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Biomedical subjects

Y Katano

Publications and source records attributed to Y Katano.

At least 19 recordsLinked to original sources

Infection of hepatitis A virus in Japanese haemophiliacs.

OBJECTIVES: Outbreaks of hepatitis A virus (HAV) infection in haemophiliacs have been reported from many countries. The aim of this study was to determine the prevalence of hepatitis A virus antibody (HAVAb) in Japanese haemophiliacs. METHODS: Sixty-seven male haemophiliacs were recruited for this study of HAV infection. We also compared the rate of HAV infection with that of human immunodeficiency virus (HIV), hepatitis C virus (HCV), and hepatitis G virus (HGV). RESULTS: Fifteen of 67 haemophiliacs (22.4%) were positive for HAVAb. Prevalence of HAVAb was significantly higher in haemophiliacs than in Japanese normal subjects previously reported (P= 0.0001). Age, alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin and prevalence of HIV, HCV, and HGV were not statistically different between HAVAb positive and HAVAb negative haemophiliacs. We suggest that the use of clotting factor concentrates is closely associated with HAV infection, but HAV infection does not have an effect on clinical course. CONCLUSIONS: Administration of clotting factor concentrates may increase risk of HAV infection in haemophiliacs.

Adolescent↗

Fatal bleeding from a residual vein at the esophageal ulcer base after successful endoscopic variceal ligation.

Endoscopic variceal band ligation (EVL) is now one of the accepted treatment options for esophageal varices, and the safety of this procedure has been proved. However, we experienced a patient who had a fatal massive bleeding after successful EVL for ruptured esophageal varix. Postmortem study revealed a residual vein at the base of the esophageal ulceration associated with the ligation, which was believed to be the site of the fatal bleeding. His platelet counts and prothrombin time were not very impaired. Our case indicates that fatal massive bleeding can occur in patients after successful EVL without specific risk factors and indicates the importance of the awareness of the possibility of these complications.

Esophageal and Gastric Varices↗

Immunologic dynamics in hemophiliac patients infected with hepatitis C virus and human immunodeficiency virus: influence of antiretroviral therapy.

Infection with hepatitis C virus (HCV) or human immunodeficiency virus (HIV) or both is common in hemophiliac patients due to putative transmission through clotting factor concentrates. Recently, highly active antiretroviral therapy (HAART) has been found to markedly improve viremia and immunologic parameters in patients infected with HIV. This report considers interactions between these viral infections, the immune system, and antiretroviral therapy. A total of 130 male hemophiliac patients were grouped according to type of viremia (HCV, HIV, both, or neither). Along with 30 healthy men age-matched to viremic patients, these groups were compared with respect to viral load and immunologic parameters. Thirty-five patients treated as above for HIV were serially followed up. HCV infection was associated with reduced peripheral B-cell and CD4(+)-cell counts and with increased serum IgG and IgM levels, whereas HIV infection was associated with reduced peripheral CD4(+)-cell counts and increased serum IgG and IgA levels. In patients with both viruses, HCV and HIV RNA load correlated inversely with peripheral B-cell and CD4(+)-cell counts, respectively. HAART reduced levels of both viruses in the blood. Of the 25 patients with both viruses, HAART eliminated HCV in 2. In conclusion, immunologic dynamics differed between hemophiliac patients infected with HCV, HIV, or both. The relative dynamics of HCV viral load, peripheral B-cell count, and serum IgM level were similar to those of HIV viral load, CD4(+)-cell count, and serum IgA. (Blood. 2000;96:4293-4299)

Adolescent↗

Vasodilator effect of urotensin II, one of the most potent vasoconstricting factors, on rat coronary arteries.

The effects of human urotensin II on coronary flow were studied in the perfused rat heart. Urotensin II transiently decreased coronary flow, then induced sustained vasodilatation. In the presence of a cyclooxygenase inhibitor, diclofenac, coronary vasodilatation was significantly inhibited. A nitric oxide synthase inhibitor, N(G)-nitro-L-arginine (L-NNA), attenuated the urotensin-induced vasodilatation. These data suggest that urotensin II modulates coronary flow through factors such as cyclooxygenase products and nitric oxide to elicit coronary vasodilatation.

Animals↗

Massive bleeding from a gastric erosion after transcatheter arterial chemoembolization for hepatocellular carcinoma in a patient with mild haemophilia A.

We observed massive bleeding from a gastric erosion following transcatheter arterial chemoembolization (TAE) in a patient with mild haemophilia A. A 78-year-old haemophiliac (factor VIII level over 60%) received TAE with farmorubicin and spongel. Haematemesis and melena with loss of consciousness occurred 3 days [corrected] after TAE, and endoscopy revealed superficial erosions with oozing. Toxic effects of the anticancer drug in conjunction with the bleeding disorder may have caused the massive bleeding. We should always consider the possibility of unexpected complications in patients with bleeding disorders; gastrointestinal bleeding can develop during treatment for liver tumours.

Aged↗

Poor response to interferon treatment for chronic hepatitis C in human immunodeficiency virus-infected haemophiliacs.

We performed a pilot study to evaluate the factors associated with response to interferon (IFN) therapy for chronic hepatitis C (CHC) with human immunodeficiency virus (HIV) coinfected haemophiliacs. Seven haemophiliacs, coinfected with HIV and hepatitis C virus (HCV), received 9 mega-units (MU) of natural IFN-alpha daily during the first 2 weeks and then three times a week for 22 weeks, all injected subcutaneously. Six patients were receiving zidovudine (AZT) 600 mg day-1 and didanosine (ddI) 200 mg day(-1) during IFN therapy. This treatment was safe and well tolerated. Four patients had no detectable serum HCV-RNA at the end of therapy, but long-term, none of the seven patients achieved a sustained response, i.e. undetectable serum HCV-RNA with persistently normal serum alanine aminotransferase (ALT) 6 months after therapy. IFN did not affect CD4-positive cell counts. Most of our patients had high HCV-RNA loads and/or low CD4 counts, both unfavourable markers for IFN therapy. In conclusion, IFN therapy did not eradicate HCV from haemophiliacs coinfected with HIV.

Adult↗

Long-term follow-up of sustained responders to interferon therapy, in patients with chronic hepatitis C.

Interferon (IFN) therapy has been proven to induce the normalization of serum alanine aminotransferase (ALT) levels and to eradicate the hepatitis C virus (HCV) in some patients with chronic hepatitis C, and these patients are usually defined as 'sustained responders'. However, there have been some reports of hepatocellular carcinoma (HCC) in these patients, and the development of HCC remains life-threatening in patients who clear HCV. We analysed the long-term prognoses of patients with chronic hepatitis C in whom HCV was eradicated with IFN. We investigated 392 sustained responders to IFN therapy, from 1,277 patients with chronic HCV infection who received IFN treatment at one of our institutions between April 1989 and March 1999. We analysed the medical records and looked for the development of HCC. About 30% of the sustained responders had been lost to follow-up 3 years after the end of IFN therapy, and the follow-up rate of sustained responders was significantly lower than that of non-sustained responders (P < 0.0001). HCC were found in eight patients: in seven patients HCC developed within 5 years after completion of IFN therapy; but in one patient, a single HCC less than 3 cm in diameter was detected between 7 and 8 years after completion of IFN. Of the five patients who had regular medical follow-up, the HCC was solitary, and the patients survived without any evidence of recurrence. Of the three patients who had not been followed-up, two died from HCC and HCC recurred in the third. These results suggest that HCC can develop in sustained responders and that sustained responders should be followed-up closely after completion of IFN so that HCC may be detected at an early stage. The optimal duration of the follow-up period of the sustained responders remains unclear. Additional prospective studies are required in order to establish an appropriate follow-up protocol for sustained responders to IFN.

Adolescent↗

Differential modulation of nitric oxide and prostacyclin release in senescent rat heart stimulated by angiotensin II.

To elucidate the mechanism of age-related changes in the cardiovascular function stimulated with angiotensin II, we examined the effects of angiotensin II on the coronary flow, production of nitric oxide (NO) and prostacyclin, and on the cardiac function in the Langendorff-perfused young and aged rats' hearts. Angiotensin II decreased coronary flow, left ventricular dP/dt and heart rate. These effects were more pronounced in aged rats. Pretreatment with a NO synthase inhibitor, N(G)-nitro-L-arginine, significantly increased the angiotensin II-induced vasoconstriction in young rats. Angiotensin II increased the concentration of NO in the coronary effluent in young but not in aged rats. In contrast, angiotensin II stimulated the release of prostacyclin to a much greater extent in aged rats than in young rats. These results suggest that impaired production of NO may contribute to the greater constrictor effect of angiotensin II in the aged rat, although aging modulated the production of prostacyclin in a different manner. This age-related endothelial dysfunction may alter the physiological regulation of coronary flow and cardiac function stimulated with angiotensin II.

Acetylcholine↗

Why is the interferon sensitivity-determining region (ISDR) system useful in Japan?

BACKGROUND/AIMS: The amino acid sequence of NS5A2209-2248, named the "interferon sensitivity-determining region" (ISDR), has been reported to correlate with responsiveness of interferon (IFN) therapy to patients with the hepatitis C virus (HCV) genotype-1b, by several Japanese authors. However, European authors have failed to find this phenomenon, suggesting a difference in HCV-1b isolates between Japan and Europe. METHODS: We compared the HCV-1b nucleotide sequences of our Japanese patients and those of other countries quoted from GenBank, using the envelope 1 sequence. RESULTS: A phylogenetic tree analysis revealed two characteristic groups from a geographical viewpoint: one group (NJ group) consists of almost entirely non-Japanese isolates, and the other (J group) of almost entirely Japanese isolates. The isolates other than the NJ and J groups are characterized by their specific nucleotide residue, constructing an individual group (W group). Japanese HCV-1b isolates consist of the J group and W group (approximately 40% and 60%, respectively). Comparative study between the two groups in Japanese patients treated with IFN revealed a strong correlation between ISDR type and IFN responsiveness only in the J group, but not in the W group. CONCLUSIONS: These observations convinced us that the existence of the Japan-specific J group is one reason why the ISDR system is useful only in Japan.

Base Sequence↗

Infection with TT virus, a novel transfusion-transmissible DNA virus, in haemophiliacs and in blood products.

We evaluated the characteristics and rate of infection with TT virus (TTV), a novel DNA virus, in Japanese haemophiliacs. TTV DNA was measured in 60 haemophiliacs by semi-nested polymerase chain reaction. Co-infection with hepatitis C virus (HCV), hepatitis G virus (HGV) and human immunodeficiency virus (HIV) was also evaluated. In addition, the rate of detection of TTV DNA in blood products was evaluated. TTV DNA was detected in 35/60 haemophiliacs (58.3%). There were no differences in the backgrounds or characteristics between haemophiliacs with and without TTV infection, except for higher levels of IgG and IgM in patients with TTV infection. In patients infected with TTV of types other than type 1, which are rarely detected in Japan, the rate of co-infection with HCV of imported types was high; TTV of types other than type 1 in Japanese haemophiliacs were probably transmitted by imported blood products. TTV DNA was detected in over half of the blood products tested, but TTV DNA concentrations in these products were lower than in the serum of haemophiliacs.

Adolescent↗

Reactive lymphoid hyperplasia of liver coexisting with chronic thyroiditis: radiographical characteristics of the disorder.

BACKGROUND: Reactive lymphoid hyperplasia of the liver is an extremely rare entity, with six cases reported so far. METHODS: We encountered a 47-year-old Japanese female with reactive lymphoid hyperplasia of the liver, which coexisted with chronic thyroiditis. The lesion was discovered incidentally as a hypo-echoic mass with a hyper-echoic rim at a routine ultrasonography examination. It increased from 12 to 17 mm diameter in 6 months. Radiological studies, such as contrast-enhanced computerized tomography (CT) and angiography demonstrated a hypervascular lesion. RESULTS: It was consequently diagnosed as a neoplasm with malignant potentiality and she underwent partial hepatectomy. The lesion was composed of small mature lymphocytes which formed prominent lymphoid follicles with germinal centres, scattered plasma cells and stromal fibrosis. Immunohistochemical study revealed polyclonal origins of the involved lymphocytes. DNA analysis for the immunoglobulin heavy gene and the T cell receptor beta gene using Southern blot hybridization showed no monoclonality. The following features have characterized the images in past cases, as well as ours: hypo-echoic mass, occasionally with a rim, in ultrasonography and hypervascularity, shown by angiography and enhanced CT.

Angiography↗

Conformational epitopes detected by cross-reactive antibodies to envelope 2 glycoprotein of the hepatitis C virus.

The prevalence of anti-E2 antibody in persons chronically infected with hepatitis C virus (HCV) is high irrespective of viral genotype, and this cross-reactive antibody is thought to react with a conformational epitope. To investigate the characteristics of this anti-E2 antibody, the immunoreactivity of sera from HCV-1b-infected patients was measured against various modified forms of E2 glycoprotein derived from HCV-H (genotype 1a) by an immunofluorescence technique. Twelve of 18 patients were positive for anti-E2 antibody, and 10 of the 12 required a minimal amino acid (aa) region including aa 406-644 for strong reactivity, suggesting that the major E2 antibody has a conformational epitope in this region. Subsequent analysis using mutant E2 glycoproteins designed to lose N-glycosylation potential at varying sites revealed seven important N-glycosylation sites in this region. Four of these (aa 423, 430, 448, and 576) are indispensable for an antibody response.

Amino Acid Sequence↗

Fatal liver failure in haemophiliacs with HIV-induced immunodeficiency: observation of six patients.

We observed six cases of haemophiliacs with HIV-induced immunodeficiency who died from fatal liver failure despite the absence of evident cirrhosis. They all had the infection with hepatitis viruses (two patients with hepatitis B and D viruses and four patients with hepatitis C virus) and their CD4 counts were severely decreased. They were much younger than cirrhotic haemophiliacs without HIV. Their serum levels of hyaluronic acid and type IV collagen were lower than those in haemophiliacs with cirrhosis, and were normal. No patients had experienced symptoms or concomitant diseases characteristic of cirrhosis, such as ascites, jaundice, oesophageal/gastric varices or hepatocellular carcinoma, except for one case who had a history of mild ascites. The characteristics of this liver failure were different from liver failure resulting from cirrhosis caused by chronic hepatitis, which suggests liver failure that is specific to patients with immunodeficiency. This kind of liver failure can be a factor threatening survival in patients with HIV infection and with hepatitis virus co-infection in an immunodeficient state.

Acquired Immunodeficiency Syndrome↗