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)

Hepatitis B virus (HBV) and hepatitis C virus (HCV) are not only hepatotropic but possibly hematotropic. Recent studies showed the presence of HBV in lymphoma cells of extrahepatic origin. In the current study, we examined the presence of HBV DNA and HCV RNA in the tumor tissues of nine patients with primary hepatic lymphoma (PHL). Immunohistochemical study using polyclonal anti-HCV antibody was possible in four cases. The age of the patients ranged from 45 to 78 years (median, 58 yr), with a male-to-female ratio of 2:1. A history of chronic hepatitis was found in three patients and of cirrhosis in one. Histologically, all of the cases were non-Hodgkin's lymphoma of B-cell phenotype, with a diffuse large cell type being the most common. Polymerase chain reaction using both the S and X region primers failed to detect HBV DNA in the lymphoma tissues. The HCV genome was detected by in situ hybridization in the tumor cells but not in the surrounding hepatocytes in the one case of cirrhosis, which probably resulted from a blood transfusion more than 20 years previous; immunohistochemical analysis revealed positive staining for anti-HCV antibody in the cytoplasm of lymphoma cells in this case. In two cases, positive signals were found only in the hepatocytes surrounding the lymphoma. This is the first report showing the presence of the HCV genome in the lymphoma cells of PHL. HCV could be involved in development of PHL directly or via exogenic antigenic stimulus from HCV-infected hepatocytes.
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PMID:Hepatitis C viral genome in a subset of primary hepatic lymphomas. 961 1

We present a case of non-Hodgkin's lymphoma of B cells in a patient with cirrhosis by hepatitis C virus. Our patient presented scarce symptomatology related with non-Hodgkin's lymphoma. A notable hyperbilirrubinaemia with hypoalbuminaemia were the only features that allowed us to suspect the diagnosis. The diagnostic was proved by necroscopic study. There are several factors involved in the etiology of non-Hodgkin's lymphoma, including infectious agents. Recent Italian studies have suggested an association between C virus infection and non-Hodgkin's lymphoma. We have carried out a bibliographical revision of this association to conclude that important geographical differencies must be pointed out.
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PMID:[A case of non Hodgkin Lymphoma in a patient with hepatic cirrhosis by the hepatitis C virus]. 964 78

At present, there is no case report of HHV8- primary effusion lymphoma (PEL) with t(9;14)(p13;q32) involving both PAX-5 and immunoglobulin heavy chain gene rearrangement, which is a rare translocation in B-cell non-Hodgkin's lymphoma, in an HIV- patient. We examined an HIV-seronegative 63-year-old Japanese man with hepatitis C virus-associated liver cirrhosis and hepatocellular carcinoma manifesting peritoneal lymphomatous effusion without tumor mass at any body site. The lymphoma cells were examined twice by light microscopy, immunohistochemistry, three-color flow cytometry, cytogenetics, and molecular analyses. The nuclear morphology of lymphoma cells was similar to that of large noncleaved cells, although the lymphoma cell size was a little smaller that of the usual large-cell lymphoma. Immunophenotyping of lymphoma cells in the ascitic fluid revealed a mature peripheral B-cell phenotype (CD5- CD10- CD19+ CD20+ CD22+ Ig G+ lambda+). Cytogenetics showed a clonal population: 45,X,-Y, der(2) t(2;6)(q31;p21.3), t(4;8)(q21;q11.2), der(6) t(2;6)(q31;p21.3) add(6)(q15), t(9;14)(p13;q32.3) [10]/47, idem, +der(6) t(2;6), +16[10]. Southern blot analysis revealed rearranged fragments with a probe for immunoglobulin heavy chain, some of which were a size similar to those with a PAX-5 gene probe. Polymorphism, not rearrangement, of the c-MYC gene, was also found. HHV8 and the Epstein-Barr virus were not detected by polymerase chain reaction. This case is the first report of an HHV8- PEL with t(9;14) involving a PAX-5 gene rearrangement in an HIV-seronegative patient. This primary effusion lymphoma manifested spontaneous regression without any therapy. These findings suggest that there may be an additional subcategory of primary effusion lymphoma that is not associated with HHV8 nor c-MYC(R) but is pathogenetically associated with the PAX-5 gene or hepatitis C virus.
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PMID:Herpes virus type 8-negative primary effusion lymphoma associated with PAX-5 gene rearrangement and hepatitis C virus: a case report and review of the literature. 1063 3

Hepatitis C virus (HCV) is a single-stranded RNA agent which expresses its genetic informations in the form of a single, large polyprotein encoded by an open reading frame (ORF) that extends through most of its genomic RNA. Proteolytic cleavage of the ORF product is essential for the virogenesis and the production of viral progeny. HCV is responsible for chronic liver disease, cirrhosis and possibly hepatocellular carcinoma. Viral persistence is considered the greatest problem in the management of HCV infection. It may result from several mechanisms, two of which are established. In the first, the high rate of genetic variations during viral replication results in the production of mutants capable of escaping the immune attack. In the second, the virus infects cells of the immune system itself, which represent a privileged site that cannot be reached by virus-specific T cell response. Involvement of lymphoid cells in the early stages of HCV infection may provide insight into the pathobiologic patterns of extrahepatic dissemination (lymph nodes, major salivary glands, kidneys, blood vessels). Dissemination of HCV-infected lymphoid cells throughout the organism is likely to maintain a mobile and extensive reservoir of the virus. In this respect, extrahepatic sites may act as a source of continuous reinfection of hepatocytes. Studies of intrahepatic B lymphocytes indicate that they are infected with HCV, clonally expanded and activated to secrete IgM molecules with rheumatoid factor activity. This strongly suggests that HCV directly stimulates B cell expansion, which may result in an indolent stage of lymphoproliferation (i.e., mixed cryoglobulinemia) or in frank B cell non-Hodgkin's lymphoma (NHL). The frequency of NHL, however, is much lower than that of HCV infection, suggesting that HCV alone is not able to induce tumors and that cellular events, in addition to the presence of virus and virus-encoded products, are necessary in order to obtain a malignant B cell phenotype. The demonstration of HCV productive infection in bone marrow-recruited and circulating pluripotent hematopoietic CD34+ stem cells indicates that HCV replication occurs in the early differentiation stages of hematopoietic progenitors. These are stable cell populations and are likely to represent the initial site of infection and a continuous source of virus production.
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PMID:Hepatitis C virus infection, mixed cryoglobulinemia, and non-Hodgkin's lymphoma: an emerging picture. 992 37

The present investigation represents an update of a previous cohort mortality study of 7543 workers who were employed at a petroleum refinery in Beaumont, Texas, for at least 1 year between 1945 and 1996. The updated study covered an observation period of 51 years, from 1946 to 1996, with a total of 208,627 person-years of observation. A total of 3020 (40.0%) cohort members were known to have died. The mortality data were analyzed in terms of cause-specific standardized mortality ratios (SMRs) and 95% confidence intervals (95% CIs). The overall mortality of the cohort was significantly lower than expected when compared with that of the general US population (SMR, 95.7; 95% CI, 92.3 to 99.2). Overall cancer mortality was also lower than expected (SMR, 85.8; 95% CI, 79.4 to 92.5). For specific cancer sites, significant mortality deficits were observed for the following: buccal cavity and pharynx, esophagus, large intestine, rectum, larynx, lung, and bladder and other urinary organs. No significant increase was reported for any site-specific cancer. A non-significant increase in acute myeloid leukemia was observed among male employees (SMR, 147.2; 95% CI, 76.1 to 257.2). Detailed analyses indicated that the excess was restricted to workers hired before 1950. No increase was detected for other leukemia cell-types, non-Hodgkin's lymphoma, or multiple myeloma. For non-malignant diseases, the majority of SMRs were below 100, and no significant increase was observed for any cause. In particular, significant mortality deficits were reported for ischemic heart disease (SMR, 91.0; 95% CI, 85.4 to 96.9), non-malignant respiratory disease (SMR, 61.5; 95% CI, 52.2 to 72.0), pulmonary fibrosis (SMR, 51.0; 95% CI, 22.0 to 100.4), cirrhosis of the liver (SMR, 47.2; 95% CI, 30.6 to 69.7), and accidents (SMR, 81.7; 95% CI, 66.3 to 99.6). Separate analyses of male workers by job classification (process and maintenance) were conducted. Mortality from acute myeloid leukemia was elevated among employees in maintenance jobs (8 observed deaths vs 4.31 expected; SMR, 185.5; 95% CI, 80.1 to 365.6). However, no upward trend by length of service was found. A detailed analysis indicated that the acute myeloid leukemia mortality excess was limited to maintenance workers who were hired before 1950. No other significant excess was detected for any cause among maintenance or process workers. These findings from the present study were discussed in conjunction with results from previous investigations of employees at the Beaumont refinery and with results from other refinery studies. Potential limitations of the study were also discussed.
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PMID:An updated mortality study of workers at a petroleum refinery in Beaumont, Texas, 1945 to 1996. 1132

We reviewed the clinical manifestations, sequential changes in cryptococcal antigen titers in serum and cerebrospinal fluid (CSF), and the antifungal drug susceptibility of Cryptococcus neoformans in three patients with cryptococcal meningitis between 1996 and 2000. Cryptococcal antigen titers were measured using the latex agglutination method with Pastrex Cryptococcus (Fuji Mebio, Tokyo) and Serodirect Cryptococcus (Eiken Chemical, Tokyo). The underlying systemic diseases in the three patients were liver cirrhosis, non-Hodgkin's lymphoma associated with miliary tuberculosis, and malignant thymoma associated with systemic lupus erythymatosus. The CSF samples showed positive indian ink staining in two of the three patients and C. neoformans was cultured from all three. The cryptococcal antigen titers in serum were higher than those in the CSF. The serum and CSF cryptococcal antigen titers measured by Serodirect Cryptococcus were higher than those measured by Pastrex Cryptococcus. The maximum titers of antigen in serum and CSF measured by Serodirect Cryptococcus were greater than 1,024 in all three patients. The treatment regimens used for the three patients were amphotericin-B (AMPH-B) and flucytosine (5-FC), fluconazole (FLCZ) and intrathecal AMPH-B, FLCZ and 5-FC, and intrathecal AMPH-B, respectively. The antigen titers in serum and CSF decreased after treatment in all three patients. The antigen titers decreased slowly over 7.3 months in the most seriously ill patient who had non-Hodgkin's lymphoma associated with miliary tuberculosis. The time between the beginning of treatment and CSF cryptococal antigen titers falling to less than 8 was 1.7 to 7.3 months in the three patients, but the serum titers did not decrease to less than 8 during this period. The minimum inhibitory concentration was 0.06-0.25 microgram/ml for AMPH-B, 4-8 micrograms/ml for 5-FC, 2-8 micrograms/ml for FLCZ, 0.125-0.5 microgram/ml for miconazole and 0.03-0.125 microgram/ml for itraconazole. The measurement of sequential changes in cryptococcal antigen titers in serum and CSF was useful for evaluating the response to treatment.
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PMID:[A clinical study of cryptococcal meningitis--sequential changes of cryptococcal antigen titers]. 1270 8

Summary Hepatitis C virus infection is often associated with extra-hepatic manifestations, secondary to the elicitation of autoimmune reactions, generalized deposition of immune complexes and lymphoproliferative disorders. The most clearly established associations are those linking chronic hepatitis C with mixed cryoglobulinaemia (and the related glomerulonephritis and cutaneous vasculitis), as well as with the presence of autoantibodies. Less well-documented disorders include non-Hodgkin's lymphoma, thrombocytopenia, sialadenitis, thyroid disease, lichen planus, porphyria cutanea tarda, rheumatoid disorders and neurological disorders. Extra-hepatic manifestations are most frequent in patients of female sex, advanced age, long-lasting infection and cirrhosis. Optimal treatment strategies should be based on the predominant manifestation of the disease. In the case of autoimmune disorders not clearly attributable to the viral infection, corticosteroids may be the most effective option. Interferon-alpha alone or in combination with ribavirin may be indicated for those disorders related to immune complex deposition, such as mixed cryoglobulinaemia, although relapses of extra-hepatic signs often occur on discontinuation of treatment. In some cases, interferon-alpha may induce or exacerbate some extra-hepatic manifestations.
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PMID:Hepatitis C virus-related extra-hepatic disease--aetiopathogenesis and management. 1523 92

Primary T-cell non-Hodgkin's lymphoma (NHL) occurring in the context of acquired immune deficiency syndrome (AIDS) is uncommon. Here, we report and discuss such a case presenting in the rectum, and review relevant literature. Although typical in some respects, the case is, in other ways, somewhat unusual for an AIDS-related NHL (ARL); ARL tends to be B cell and advanced stage and our case was T cell and stage IE. In addition, the patient suffered from concomitant cirrhosis related to hepatitis C. Chemotherapeutic options for ARL were limited early in the AIDS epidemic due to poor tolerability. Although this has largely been mitigated by the advent of highly active antiretroviral therapy, our patient eventually suffered complications of chemotherapy, apparently related more to his liver disease than to either his lymphoma or AIDS, that ultimately brought about his demise.
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PMID:T-cell lymphoma of the rectum in a patient with AIDS and hepatitis C: a case report and discussion. 1582 Dec 49

We report here on a case of non-Hodgkin's lymphoma in which liver involvement was the predominant clinical manifestation. A healthy 44-year-old man presented with upper abdominal pain, hepatosplenomegaly, thrombocytopenia, elevated AST, ALT and bilirubin, and marked elevation of lactate dehydrogenase and alkaline phosphatase. The abdominal CT scan showed only diffuse hepatosplenomegaly and uneven contrast enhancement of the spleen without any definite mass of the liver and spleen. US-guided aspiration biopsy of liver and the histologic examination confirmed a diagnosis of non-Hodgkin's lymphoma, the diffuse large B cell type. Bone marrow biopsy showed the infiltration of malignant lymphoma cells. PET-CT showed an increased FDG uptake of the liver, spleen and long bones. The patient was treated with combination regimen of cyclophosphamide, doxorubicin, vincristine and prednisone chemotherapy. Even in the absence of a mass lesion or lymphadenopathy, primary hepatic or hepatosplenic lymphoma should be considered in differential diagnosis of hepatitis or liver cirrhosis, especially for patients with diffuse hepatosplenomegaly and markedly elevated LDH.
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PMID:[A case of primary hepatic lymphoma mimicking hepatitis]. 1617 55

Hepatitis C virus (HCV) causes hepatitis, liver cirrhosis and hepatocellular carcinoma, and may also induce type II mixed cryoglobulinemia syndrome (MC), a disease characterized by clonal B-cell lymphoproliferations that can evolve into non-Hodgkin's lymphoma (NHL). Interleukin-1 (IL-1) is a cytokine that plays an important role in initiating the cascade of events of immunoinflammatory responses through costimulation of T lymphocytes, B-cell proliferation, induction of adhesion molecules and stimulation of the production of other inflammatory cytokines. The role of IL-1 in immunoinflammatory responses is highlighted by the presence of endogenous regulators (IL-1 receptor antagonist, soluble receptors type 1 and II, human IL-1 accessory protein) that, when secreted into the blood stream may serve as endogenous regulators of IL-1 action. The aim of this study was to evaluate whether abnormalities in the blood levels of IL-1beta IL-1 receptor antagonist, soluble IL-1 receptor type II and human IL-1 accessory protein in HCV+ patients are associated with development of MC and/or NHL. Relative to healthy controls, we observed: i) an increase in the circulating levels of IL-1beta in HCV+ patients simultaneously affected by NHL; ii) increased levels of IL-1 accessory protein in patients singly infected by HCV; iii) increase of IL-1 receptor antagonist in HCV+ patients and in those affected also by NHL with or without MC; iv) a homogeneous increase of sIL-1R type II in all the subgroup of patients. These data indicate that an attempt to increased circulating levels of IL-1 inhibitors occurs at different extent in the course of HCV infection as well as in its progression to NHL and/or MC.
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PMID:Analysis of interleukin (IL)-1beta IL-1 receptor antagonist, soluble IL-1 receptor type II and IL-1 accessory protein in HCV-associated lymphoproliferative disorders. 1659 2


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