Anti-HBc in hepatocellular carcinoma without HBsAg, HBV DNA, anti-HCV, and HCV RNA.
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Aged↗
Biomedical subjects
M Sata
Publications and source records attributed to M Sata.
Chemotherapy for hepatocellular carcinoma with portal hypertension due to tumor thrombus.
A case of hepatocellular carcinoma (HCC) complicated by tumor thrombosis of the main trunk is presented. Four courses of hepatic arterial infusion therapy, via a subcutaneously implanted injection port, were performed using cisplatin (10 mg for 1 hour on days 1-5) and 5-fluorouracil (250 mg for 5 hours on days 1-5). After four courses of the chemotherapy, marked reduction in size of HCC and the tumor markers were noted. The esophageal varices and ascites were improved after the chemotherapy with a recanalization of the left branch of the portal vein. The patient was doing well with a survival period of 28 months after the chemotherapy. These encouraging results suggested that the present therapy, based on the biochemical modulation, was a useful option for advanced HCC with portal hypertension due to tumor thrombosis of the main portal vein.
Aged↗
[Evaluation of serological response to Bartonella henselae by enzyme immunoassay in cat scratch disease].
The IgG and IgM titers to Bartonella henselae were determined by an enzyme immunoassay (EIA). The EIA test for detection of IgG and IgM antibodies to B. henselae concerning CSD showed that 8 (40%) of 20 patients with CSD had a serum IgG antibody titer of 12 EIA unit or more and that 5 (25%) patients had a serum IgM titer of 12 EIA unit or more. Totally 12 (60%) of the 20 patients with CSD were seropositive for B. henselae. The mean age of IgG positive patients were higher than IgM positive patients. The IgM antibodies to B. henselae disappeared within 4 to 12 weeks after onset of disease. The IgG antibodies to B. henselae disappeared within 3 to 8 weeks after onset of the symptoms in 2 cases of CSD. Another 2 cases CSD produced high levels of IgG antibodies in the acute phase of the disease. Different course of IgG and IgM antibody titers were found in sera from patients.
Adult↗
Detection of hepatitis C virus in saliva before and after scaling of dental calculus.
Dentists and dental health care workers are at risk of contracting hepatitis C virus (HCV) through dental treatment, since HCV RNA was reported to be easily detectable in the saliva of patients with chronic HCV liver disease. We tested for the presence of HCV RNA in saliva before and after removal of dental calculus, and in splashes on the chin-length face shields of dentists following treatment of six patients with HCV chronic liver diseases. We used a sensitive reverse transcription polymerase chain reaction (RT-PCR) method, to estimate exposure to HCV. All patients were anti-HCV and HCV RNA seropositive. HCV RNAs in saliva before or after scaling treatment were detected in three of the six, but none of the face shields showed positive samples. In conclusion, dentists and dental health care workers should be aware of the possibility of HCV infection via contact with serum and saliva during dental practice.
Dental Calculus↗
Vascular endothelial cells and smooth muscle cells differ in expression of Fas and Fas ligand and in sensitivity to Fas ligand-induced cell death: implications for vascular disease and therapy.
Fas ligand (FasL) is a death factor that induces apoptosis in cells bearing its receptor, Fas. Fas and FasL have been detected in the vessel wall, and it has been proposed that Fas-mediated apoptosis has a role in physiological and pathological cell turnover in the vasculature. Here, we evaluated the expression of Fas in the presence and absence of cytokines on both endothelial cells (ECs) and vascular smooth muscle cells (VSMCs). We also examined the sensitivity of ECs and VSMCs to Fas-mediated apoptosis induced by exposure to multiple Fas agonists: soluble FasL, anti-Fas antibody, and membrane-bound FasL resulting from transduction with a replication-defective adenovirus expressing FasL (Adeno-FasL). Cell-surface FasL expression was detected on human ECs with the use of 4 anti-FasL antibodies, whereas cell-surface FasL expression was not detected on VSMCs. Unstimulated ECs expressed relatively low levels of Fas, but expression was upregulated after treatment with tumor necrosis factor-alpha (TNF-alpha) or interferon gamma (IFN-gamma). In contrast, VSMCs expressed relatively high levels of Fas, and treatment with TNF-alpha or IFN-gamma induced little or no upregulation under the conditions of these assays. ECs were resistant to death after exposure to soluble FasL or agonist anti-Fas antibody and also after infection with Adeno-FasL in the presence or absence of cytokine treatment. In contrast, VSMCs remained viable in the presence of soluble FasL or agonist anti-Fas antibody, but they underwent apoptosis after infection with Adeno-FasL. IFN-gamma enhanced Adeno-FasL-induced death of VSMCs, but TNF-alpha did not. These findings provide insights about the potential role of Fas-mediated apoptosis in the vessel wall and suggest strategies to treat proliferative vascular diseases by exploiting the differential sensitivity of ECs and VSMCs to FasL-induced cell death.
Apoptosis↗
Adrenomedullin and nitric oxide inhibit human endothelial cell apoptosis via a cyclic GMP-independent mechanism.
Adrenomedullin, which was discovered as a vasodilating peptide, has been reported to be produced in various organs, in which adrenomedullin regulates not only vascular tone but also cell proliferation and differentiation in an autocrine/paracrine manner. We evaluated the effect of adrenomedullin on endothelial cell apoptosis. Human umbilical vein endothelial cells underwent apoptosis when cultured in serum-free medium. Treatment with adrenomedullin reduced the number of cells with pyknotic nuclei (Hoechst 33258 staining) and inhibited cell death (dimethylthiazol-diphenyltetrazolium bromide assay) in a dose-dependent manner. The administration of adrenomedullin did not alter the expression levels of Bcl-2 family proteins. Experiments with analogs of cAMP or a cAMP-elevating agonist demonstrated that elevation of the intracellular cAMP concentration does not mediate the antiapoptotic effect of adrenomedullin. The coadministration of N-nitro-L-arginine methyl ester (2 mmol/L), an inhibitor of nitric oxide synthase, abrogated the effect of adrenomedullin. Lower doses of sodium nitroprusside (1 to 10 micromol/L), a nitric oxide donor, mimicked the antiapoptotic effect of adrenomedullin. The antiapoptotic effect of sodium nitroprusside was not attenuated by the inhibition of soluble guanylyl cyclase with 1 micromol/L oxadiazolo-quinoxalin-1-one nor could apoptosis be inhibited by the incubation of human umbilical vein endothelial cells with 1 mmol/L 8-bromo-cGMP, a cell-permeant cGMP analog. These results indicate that adrenomedullin and nitric oxide inhibit endothelial cell apoptosis via a cGMP-independent mechanism.
Adrenomedullin↗
Cytokine-targeted therapeutic approaches for inflammatory bowel disease.
Although the causes of inflammatory bowel disease currently are not fully understood, increasing evidence implicates cytokines as key factors in the development of this disorder. The rationale for cytokine-targeted therapy for inflammatory bowel disease has been refined significantly and clinical studies have been initiated. Efficacy of therapy with antitumor necrosis factor-alpha antibody has already been established and clinical trials of recombinant interleukin-10 and interleukin-11 are in progress. Recent investigations have also focused on intracellular signaling pathways and transcription factors that regulate production and activation of cytokines. Further elucidation of the immune response and the role of cytokines in inflammatory bowel disease may lead to identification of additional possible targets for therapeutic intervention that could improve management of the disease.
Journal Article↗
Epidemiological study on food intake and Helicobacter pylori infection.
We conducted an epidemiological study to investigate the relation of food intake to Helicobacter pylori (H. pylori) infection in an area endemic for H. pylori. In this study, 365 subjects, 104 men and 261 women, were randomly selected from 7,389 adult (over age 20) inhabitants of town A, Japan. The prevalence of immunoglobulin G (IgG) class antibody to H. pylori (anti-H. pylori) was 83.7% and the prevalence of anti-H. pylori increased with age significantly (P < 0.05). Subjects with anamnesis of gastritis, gastroduodenal ulcer and gastric cancer tended to have a higher anti-H. pylori positive ratio (93.5%) than those without (81.0%). But there was no relationship between anti-H. pylori prevalence and sex, blood type, smoking or drinking habits. Daily intake of foods by food groups, nutrients and the concentrations of serum ingredients were compared between 37 anti-H. pylori-positive and 40 negative subjects selected from 365 inhabitants by matching up according to sex and age. The daily intake of cereals, potatoes and starches, and milks tended to be higher in positive than negative subjects, while the daily intake of algae and tea appeared to be a little higher in negative than in positive subjects. The daily zinc intake of antibody-positive subjects was significantly higher (P < 0.05) than in antibody negative subjects. On the other hand, the daily iron intake in negative subjects was significantly higher (P < 0.05) than in positive subjects. The serum concentrations of copper, zinc, and vitamin E tended to be higher in positive than negative subjects. But there were no significant differences in serum ingredients concentrations between antibody negative and positive subjects. Our findings suggest that iron and zinc intakes may effect on H. pylori infection.
Adult↗
HBV DNA can be detected from nail clippings of HBs Ag positive patients.
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DNA, Viral↗
Angiogenesis inhibitor TNP-470 suppresses the progression of experimentally-induced hepatocellular carcinoma in rats.
We evaluated the effects of angiogenesis inhibitor, TNP-470, on hepatocellular carcinoma (HCCs) induced by a choline-deficient L-amino acid defined (CDAA) diet in rats. Male Fisher 344 rats were fed CDAA for 68 weeks. Rats were treated by subcutaneous injection of TNP-470 (15 mg/kg) or saline (control) three times per week from 53 to 68 weeks. At the end of the experiment, we determined the frequency and size of HCCs and glutathione S-transferase placental form (GSTP)-positive lesions, histology of liver cirrhosis, liver function, and liver weight per body weight. We also determined, using histologic and immunohistochemical semiquantification analyses, the degree of vascularity, apoptosis and proliferation in HCC and adjacent tissues. Treatment with TNP-470 resulted in a reduction of the size and frequency of HCC compared to untreated rats. However, TNP-470 did not influence the histology of liver cirrhosis and liver function. The liver weight per body weight of TNP-470-treated rats was slightly heavier in comparison with that of the controls. Treatment with TNP-470 significantly reduced tumor vascularity relative to the controls. There were no significant differences in the Ki-67 labeling index of HCCs between TNP-470 treated and control rats. The frequency of apoptotic hepatoma cells in TNP-470-treated rats was higher than in control rats. Our results indicate that TNP-470 suppresses the progression of CDAA-induced HCCs in rats through inhibition of angiogenesis, and suggest that TNP-470 might be useful clinically for HCCs.
Angiogenesis Inhibitors↗
Clinical characteristics of patients in their 40s with HCV antibody-positive hepatocellular carcinoma.
BACKGROUND: We investigated the clinical characteristics of hepatitis C virus (HCV) antibody-positive hepatocellular carcinoma (HCC) patients who developed HCC at a relatively young age. METHODS: Clinical characteristics of patients in their 40s were investigated and were compared with those of patients 50 years and older. The subjects were 648 HCC patients, 469 men (72%) and 179 women (28%), who were treated at our hospital between 1991 and 1997. RESULTS: No patient was under 40 years of age. Eighteen patients (3%) were in their 40s, 137 patients (21%) were in their 50s, 338 patients (52%) were in their 60s, 143 patients (22%) were in their 70s, and 12 patients (2%) were in their 80s. Fifteen of the patients (83%) in their 40s were male. The proportion of men in their 40s was higher than that of all men. Eight of the 15 men in their 40s (53%) were heavy drinkers, and 2 (14%) were habitual drinkers. Three of the 15 men (20%) were HBV carriers, and these 3 HBV carriers were not drinkers. The proportion of heavy drinkers and HBV carriers was significantly higher among the patients in their 40s than in the 60 patients randomly sampled from the patients 50 years of age and older. The mean ages of male patients with HCC who were heavy drinkers, habitual drinkers, occasional drinkers, or nondrinkers were 52.3, 58.9, 62.0, and 61.7 years, respectively. HCC occurred significantly earlier in heavy drinkers than in the other 3 groups. We compared laboratory data of the patients in their 40s with data of all of the patients of 50 years and older. Serum total bilirubin, prothrombin time, and platelet counts were significantly worse in the patients in their 40s. CONCLUSIONS: Logistic regression analysis revealed that heavy drinking and presence of HBV infection were independently related to HCV antibody-positive HCC development at a younger age.
Adult↗
A case of normotensive scleroderma renal crisis after high-dose methylprednisolone treatment.
A 68-year-old male was admitted for interstitial pneumonia associated with scleroderma. High-dose methylprednisolone was administered for treatment of the pneumonitis. Two weeks later, anemia, thrombocytopenia and progressive increase in BUN, creatinine and LDH were observed. Although the blood pressure remained normotensive, renal biopsy showed thrombosis of the polar arterioles and glomerular capillaries. The affected interlobular artery included concentric intimal thickening and thrombosis in the lumen. Our findings suggested that the antecedent use of high-dose corticosteroids is involved in precipitating normotensive renal crisis. Corticosteroids should be used in low doses and with great caution in scleroderma patients.
Aged↗
[A case of microscopic polyarteritis nodosa associated with autoimmune hepatitis complicated with rheumatoid arthritis and chronic thyroiditis].
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Arthritis, Rheumatoid↗
[Clinical evaluation of the relationship between interferon therapy and oral lichen planus in patients with type C chronic hepatitis].
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Hepatitis C, Chronic↗
[Autoimmune thrombocytopenia and erythroid hypoplasia associated with hepatitis A].
A 53-year-old woman developed fever and fatigue after eating raw oysters, and consulted a local clinic. She exhibited liver dysfunction and jaundice, and was therefore referred and admitted to our hospital. Hepatitis A was diagnosed based on virus markers, and palliative therapy was administered. After admission, the increased levels of transaminases and lactic acid dehydrogenase (LDH) normalized rapidly. However, marked thrombocytopenia was observed, and steroid pulse therapy was administered. Thereafter, idiopathic anemia developed, and a bone marrow puncture was performed. Bone marrow smears showed marked depletion of cells of the erythroblastic and megakaryocytic series. Parvovirus B19 infection was ruled out, and an additional steroid was administered. However, the patient's anemia and thrombocytopenia persisted. She suffered a prolonged period of cholestasis and died of acute renal failure. At autopsy, the bone marrow revealed severe erythroblastopenia. A diagnosis of thrombocytopenia due to an autoimmune mechanism was made on the basis of elevated levels of platelet-associated immunoglobulin G (PAIgG) and immune complex. Furthermore, the advanced anemia was complicated by concurrent hemolysis. This case may provide information useful for clarifying the pathogenesis of hematopoietic disorders complicated by hepatitis.
Female↗
Cyclosporine downregulates Fas ligand expression on vascular endothelial cells: implication for accelerated vasculopathy by immunosuppressive therapy.
Although the introduction of cyclosporine A (CyA) and FK506 for immunosuppressive therapy has dramatically enhanced the early survival of organ transplant recipients, administration of these immunosuppresants is correlated with high incidence of transplant arteriosclerosis. Transplant-associated arteriosclerosis is believed to result from recipient inflammatory responses to the allograft, as it is characterized by early mononuclear cell infiltration of the transplanted vessel. We reported that vascular endothelial cells naturally express a death factor, Fas ligand, that may function to inhibit detrimental leukocyte infiltration. Here, we show that CyA or FK506 downregulates FasL expression on endothelial cells with accompanying decrease in the cytotoxicity toward Fas-bearing cells. Our findings not only demonstrate a novel biological action of these drugs, but also suggest a mechanism by which immunosupressive treatment contributes to atherogenesis.
Arteriosclerosis↗
Interferon therapy reduces the risk for hepatocellular carcinoma: national surveillance program of cirrhotic and noncirrhotic patients with chronic hepatitis C in Japan. IHIT Study Group. Inhibition of Hepatocarcinogenesis by Interferon Therapy.
BACKGROUND: Previous studies on the effect of interferon therapy on the incidence of hepatocellular carcinoma have not sufficiently assessed degree of liver fibrosis, a major risk factor for hepatocellular carcinoma. OBJECTIVE: To evaluate the effect of interferon therapy on incidence of hepatocellular carcinoma, adjusting for risk factors, including the degree of liver fibrosis. DESIGN: Retrospective cohort study. SETTING: Seven university hospitals and one regional core hospital in Japan. PATIENTS: 2890 patients with chronic hepatitis C who had undergone liver biopsy since 1986. Of these patients, 2400 received interferon and 490 were untreated. MEASUREMENTS: The degree of liver fibrosis was assessed from stage F0 (no fibrosis) to stage F4 (cirrhosis). Response to interferon was determined virologically and biochemically. Screening for development of hepatocellular carcinoma was performed periodically during an average follow-up of 4.3 years. Effect of interferon therapy on the risk for hepatocellular carcinoma was analyzed by using Cox proportional hazards regression. RESULTS: Hepatocellular carcinoma developed in 89 interferon-treated patients and in 59 untreated patients. Among untreated patients, the annual incidence of hepatocellular carcinoma increased with the degree of liver fibrosis, from 0.5% among patients with stage F0 or F1 fibrosis to 7.9% among patients with stage F4 fibrosis. The cumulative incidence in treated and untreated patients differed significantly for patients with stage F2 fibrosis (P = 0.0128) and for those with stage F3 fibrosis (P = 0.0011). In multivariate analysis, interferon therapy was associated with a reduced risk for hepatocellular carcinoma (adjusted risk ratio, 0.516 [95% CI, 0.358 to 0.742]; P < 0.001), especially among patients with sustained virologic response (risk ratio, 0.197 [CI, 0.099 to 0.392]), among those with persistently normal serum alanine aminotransferase levels (risk ratio, 0.197 [CI, 0.104 to 0.375]), and among those with alanine aminotransferase levels less than two times the upper limit of normal (risk ratio, 0.358 [CI, 0.206 to 0.622]). CONCLUSIONS: Interferon therapy significantly reducesthe risk for hepatocellular carcinoma, especially among virologic or biochemical responders.
Alanine Transaminase↗
Adenovirus-mediated delivery of fas ligand inhibits intimal hyperplasia after balloon injury in immunologically primed animals.
BACKGROUND: Adenoviral constructs have been used for studies of injury-induced vascular hyperplasia in immunologically naive laboratory animals, but their usefulness for intra-arterial gene therapy may be limited by the prevalence of preexisting immunity to adenovirus in the patient population. Here, we explored the efficacy of adenovirus-mediated transfer of Fas ligand, a cytotoxic gene with immunomodulatory properties, in inhibiting injury-induced vascular lesion formation in both naive and immunologically primed animals. METHODS AND RESULTS: Lesion formation was evaluated in balloon-injured carotid arteries of naive and adenovirus-immunized rats that were infected with adenoviral constructs expressing Fas ligand (Ad-FasL), the cyclin-dependent kinase inhibitor p21 (Ad-p21), or beta-galactosidase (Ad-betagal). In naive rats, Ad-FasL induced apoptosis in medial vascular smooth muscle cells and inhibited intimal hyperplasia by 60% relative to Ad-betagal-treated vessels (P<0.05), whereas the cytostatic agent Ad-p21 decreased lesion size by 58% (P<0.05). In animals preimmunized with an adenoviral vector containing no transgene, Ad-FasL significantly inhibited neointima formation (73% reduction, P<0.05), but Ad-p21 failed to inhibit neointima formation relative to controls. Immunologically primed rats displayed robust T-cell infiltration in Ad-p21- and Ad-betagal-treated vessels, but T-cell infiltration was markedly attenuated in Ad-FasL-treated vessels. CONCLUSIONS: Our data demonstrate that adenovirus-mediated Fas ligand delivery can inhibit intimal hyperplasia in both immunologically primed and naive animals, whereas the efficacy of an adenovirus-mediated p21 delivery is limited to immunologically naive animals. This study documents, for the first time, the therapeutic efficacy of intravascular adenoviral gene transfer in animals with preexisting immunity to adenovirus.
Adenoviridae↗