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

We evaluated the risk of development of second primary cancers, with particular reference to subsequent hepatocellular carcinoma (HCC), in 592 patients diagnosed as non-Hodgkin's lymphoma (NHL), at Osaka Medical Center for Cancer and Cardiovascular Diseases. During 1978-1994, 2,163 person-years of observation were accrued, and 27 of the patients developed a second primary cancer, yielding an observed-to-expected ratio (O/E) of 1.53 [95% confidence interval (CI) = 1.01-2.23]. Significant excess risk was noted for primary liver cancer (PLC; O/E = 4.36, 95% CI = 1.99-8.28; O = 9) and non-lymphocytic leukemia (O/E = 26.17, 95% CI = 5.26-76.46; O = 3). The excess risk of PLC was relatively constant within the first 10 years after the NHL diagnosis. Patients who received chemotherapy as the NHL treatment had a significantly increased risk of PLC (O/E = 5.91, 95% CI = 2.70-11.23; O = 9). Their clinical reports indicated that all nine patients with PLC were diagnosed as HCC, and eight of them had clinical and/or histologic evidence of cirrhosis at the time of HCC diagnosis. None of the nine patients had a history of blood transfusion between the first NHL treatment and the diagnosis of HCC. These findings suggested that Japanese NHL patients might have an increased risk of developing HCC, and they indicated the importance of medical surveillance for liver malignancies, as well as subsequent leukemias. Possible explanations for the excess risk of subsequent HCC are discussed.
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PMID:Second primary cancers following non-Hodgkin's lymphoma in Japan: increased risk of hepatocellular carcinoma. 926 30

Oncogenesis is a multifactorial process in which environmental, genetic and infectious factors are variably involved. A possible role of specific viruses has been suggested in at least 15% of human cancers. Hepatitis C virus (HCV), which is both hepato- and lymphotropic, is responsible for various liver disorders, i.e. chronic hepatitis, cirrhosis and hepatocelluar carcinoma, as well as for a constellation of extrahepatic immune-mediated manifestations, among which is mixed cryoglobulinaemia. This is a systemic disorder secondary to a chronic, benign B-lymphocyte proliferation, which in some subjects may evolve to a malignant non-Hodgkin's lymphoma (NHL). Interestingly, recent studies reported the appearance of malignant B-cell neoplasias in patients with type C chronic hepatitis; moreover, in a significant number (from 22% to 50%) of 'idiopathic' NHLs, the presence of HCV infection has been demonstrated. The presence of a geographical etherogeneity in the prevalence of HCV-positive NHL suggests that other co-factors, i.e. genetic and environmental, could be involved in the lymphomagenesis. HCV may exert its oncogenic potential in two different directions, leading to liver cancer or B-cell lymphoma.
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PMID:Viruses and cancers: possible role of hepatitis C virus. 935 39

The objective of this study was to test the hypothesis of a lower mortality from cancer and cardiovascular diseases among men expressing glucose-6-phosphate dehydrogenase (G6PD) deficiency. We designed a mortality study based on death certificates from January 1, 1982 through December 31, 1992 in a cohort of G6PD-deficient men. Cohort members were 1,756 men, identified as expressing the G6PD-deficient phenotype during a 1981 population screening of the G6PD polymorphism. The setting was the island of Sardinia, Italy. Outcome measures were cause-specific standardized mortality ratios (SMRs), which were computed as 100 times the observed/expected ratio, with the general Sardinian male population as the reference. Deaths from all causes were significantly less than expected due to decreased SMRs for ischemic heart disease (SMR, 28; 95% confidence interval [CI], 10 to 62), cerebrovascular disease (SMR, 22; 95% CI, 6 to 55), and liver cirrhosis (SMR, 12; 95% CI, 0 to 66), which explained 95.6% of the deficit in total mortality. All cancer mortality was close to the expectation, with a significant increase in the SMR for non-Hodgkin's lymphoma (SMR, 545; 95% CI, 147 to 1,395). A decrease in mortality from cardiovascular diseases was one of the study hypotheses, based on an earlier human report and experimental evidence. However, selection bias is also a likely explanation. Further analytic studies are warranted to confirm whether subjects expressing the G6PD-deficient phenotype are protected against ischemic heart disease and cerebrovascular disease. This cohort study is consistent with more recent case-control studies in rejecting the hypothesis of a decreased cancer risk among G6PD-deficient subjects. The observed increase in mortality from non-Hodgkin's lymphoma and decrease in mortality from liver cirrhosis were not previously reported.
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PMID:Mortality in a cohort of men expressing the glucose-6-phosphate dehydrogenase deficiency. 942 29

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


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