UMLS:C0023890 - FACTA Search

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)

Lymphocytic dipeptidylaminopeptidase IV (DP-IV; E.C.3.4.14.5.) is described as a marker enzyme of immunostimulant T-lymphocytes as well as functional characteristic of IL-2-producing cells. Mononuclear cells of periphere blood (MNC) were isolated by density gradient centrifugation followed by enzymcytochemical staining of DP-IV positive cells and measuring of DP-IV enzyme activity using chromogenic substrates. As relative sign of single cell DP-IV activity we calculated average DP-IV activities of DP-IV positive cells. Blood samples from 14 patients with acute virus hepatitis, 30 cases of chronic active liver disease, 61 cases with liver cirrhosis of various kind and 19 patients with fatty liver and toxic hepatitis were investigated. As standard of comparison we used a group of healthy blood donors. By this way significant differences of described DP-IV parameters between some groups of liver disease were evident. Using an aetiologic classification of investigated liver diseases we found highly significant increased single cell activities in hepatitis-B associated cases in comparison to remarkable lower lower values in autoimmune cases. Different hypothesis about changes of lymphocytic dipeptidylaminopeptidase IV as a part of disturbed immunoregulation in chronic liver diseases were discussed.
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PMID:[Dipeptidylpeptidase IV activity in human lymphocytes in hepatobiliary diseases]. 197 80

Interleukin-2 has proved to be effective for the intralesional treatment of tumors of the bladder. There are examples in literature of hepatocellular carcinoma (HCC) treatment with lymphokine-activated killer (LAK) cells infused in the hepatic artery. We decided to check the effects of echo-guided intralesional injection of these cells in this disease. We treated 5 patients with inoperable hepatocellular carcinoma, following cirrhosis; in 4 cases the mass had a diameter less than 3 cm (small HCC) while in the remaining case it measured 7 cm. Tumor size remained unchanged in 3 of the 4 small HCC, and increased only slightly in the other (over a period of 10 months). This would appear to indicate that treatment halted neoplasm growth or at least slowed it down. The echo pattern of the lesions changed, with a constant reduction in echogenicity. Finally, in multiple control biopsies, fibrosis, present in only one case before treatment, was found fairly constantly after treatment. There were no significant side effects, apart from slight water retention in one patient. On the basis of our preliminary results, we consider it worthwhile continuing this study to establish the most suitable IL-2 doses and analyze in more detail the modifications induced in the neoplasm.
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PMID:Intratumoral echo-guided injection of interleukin-2 and lymphokine-activated killer cells in hepatocellular carcinoma. 255 85

To investigate whether disordered immune function, as shown by abnormalities in lymphokine production, is present in alcoholic liver disease, interleukin-1 and interleukin-2 activity were assayed in a group of patients with acute alcoholic hepatitis in the absence of underlying cirrhosis, and a group of patients with inactive alcoholic cirrhosis. Activities of both IL-1 and IL-2 in alcoholic hepatitis were similar to those of normal individuals, although in abstinent patients with alcoholic cirrhosis, IL-1 activity was increased and IL-2 activity decreased. Lymphocyte transformation in response to PHA in patients with alcoholic hepatitis was significantly impaired when compared with normal controls, and addition of exogenous IL-2 did not correct this impaired response over a wide range of concentrations of both PHA and IL-2. These observations suggest the underlying defects in cell mediated immunity in acute alcoholic hepatitis, as assessed by blast transformation, could be fundamentally different from those of alcoholic cirrhosis and could be secondary to the metabolic effects of acetaldehyde or altered redox potentials on the behaviour of proliferating cells.
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PMID:Contrasts in interleukin-1 and interleukin-2 activity in alcoholic hepatitis and cirrhosis. 262 42

Cytokines constitute a complex network of molecules involved in the regulation of the inflammatory response and the homeostasis of organ functions. Cytokines coordinate physiologic and pathologic processes going on in the liver, such as liver growth and regeneration, inflammatory processes including viral liver disease, liver fibrosis and cirrhosis. Liver growth and regeneration are regulated by several cytokines. The platelet-derived hepatocyte growth factor, in particular, delivers a strong mitogenic stimulus for hepatocyte regeneration. The cell-mediated immune response plays a central role in hepatocellular necrosis and in the immunopathogenetic mechanisms involved in viral clearance and persistence in liver disease of viral etiology. In this context, cytokines modulate the immune system and exert direct antiviral activity by cytopathic and non-cytopathic mechanisms, as demonstrated in a transgenic mouse model. IL-6, TNF-alpha, IL-1 and IL-2 increase in acute fulminant viral hepatitis; in fact, they have pro-inflammatory and cytotoxic effects. Reduced IL-2 and IFN-alpha synthesis and increased serum levels of IL-1 and IL-2 soluble receptor (IL-2R) have been observed in HBV chronic liver disease. In HCV chronic hepatitis, IL-2R increases as well, while IFN-gamma and IL-2 decrease. In personal experimental observations, intra-hepatic messenger RNA expression of several cytokines was measured in liver specimens of patients with chronic HBV and HCV infections: patients with HCV chronic liver disease had higher levels of IL-2, IL-6, IL-10, and IFN-gamma. These data are in accordance with immunological studies showing a vigorous cell-mediated immune response in HCV chronic liver disease and a deficient immune response in HBV chronic hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cytokine mediators in acute inflammation and chronic course of viral hepatitis]. 772 1

Cytokine response to viral infection can be of critical importance in the host defense against virus. Interferon (IFN)-gamma and interleukin (IL)-2 have wide ranges of activities in host defense mechanisms. Therefore, these cytokine genes in the liver were investigated in a series of patients with hepatitis C virus (HCV) infection using a reverse transcribed-polymerase chain reaction (RT-PCR). Total RNA was purified from liver biopsies, reverse transcribed to cDNA, amplified by specific primers, and the products were detected by agarose gel and slot blot hybridization. All samples from acute hepatitis (AH; n = 4) and chronic hepatitis patients (CH; n = 19) were positive for IFN-gamma at varying degrees. AH patients showed strong signals compared to CH patients, liver cirrhosis (LC; n = 12; 72% positive) patients, and hepatocellular carcinoma (HCC; n = 21; 19% positive) patients. IL-2 gene was undetectable in all patients tested. IL-2 receptor (IL-2R) was detectable in AH, CH and LC patients but not in HCC patients. We conclude that IFN-gamma has important roles in the cytokine network that indeed present in the liver of HCV patients while the presence of IL-2R gene may indicate that the signaling pathway for IL-2 is intact.
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PMID:Interferon-gamma, interleukin (IL)-2 and IL-2 receptor expressions in hepatitis C virus-infected liver. 839 42

An imbalance between T helper cell (Th)1 and Th2-like cytokines has been described in several chronic infectious diseases. We therefore analyzed the intrahepatic messenger RNA (mRNA) expression of Th1-like (interleukin [IL]-2, interferon [IFN]-gamma) and Th2-like (IL-4, IL-10) cytokines in chronic hepatitis C patients (n = 17) and controls (n = 6) and correlated the results with liver histology and intrahepatic viral load. Intrahepatic cytokine mRNA and hepatitis C virus (HCV) RNA were quantitatively assessed by polymerase chain reaction (PCR) using a dot-blot hybridization technique. Liver biopsy specimens were histologically graded using the Scheuer Score. IFN-gamma and IL-2 mRNA expression were significantly upregulated in chronic HCV vs. controls (P < .002, P < .04, respectively). Both correlated significantly with histological fibrosis and portal tract inflammation. In contrast, the expression of IL-10 mRNA was decreased in cirrhosis and chronic HCV compared with controls (P < .02, P < .0001, respectively). IL-4 mRNA was detected inconsistently at low levels in all groups. Intrahepatic viral load did not correlate with either cytokine expression or tissue injury. In conclusion, the progressive liver injury seen in chronic HCV is associated with the upregulation of intrahepatic Th1-like cytokines and the downregulation of IL-10, a Th2-like cytokine. These results suggest a role for delayed-type hypersensitivity immune reactions in HCV related liver injury.
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PMID:Progressive liver injury in chronic hepatitis C infection correlates with increased intrahepatic expression of Th1-associated cytokines. 885 73

Patients with cirrhosis of the liver frequently demonstrate anergy in intracutaneous tests and fail to respond to vaccination, suggesting impaired delayed hypersensitivity and other T cell-dependent functions in vivo. T cell activation through the coordinated interaction of different cells of the immune system (B cell, antigen-presenting cells (APC)) is an important step in the induction of cellular and humoral immune responses. Impaired T cell-dependent functions in patients with liver cirrhosis may thus be explained by defective T cell activation. We prospectively investigated T cell activation pathways in 12 patients (nine males, three females) with alcoholic liver cirrhosis (seven Child Pugh stage A and B (CP A + B), five Child Pugh stage C (CP C)) and five healthy controls and compared the in vitro results of T cell activation with data obtained in vivo, e.g. intracutaneous tests and vaccination against hepatitis B surface antigen (HBs-Ag). Five out of eight patients who completed vaccination against hepatitis B virus infection were non-responders; one of the three responders had a non-protective anti-HBs titre. Moreover, three of five patients with alcoholic liver cirrhosis CP A + B, and two out of three with CP C were anergic in intracutaneous tests to a set of diverse antigens. All parameters of T cell activation were normal, including proliferation mediated by CD2, CD3-T cell receptor (TCR) complex, and CD28; acquisition of responsiveness to exogenous IL-2 and IL-4; activation of proteinkinase C (PKC) by phorbol ester and calcium influx by addition of ionomycin. The ability of monocytes to deliver costimulatory signals was preserved in patients with alcoholic cirrhosis. In addition, serum of patients with alcoholic liver disease did not inhibit T cell proliferation. We conclude that, although in patients with alcoholic liver cirrhosis T cell-dependent functions are impaired in vivo, T cell activation pathways are not responsible for the observed immune defect.
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PMID:Analysis of T cell activation pathways in patients with liver cirrhosis, impaired delayed hypersensitivity and other T cell-dependent functions. 909 23

Idiopathic portal hypertension (IPH) was diagnosed in a 30-year-old man. Clinical signs were splenomegaly, leucothrombocytopenia, and esophageal varices of fourth degree. The histology of the liver biopsy showed portal fibrosis with no evidence of cirrhosis. No causing agent or known disease could be found for the histopathological and clinical features. Due to a severe deterioration of general condition and a decline of synthetic liver function, liver transplantation and splenectomy were performed. The histological examination of the explanted liver revealed features of IPH, demonstrating portal fibrosis and dilated vessels adjacent to portal tracts; no cirrhosis was found. The postoperative recovery was without any severe complications. The duration of hospitalization was 28 days. Following liver transplantation, the esophageal varices disappeared and leucocytes, platelets as well as parameters of hepatic synthesis reached normal values. Initially, the immunosuppression was composed of prednisolon, tacrolimus, and antibodies against IL-2 receptors (BT 563) and was later continued with prednisolon and tacrolimus. Within the follow-up observation of 26 months, there was no evidence for graft rejection, severe infection, or occurrence of portal hypertension. Up till now the patient is in good condition with normal graft function. Liver transplantation may be a curative therapy for patients with advanced disease of IPH but the long-term follow-up after transplantation has to show whether IPH can reoccur.
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PMID:[Liver transplantation and splenectomy in idiopathic portal hypertension]. 926 93

We previously reported that the number of TNF-alpha-producing cells was increased in the liver of patients with type C chronic liver disease. To understand further the pathophysiology of this change, we examined serum levels of two soluble TNF receptors, TNF-alphaRI (p55) and -alphaRII (p75), and IL-10, all of which act as TNF-alpha buffer, and IL-15, a novel cytokine sharing many immunological activities with IL-2, using ELISA methods. We studied control individuals and patients with type C chronic liver disease, including asymptomatic hepatitis C virus (HCV) carriers with persistently normal serum ALT values, and those with chronic hepatitis (CH), liver cirrhosis (LC) and hepatocellular carcinoma (HCC). Both types of sTNF-alphaR closely correlated with disease progression. Patients with LC and HCC had significantly elevated levels for sTNF-alphaRII compared with the other patient groups and controls. Serum IL-10 levels were significantly greater in all chronic liver disease groups than in controls. With respect to IL-15, the values were high in CH, LC and HCC compared with those of controls. Notably, HCC patients showed highest values for both IL-10 and IL-15, with significant differences from the other patient groups. Serial determinations revealed that interferon (IFN) treatment for CH patients resulted in the suppression of circulating IL-10 and IL-15 levels along with decrease in serum aminotransferase values. Both cytokines remained at decreased levels after cessation of therapy in patients who went into clinical and virological remission. On the other hand, treatment did not affect serum levels of sTNF-alphaRs. These findings indicate that serum levels of these molecules correlated with disease progress in chronic HCV infection, and that IL-10 and IL-15 may reflect the degree of inflammation in the liver. It is also suggested that both cytokines may be related to the development of HCC.
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PMID:Serum levels of IL-10, IL-15 and soluble tumour necrosis factor-alpha (TNF-alpha) receptors in type C chronic liver disease. 932 22

No previous studies have been reported on human alcoholism in which the pattern of cytokine secretion by natural killer (NK) cells is explored. The goal of the present study was to evaluate the role of NK cells in the production of cytokines in patients with chronic alcoholism, analyzing at the same time the possible relationship between cytokine production and both alcoholic liver disease and ethanol (EtOH) intake. A total of 30 chronic alcoholic patients-11 without liver disease [alcoholics without liver disease (AWLD) group] and 19 diagnosed of alcoholic liver cirrhosis-were included in this study. Twenty-five age- and sex-matched healthy volunteers were analyzed as controls. Production of interferon (IFN)-gamma, tumor necrosis factor-alpha (TNF-alpha), and interleukin (IL)-6 was performed on NK-enriched peripheral blood mononuclear cells (PBMC) after stimulation with IL-2 and IFN-alpha. In AWLD patients, the production of TNF-alpha was significantly reduced, compared with normal controls, under both IFN-alpha (p < 0.01) and IL-2 (p < 0.05) stimulation. In patients with cirrhosis, TNF-alpha production by PBMC enriched in NK cells varied depending on the EtOH intake status at the moment of evaluation. Accordingly, an increased concentration of this cytokine was detected in the supernatants of cirrhotic patients and active EtOH intake, particularly after IFN-alpha stimulation (p < 0.05); whereas, in patients with at least 1 year of alcohol withdrawal, TNF-alpha levels remained within normal range. The results on the production of IL-6 and IFN-gamma in AWLD and cirrhotic patients showed that only cirrhotic patients with a prolonged EtOH withdrawal period display abnormal production. Accordingly, in this group of patients, a significantly increased release of IL-6 was observed after both IFN-alpha and IL-2 stimulation (p < 0.01 and p < 0.05, respectively). By contrast, a lower IFN-gamma production (p < 0.005) was detected with respect to the control group. Our results point to the existence of an abnormal cytokine secretion by NK cells from chronic alcoholism patients, which depend on both the existence of liver disease and the status of EtOH intake.
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PMID:Alterations in tumor necrosis factor-alpha, interferon-gamma, and interleukin-6 production by natural killer cell-enriched peripheral blood mononuclear cells in chronic alcoholism: relationship with liver disease and ethanol intake. 934 83

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