Biomedical subjects

M Sata

Publications and source records attributed to M Sata.

336 records · Page 19Linked to original sources

PubMedDate not supplied

A simultaneous monitoring of Lens culinaris agglutinin A-reactive alpha-fetoprotein and des-gamma-carboxy prothrombin as an early diagnosis of hepatocellular carcinoma in the follow-up of cirrhotic patients.

To elucidate the risk factors for developing hepatocellular carcinoma (HCC) during the follow-up of patients with liver cirrhosis (LC), outpatients with LC were examined periodically by means of serum biochemical assessments, ultrasonography, and computed tomography. Risk factors for HCC were statistically analyzed. We also examined an efficacy of Lens culinaris agglutinin A-reactive profiles of alpha-fetoprotein (AFP-L3%) and des-gamma-carboxy prothrombin (DCP) value using a highly sensitive DCP determination kit (ED036) for the early recognition of HCC. The AFP-L3% and the ED036 value were retrospectively determined with stored serum samples. HCC was diagnosed in 21 of the 78 patients with LC during the follow-up period (mean follow-up period: 42 months). The estimated cumulative incidence of HCC was 25% with 3 years and 48% with 5 years. The most significant risk factor for the development of HCC in LC patients was found to be the mean serum AFP concentration from the year before the HCC detection (p=0.02). At the time of the recognition of HCC, the positive rates of the tumor markers were: serum AFP concentration 14%, serum DCP value 5%, AFP-L3% was 33%, and that of ED036 43%. The positive rate in collaborative use of AFP-L3% and ED036 was 67%. The simultaneous determination of the AFP-L3% and the ED036 value was shown to be effective for the early detection of HCC.

Aged↗

PubMedDate not supplied

Bright loop appearance; a characteristic ultrasonography sign of early hepatocellular carcinoma.

Ultrasonography (US) and computed tomography (CT) are the most effective screening methodologies for hepatocellular carcinoma (HCC). In our US screening, 20% of small HCC nodules less than 20 mm in diameter were detected as hyperechoic tumors. Among these hyperechoic HCC nodules, we have often observed (BL) which is defined as hypoechoic nodules in the hyperechoic tumor. In this study, we report that the BL is a sign of dedifferentiation of early stage of HCC with fatty change by US. From 1994 to 1998, we performed tumor targeting needle biopsy in 938 hepatic nodular lesions. Among them, 284 nodules <20 mm in diameter, histologically diagnosed as HCC, were studied. BL is defined as a hyperechoic tumor containing a hypoechoic nodule >4 mm in diameter by US. Among 284 nodules, well, moderately and poorly differentiated HCC were 183 (64.4%), 100 (35.2%) and 1 (0.4%), respectively. On US, hypoechoic, isoechoic, and hyperechoic nodules were 188 (66.2%), 32 (11.3%) and 64 (22.5%), respectively. Forty-seven nodules of 64 hyperechoic HCC nodules <20 mm in diameter, 47 nodules (73.4%) showed fatty changes. Of 64 hyperechoic HCC nodules, we recognized 22 nodules (34.4%) as BL. The proportion of BL type hyperechoic nodules increased with the tumor size. Two hyperechoic nodules followed by US changed to BL with tumor enlargement. Histologic examination of a resected HCC with BL showed that hyperechoic HCC nodule represented well-differentiated HCC with fatty change and inner hypoechoic lesion represented moderately differentiated HCC without fatty change. In US screening for HCC, BL was often observed in HCC nodules from 11 to 20 mm in diameter. Histologic examination revealed that BL of HCC on US was associated with tumor progression and indicated dedifferentiation showing moderately differentiated HCC in well-differentiated HCC with fatty change.

Adult↗

PubMedDate not supplied

Expression of the SART1 tumor-rejection antigen in hepatocellular carcinomas.

We previously reported a tumor-rejection antigen, SART1259, possessing tumor epitopes capable of inducing cytotoxic T lymphocytes (CTL) in epithelial cancer patients. The present study investigated the expression of the SART1259 antigen in hepatocellular carcinomas (HCC) in order to explore for a potential molecule for use in specific immunotherapy of HCC patients. Expression of the SART1 antigens in samples was analyzed by western blot analysis with anti-SART1259 and anti-SART1800 polyclonal antibodies. In addition HLA-A24- restricted CTLs were induced from peripheral blood mononuclear cells (PBMCs) of HLA-A24+ HCC patients by the SART1690-698 (EYRGFTQDF) peptide with an HLA-A24 binding motif. The SART1259 antigen was detected in the cytoplasmic fraction of 6 of 8 HCC cell lines and 12 of 23 (52%) HCC tissues, but in none of the normal liver tissues or those of chronic hepatitis or cirrhosis. The HLA-A24 restricted and SART1-specific CTLs recognized the HLA-A24+ and SART1259+ HCC cells. Further, in peripheral blood mononuclear cells of HCC patients, the SART1690-698 peptide induced CTLs that reacted to the HCC cells in an HLA-A24-restricted manner. These results suggest that the SART1259 antigen could be an appropriate target molecule for use in specific immunotherapy of HCC patients.

Antibodies↗

PubMedDate not supplied

A novel strategy for remission induction and maintenance in cancer therapy.

The p53 tumor suppressor gene plays an important role in protecting cells from developing undesirable proliferation. The mutant p53 gene or malfunctioning p53 protein found in more than 50% of cancer cells impedes DNA repair or apoptosis induction. This may be why some cancers gain resistance to chemotherapy and radiation and become more resistant after frequent cancer treatments. A non-toxic p53 gene activator would induce cancer cell apoptosis and help damaged cancer cells to recover. Therefore, the combination use of chemotherapeutics or radiation with a non-toxic p53 gene activator will be crucial in cancer therapy, damaging DNA with chemotherapeutics or radiation on the one hand and promoting apoptosis induction with p53 gene activator on the other. This strategy would be most efficient for remission induction and maintenance in cancer therapy. Antineoplastons are naturally occurring peptides and amino acid derivatives that control neoplastic growth. Antineoplaston A10 and AS2-1 are chemically identified and synthesized antineoplastons proven to inhibit cancer cell growth by arresting the cell cycle in the G1 phase and inhibiting tumor growth by reducing mitosis. These agents are thought to be good candidates for clinically easily applicable non-toxic p53 gene activators. Our cases of advanced cancer responded well to combination treatment using chemotherapeutics and irradiation with antineoplaston A10 and AS2-1 in clinical trials being conducted in Kurume University Hospital. We describe herein the clinical cases and discuss the possible mechanism of action of this combination therapy.

Adult↗

PubMedDate not supplied

Budd-Chiari syndrome complicated by hepatocellular carcinoma with no evidence of infection with hepatitis virus: a case report.

Hepatocellular carcinoma occurs in patients with Budd-Chiari syndrome. However, the etiology of hepatocellular carcinoma accompanied with Budd-Chiari syndrome has not been elucidated. We report a case of Budd-Chiari syndrome with membranous obstruction of the inferior vena cava complicated by hepatocellular carcinoma in an 80 year-old man. There was no evidence of co-infection with hepatitis A, B, C, D, E, and G virus. Histologically, the non-cancerous liver tissue showed chronic venous congestion with no evidence of hepatitis virus-associated liver cirrhosis. This case suggests that chronic venous congestion of the liver may be one of the pathologic conditions that occurs in hepatocellular carcinoma.

Aged↗

PubMedDate not supplied

Successful treatment for bronchial bleeding from invasive pulmonary metastasis of hepatocellular carcinoma: a case report.

Pulmonary metastasis is frequently seen in patients with advanced hepatocellular carcinoma. However, information is limited concerning life-threatening complications and effective treatment of pulmonary metastasis because of the poor prognosis of patients with advanced hepatocellular carcinoma. Recent remarkable progress in detection and treatment of hepatocellular carcinoma has improved prognosis, making management of pulmonary metastasis an important clinical issue. We describe a 68-year-old man with pulmonary metastasis of hepatocellular carcinoma and sudden onset of hemoptysis from bronchial invasion. Transcatheter embolization was performed successfully via the bronchial artery with disappearance of bloody sputum. Peribronchial pulmonary metastasis of hepatocellular carcinoma can cause life-threatening hemoptysis. Transcatheter arterial embolization may be one of therapeutics for hemoptysis from invasive pulmonary metastasis of hepatocellular carcinoma.

Aged↗

PubMedDate not supplied

Long-term follow-up of interferon-treated chronic hepatitis C and serum hepatic fibrosis markers.

BACKGROUND/AIMS: We investigated the clinical application of serum fibrosis markers in a long-term follow-up of patients with chronic hepatitis C treated with interferon-alpha. METHODOLOGY: This study included 52 patients treated with interferon-alpha (total: 480 MU) for 6 months. They each underwent liver biopsy before and after treatment. Twenty-eight patients who underwent liver biopsy less than 2 years after treatment were classified as group 1, and 24 patients as group 2. The two groups were subdivided into HCV RNA-negative responders and HCV RNA-positive nonresponders. Liver specimens were estimated using grading and staging scores. Serum hyaluronan, PIIIP, and type IV collagen levels were measured before and after treatment. RESULTS: In the responders of groups 1 and 2, grading score after treatment was significantly decreased compared with that before treatment. Staging score after treatment was significantly improved only in the responders of group 2. In the responders of group 2, serum hyaluronan level was significantly decreased compared with that before treatment. In group 2, the grading score was significantly correlated with serum PIIIP and type IV collagen levels, and the staging score was significantly correlated with only serum hyaluronan level. CONCLUSIONS: These findings indicate that the serum PIIIP and type IV collagen levels reflect the activity, and serum hyaluronan reflects the degree of fibrosis in liver specimens of HCV RNA-negative patients in a long-term follow-up of patients after interferon-alpha treatment.

Adult↗

PubMedDate not supplied

Serum hyaluronate predicts response to interferon-alpha therapy in patients with chronic hepatitis C.

BACKGROUND/AIMS: The response to interferon therapy for chronic hepatitis is known to decrease with progression of the hepatic fibrosis. On the other hand, serum hyaluronate reflects hepatic sinusoidal capillarization or liver cirrhosis, and also serum type IV collagen, which is one of the main components of the basement membrane, rises with the progression of hepatic fibrosis. In this study, the relationship between the degree of hepatic fibrosis and the response to interferon-alpha was determined retrospectively in patients with chronic hepatitis C. In addition, whether the measurement of serum hyaluronate and type IV collagen before interferon-alpha therapy was useful for predicting the response to interferon-alpha therapy in chronic hepatitis C was determined. MATERIALS AND METHODS: Thirty-seven patients with elevated serum ALT levels for at least 6 months and histologically determined chronic hepatitis were studied. All patients were positive for anti-HCV and negative for hepatitis B surface antigen. Twenty-eight healthy adults with normal blood biochemical data, who were negative for hepatitis B antigen and HCV antibody tests, had limited alcohol intake were used as controls. The test group was given IFN-alpha by intramuscular injection for 14 days, and then were treated 3 times per week for 24 weeks. RESULTS: The extent of hepatic fibrosis, particularly, perisinusoidal fibrosis (P < 0.01) was significantly greater in nonresponders than in responders. The mean serum hyaluronate and type IV collagen levels were more elevated in nonresponders than in responders, especially, the serum hyaluronate level showed a significant difference (P < 0.01). Most of the patients having a serum hyaluronate level of more than 100 ng/ml were nonresponders who had chronic active hepatitis with bridging necrosis on liver biopsy. Serum hyaluronate and type IV collagen levels showed significant positive correlation with degree of the portal fibrosis (P < 0.01), perisinusoidal fibrosis (P < 0.001) and focal necrosis (P < 0.01) in histological findings of liver biopsy specimens. CONCLUSION: These results suggest that serum hyaluronate and type IV collagen levels reflect the extent of the hepatic fibrosis in chronic hepatitis C and also that serum hyaluronate level predicts the response to interferon-alpha therapy in patients with chronic hepatitis C.

Adult↗

PubMedDate not supplied

Increased serum IgM class anti-lipid A antibody and therapeutic effect of ursodeoxycholic acid in primary biliary cirrhosis.

BACKGROUND/AIMS: There is as yet no explanation for the increased serum IgM level observed in patients with primary biliary cirrhosis. METHODOLOGY: The serum IgM class anti-lipid A antibody was determined in patients with primary biliary cirrhosis using Elisa and Western blot techniques. RESULTS: Using enzyme-linked immunosorbent assay, we found the concentration of serum IgM class anti-lipid A antibody was the highest in 21 patients with PBC as compared to 29 patients with other liver diseases and 19 controls. Using western blotting, IgM class anti-lipid A antibody was detected as a clear band in patients with primary biliary cirrhosis. The level of this antibody correlated significantly (p < 0.005) with that of total IgM. Treatment with ursodeoxycholic acid improved not only the routine biochemical profile but also the level of IgM class anti-lipid A antibody (p < 0.005). CONCLUSIONS: Since the lipid A plays a primary role in the biological activities of lipopolysaccharide (a component of gram-negative bacteria), bacterial antigen may participate in the elevation of serum IgM levels in patients with primary biliary cirrhosis. Ursodeoxycholic acid treatment may improve the cholestasis, and this may have altered the response to stimulation by gut derived bacterial antigens.

Antibodies, Bacterial↗

PubMedDate not supplied

The incidence of hepatocellular carcinoma in patients with chronic hepatitis C after interferon treatment.

To determine whether serum hepatitis C virus (HCV) RNA disappearance after interferon (IFN) treatment prevents development of hepatocellular carcinoma (HCC), we evaluated retrospectively the incidence of HCC in patients with chronic hepatitis C. A total of 213 patients were monitored for more than 6 months after completion of IFN treatment. Sixty-three of the 213 patients (29.6%) achieved a complete response (CR) to treatment and 150 (70.4%) had no response (NR). HCC developed in 12 (5.6%), all of whom were NR. Logistic analysis showed age, alpha -fetoprotein, and staging of histological finding before IFN treatment were independent factors to development of HCC. The fact that there was no HCC development from CR provides a basis for IFN treatment in chronic HCV infection.

Adult↗

PubMedDate not supplied

Long-term evaluation of interferon therapy in hepatitis C virus-associated cirrhosis: does IFN prevent development of hepatocellular carcinoma?

During the course of long-term follow-up, we examined the efficacy of interferon (IFN) in the improvement of liver function and prevention of hepatocellular carcinoma (HCC) in hepatitis C virus (HCV) associated cirrhosis patients. Fifty-five cirrhotic patients, in whom HCC nodules in the liver were not detected by ultrasonography (US) or computed tomography (CT), received 3 or 6 million units of human lymphoblastoid IFN daily for two weeks and 3 times a week for 22 weeks. Complete response (CR) was defined as normalization of serum alanine aminotransferase (ALT) together with negative HCV RNA at 6 months after IFN therapy completion. Any other pattern of response was defined as non-response (NR). After IFN therapy the patients were followed up every 1-3 months for at least 1 year (average follow-up period, about 40 months) with serological tests and US or CT. In the 8 CR patients, the serum ALT levels remained normal and HCV RNA remained negative. Platelet count, white blood cell count, serum albumin and zinc turbidity test have recovered to the normal range at final follow-up. Ten of the 47 patients with NR have developed HCC, whereas no patients with CR has developed HCC during follow-up. We conclude that IFN improves the liver function and may prevent the development of HCC even in cirrhotic patients who show CR to IFN therapy.

Carcinoma, Hepatocellular↗

PubMedDate not supplied

Monitoring of serum levels of HCV RNA in early phase of IFN therapy; as a predictive marker of subsequent response.

BACKGROUND/AIMS: To determine whether the initial response to interferon (IFN) therapy predicts the long-term response, monitoring of HCV RNA level in the early phase of IFN therapy was performed. METHODOLOGY: Sixty-seven patients with chronic hepatitis C virus (HCV) infection were investigated. Patients received 6 MU of human lymphoblastoid IFN daily for 2 weeks and then three times weekly for 22 weeks (total dose; 480 U). These were 34 complete responders (CR) and 33 non-responders (NR). Serum levels of HCV RNA were assayed before therapy and at weeks 1 and 2, using the AMPLICOR HCV Monitor kit. RESULTS: Serum levels of HCV RNA were below the detection limit in 33 (97.1%) of 34 CR compared with 13 (39.4%) of 33 NR at week 1, and in 100% of CR compared with 17 (51.5%) of NR at week 2 (P < P0.05). These observations were independent with viral genotypes. CONCLUSION: A complete response to IFN therapy results primarily from a rapid decrease in the serum levels of HCV RNA and a further decrease to below the detection limit by week 2 of the therapy. In spite of a viral genotype, early monitoring of serum levels of HCV RNA during IFN therapy are predictive of a subsequent long-term response to IFN in patients with chronic HCV infection.

Adult↗