1/473. Wilson's disease coexisting with viral hepatitis type C: a case report with histological and ultrastructural studies of the liver.Histopathological and ultrastructural findings in the liver of a female patient who suffered from Wilson's disease (WD) and viral hepatitis type C (HCV) are reported. light and electron microscopy examinations demonstrated a variety of morphological alterations--many of them frequently seen in livers of patients with WD and others that can be found in cases presenting HCV infection. The influence of coexistence of these two diseases on morphological changes is discussed.- - - - - - - - - - ranking = 1keywords = infection (Clic here for more details about this article) |
2/473. Combining IgG and interferon alpha-2b in chronic hepatitis c virus infection.Treatment of chronic active hepatitis c virus (HCV) liver disease remains unsatisfactory. Interferon alpha 2b (IFN) has shown favorable though often unsustained effects. Besides its antiviral properties, IFN is a recognized immune modulator. We present data showing the favorable evolution of a case treated with IFN and IgG. Besides the antibody repertoire, the influence of IgG on the immune network is increasingly considered. The complex interactions resulting from combining drugs with immunomodulatory properties, such as IFN and different IgG preparations, may sound confusing. However, it might provide an insight into the outcome of chronic HCV infection, in which, evidently, immune components are heavily implicated. Prolonged treatment, with high-dose intravenous immunoglobulin (IVIG) seemed to be effective, either independently or by potentiating IFN.- - - - - - - - - - ranking = 5keywords = infection (Clic here for more details about this article) |
3/473. Highly active antiretroviral therapy leading to resolution of porphyria cutanea tarda in a patient with AIDS and hepatitis c.The association between hiv infection and porphyria cutanea tarda (PCT) is not well established. Since almost all hiv-infected patients with PCT previously described in the literature had additional risk factors for PCT, it is still unclear if hiv infection and not a cofactor such as hepatitis c virus is the trigger for PCT in this population. We describe a patient with AIDS and hepatitis c who developed bullous lesions due to PCT. The cutaneous lesions persisted for 18 months and resolved after he was placed on highly active antiretroviral therapy for hiv. No other therapeutic interventions were undertaken, while exposure to other known precipitants remained unchanged. During follow-up, skin lesions reappeared when the patient discontinued antiretroviral therapy, but PCT lesions again resolved after he restarted highly active antiretroviral therapy and hiv infection was controlled. This case supports the hypothesis that a direct causative relationship exists between hiv and the development of PCT.- - - - - - - - - - ranking = 3keywords = infection (Clic here for more details about this article) |
4/473. interferon-alpha may exacerbate cryoblobulinemia-related ischemic manifestations: an adverse effect potentially related to its anti-angiogenic activity.The discovery of the strong association between hepatitis c virus (HCV) infection and the development of mixed cryoglobulinemia has motivated active testing of antiviral-directed alternative therapies. Several trials have demonstrated that classic cryoglobulinemia-associated manifestations improve with interferon-alpha (IFNalpha) treatment. Herein we report on 3 HCV-infected patients with severe cryoglobulinemia-related ischemic manifestations who were closely followed up during IFNalpha therapy. Clinical evaluations with special attention to ischemic lesions, liver function tests, and cryocrit determinations were serially performed. In addition to prednisone and immunosuppressive agents, the patients received IFNalpha at 3 x 10(6) units, 3 times per week for 2 months, 3 months, and 4 months, respectively. In all 3 patients, systemic features improved, liver function results returned to normal, and cryocrit values decreased. However, ischemic lesions became less vascularized and ischemia progressed, leading to transmetatarsal and subcondylar amputation, respectively, in 2 of the patients and fingertip necrosis and ulcer enlargement in the third. skin biopsies performed before IFNalpha therapy and after 2 months of IFNalpha therapy in the third patient showed a significant decrease in subepidermal microvessels. When IFNalpha was discontinued, the lesions finally healed. cryoglobulinemia-related ischemic lesions may worsen during IFNalpha treatment, presumably through a decrease in inflammation-induced angiogenesis. The anti-angiogenic activity of IFNalpha may delay the appropriate healing of ischemic lesions.- - - - - - - - - - ranking = 1keywords = infection (Clic here for more details about this article) |
5/473. Fatal virus-associated hemophagocytic syndrome associated with coexistent chronic active hepatitis B and acute hepatitis c virus infection.A 28-year-old man was admitted to our department with intermittent fever, hepatosplenomegaly and pancytopenia. Liver parameters and serum ferritin were markedly elevated. bone marrow biopsy showed hypocellularity, histiocytic hyperplasia, and hemophagocytosis consistent with a virus-associated hemophagocytic syndrome (VAHS). There was serological evidence of chronic active hepatitis B and acute hepatitis c virus infection. The patient died despite aggressive immunosuppressive and supportive treatment. autopsy revealed signs of acute viral hepatitis with cholestasis. histiocytes engaged in hemophagocytosis were observed in bone marrow and spleen. The condition was interpreted as VAHS associated with chronic active hepatitis B and acute hepatitis c virus infection. To our knowledge this is the first report of a hemophagocytic syndrome in that setting.- - - - - - - - - - ranking = 6keywords = infection (Clic here for more details about this article) |
6/473. Fibrosing cholestatic hepatitis in renal transplant recipients with hepatitis c virus infection.Fibrosing cholestatic hepatitis (FCH) has been described as a specific manifestation of hepatitis b virus (HBV) infection in liver allograft recipients characterized by a rapid progression to liver failure. Only sporadic cases have been reported in other immunocompromised groups infected with HBV and in a few transplant recipients with hepatitis c virus (HCV) infection. We present the occurrence of FCH in 4 HCV-infected renal transplant recipients within a series of 73 renal transplant recipients with HCV infection followed up closely serologically and with consecutive liver biopsies. All 4 patients received the triple-immunosuppressive regimen (azathioprine, cyclosporine A, methylprednisolone). The interval from transplantation to the appearance of liver dysfunction was 1 to 4 months and to histological diagnosis, 3 to 11 months. The biochemical profile was analogous to a progressive cholestatic syndrome in 3 patients, whereas the fourth patient had only slightly increased alanine aminotransferase and gamma-glutamyl transferase (gammaGT) levels. Liver histological examination showed the characteristic pattern of FCH in 2 patients, whereas the other 2 patients had changes compatible with an early stage. All patients were anti-HCV negative at the time of transplantation, whereas 2 patients, 1 with incomplete and 1with complete histological FCH features, seroconverted after 3 and 31 months, respectively. The patients were HCV rna positive at the time of the first liver biopsy and showed high serum HCV rna levels (14 to 58 x 10(6) Eq/mL, branched dna). HCV genotype was 1b in 3 patients and 3a in 1 patient. After histological diagnosis, immunosuppression was drastically reduced. Two patients died of sepsis and liver failure 16 and 18 months posttransplantation, whereas the seroconverted patients showed marked improvement of their liver disease, which was histologically verified in 1 patient. In conclusion, FCH can occur in HCV-infected renal transplant recipients. It seems to develop as a complication of a recent HCV infection during the period of maximal immunosuppression and is associated with high HCV viremia levels. There are indications that drastic reduction of immunosuppression may have a beneficial effect on the outcome of the disease.- - - - - - - - - - ranking = 8keywords = infection (Clic here for more details about this article) |
7/473. hepatitis c virus-related fibrosing cholestatic hepatitis after cardiac transplantation: is azathioprine a contributory factor?We report a patient who acquired hepatitis c virus (HCV) infection at cardiac transplantation, developing fibrosing cholestatic hepatitis (FCH) with early liver failure and a fatal outcome. FCH is a recently described clinicopathological entity characterized by a cholestatic pattern of serum liver enzyme abnormalities, a progressive course leading to liver failure, and a pathological picture defined by periportal fibrosis, neutrophilic infiltrates and signs of histological cholestasis. Although it was initially described secondary to hepatitis b virus infection, it has also been recently related to HCV infection. Some histopathological features consistent with azathioprine hepatotoxicity like cholestasis, perisinusoidal fibrosis, veno-subocclusive lesions and nodular regenerative hyperplasia were also observed in this case. Therefore, a direct cytopathic effect of HCV and the concurrent pathogenic role of azathioprine hepatotoxicity may be involved in the development of this complication of transplantation.- - - - - - - - - - ranking = 3keywords = infection (Clic here for more details about this article) |
8/473. Transplantation of allogeneic CD34-selected peripheral stem cells does not prevent transmission of hepatitis c virus from an infected donor.There is little information on the clinical course of transplantation from HCV-positive donors. However, it seems that there is no increased risk of acute liver failure after the procedure and that the presence of HCV-rna in serum is necessary for transmission to take place. We report a case of allogeneic CD34-selected peripheral stem cell transplantation from an HCV-infected donor with viremia with a special clinical and virological course. After the selection procedure and cell washing we could not detect HCV-rna by PCR in the wash buffer, but HCV-rna was positive by PCR in the selected cells. Once the patient received the transfusion of the selected product HCV was detected in the PBMCs and at very low concentration in serum. HCV was also demonstrated in the hepatocytes with the in situ hybridization technique. In conclusion, we have shown that CD34 cell selection from an HCV-positive allogeneic donor does not prevent HCV infection in the recipient. Our results also suggest that HCV replicates in PBMCs in vivo and that these cells release viral particles that can infect the liver.- - - - - - - - - - ranking = 1keywords = infection (Clic here for more details about this article) |
9/473. Transmission of hepatitis c within Australian prisons.Transmission of hepatitis c virus (HCV) within prisons has long been suspected but has not been satisfactorily documented. We present four cases of HCV infection occurring during periods of continuous imprisonment. Each subject was HCV seronegative on entering prison and on repeat testing after 4-52 months in prison, but subsequently became seropositive. Two subjects gave a history of injecting drug use, and the most likely means of infection in the other two subjects were lacerations from barbers shears and lacerations arising from physical assault. There is an urgent need for detailed study of the incidence of HCV infection and the modes of transmission in prisons.- - - - - - - - - - ranking = 3keywords = infection (Clic here for more details about this article) |
10/473. Identification of hepatitis c virus seroconversion resulting from nosocomial transmission on a haemodialysis unit: implications for infection control and laboratory screening.hepatitis c virus (HCV) seroconversion was detected by routine screening in a haemodialysis patient, Patient 1. Serological investigations were undertaken over the following 3 months to determine if further transmission to other patients on the unit had occurred. No additional cases were identified. Twenty-two haemodialysis patients known to have HCV infection were investigated using molecular epidemiological methods to determine if transmission between patients had occurred. HCV viraemia was demonstrated by polymerase chain reaction in 19 of 22 patients (86%). Genotyping showed that eight patients were infected with genotype 1, three with genotype 3 and eight, including Patient 1, with genotype 2. Phylogenetic analysis of viral sequences from the eight patients with genotype 2 revealed three, including Patient 1,with a novel subtype of HCV type 2, and revealed close similarity between viral sequences from patient 1 and those from one other patient, suggesting transmission. This was consistent with haemodialysis histories. Among other patients with genotype 2, there were two with subtype 2a and three others with three separate novel subtypes, as yet undesignated. With the exception of patient 1, all patients infected with novel subtypes were of Afro-Caribbean origin. The HCV prevalence among patients on the haemodialysis unit was high (14%), which may reflect the ethnicity of our haemodialysis population. This case emphasises the risk of nosocomial transmission and the importance of infection control procedures on haemodialysis units, and highlights the usefulness of molecular epidemiological techniques for the investigation of outbreaks of HCV infection.- - - - - - - - - - ranking = 7keywords = infection (Clic here for more details about this article) |
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