[Nursing of a patient with fracture of the right femoral neck and Colles' fracture of the same side].
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Biomedical subjects
Publications and source records attributed to I Tamura.
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For the purpose of clarifying the relation between hepatitis B virus (HBV) and hepatocellular carcinoma (HCC), a follow-up study of 1,614 HBV carriers (910 males and 704 females) was conducted at Kure National Hospital from 1970 to 1984. During the follow-up period (40.3 months on average), 247 HBV carriers died. Deaths from HCC and liver cirrhosis (LC) numbered 99 of 168 males (58.9%) and 38 of 79 females (48.2%), the chi-square test revealing no sex difference. Of 142 deaths from malignant neoplasm, HCC accounted for 52 of 96 males (54.2%) and 19 of 46 females (41.3%), the chi-square test again revealing no sex difference. The adjusted odds ratio of death from HCC among HBV carriers (1,614) with respect to HBV non-carriers (176,909) in this hospital during the study period (14-years) was 9.52 (males 7.94, females 13.39). The expected number of deaths was calculated based on the population of Hiroshima Prefecture (1978-1980) as a standard. The adjusted O/E (observed number/expected number) ratio of death from HCC was 6.66 for males and 12.13 for females, and the adjusted O/E ratio of death from LC was 5.41 for males and 11.02 for females. These findings suggest that HBV is a high risk factor of both HCC and LC, and, unlike the general population, female HBV carriers may have a rather higher risk of death from HCC and LC than male HBV carriers.
Cerebrospinal fluids (CSFs) and sera from 20 patients with echovirus 30 (E 30) meningitis, 4 patients with enterovirus 71 (EV 71) meningitis, and 5 patients with acute aseptic meningitis (AM) of unknown etiology were investigated at the acute and the convalescent phases of the disease to elucidate the roles of neutralizing antibody (NT) and interferon-alpha (IFN-alpha) in the central nervous system (CNS) in cases of AM in humans. Viruses were isolated from the CSFs at the acute phase of AM, but not at the convalescent phase. There was a fourfold or greater rise in NT titer between paired sera to E 30 or EV 71 but only a slight rise between paired CSFs. IFN-alpha was detected in the CSFs ranging from less than 10 to 25.5 IU/ml but not in the sera, and the IFN-alpha level in the CSF was significantly higher in the acute phase than in the convalescent phase. These results suggest that in cases of acute enteroviral infections in the CNS, NT plays only a small role in the recovery from AM, and IFN-alpha plays a direct or indirect role in curbing the local spread of the virus and eliminating the virus from the CNS at the acute phase of AM.
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Four-hundred and seventy-eight hepatitis B virus (HBV) carriers were followed for more than 60 months. In thirty-six cases the hepatitis B surface antigen (HBsAg) was cleared from serum during the observation period. In one case hepatitis B e antigen (HBeAg) was detectable for more than 66 months even after the appearance of antibody against hepatitis B surface antigen (anti-HBs). HBeAg was detected not only by radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA), but also by reversed passive haemagglutination (RPHA) method which has been believed to be far less sensitive than RIA or ELISA tests. HBV DNA was demonstrated in the serum even after the appearance of anti-HBs. Therefore, it is suggested that HBV (Dane particles) remains or reappears intermittently in the serum after seroconversion of HBsAg antigenaemia to anti-HBs complexes.
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A total of 336 hepatitis B virus (HBV) carriers were followed for more than 3 years with serial measurements of serological markers of HBV to determine the correlation between their clinical course and the HBeAg-anti-HBe system. In all, 139 had hepatitis B e antigen (HBeAg) at the beginning of the study. During the study, 30 of 139 HBeAg-positive carriers became HBeAg negative and subsequently gave a positive reaction for antibody to HBeAg (anti-HBe). The rate of seroconversion was 3.6% per year. Two types of profile of seroconversion were observed, rapid and gradual. No significant differences were observed in the incidences of HBeAg and anti-HBe in HBV carriers with or without liver cirrhosis (LC) and hepatocellular carcinoma (HCC). These findings do not support the report by Chung et al. (1983, J. Med. Virol. 11: 99-104) that a prolonged replicative phase of chronic HBV infection is essential for the occurrence of HCC. Two HBV carriers were diagnosed as having HCC at the time of seroconversion from HBeAg to anti-HBe. This finding supports the reports by Coursaget et al. (1978, J. Clin. Microbiol. 7: 394-395) and Musca et al. (1983, Hepatogastroenterology 30: 3-5) that actively replicating HBV sometimes becomes defective during the course of malignant transformation.
An enzyme-linked immunosorbent assay (ELISA) using microplates as solid phase, rabbit antiserum against human rotavirus Wa strain as catching antibody, and the same reagent labeled with beta-D-galactosidase as conjugate, has been developed for detection of human rotavirus antigen(s) in stool specimens from patients with acute gastroenteritis. The limit of detection of purified human rotavirus by ELISA was 15.6 ng/ml (1.56 ng/well) of viral protein. The sensitivities of ELISA, electron microscopy, and the reversed passive haemagglutination method (ROTA-CELL) were compared. ELISA was more sensitive than electron microscopy and the reversed passive haemagglutination method. The ELISA blocking assay was useful for detection of an antibody response to human rotavirus in paired sera from children in two institutions during outbreaks of rotavirus gastroenteritis.
Pleural effusions and sera of two patients with lung cancer were tested after intrapleural injection of OK-432 as an anticancer drug for IFN-alpha activity by biological assay and for IFN-alpha as an antigen by radioimmunoassay. The titers by radioimmunoassay were fairly consistent with those by biological assay, but were usually higher. In Case 1, IFN-alpha was observed fairly early after administration of OK-432 and only in pleural effusions. In Case 2, induction of IFN-alpha at low level was observed late after the first administration of OK-432 both in the pleural effusion and serum and was detected only by radioimmunoassay.
To investigate the prevalence of hepatitis delta virus (HDV) infection in different time periods between 1973 and 1988, antibody to hepatitis delta antigen (anti-HD) was tested for in sera collected from 1088 cases with acute or chronic hepatitis B virus (HBV) infection treated at Kure National Hospital. Between 1979 and 1983, anti-HD was first detected in 16% (four of 25 cases) of patients with acute hepatitis B, in 6.8% (11 of 161 cases) of asymptomatic HBV carriers and 26% (51 of 196 cases) of those with chronic liver disease. Except for this time period anti-HD was hardly detected. These findings indicate that sporadic HDV infections existed in this area between 1979 and 1983.
In this study, the diagnostic significance of PIVKA-II concentrations in various liver diseases was evaluated, and the use of PIVKA-II as a tumour marker for hepatocellular carcinoma (HCC) was discussed. Also, the location of abnormal prothrombin (PIVKA-II) production in HCC by indirect immunoperoxidase staining was examined. There was a good correlation between plasma and serum PIVKA-II concentrations, indicating that serum samples are adequate for PIVKA-II measurements. Fifty-four of 97 (55.7%) patients with HCC, one of 10 (10%) patients with metastatic liver cancer and two of 47 (4.3%) patients with liver cirrhosis had positive serum PIVKA-II concentrations. Positive serum PIVKA-II concentrations were found more frequently in patients with HCC than in any other liver disease (P < 0.01). Of the 97 patients with HCC, 54 (55.7%) were PIVKA-II positive, 76.3% had serum concentrations of either PIVKA-II or alpha-fetoprotein, indicating the usefulness of both tumour markers in the diagnosis of HCC. Using frozen sections of tissue specimens obtained at autopsy or during surgery, the localization of PIVKA-II was examined by indirect immunoperoxidase staining with specific anti-PIVKA-II antibodies. Tissues from 12 of 22 patients with HCC had positive PIVKA-II indirect immunoperoxidase staining only in the cancer cells. Cells with greater atypia tended to have stronger cytoplasmic staining. No specific staining was observed in non-cancerous cells. These findings suggest that PIVKA-II is synthesized specifically in hepatic cancer cells.
To investigate the effect of hepatitis delta virus (HDV) superinfection on the long-term outcome of Japanese subjects with chronic hepatitis B virus (HBV) infection, we examined the presence of antibodies to hepatitis delta antigen (anti-HD) in serial serum samples collected from 1127 subjects with chronic HBV infection. The subjects were followed for at least 36 months (mean: 121.3 months) between 1973 and 1991. Among 69 cases where anti-HD was detected, eight (12%) developed liver cirrhosis (LC) and six (9%) developed hepatocellular carcinoma (HCC). However, among 1058 cases without anti-HD, there were 43 patients (4%) who developed LC and 29 (3%) who developed HCC. The prevalence of LC and HCC was significantly higher among the cases with anti-HD than those without anti-HD. The proportion of LC and HCC per 1000 person years was 10.46 and 7.84, respectively among cases with anti-HD, and 4.05 and 2.73 among those without anti-HD, respectively. The overall relative risk of LC and HCC was 2.58 and 2.87, respectively; 95% confidence interval (CI): LC, 1.14-5.13; HCC, 1.03-6.23. These results indicate that in the Kure district in Japan, where HDV infection of persons infected with HBV is about 6%, such superinfection increases the risk of LC and HCC.
From 1973 to 1989 five patients with hepatitis delta virus having anti-hepatitis delta antibodies continuously in the serum for more than 5 years were identified among 1019 hepatitis B virus carriers who were being followed-up for more than 3 years (mean 8.9 years). Of the five patients with antibodies, three had a history of blood transfusion, in two cases the transfusion was massive, and one patient had been addicted to narcotics given intravenously 35 years before. In the remaining patient, the route of superinfection could not be determined. Hepatitis delta antigen was detected in hepatocyte nuclei of one of the three patients in whom liver biopsies were performed and there was chronic persistent hepatitis detected by an indirect immunoperoxidase technique. During the follow-up, hepatocellular carcinoma developed in one case but the clinical prognosis was favourable in the remaining four cases.
We investigated the prevalence of human immunodeficiency viruses-1 and 2 (HIV-1 and HIV-2), human T-lymphotropic virus type I and II, hepatitis B virus (HBV), hepatitis C virus (HCV) and hepatitis D virus among intravenous drug users (IVDU) in Hiroshima, Japan, where little is known about their present levels. From June to December 1993, serum samples were collected from 47 IVDU and 98 alcoholics in Hiroshima, Japan, and examined for markers of virus infection. The prevalence of antibody to HCV (anti-HCV) and/or HCV-RNA was significantly higher in IVDU than alcoholics (74.5% vs 20.4%, 44.7% vs 10.2% respectively, P < 0.001). In contrast, the prevalence of antibody to hepatitis B surface antigen and/or core antigen (anti-HBs and/or anti-HBc) showed no significant difference between the 2 groups (57.4% vs 66.3%). HIV-1 infection was found in one (2.1%) IVDU and genome analysis indicated that it was subtype B according to Myers' classification. Thus, an extremely low level of HIV infection and a high level of HCV infection was found in IVDU. Careful follow-up of this group is thought to be needed to minimize an outbreak of HIV-1 infection in Japan.
We compared the levels of type IV collagen (IV-C) in vitreous fluid and serum and the levels of glycosylated haemoglobin in 47 patients with proliferative diabetic retinopathy (DR) and 21 patients with non-inflammatory retinopathies. Levels of IV-C were found to be higher in the vitreous fluid in patients with DR than in patients with non-inflammatory retinopathy (53.2 +/- 14.9 microg/l versus 14.7 +/- 4.5 microg/l). Serum levels were likewise higher in patients with DR (349.7 +/- 106.2 microg/l versus 97.7 +/- 13.1 microg/l) as were glycosylated haemoglobin levels (8.3 +/- 0.3% versus 5.2 +/- 0.4%). In addition, levels of type IV collagen in the vitreous fluid were found to be higher in the patients who had been diabetic for > or = 10 years than in patients who had been diabetic for < 10 years (54.8 +/- 15.5 microg/l versus 16.8 +/- 4.6 microg/l). We conclude that accumulation of vitreous fluid IV-C may relate to high levels of glycosylated haemoglobin and long duration of diabetes. This suggests that the concentration of IV-C in vitreous fluid, and possibly also the serum levels of IV-C, reflects the progression of DR. Further investigation is needed to verify this and to investigate whether or not measuring IV-C levels is a useful means to assess therapeutic effects and/or prognosis of diabetic microangiopathy.