PubMed HealthSearch

Biomedical subjects

T Suou

Publications and source records attributed to T Suou.

At least 19 recordsLinked to original sources

Plasma vitronectin concentrations in patients with chronic hepatitis C treated with interferon alpha.

Plasma vitronectin concentration was measured in 60 patients with chronic hepatitis C before and after interferon alpha treatment. The plasma pretreatment levels of vitronectin in the interferon non-responders was significantly lower than those in the interferon sustained and transient responders, but the levels were not different in the latter two groups. After interferon therapy, the plasma levels of vitronectin were significantly increased in all three groups, and they were correlated with the albumin levels. Absolute changes of plasma vitronectin before and after interferon treatment were significantly related to initial levels, but they were not related to those of albumin or alanine aminotransferase levels. The values of sensitivity and specificity for plasma vitronectin in the sustained responder and non-responder were 45% and 95% for each. These results suggest that chronic hepatitis C patients with low levels of plasma vitronectin may have a weak response in interferon therapy.

Alanine Transaminase

Prognostic significance of serum anti-p53 antibody in patients with hepatocellular carcinoma.

BACKGROUND/AIMS: Abnormalities of the p53 gene can lead to the production of anti-p53 antibody in the serum of cancer patients. We evaluated the prognostic significance of anti-p53 antibody in 86 patients with hepatocellular carcinoma (HCC) in comparison with clinicopathological factors: age, sex, etiology, smoking and drinking habits, history of blood transfusion, presence of encephalopathy and ascites, Child classification, Pugh score, bilirubin, albumin, prothrombin time, indocyanine green retention time at 15 min (ICG), underlying liver disease, alpha-fetoprotein (AFP), tumor size, number of tumors, differentiation degree of HCC, presence of extrahepatic metastasis and therapy for HCC. METHODS: The serum anti-p53 antibody in 86 patients with HCC, 20 with chronic hepatitis (CH) and 20 with liver cirrhosis (LC) was measured by an enzyme-linked immunosorbent assay (ELISA). A single-strand conformation polymorphism-polymerase chain reaction (SSCP-PCR) analysis and loss of heterozygosity (LOH) study of the p53 gene were performed using 8 tissue samples of 8 HCC from four antibody-positive and four antibody-negative patients. The survival probabilities were assessed by the Kaplan-Meier technique, and a Cox regression analysis was used to identify the independent factors for prognosis. RESULTS: Anti-p53 antibody was positive in 32% (28 of 86) of the sera from patients with HCC, but in none of the 20 with CH and 20 with LC. p53 antibody positivity was associated with bilirubin and the number of tumors (p=0.027 and p=0.018, respectively). Overall survival was shorter in the HCC patients with p53 antibody than in those without p53 antibody (p<0.02). Bilirubin, p53 antibody, AFP and ICG were found to be significant prognostic factors by univariate analysis. A Cox multivariate analysis showed that bilirubin and p53 antibody were independent prognostic variables (p<0.0001 and p=0.003, respectively). In four antibody-positive patients, mutation and LOH of the p53 gene were detected in one patient and two patients, respectively. In contrast, only one of four antibody-negative patients exhibited LOH of the p53 gene. CONCLUSIONS: Serum anti-p53 antibody could be a useful prognostic factor in patients with HCC.

Adult

Collagen-binding activity of plasma vitronectin in chronic liver disease.

The collagen-binding activity of plasma vitronectin was measured in 15 control subjects and 64 subjects with chronic liver disease. The assay of collagen-binding vitronectin was performed by an enzyme immunoassay using a monoclonal antibody to human vitronectin and type I collagen from human placenta. The plasma collagen-binding vitronectin concentration (mean +/- S.D.) was 5.6 +/- 1.9 micrograms/ml in the controls, 8.3 +/- 1.1 micrograms/ml in chronic persistent hepatitis, 8.3 +/- 2.9 micrograms/ml in chronic active hepatitis, 7.8 +/- 2.9 micrograms/ml in liver cirrhosis and 8.2 +/- 2.1 micrograms/ml in hepatocellular carcinoma with cirrhosis. The percent collagen-binding vitronectin to total plasma vitronectin was 2.2 +/- 0.8% in the controls, 3.9 +/- 2.2% in chronic persistent hepatitis, 3.9 +/- 1.2% in chronic active hepatitis, 5.8 +/- 3.3% in liver cirrhosis and 4.1 +/- 1.2% in hepatocellular carcinoma with cirrhosis. The plasma collagen-binding vitronectin also correlated with the serum levels of 7S collagen and hyaluronic acid. These findings suggest that vitronectin may play an important role in the progression of liver disease and/or in hepatic fibrosis through its collagen-binding domain.

Aged

Frequent loss in chromosome 8p loci in liver cirrhosis accompanying hepatocellular carcinoma.

Most hepatocellular carcinoma (HCC) is preceded by liver cirrhosis, but the genetic changes involved in cirrhosis are not well understood. We therefore studied loss of heterozygosity (LOH) in cirrhotic and neoplastic foci in livers of 14 patients with HCC. The samples, microdissected from paraffin-embedded tissues, were analyzed using a polymerase-chain-reaction-based assay for dinucleotide repeat polymorphisms on 8p. Of the 14 cases, 13 showed constitutional heterozygosity for the microsatellite markers. In 7 (54%) of these 13 informative cases, LOH was detected in the primary HCC and, in these 7 doubly informative (informative and LOH-positive in primary HCC) cases, LOH was found in 16 (70%) of 23 liver cirrhotic foci. The pattern of 8p allelic loss was identical in each doubly informative tumor; however, some of the liver cirrhotic foci harbored an 8p loss identical to that seen in the primary HCC, some harbored a different 8p loss, and some did not harbor any 8p loss. The remaining 6 cases without LOH on 8p in HCC showed no 8p loss in any cirrhotic foci. Presumably HCC could develop from cirrhotic cells harboring 8p loss.

Adult

Relationship between serum and hepatic 7S fragments of type IV collagen in chronic liver disease.

We evaluated the mechanism of increased serum concentrations of the 7S fragment of the N-terminal domain of type IV collagen (7S collagen) in chronic liver disease. We measured the concentrations of hepatic-free and deposited 7S collagens after extraction with Tris-HCl buffer and bacterial collagenase, then compared them with the serum levels in 8 normal controls and 48 patients with chronic liver disease. The hepatic 7S collagen levels extracted with Tris-HCl buffer and collagenase accounted for 7% and 93%, respectively, of the total 7S collagen levels in normal controls. Both hepatic 7S collagen levels as well as serum levels increased in accordance with the progress of liver disease. Serum levels of 7S collagen showed a closer correlation with the hepatic 7S collagen levels extracted with Tris-HCl buffer (r = .822), compared with those extracted with collagenase (r = .382). On the other hand, the histological degrees of liver fibrosis were highly correlated with the hepatic collagenase-extracted 7S collagen levels (r = .822), compared with serum and the hepatic Tris-HCl buffer-extracted levels (r = .478 and r = .537, respectively). Although there was no difference in serum and hepatic 7S collagen levels between B and C viral patients, the serum and hepatic Tris-HCl buffer-extracted 7S collagen levels were higher in patients with alcoholic cirrhosis than patients with viral cirrhosis. However, the hepatic collagenase-extracted levels were similar in both groups. Gel filtration demonstrated that the serum and hepatic Tris-HCl buffer-extracted 7S collagens were mainly eluted in the macromolecular 7S collagen-reactive fraction in cirrhosis, whereas the hepatic collagenase-extracted 7S collagen was eluted in the authentic 7S collagen-reactive fraction. The results suggest that serum 7S collagen levels are not a particularly reliable measure of hepatic fibrosis but reflect the enhanced metabolism, especially synthesis of type IV collagen in the liver.

Adolescent

Rupture of metastatic nodule on the peritoneal surface secondary to hepatocellular carcinoma.

A 20-year-old man with hepatocellular carcinoma (HCC) died of intraperitoneal bleeding from ruptured HCC, which was diagnostic from hemorrhagic ascites. At autopsy, a small nodule covered with hematogenous deposits was noted in the pelvic cavity near the left iliac artery. Microscopic findings showed that this was a ruptured metastatic nodule from HCC. Rupture of a metastatic nodule from HCC, especially one located on the peritoneal surface, has rarely been reported in the literature.

Adult

Clinical evaluation of a monoclonal antibody to serum KM01 for the diagnosis of hepatocellular carcinoma.

In order to evaluate a monoclonal antibody KM01 which was developed in mice immunized against a human colon carcinoma cell line, serum levels of KM01 and other tumor markers were studied in patients with both hepatocellular carcinoma and liver cirrhosis and in patients with liver cirrhosis alone. The KM01 levels in the sera of 50 patients with hepatocellular carcinoma plus liver cirrhosis and 50 patients with liver cirrhosis were measured using an enzyme immunoassay method and compared with various tumor markers including alpha-fetoprotein (AFP), DUPAN-2, and protein induced vitamin K absence or antagonist-II (PIVKA-II). The mean serum level (+/- S.D.) and sensitivity of KM01 in patients with hepatocellular carcinoma plus liver cirrhosis were 734 (+/- 716) units/ml and 64%, respectively, and they were significantly higher than those of liver cirrhosis patients (P < 0.001). Three out of 9 cases showing negative serum AFP levels had positive serum KM01 levels. Although the sensitivity of serum KM01 level for hepatocellular carcinoma was inferior to serum AFP and plasma PIVKA-II values, the sensitivity of a combination assay of serum KM01 or AFP was increased to 88%. Clinical data of the patients with markedly elevated serum KM01 levels (more than 1000 units/ml) were compared with patients with moderately elevated levels (530-1000 units/ml); serum bilirubin and alkaline-phosphatase were statistically higher in the former group (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Effects of bathing in hot water on portal hemodynamics in healthy subjects and in patients with compensated liver cirrhosis.

Bathing in hot water induces vasodilatation of the peripheral vessels and alteration of blood distribution. Using a Doppler flowmeter, we evaluated the effect of bathing in hot water on portal hemodynamics. Eight controls and 8 patients with compensated liver cirrhosis remained immersed in hot water at 42 degrees C for 5 minutes. Portal flow significantly decreased from 811 +/- 141 (ml/min) at the baseline to 530 +/- 98 in the controls and from 855 +/- 308 to 642 +/- 208 in cirrhotics immediately after bathing. This decrease (25%) in cirrhotics was significantly less than that (35%) in controls because vessel diameter did not decrease as rapidly as it did in controls. Portal flow after 30 minutes returned to the baseline values in controls but remained low in cirrhotics. These findings suggest that cirrhotics have a lower hemodynamic response to bathing in hot water compared with that in controls.

Adult

Long-term decrease in serum N-terminal propeptide of type III procollagen in patients with chronic hepatitis C treated with interferon alfa.

To evaluate the effect of interferon alfa (IFN-alpha) on the hepatic extracellular matrix, we investigated the changes in serum N-terminal propeptide of type III procollagen during and after 4 months of INF-alpha treatment in 178 treated and 45 nontreated patients with chronic hepatitis C. Serum pretreatment levels in nonresponders were significantly higher than those in long-term and short-term responders, but those levels were not different in the latter two groups. Serum propeptide levels decreased significantly during and after IFN-alpha therapy in the treated patients, although those levels were unchanged in the nontreated patients. This decrease was sustained for 12 months after IFN-alpha was completed not only in long-but also in short-term responders and nonresponders. Serum propeptide levels decreased in those with elevated pretreatment levels, but not in those with normal initial levels, whereas serum transaminase levels decreased similarly in both groups. The changes in serum propeptide levels during and after treatment were more closely correlated with the initial levels compared with those in serum transaminase levels. These results suggested that IFN-alpha treatment induces the long-term suppression of active fibrogenesis in chronic hepatitis C independent of antiviral and anti-necroinflammatory effects, thus preventing progression to cirrhosis.

Alanine Transaminase

[Fascioliasis].

Explore the source record for details and available documents.

Animals

Reduced numbers of CD8+ T cells and B cell-expression of Leu-8 antigen in peripheral blood of patients with primary biliary cirrhosis.

The presence of Leu-8 antigen, the human homologue of the murine MEL-14 peripheral lymph node homing receptor, defines subsets of peripheral blood mononuclear cells (PBMC) with different functions. Since it has been suggested that abnormal function of Leu-8 subsets may contribute to the immunopathogenesis of primary biliary cirrhosis (PBC), this study was undertaken to define whether abnormal expression of the Leu-8 antigen occurs in this disease. We studied 25 PBC patients, 12 with other chronic liver diseases, and 21 normal controls. PBMC were tested by direct immunofluorescence using monoclonal antibodies and flow cytometry. In PBC the proportion of PBMC that were CD4+ was normal; in contrast, the proportion that were CD8+ was decreased (p < 0.01). A negative correlation was found between absolute numbers of CD8+ T cells and total serum bilirubin levels (r = -0.50, p < 0.05). The distribution of Leu-8 antigen on T cells was normal; however, the proportion of PBMC that were B cells was increased (p < 0.01) and the fraction of these that were Leu-8 negative was also increased (p < 0.01). The expression of antigens of activation on B cells was similar to that for normal controls. These findings suggest that in peripheral blood of PBC patients reduced numbers of T cells may occur due to a selective intrahepatic sequestration of CD8+ T cells, and that the decreased expression of Leu-8 antigen by B cells may be associated with their participation in autoimmune processes.

Adult

Serum and urinary neopterin levels in patients with chronic active hepatitis B treated with interferon.

Serum and urinary neopterin levels and serum 2',5'-oligoadenylate synthetase and DNA polymerase activities were measured in 14 patients with HBeAg-positive chronic hepatitis B treated with interferon. Treatment with interferon brought about a threefold increase over basal levels in serum and urinary neopterin levels one week after the start of treatment. Both neopterin levels remained significantly elevated during treatment but rapidly returned to basal levels after the completion of treatment. Serum and urinary neopterin levels changed with a pattern similar to that of serum 2',5'-oligoadenylate synthetase activity and with a mirror image to serum DNA polymerase activity. It is indicated that measurement of serum and urinary neopterin can be used as a marker for cell-mediated immunity during interferon therapy for chronic hepatitis B, but can not be used to predict the short-term clinical effects of interferon treatment as in the case of serum 2',5'-oligoadenylate synthetase.

2',5'-Oligoadenylate Synthetase

[Clinical significance of serum and urinary neopterins after transcatheter arterial embolization for hepatocellular carcinoma].

To elucidate the immunological effects of transcatheter arterial embolization (TAE) for hepatocellular carcinoma (HCC), serum and urinary neopterins were measured using the radioimmunoassay in patients with HCC before and after TAE (n = 11), and compared with one shot arterial injection (AI)(n = 8). At the third day after TAE, serum and urinary neopterin levels were maximally elevated up to 164% and 158% from their respective baselines (p < 0.01). By contrast, these levels were unaffected after AI. In considering the changes of natural killer cell activity, C-reactive protein, transaminase and alpha-fetoprotein, these results suggest that the determination of neopterin levels after TAE may be not only valuable to assess the necrotic effect of TAE, but also be useful for evaluating cellular immunity after TAE.

Adult

Combination therapy with transcatheter arterial embolization and percutaneous ethanol injection for advanced hepatocellular carcinoma.

The effectiveness of transcatheter arterial embolization (TAE) combined with percutaneous ethanol injection (PEI) was investigated in 18 patients with advanced hepatocellular carcinoma (HCC), and compared with 18 patients with HCC treated by TAE therapy alone. In both groups, patients had multiple lesions or a single lesion larger than 3 cm. The pretreatment characteristics of the patients in the two groups showed that serum bilirubin in the TAE-PEI group was significantly higher than that in the TAE-only group, but that the patients in the two groups were comparable in all other respects. The cumulative survival rate of the TAE-PEI group estimated by the Kaplan-Meier method was 100% for 10 months, 82% for 20 months, 53% for 30 months and 18% for 40 months, whereas that of the TAE-only group was 75% for 10 months, 50% for 20 months, 30% for 30 months and 30% for 40 months. The survival rate in the TAE-PEI group was significantly higher than that in the TAE group. Moreover, the survival rate of patients whose main tumor was 4 cm or larger, was significantly higher in the TAE-PEI group than that in the TAE-only group. The average survival period of these patients in the TAE-PEI group was five times as long as that in the TAE-only group. The survival rate of Child's B and C patients in the TAE-PEI group was significantly higher than that in the TAE-only group.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged

Changes of serum 7S fragment of type IV collagen and N-terminal propeptide of type III procollagen after transcatheter arterial embolization as a model of acute liver injury.

To evaluate the mechanism of increased serum concentrations of the N-terminal propeptide of type III procollagen and the 7S fragment of type IV collagen in acute liver injury, we serially measured serum levels of these substances after transcatheter arterial embolization in patients with hepatocellular carcinoma. The results demonstrated marked increases in serum levels of the 7S fragment of type IV collagen in accordance with increased serum levels of transaminase after transcatheter arterial embolization. In contrast, a transient decrease in serum levels of the N-terminal propeptide of type III procollagen was found after transcatheter arterial embolization and transcatheter arterial infusion, although no significant changes in serum levels of the N-terminal propeptide and 7S fragment were seen after hepatic arteriography alone. The absolute change in serum levels of the 7S fragment after treatment showed positive correlation with serum transaminase levels and negative correlation with the decrease in serum levels of alpha-fetoprotein, although serum levels of N-terminal peptide did not demonstrate such a correlation. The results suggest that in acute liver injury induced by transcatheter arterial embolization, at least in part, increased in serum levels of the 7S fragment of type IV collagen reflect accelerated liberation of type IV collagen from the destroyed surrounding nontumorous tissues and that decreased serum N-terminal propeptide of type III procollagen reflects diminished synthesis of type III collagen caused by anticancer drugs.

Adult