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Background: Data on the prevalence and compliance with management of viral hepatitis in the street-involved population are limited. Method: Hepatitis A (HAV), B (HBV) and C (HCV) serology and compliance with HBV vaccination were documented in 533 street-involved individuals. Results: The mean age of the study population was 25.7 years (range: 11–65) and 53% were female. Serologic evidence of HAV infection was present in 53%; HBV, 12% (3% ongoing infection); and HCV, 17%. HAV infections were associated with Aboriginal/Metis ethnicity and age over 25 years; HBV with injection drug use (IDU); and HCV with IDU, sex trade work and age over 25 years. Compliance with three-step HBV vaccination was 98%, 77% and 63%. Conclusions: HAV, HBV and HCV are common infections in urban street-involved persons. Successful HBV (and presumably HAV) vaccination can be achieved in the majority of this population, but concerns exist regarding compliance with more long-term, parenterally-based antiviral therapies.

In vitro 1H MRS of human bile has shown potential in the diagnosis of various hepatopancreatobiliary (HPB) diseases. Previously, in vivo 1H MRS of human bile in gallbladder using a 1.5T scanner demonstrated the possibility of quantification of choline-containing phospholipids (chol-PLs). However, other lipid components such as bile acids play an important role in the pathophysiology of the HPB system. We have employed a higher magnetic field strength (3T), and a custom-built receive array coil, to improve the quality of in vivo 1H MRS of human bile in the gallbladder. We obtained significant improvement in the quality of 1D spectra (17 healthy volunteers) using a respiratory-gated PRESS sequence with well distinguished signals for total bile acids (TBAs) plus cholesterol resonating at 0.66ppm, taurine-conjugated bile acids (TCBAs) at 3.08ppm, chol-PLs at 3.22ppm, glycine-conjugated bile acids (GCBAs) at 3.74ppm, and the amide proton (-NH) arising from GCBAs and TCBAs in the region 7.76-8.05ppm. The peak areas of these signals were measured by deconvolution, and subsequently the molar concentrations of metabolites were estimated with good accuracy, except for that of TBAs plus cholesterol. The concentration of TBAs plus cholesterol was overestimated in some cases, which could be due to lipid contamination. In addition, we report the first 2D L-COSY spectra of human gallbladder bile in vivo (obtained in 15 healthy volunteers). 2D L-COSY spectra will be helpful in differentiating various biliary chol-PLs in pathological conditions of the HPB system. © 2014 John Wiley & Sons, Ltd.

© 2014 John Wiley & Sons, Ltd. In vitro1H MRS of human bile has shown potential in the diagnosis of various hepatopancreatobiliary (HPB) diseases. Previously, in vivo1H MRS of human bile in gallbladder using a 1.5 T scanner demonstrated the possibility of quantification of choline-containing phospholipids (chol-PLs). However, other lipid components such as bile acids play an important role in the pathophysiology of the HPB system. We have employed a higher magnetic field strength (3 T), and a custom-built receive array coil, to improve the quality of in vivo1H MRS of human bile in the gallbladder. We obtained significant improvement in the quality of 1D spectra (17 healthy volunteers) using a respiratory-gated PRESS sequence with well distinguished signals for total bile acids (TBAs) plus cholesterol resonating at 0.66 ppm, taurine-conjugated bile acids (TCBAs) at 3.08 ppm, chol-PLs at 3.22 ppm, glycineconjugated bile acids (GCBAs) at 3.74 ppm, and the amide proton (-NH) arising from GCBAs and TCBAs in the region 7.76-8.05 ppm. The peak areas of these signals were measured by deconvolution, and subsequently the molar concentrations of metabolites were estimated with good accuracy, except for that of TBAs plus cholesterol. The concentration of TBAs plus cholesterol was overestimated in some cases, which could be due to lipid contamination. In addition, we report the first 2D L-COSY spectra of human gallbladder bile in vivo (obtained in 15 healthy volunteers). 2D L-COSY spectra will be helpful in differentiating various biliary chol-PLs in pathological conditions of the HPB system.

OBJECTIVE: To document the frequency of admissions and the outcome of patients with a diagnosis of intentional iron overdose to a large urban hospital. DESIGN: Retrospective review of hospital records. SETTING: Health Sciences Centre, Winnipeg, an 1100-bed primary and tertiary care centre serving a regional population of about 1.2 million. PATIENTS: All patients with a discharge diagnosis of iron overdose who were admitted from Jan. 1, 1979, to July 1, 1991. Of these 113 cases 66 (58%) represented an intentional iron overdose on the basis of information derived from the patient, family or friends. MAIN OUTCOME MEASURES: Frequency of admissions, length of hospital stay and survival rate. RESULTS: Most (53 [80%]) of the 66 patients were females. The mean age was 19.8 (standard deviation [SD] 6.1) years (range 9 to 48 years). One third of the cases were associated with excess alcohol intake. The frequency of hospital admissions increased during the study period (1.4 cases per year in the first 5 years and 9.8 cases per year in the last 5; 5.3 cases per year overall). The mean length of hospital stay was 6.8 (SD 12.1) days, and the mortality rate was 10%. CONCLUSIONS: Hospital admissions because of intentional iron overdose are becoming more frequent in this centre and are associated with appreciable morbidity and mortality rates. Prospective studies are required to delineate clearly the signs, symptoms and abnormal laboratory findings associated with this problem.

Background Liver fibrosis is the common sequel of chronic liver diseases. Recent studies have identified hepatic stellate cells as the primary cell type mediating hepatic fibrogenesis. It has been demonstrated that hepatic stellate cells undergo a process of activation during the development of liver fibrosis. During the activation process, hepatic stellate cells acquire myofibroblast-like phenotype featuring the expression of smooth muscle alpha actin. Interferons have been employed for the treatment of viral hepatitis. However, it is unclear what is the effect of interferons on the prevention and treatment of liver fibrosis. Moreover, it is not clear whether there are any differences among interferon alpha, interferon beta, and interferon gamma in the treatment of liver fibrosis. Therefore, our objective in current study is to investigate the effects of rat interferon-α, interferon-β, and interferon-γ on the proliferation and activation of rat hepatic stellate cells. Results Rat interferon-β and interferon-γ significantly inhibited rat hepatic stellate cell proliferation while rat interferon-α did not affect the cell proliferation under the same culture condition. Inhibition of cell proliferation was confirmed by both WST-1 cell proliferation assay and 5-bromo-2'-deoxy-uridine incorporation assay. Similar results were observed regarding interferons regulation of hepatic stellate cell activation. Both rat interferon-β and interferon-γ reduced smooth muscle α-actin abundance after 6 days treatment, but rat interferon-α did not alter smooth muscle α-actin level. Conclusions Our results indicate that rat interferon-α and interferon-β have different biological effects on rat hepatic stellate cells and suggest that there are different signaling events between interferon-α and interferon-β in hepatic stellate cells.

An aqueous preparation of hepatitis B virus (HBV) vaccine was used as an intradermal skin test antigen to assess delayed hypersensitivity to hepatitis B surface antigen (HBsAg). Thirty-five persons were tested including 10 individuals seronegative for all HBV markers, 10 positive for HBsAg (chronic carriers) and 15 positive for antibody to HBsAg (anti-HBs), five of whom had received the HBV vaccine. All patients were also studied for lymphocyte blastogenic responses to phytohaemagglutinin, concanavalin A, pokeweed mitogen and purified HBsAg. Only one individual had a positive delayed skin test reaction to HBsAg. This person had received the HBV vaccine and had high titres of anti-HBs in serum. However, neither this individual nor any other subject exhibited a positive lymphocyte blastogenic response to HBsAg in vitro. Thus, delayed hypersensitivity skin test reactivity to HBsAg was not detected after natural infection with HBV and was rarely present in hyperimmunized individuals. In vitro assays of immune responsiveness failed to demonstrate cellular immunity to HBsAg even in hyperimmunized persons. These studies provide no evidence that cell-mediated immunity to HBsAg plays a role in the immunopathogenesis of acute or chronic type B hepatitis.

To determine the prevalence of hepatitis A in a Canadian Inuit population, serum from 85% of the 850 inhabitants of Baker Lake, Northwest Territories, was tested by radioimmunoassay for antibody to the hepatitis A virus (anti-HAV). The overall prevalence of anti-HAV in the community was 71%. Exposure to the virus occurred early in life, such that by the age of 6 years 53% of the children had anti-HAV in their serum. The rate approached 100% by the age of 50 years. These findings document the ubiquitous nature of the hepatitis A virus in this northern Inuit settlement and suggest that immunoprophylaxis be considered for individuals taking short-term employment in such places.

THREE VIRUSES COMMONLY INFECT THE LIVER: hepatitis A virus (HAV), hepatitis B virus (HBV) and the virus(es) responsible for non A non B hepatitis (nAnB). HAV infection occurs predominantly by the fecal-oral route and thus is more common in areas where living conditions are poor and personal hygiene suboptimal. Immune serum globulin (ISG) prevents this form of hepatitis. HBV infection can be spread by either parenteral (e.g. drug abuse) or non-parenteral (e.g. intimate contact) routes. High risk, susceptible individuals should be vaccinated with the HBV vaccine for longterm protection. Hepatitis B immune globulin (HBIG) remains the treatment of choice after exposure, but its protective effect does not exceed three to four months. The nAnB agent is spread by the same routes as HBV infection. At present there is no convincing evidence that any form of active or passive prophylaxis is beneficial for this form of hepatitis.