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)

In a consecutive series of 317 patients with hepatocellular carcinoma (HCC), 32 (10.1%) had 35 extrahepatic primary malignant neoplasms (PMNs) (3 patients had triple cancers). Twenty-five PMNs occurred before the diagnosis of HCC, 7 were synchronous and 3 metachronous. These 35 PMNs were: 6 cancers of the colon, 3 of the stomach, 1 of the rectum, 4 of the breast, 2 of the lung, 1 of the larynx, 3 of the prostate, 1 of the penis, 1 of the urinary bladder, 1 of the uterus, 2 of the skin, and the remaining 10 were immunoproliferative cancers, all of B cell origin (7 non-Hodgkin's lymphoma, 2 multiple myeloma, and 1 chronic lymphocytic leukemia). Thus, in this series, B-lymphocyte-derived neoplasms were the most frequent PMNs associated with HCC. These 10 patients showed no difference for age, male:female ratio, HCC cytotype, presence of cirrhosis, alcohol abuse, markers related to hepatitis B and C virus, and serum level of alpha-fetoprotein when compared with the 22 patients with HCC and other PMNs and the 285 with HCC alone. B cell neoplasms constitute half of the synchronous or metachronous cancers, and must, therefore, be kept in mind in the management of HCC patients.
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PMID:Extrahepatic primary malignant neoplasms associated with hepatocellular carcinoma: high occurrence of B cell tumors. 805 89

Thirty-nine patients with non-Hodgkin's lymphoma were treated with weekly alternating non-cross-resistant chemotherapy (CAMBO-VIP). We obtained a high response rate, and prolonged disease-free survival with side effects and complications of various severity were observed. Three patients were withdrawn from the study due to aggravation of liver cirrhosis, cerebral infarction, and poor tolerance. Thirty-six patients completed this 12-week intensive chemotherapy. The median treatment delay in all patients was 3 days (-4 to 29 days), and a delay of over 15 days was seen in 5 patients. The nadir of the neutrophil count was 0 to 2,100/microliters (median 140/microliters), and 15 patients were below 100/microliters. Two patients had pneumonia and 4 had herpes zoster infection. The platelet count nadir was 20,000 to 240,000/microliters (median 90,000/microliters). Ten patients were below 50,000/microliters, but none required platelet transfusion. Red cell transfusion was given in 6 patients. Elevation of transaminases was seen in 25 patients, but it was not serious except for a patient with liver cirrhosis. The elevation of serum LDH level and decrease of serum haptoglobin level seen shortly after completion of treatment seemed due to the increased blood cell destruction. Stomatitis was observed in 32 patients, 17 of whom showed more than grade 3 toxicity. Blister formation on palms and/or soles was noted in 6 patients. There was no treatment-related death observed.
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PMID:[A study of toxicities and complications observed in alternating non-cross-resistant chemotherapy (CAMBO-VIP) for non-Hodgkin's lymphoma]. 833 48

The main goal of our study was to test dynamic CT capability to characterize focal liver lesions. We examined 57 patients: 6 were affected with focal nodular hyperplasia (FNH), 19 with hepatocellular carcinoma (HCC), 1 with a regenerating nodule on cirrhosis; 14 patients had metastases, 3 focal fatty infiltration, 1 a necrotic nodule, 1 a non-Hodgkin's lymphoma, 1 a cysto-adeno-cholangiocarcinoma and 11 hemangiomas. All lesions were identified with US and the diagnosis was confirmed with the gold standard technique--that is, biopsy or surgery, and red blood cell SPECT for hemangiomas. All lesions were studied with a CT multiphase protocol consisting of a single-level dynamic phase followed by an incremental dynamic phase and finally by a delayed phase to study prolonged and delayed enhancement. Single-level dynamic bolus CT requires an injection of 60 ml nonionic contrast agent administered with a power injector into a cubital vein, at a rate of 5 ml/s. Scanning begins 10 seconds after the injection and consists of 6 series of 2 scans each; each scan lasts 2 seconds and is obtained during the same respiratory apnea, with a 5-second interscan pause. In this phase, 12 scans 5 mm thick are obtained, lasting 24 seconds in all, with pauses lasting 25 seconds--in all, 49 seconds. The next phase is the dynamic incremental scanning, to study the whole liver: this phase requires a 50-ml contrast agent injection at a rate of 4 ml/s, followed by 70 ml at a rate of 1 ml/sec, using 5 mm slice thickness and 8 mm scan interval. This results in 16 scans, beginning 20 seconds after the injection, with a scan time of 2 seconds and 4 seconds of interscan delay, 92 seconds in all. In the last phase, scanning begins 5 minutes after the injection, with a maximum delay of 10-15 minutes. Enhancement variations in both the lesions and the surroundings parenchyma, as related to time, were collected together with morphological data. Time density curves were grouped according to histologic classification and red blood cells SPECT findings; the curves were analyzed with the regression analysis. The results were obtained by analyzing a series of equations describing the different densities of the lesion and the surrounding parenchyma at fixed time intervals, integrated with morphological data, and then comparing the groups of lesions with each other. The regression analysis of the density curves and of the morphological data allowed us to correctly differentiate the 4 most frequent types of lesions--that is, hemangioma, HCC, FNH and metastasis--in 89% of the patients.
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PMID:[Dynamic computed tomography in the characterization of focal hepatic lesions]. 861 39

We studied hepatitis C virus (HCV)-related disease in older people because the treatment rationale for younger asymptomatic patients is based on the long-term prognosis of infection. Of the HCV-antibody-positive patients seen at Freeman Hospital 1990-1994, 25 were > 65 years old; 24 were Caucasian and one was Afro-Caribbean. Median age at presentation was 67 years, and five were female. Nine were asymptomatic at presentation, six presented with varices, five with malaise, three with abdominal pain, one with pruritus and one with oedema. Risk factors identified were: transfusion (7), haemodialysis (1), health care worker (dentist) (1), and tattoos (2). There was no recognized risk factor for infection in 14, but five of these had done military service in areas of high HCV prevalence. Liver biopsy in 20 showed chronic hepatitis in two, cirrhosis in 12, and cirrhosis and hepatocellular carcinoma in six. Three additional patients also developed hepatocellular carcinoma. HCV genotyping was done in 19 and all were type 1 (1a, 4; 1b, 14; 1 untypable, 1). Eleven died, at median age 71 years (range 65-94 years), five of HCV liver-related deaths and two from HCV-associated non-hepatic disorders (non-Hodgkin's lymphoma and fibrosing alveolitis).
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PMID:Hepatitis C virus infection in the elderly. 873 16

The autopsy findings of 80 human immunodeficiency virus (HIV)-infected adults, who died between 1982-1995, are presented with special emphasis on the risk factor of hemophilia. The study included 23 blood product recipients (hemophiliacs n = 21; non-hemophiliacs n = 2), 34 homosexuals, four intravenous drug abusers, and 19 patients with no known risk factor. Nearly all individuals (93%) showed the late stage of acquired immunodeficiency syndrome (AIDS). Blood product recipients had a significantly lower overall frequency of opportunistic infections (p < 0.05). Homosexuality was associated with the highest overall frequency of opportunistic infections and HIV-associated malignancies, such as Kaposi's sarcoma and malignant non-Hodgkin's lymphoma. Exclusive visceral involvement of Kaposi's sarcoma was frequent, and no decrease of Kaposi's sarcoma was observed during the study period. Pneumocystis infections, atypical mycobacteriosis, and non-Hodgkin's lymphoma showed a significant increase during the last five years (1991-1995) of the observation interval. Opportunistic infections and malignancies were the cause of death in approximately one-half of the patients. In blood product recipients, hepatic failure due to posthepatitic cirrhosis and hemorrhage due to hepatic failure with subsequent coagulopathy and in non-blood product recipients, bacterial bronchopneumonia, and diffuse alveolar damage were additional major causes of death. The data suggest a lower risk for HIV-infected blood product recipients, particularly hemophiliacs, to acquire opportunistic infections and malignant neoplasms.
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PMID:Autopsy findings in patients with human immunodeficiency virus infection with emphasis on the risk factor of hemophilia. 878 Sep 28

Hepatitis C virus (HCV) infection may be complicated by non-Hodgkin's lymphoma through yet unknown pathogenetic mechanisms. We describe the case of a patient with HCV-related cirrhosis who developed a primary effusion lymphoma (PEL) of Burkitt's type confined to the peritoneal cavity, in the absence of immunodeficiency or autoimmunity. Paracentesis followed by immunophenotyping, karyotyping, and molecular studies allowed us to diagnose a small noncleaved B-cell lymphoma (CD20+, CD24+, CD10+, CD5-, CD23-, lambda+) with the t(8;22) (q24;q11) translocation and clonal rearrangement of the immunoglobulin heavy chain gene. HCV-RNA, Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus were not identified within lymphoma cells. The finding of HCV-RNA in the ascitic fluid suggests a link between HCV and development of lymphoma with HCV playing the role of persistent antigenic stimulation to intraperitoneal B-cell clonal expansion(s).
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PMID:Primary effusion Burkitt's lymphoma with t(8;22) in a patient with hepatitis C virus-related cirrhosis. 941 5

Like other viruses (i.e Epstein'Barr virus), the role of hepatitis C virus is suspected in the pathogenesis of lymphoproliferative disorders. We report one case of primary hepatic malignant lymphoma associated with chronic hepatitis C viral infection. The diagnosis was obtained by percutaneous liver biopsy showing a non-Hodgkin's diffuse large cell lymphoma and micronodular cirrhosis. Serology for hepatitis C virus positivity was known three years before lymphoma diagnosis. Staging of the lymphoma confirmed multinodular primary hepatic lymphoma with no other detectable localisation. Complete remission has been obtained with aggressive chemotherapy. The role of hepatitis C virus in the pathogenesis of the lymphoma is unknown. An indirect mechanism is suspected. Chronic inflammation may evolve from polyclonal lymphocytic proliferation to true non-Hodgkin's lymphoma, as it has been suggested for non-Hodgkin's lymphoma in the emergence of cryoglobulinemia in hepatitis C positive patients.
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PMID:Primary hepatic lymphoma associated with chronic hepatitis C. 925 39

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


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