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 blood pressure responses to intravenous infusions of norepinephrine and angiotensin II, sympathetic and nonsympathetic vasoconstricting agents, respectively, were measured in 20 patients with cirrhosis (10 Child-Pugh grade A and 10 Child-Pugh grades B or C) and in 20 healthy subjects. The log PD20 (dose of agonist required to raise blood pressure by 20 mm Hg) for norepinephrine was 4.78 +/- 0.36 (mean +/- S.D.) in patients with severe cirrhosis and 4.36 +/- 0.37 in controls, p less than 0.01. Log PD20 for angiotensin II was 3.16 +/- 1.06 in patients with severe cirrhosis and 1.97 +/- 0.74 in controls, p less than 0.01. Cardiovascular responses to selective sympathetic agonists were measured in 10 other cirrhotic patients (all Child-Pugh grades B or C) and in 10 healthy controls. Log PD20s for phenylephrine, an alpha-1 adrenoceptor agonist, and for alphamethylnorepinephrine; an alpha-2 adrenoceptor agonist, were increased in cirrhosis (phenylephrine = 5.35 +/- 0.49 vs. 4.95 +/- 0.35, p less than 0.05; alphamethylnorepinephrine = 4.05 +/- 0.26 vs. 3.44 +/- 0.55, p less than 0.001). In contrast, log CD20 (dose of agonist required to raise the heart rate by 20 beats/min) for isoproterenol, a beta-adrenoceptor agonist, was similar in cirrhotic patients and controls (2.81 +/- 0.38 vs. 2.94 +/- 0.45, p = 0.49). These studies demonstrate that pressor reactivity to both sympathetic and nonsympathetic agonists is impaired in severe cirrhosis, that the impaired sympathetic responses are not caused by generalized sympathetic desensitization and that the site common to the four agonists with impaired responses is the peripheral vascular smooth muscle.
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PMID:Impaired pressor reactivity in cirrhosis: evidence for a peripheral vascular defect. 201 Jan 64

In the peripheral blood (PB) we detected so-called early plasma cells that might already be committed to entering the bone marrow (BM). By two-colour staining with FITC-anti-CD38 antibody, their intensity (CD38++) of expression of CD38 antigen was between that of germinal centre (GC) B cells (low expression (CD38+)) and that of BM plasma cells (high expression (CD38++)), and their phenotype was CD38++ CD19+ CD10- CD20- CD21+ CD24- CD39+ CD5- VLA-4+ VLA-5- MPC-1- without expression of surface membrane IgM (SmIgM). Morphological and immunological examination of the sorted cells confirmed that they were plasmacytoid cells with expression of cytoplasmic IgG (cIgG). Variations of these early plasma cells were examined in various diseases. In active systemic lupus erythematosus, bacterial septicaemia and liver cirrhosis, early plasma cell levels were significantly increased in PB, and after subsidence of such inflammation (inactive states) these cells returned to normal levels. In contrast, normal early plasma cells were significantly suppressed in myelomas, whilst normal or slightly increased numbers of early plasma cells was found in benign monoclonal gammopathy (BMG). In addition, the number of normal early plasma cells returned to a normal level in myeloma cases with complete responses. Therefore, early plasma cells were identified phenotypically, and an increase and decrease in these cells in PB may reflect mobilization and suppression, respectively, of activated B cells into BM plasma cells.
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PMID:Identification of early plasma cells in peripheral blood and their clinical significance. 856 94

Immunological disturbances with impairment of immune function and a higher incidence of lymphoproliferative disorders and other malignancies have been described in liver cirrhosis patients. To investigate the pathogenetic mechanism(s) involved in such associated we looked for a possible imbalance in peripheral blood T-lymphocyte subpopulations in patients with liver cirrhosis of differing severity. Immunophenotyping and counts of peripheral blood T-lymphocyte subpopulations were carried out using monoclonal antibodies conjugated with different fluorochromes in 31 consecutive cirrhotic patients and 23 matched healthy volunteers. Univariate and multivariate analyses of lymphocyte phenotype counts were performed and odds ratios were computed. Statistically significant associations, according to both univariate and multivariate analyses, were found between case/control status and mean CD3 and CD4 T-lymphocyte counts (P < 0.0001). A strong correlation was found between the Pugh's index and CD3 and CD4 lymphocyte counts, with a clear reduction of these phenotypes with increasing liver cirrhosis. Median CD3 and CD4 values were 2,283 and 1,329/microliters respectively among controls and 896, 801, and 492/microliters and 515, 514, and 307/microliters, respectively in categories A, B, and C of Pugh's classification. Very high odds ratios were found using the median values of CD3 and CD4 as a threshold. There was a statistically significant decrease for each of the T-cell phenotypes studied (CD2, CD3, CD4, CD8, CD16, CD19, CD20, CD56, CD57) between patients and controls (P < 0.0001). The progressive and severity-related decrease in mean peripheral blood CD3 and CD4 counts in liver cirrhosis suggests a progressive impairment of protective immune function and may be a factor facilitating malignancy in cirrhotic patients.
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PMID:Peripheral blood CD3 and CD4 T-lymphocyte reduction correlates with severity of liver cirrhosis. 856 79

This study was aimed to evaluate the source of endothelin-1 (ET-1) in cirrhotic patients. ET-1 is implicated in the pathogenesis of portal hypertension. However, the mechanism and source for increased plasma ET-1 in cirrhotic patients are still obscure. Plasma ET-1 levels in systemic (SV), superior mesenteric (SMV), and splenic venous (SPV) blood were measured in 23 patients with cirrhosis and 8 controls with normal liver. Fourteen removed spleens were immunohistochemically studied for ET-1, CD34, CD68, and CD20. In situ hybridization was done to localize ET-1 messenger RNA (mRNA). In cirrhosis, ET-1 levels in both SMV and SPV were higher than in SV. ET-1 in SV and SPV were significantly higher in cirrhotic patients than in control patients. Three groups of cells in the spleen expressed both protein and mRNA of ET-1: endothelial cells in the sinus, which were also stained for CD34; cells in the germinal center; and cells in the marginal zone of lymphoid sheaths and follicles, which were also stained for CD20 but not for CD34 and CD68. The ET-1 concentration released from the spleen was in parallel with the grade of ET-1 expression in the spleen. The spleen is one of the major sites of ET-1 release in cirrhotic patients. Endothelial cells of the splenic sinus and possibly B lymphocytes in the germinal center and marginal zone of lymphoid sheaths and follicles seem to be the sites of ET-1 production in the spleen.
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PMID:Production and release of endothelin-1 from the gut and spleen in portal hypertension due to cirrhosis. 1079 86

Monitoring of posttransplantation lymphoproliferative disorder (LPD) is usually based on imaging, which lacks sensitivity. A prospective study in 911 consecutive recipients of liver transplants was conducted to assess the value of gammopathy monitoring by serum protein electrophoresis (SPE) and to compare it with conventional follow-up methods. Patients systematically underwent SPE testing just before transplantation, at least twice during the first year after transplantation, and once a year thereafter. Patients with LPD underwent SPE testing every month. Immunofixation was done if abnormalities were detected by SPE. Gammopathy was observed in 114 patients, 18 of whom had onset of LPD. In 3 other patients, LPD developed, but no gammopathy was detected before onset of LPD or while LPD was present. Multivariate analyses showed gammopathy (relative risk [RR], 65.3), more than one transplantation (RR, 7.5), and viral cirrhosis (RR, 2.8) to be independent prognostic factors associated with occurrence of LPD. LPD was treated by reducing immunosuppression, with or without chemotherapy, administration of anti-CD20 monoclonal antibody, or surgery. The mortality rate was 24% (5 of 21 patients). Remission, which occurred in 13 patients, was associated with disappearance of gammopathy in 10 patients. In 5 patients, normalization of SPE results preceded the diagnosis of remission based on imaging, by a mean of 4 months. For diagnosis of LPD remission, the positive and negative predictive values of disappearance of gammopathy were 91% and 100%, respectively; and gammopathy monitoring was more sensitive than imaging (100% and 38%, respectively). Gammopathy monitoring is an inexpensive, noninvasive, sensitive way to detect LPD and assess the efficacy of treatment. It could be used routinely in follow-up of recipients of transplants.
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PMID:Detection of gammopathy by serum protein electrophoresis for predicting and managing therapy of lymphoproliferative disorder in 911 recipients of liver transplants. 1152 Jul 79

Primary effusion lymphoma (PEL) or body cavity-based lymphoma (BCBL) is a unique subgroup of B-cell lymphomas that exhibits exclusive or dominant involvement of serous body cavities without a detectable tumor mass. We present a case of a PEL/BCBL that exclusively involved the peritoneal cavity of a 58-year-old immunocompetent male with hepatitis C virus (HCV)-related liver cirrhosis. The lymphoma cells were large, highly atypical and expressed CD19, CD20, CD22, CD10, HLA-DR, and CD45 with kappa light chain restriction. Unlike typical PEL/BCBL, human herpesvirus type 8/Kaposi sarcoma herpes virus (HHV-8/KSHV) genomic sequence was not present in the lymphoma cells and there was no serologic evidence of human immunodeficiency virus (HIV) infection. This is the fourth reported case of HHV-8 negative, HIV negative PEL/BCBL in a patient with associated HCV-related cirrhosis and review of these cases showed some consistent clinicopathological features, i.e. exclusive involvement of the peritoneal cavity and phenotypic expression of B-cell associated antigens in contrast to the generally null phenotype PEL/BCBL. The occurrence of these cases suggests that HCV may play an etiological role in a subcategory of PEL/BCBL not associated with HHV-8.
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PMID:HIV and HHV-8 negative primary effusion lymphoma in a patient with hepatitis C virus-related liver cirrhosis. 1469 39

Primary gastric lymphoma is relatively rare in the scope of gastric malignancies. Here we report a case of diffuse large B-cell primary gastric lymphoma treated successfully with the CD20 monoclonal antibody, rituximab, alone. Because the patient had a complication of severe liver dysfunction due to hepatitis C virus induced-liver cirrhosis and hepatocellular carcinoma, it was difficult to treat the primary gastric lymphoma using standard therapy such as surgical resection and cocktail chemotherapy. Therefore, rituximab was administered to the patient, resulting in complete remission of the primary gastric lymphoma. This case indicates that monotherapy using only rituximab may be a promising option for the treatment of patients with diffuse large B-cell lymphoma accompanied by severe liver dysfunction.
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PMID:Diffuse large B-cell primary gastric lymphoma treated successfully with the CD20 monoclonal antibody (rituximab): a case with severe liver dysfunction due to liver cirrhosis and hepatocellular carcinoma. 1587 Sep 22

Hepatocellular carcinoma (HCC) is one of the most common malignant tumours in the world, especially in Guangxi, China. The causes and mechanism of its tumourigenesis and development have not been completely clarified Some studies revealed that the hepatic local cellular immune function was one of the factors. In the present study, the local micro-environmental immune status was explored by investigating the number, distribution and function of CD3, CD57, CD20, CD68, and granzyme B (GrB) positive cells in 60 patients with HCC and 62 patients with liver cirrhosis (LC) and its relationship with the prognosis of the patients. The results showed that the number of T and B lymphocytes and natural killer (NK) cells in the liver of HCC patients was significantly higher than that in the LC and normal controls; while the number of macrophages (Mphi) was significantly lower The number of Mphi in the tissues decreased successively with the decrease of HCC differentiation; GrB-expressing cells in the liver predominantly consisted of CD57 positive cells. The number of NK cells, B lymphocytes and GrB-expressing cells in the cancerous tissues of stage I and II was significantly higher than that of stages III and IV. The number of T lymphocytes, NK cells, Mphi, and GrB-expressing lymphocytes in HCC cases without metastasis in 15 months was significantly higher than in the metastatic counterparts. The number of T and B lymphocytes, NK cells, and GrB-expressing cells decreased in patients with the progression of the HCC. These results suggest that the number of T and B lymphocytes, NK cells, Mphi and GrB-positive lymphocytes might be important markers in the estimation of hepatic local immune status and be useful factors for predicting the prognosis of HCC patients.
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PMID:Hepatic local micro-environmental immune status in hepatocellular carcinoma and cirrhotic tissues. 1769 Dec 35

Mixed cryoglobulinemia (MC) is the most strictly virus-related extrahepatic HCV disease. Antiviral therapy is considered the first therapeutic option; however, MC patients are frequently excluded from treatment due to contraindications. The effectiveness of B-cell depletion by anti-CD20 monoclonal antibody (rituximab) has recently been described, but the possibility of an immunodepression- related increase in viral replication and aminotransferase values limits its use in patients with advanced liver disease. Unfortunately, MC patients frequently also have cirrhosis. To our knowledge, no data are available regarding the effect of rituximab therapy in patients with decompensated cirrhosis. We report the successful treatment with rituximab (4 weekly infusions of 375 mg/m 2) of two patients (a 58-year-old man, and a 65-year-old woman) with HCV-related MC syndrome and decompensated liver cirrhosis. These patients underwent at least 6 months of post-treatment follow-up. In both cases a consistent improvement of MC syndrome was evident after treatment. In addition, improvement of liver protidosynthetic activity, increased prothrombin time, impressive reduction or disappearance of ascites and encephalopathy were also observed, in spite of some increase in viral titers or in ALT values. The Child-Pugh score improved from B8 to A6 and from Cll to B7, respectively. Pre- and post-treatment transjugular liver biopsies were available in 1 patient, showing disappearance of lymphocytic infiltration after treatment. These case reports show the effectiveness and safety of rituximab in patients with HCV-related MC and advanced cirrhosis, and strongly suggest that the depletion of CD20+ B-cells induced by rituximab treatment may be responsible for liver function improvement. The mechanisms involved are unknown. Interesting working hypotheses may implicate a role played by B-cell infiltrates in conditioning liver damage. The improvement of Kupffer cell function due to the cryocrit value reduction might also play a role.
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PMID:Improvement in liver cirrhosis after treatment of HCV-related mixed cryoglobulinemia with rituximab. 1793 14

Chronic hepatitis C virus (HCV) infection has been associated with a wide number of immunologic disorders, ranging from clinically silent laboratory abnormalities (eg, autoantibody positivity) to severe systemic diseases (eg, cryoglobulinemic vasculitis). Autoimmune hemolytic anemia (AIHA), due to the production of antibodies against erythrocyte membrane antigens, is an uncommon extrahepatic manifestation in the setting of chronic hepatitis C. Herein we have reported the case of a 57-year-old woman with decompensated HCV-related cirrhosis awaiting orthotopic liver transplantation (OLT) who experienced severe AIHA. After 1 month of treatment with prednisone (1 mg/kg body weight/d), there was no significant amelioration of anemia. Rituximab, an anti-CD20 monoclonal antibody that depletes B-lymphocytes reducing serum immunoglobulins, was initiated (375 mg/m(2) IV, weekly for 4 weeks) with a prompt, sustained increase in hemoglobin. The drug was well tolerated; it did not interfere with the course of the liver disease. Thirty-one months after rituximab therapy with resolution of AIHA, the patient successfully underwent OLT using immunosuppression with tacrolimus and low-dose steroids. The patient was discharged on postoperative day 36. No infectious event occurred in the postoperative period. At 18 months follow-up after OLT, there has been no infectious or hematological event. Our experience supported the safety of rituximab use in patients with advanced HCV-related liver disease before OLT.
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PMID:Orthotopic liver transplantation after successful treatment with anti-CD20 monoclonal antibody (rituximab) for severe steroid-resistant autoimmune hemolytic anemia: a case report. 1946 May 65


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