2)/dT amounted to 0.028, 0.024, and 0.020 respectively. The fact that ions play an role in regulating the position of the ODC of patients with ionic disorders may have therapeutical implications, preventive or curative.
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PMID:Effect of inorganic ions on the oxyhemoglobin dissociation curve of severely ill patients. 976 30

The expected explosion of costs in transfusion medicine due to the shortfall of healthy donors and the more frequent treatment of transfusion-associated complications (chronic hepatitis, cirrhosis, wound infection, tumor recurrence) increases the socio-economic importance of the development of safe and effective synthetic oxygen carriers as an alternative to the transfusion of homologous red blood cells. Currently two types of artificial oxygen carriers are experimentally and clinically investigated for their capacity to ensure adequate tissue oxygenation in the case of severe anemia. In addition to their oxygen transport capacity solutions based on free human or bovine hemoglobin provide vasoconstrictor properties. Their hyperoncotic properties make them particularly attractive for the treatment of severe hemorrhagic shock. Perfluorocarbon (PFC) emulsions allow an increase of the physically dissolved portion of arterial oxygen content. Due to their particulate nature (emulsion droplets) PFC may only be infused in low doses. Otherwise there is risk of overload and malfunction of phagocytic cells of the reticulo-endothelial system. In the case of an intraoperative blood-loss in preoperatively hemodiluted patients, bolus infusion of PFC represents an effective means to avoid immediate retransfusion of autologous blood and allows for further, extreme hemodilution without risking tissue hypoxia.
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PMID:[Artificial oxygen carriers. Alternatives to homologous blood transfusion?]. 1035 79

We studied peripheral blood erythrocyte parameters and HFE genotypes in 94 hemochromatosis probands and 132 white, normal control subjects. Mean red blood cell counts in probands and control subjects were not significantly different. However, mean values of hemoglobin, hematocrit, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC) were significantly higher in C282Y/C282Y probands (n = 60) than in wild-type control subjects (n = 65). Probands with other HFE genotypes also had increased mean erythrocyte parameters (other than red blood cell count). Peripheral blood smears prepared before therapeutic phlebotomy revealed that erythrocytes in many probands had increased diameters and were well filled with hemoglobin. Erythrocyte parameters were similar in C282Y/C282Y probands with and without hepatomegaly, elevated serum concentrations of hepatic enzymes, hepatic cirrhosis, diabetes mellitus, arthropathy, or hypogonadism. Among C282Y/C282Y probands, significantly greater values of MCV (but not other erythrocyte parameters) occurred among those who had transferrin saturation values of 75% or greater or iron overload at diagnosis. After iron depletion, the mean MCV, MCH, and MCHC values of C282Y/C282Y probands decreased but remained significantly greater than values in wild-type control subjects. Mean values of prephlebotomy MCH and MCHC concentrations were lower in HLA-A3-positive than in HLA-A3-negative C282Y/C282Y probands. We conclude that increased values of mean hemoglobin, hematocrit, MCV, MCH, and MCHC in hemochromatosis probands are caused primarily by increased iron uptake and hemoglobin synthesis by immature erythroid cells. Mechanisms of iron uptake by erythrocytes that could explain these results are discussed.
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PMID:Peripheral blood erythrocyte parameters in hemochromatosis: evidence for increased erythrocyte hemoglobin content. 1063

The genotoxic effects of 2-acetylaminofluorene (AAF) alone cannot explain the formation of rat liver tumors. It has been proposed that mitochondrial effects are associated with its tumor-promoting properties. These mitochondrial effects are thought to trigger apoptosis and regenerative proliferation, which alters the liver lobule in a cirrhosis-like manner. A situation is generated which favors the growth of initiated cells. To test this sequence of events, the dose dependence of early effects with time was studied. Male Wistar rats received 50, 100, 200, 400, or 800 ppm AAF in the diet and the following endpoints were analyzed at 2, 4, 8, and 16 weeks of feeding: apoptotic cell death, cell proliferation, GST-P-positive foci (placental form of glutathione S-transferase), and morphological alterations. Hydrolyzable hemoglobin adducts were used as a dosimeter for metabolic activation after 2 weeks of feeding. The hemoglobin adduct levels increased linearly with dose. With the conventional carcinogenic concentration of 200-ppm AAF in the diet, the number of apoptoses increased first, predominantly in the periportal area (2 weeks). Cell proliferation followed with some delay (4 weeks). This reflects regenerative tissue response and not the growth of initiated cells, because the number of enzyme-altered foci was still extremely low at that time. Foci developed only later when the morphology had changed. With 50 ppm AAF in the diet, a no-effect level had not been reached for any of the endpoints, but foci developed much more gradually than with higher doses. Unexpectedly, the proliferative response stabilized at 8 weeks with a labeling index of 12-17, with all AAF concentrations. The observed sequence of events supports the hypothesis. It is concluded that (1) The proliferation of initiated cells-defined as promotable cells-is largely determined by the cellular environment, such as morphologically altered liver. (2) The morphological alterations in rat liver result from imperfect regeneration from toxic effects. (3) Imperfect regeneration results from limitations in the possibilities to adapt to chemical stress. (4) If these limits are overwhelmed and morphology has changed to a certain extent, preneoplastic foci develop; this occurs much faster, at least, than without these changes.
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PMID:Dose response of early effects related to tumor promotion of 2-acetylaminofluorene. 1078 58

The aims of the study were to determine the prevalence of protein calorie malnutrition (PCM) in Thai cirrhotic patients and to evaluate nutritional and immunological status in various stages of cirrhosis. Subjective Global Assessment (SGA) and anthropometric measurement were used as nutritional assessment in sixty cirrhotic patients. Delayed-type hypersensitivity skin test, lymphocyte count, immunoglobulin and complement were assessed for immune status. Blood samples were sent for routine tests, prealbumin, thiamine and riboflavin level. There were 7/60 (11.7%) patients with percentage of ideal body weight (%IBW) less than 90 per cent. SGA, hemoglobin, protein indices and cholesterol level showed the deterioration of nutritional status in the late stage of the disease. Five (8.3%) patients with thiamine deficiency, and thirteen (21.7%) patients with riboflavine deficiency were detected. Lowest levels of complement and highest levels of immunoglobulin also occurred in the late stage of the disease. In conclusion, defining %IBW <90 per cent as malnutrition, the prevalence of malnutrition in Thai cirrhotic patients was 11.7 per cent. Nutritional and immunological status deteriorated according to the advanced stage of disease. If nutritional support is given in the early stage, it may improve nutritional status and reduce morbidity and mortality in cirrhotic patients.
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PMID:Impact of liver cirrhosis on nutritional and immunological status. 1175 79

AIM:To investigate the pathophysiology of the digestive tract in patients with liver cirrhosis.METHODS:In 42 cirrhotic patients and 20 control subjects, the following fecal proteins were measured by enzyme-linked immunosorbent assay: albumin (Alb), transferrin (Tf), and alpha(1)antitrypsin (alpha(1)-AT) as a marker for intestinal protein loss, hemoglobin (Hb) for bleeding, PMN-elastase for intestinal inflammation, and secretory IgA for intestinal immunity.RESULTS:The fecal concentrations of Hb, Alb, Tf,alpha(1)-AT, and PMN-elastase were increased in 13 (31%), 8(19%), 10(24%), 6(14%), and 11 (26%) cases among 42 patients, respectively. Fecal concentration of secretory IgA was decreased in 7 (17%) of 42 patients. However, these fecal concentrations were not related to the severity or etiology of liver cirrhosis. The serum Alb level was significantly decreased in patients with intestinal protein loss compared to that in patients without intestinal protein loss.CONCLUSION:These findings suggest that: (1)besides the well-known pathological conditions, such as bleeding and protein loss, intestinal inflammation and decreased intestinal immunity are found in cirrhotic patients; (2)intestinal protein loss contributes to hypoalbuminemia in cirrhotic patients, and (3) intestinal inflammation should not be over looked in cirrhotic patients, since it may contribute to or cause intestinal protein loss and other various pathological conditions.
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PMID:Increased prevalence of intestinal inflammation in patients with liver cirrhosis. 1181 75

We analyzed rheologic parameters, including erythrocyte rigidity (ER), whole blood and plasma viscosity, erythrocyte and platelet count, hemoglobin, hematocrit, mean corpuscular volume (MCV), fibrinogen, erythrocyte sedimentation rate (ESR), cholesterol, triglyceride, high-density lipoprotein (HDL), low-density lipoprotein (LDL), very-low density lipoprotein (VLDL), and gamma globulin levels in 18 patients with chronic liver disease and 20 healthy volunteers. Fifteen patients had cryptogenic cirrhosis while 3 had chronic active hepatitis. ER and MCV was significantly higher in the patient group than the control group while whole blood and plasma viscosities were significantly lower. There were significant correlations between ER and blood and plasma viscosity, ER and MCV, plasma and blood viscosity, HDL and plasma viscosity and a negative correlation between ER and ESR. Our results demonstrate that erythrocytes become more rigid in chronic liver disease. We suggest that erythrocytes with increased rigidity can impair hepatic microvascular circulation and thus contribute to liver dysfunction.
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PMID:Rheological properties of blood in patients with chronic liver disease. 1190 66

Recurrence of hepatitis C virus (HCV) infection after orthotopic liver transplantation is a major cause of graft failure. The aim of our study was to determine the safety, efficacy, and tolerability of combination therapy with interferon and ribavirin in the treatment of recurrent hepatitis after liver transplantation. Twenty-six patients (18 men) with histologically established HCV recurrence after liver transplantation for cirrhosis secondary to chronic HCV infection were treated with a combination of interferon alfa-2b (3 million units three times weekly) and ribavirin (800 to 1,000 mg/d). Dosage modifications were according to a standard protocol incorporating laboratory values and clinical side effects. Fifty percent of patients completed 1 year or more of therapy. On an intention-to-treat basis, nine patients (35%) showed an end-of-treatment virological response. Six of these nine patients completed greater than 6 additional months of follow-up, and all have had sustained virological responses. A histological response (decrease in histological activity index > or = 2) was seen in 75% of virological responders and 67% of nonresponders. Adverse events requiring dose modification or cessation of therapy occurred in 66% of patients. Adjuvant therapies used to support hemoglobin levels included erythropoietin and red blood cell transfusions. There were no independent pretreatment predictors of a virological response, perhaps because of the small sample size. Combination therapy with interferon and ribavirin may be beneficial in patients with recurrent HCV after liver transplantation. The majority of patients require dose modifications because of side effects. Histological response is common in virological nonresponders.
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PMID:Treatment of posttransplantation recurrence of hepatitis C with interferon and ribavirin: lessons on tolerability and efficacy. 1208 17


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