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S Pol

Publications and source records attributed to S Pol.

At least 127 records · Page 7Linked to original sources
PubMed1994

Impact and evolution of peliosis hepatis in renal transplant recipients.

Peliosis hepatis and hepatic sinusoidal dilatations are rare vascular liver diseases that occur at increased frequency in kidney transplant recipients. We retrospectively evaluated in kidney transplant recipients the natural history of vascular liver diseases, their impact on patient and graft survival, and the influence of AZA withdrawal. Between 1970 and 1990, vascular liver disease was diagnosed in 32 cadaver kidney transplant recipients 1-128 months after transplantation (mean 41 months). Diagnosis was based on histology in all cases. Patients received conventional immunosuppression (high dose steroids and AZA). Twenty patients had a minor form (sinusoidal dilatations or focal peliosis), while 12 had a major form (diffuse peliosis) of vascular hepatic disease. Two patients were lost to follow-up and 1 died at the time of diagnosis. In 12 patients (group 1), AZA dosage remained unchanged, while it was interrupted at the time of diagnosis in 17 patients (group 2). Five group 1 patients underwent serial liver biopsies, which showed persistence of vascular hepatic disease in 3 (with regenerative nodular hyperplasia in 1) and disappearance in 2 patients. Eight group 2 patients underwent serial liver biopsies, which showed disappearance of vascular hepatic disease in 6 patients and persistence in 2. Moreover, regenerative nodular hyperplasia was noted in 1 case, perisinusoidal fibrosis in 1 case, and cirrhosis in 6 cases. Three patients of group 1 and 11 patients of group 2 returned to dialysis a mean of 21 and 39 months after diagnosis, respectively. Eight patients died and death was clearly associated with major peliosis in 2 cases. In kidney transplant recipients, vascular hepatic disease may be associated with high mortality, especially in major forms. Our findings indicate that peliosis hepatis may lead to severe fibrosing liver lesions. The course of vascular hepatic disease is not clearly modified by AZA withdrawal.

Adolescent↗
PubMed1994

Detection of hepatitis C virus RNA in peripheral blood mononuclear cells of infected patients by in situ hybridization.

We used in situ hybridization to detect hepatitis C virus (HCV) infection of peripheral blood mononuclear cells (PBMNC) from 11 patients with chronic active hepatitis. Using 35S-labeled HCV-RNA probe, HCV-RNA-positive and -negative strands were observed in unstimulated PBMNC from three patients, all of whom were receiving immunosuppressive drugs after orthotopic liver transplantation (OLT). HCV-RNA sequences were also identified in PBMNC from three patients who were not undergoing immunosuppression, after stimulation with either phytohemagglutinin (PHA) or pokeweed mitogen (PWM). In contrast, HCV-RNA was not found in the remaining five patients, who had not undergone OLT and whose cells were not stimulated with mitogens. These results show that mononuclear cells can be infected by HCV and that mitogenic stimulation of infected cells increases HCV-RNA replication.

Adult↗
PubMed1994

Absence of association between HLA antigens and chronicity of viral hepatitis in haemodialyzed patients.

The role of HLA antigens in the chronicity of viral hepatitis is still being debated. We analyzed the relation between HLA status and viral hepatitis in 558 consecutive haemodialyzed patients who underwent kidney transplantation. HLA A, B, DR status, ABO-Rh blood group, duration of haemodialysis, and number of blood units transfused during the dialysis period were known for all patients. Serological status for hepatitis B virus and hepatitis C virus and results of liver biopsies were available in 495, 300 and 316 patients, respectively. After correction for the number of tests performed, frequencies of HLA antigens did not differ significantly for: 1. hepatitis B virus infection (compared to HBsAg-positive and anti-HBc and/or anti-HBs-positive nonvaccinated patients); 2. hepatitis C virus infection (compared to anti-HCV-negative and -positive patients); 3. histopathological status (compared to patients who had chronic viral hepatitis and those who did not). These results suggest that there is no evidence for a significant role of a particular HLA antigen in the development of chronic viral hepatitis in haemodialysis patients with similar underlying immunosuppression and exposure to infection by hepatotropic viruses.

Adult↗
PubMed1994

Influence of human immunodeficiency virus infection on hepatitis delta virus superinfection in chronic HBsAg carriers.

It is generally agreed that hepatitis B virus (HBV) replication is reduced by hepatitis delta virus infection (HDV) and augmented by human immunodeficiency virus (HIV) infection. However, the precise nature of the interactions between HBV, HDV and HIV is controversial. The aim of this study was to evaluate the impact of HIV infection on HBV and HDV replication, and on histological scores during delta virus superinfection in HDV-positive, chronic carriers of hepatitis B surface antigen (HBsAg). We studied 38 men and six women, 15 of whom were HIV-positive and all of whom had at least one marker of HDV infection. Serum hepatitis B e antigen (HBeAg), HBV DNA, HDV RNA, anti-delta antigen antibodies (anti-HD) IgM, anti-HD IgG and hepatitis delta antigen (HDAg) were tested for in the serum and liver, respectively; anti-hepatitis C virus (HCV) antibodies were detected using a second-generation recombinant immunoblot assay. Histological specimens were scored blindly according to Knodell's classification for periportal and intralobular necrosis, portal inflammation and fibrosis. HBV DNA was detected more frequently in the HIV-positive patients than in those who were HIV-negative (25 vs 0%; P = 0.01), while markers of HDV replication (serum anti-HD IgM, serum HDV RNA and liver HDAg) were as frequent in the HIV-positive patients (69%, 40% and 50%, respectively) as in those who were HIV-negative (75%, 52% and 30%, respectively; P > 0.05). By contrast, 31% of the HIV-positive patients were serum HDAg-positive compared to only 6% of the HIV-negative patients (P = 0.001). HDV antigenaemia and anti-HD antibodies usually fluctuated in the HIV-positive patients during follow-up. The mean Knodell score was similar in the HIV-positive (11.5 +/- 3.2) and HIV-negative (10.7 +/- 2) subgroups, as was the mean semi-quantitative index of hepatic necrosis, inflammation and fibrosis. Our results provide evidence that in HDV-positive patients: (1) HIV infection counters the inhibitory effect of HDV superinfection on HBV replication; (2) serum anti-HD IgM. HDV RNA and liver HDAg are not more frequent in HIV-positive than in HIV-negative patients, suggesting that HIV infection has no effect on HDV replication (although the significance of the increased frequency of HD antigenaemia remains unclear); (3) the histological severity of liver disease is not influenced by HIV status.

Adult↗
PubMed1994

Effectiveness of adenine arabinoside 5'-monophosphate in kidney transplant recipients with chronic active hepatitis B.

Hepatitis B virus infection is responsible for both morbidity and mortality in kidney transplant recipients. Adenine arabinoside 5'-monophosphate (ARA-AMP), a synthetic purine nucleotide with anti-viral activity, leads to a sustained interruption of HBV replication in approximately 40% of immunocompetent patients. We report the results of a pilot study using ARA-AMP to treat HBV-related chronic active hepatitis in kidney transplant recipients. Ten patients (2 females and 8 males, mean age 44 years, mean time post-transplantation 163 months) received a 28-day course of ARA-AMP intramuscularly: 5 mg/kg twice daily for the first 5 days during hospitalization and subsequently 5 mg/kg once daily at home for the remaining 23 days. Mean follow-up was 18 months, ranging from 7 to 28 months. All patients but one had biopsy-proven chronic hepatitis, including five cases of cirrhosis. All patients had been chronic HBs Ag carriers for more than 1 year and had active replication as assessed by the presence of serum HBV DNA (mean titre, 270 pg/ml, ranging from 12 to 997 pg/ml, Genostics method). HBe Ag was present in 7 of the 10 patients. Pretreatment creatinine was normal. In four of the 10 patients, HBV DNA became undetectable respectively 1, 1, 5, and 11 months after beginning ARA-AMP. In five patients, HBV DNA decreased during ARA-AMP therapy but subsequently increased although no change was noted during the follow-up period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[Viral hepatitis in hemodialysis and renal transplantation patients].

In patients with chronic renal failure be they hemodialysed or transplanted, viral hepatitis B and C tend to progress towards chronicity, in spite of both a frequent silent clinical presentation and an atypical course of viral markers. Therefore, only liver biopsy will allow a precise diagnosis of liver disease in these patients. Immunosuppression clearly modifies natural history of B and C viral hepatitis, but their real impact at mid and long-term on patient survival is still a matter of debate. Treatment is firstly preventive (vaccination and isolation of infected patients in dialysis units) and secondly curative. Preliminary data suggest that antiviral drugs such as ARA-AMP and interferon-alpha may have the same efficacy as in non-immunosuppressed patients. It is therefore of urgent need to evaluate both efficacy and tolerance of these antiviral drugs in patients on hemodialysis and in kidney transplant recipients.

Actuarial Analysis↗
PubMed1993

Microsporidia infection in patients with the human immunodeficiency virus and unexplained cholangitis.

BACKGROUND: Cholangitis in patients with the acquired immunodeficiency syndrome (AIDS) is usually associated with opportunistic infections by cryptosporidium species or cytomegalovirus, but in about a third of cases no opportunistic agent is identified. We suspected some of these cases of biliary disease might be explained by infection with the microsporidia species Enterocytozoon bieneusi, an obligate intracellular protozoan that causes chronic diarrhea in patients infected with the human immunodeficiency virus (HIV). METHODS: We studied eight HIV-infected homosexual men (in either group IV of the classification of the Centers for Disease Control and Prevention or group II, with a CD4 cell count of < or = 10 per cubic millimeter) who were referred because of cholangitis for which no causative agent had been found by standard tests. All the patients underwent abdominal ultrasonography and endoscopic ultrasonography or endoscopic retrograde cholangiopancreatography with collection of bile from the common bile duct. One patient had transhepatic biliary catheterization, and two others had cholecystectomy. Bile samples, duodenal- and liver-biopsy specimens, and gallbladder tissue were studied by light and electron microscopy. RESULTS: All eight patients with unexplained AIDS-related cholangitis had biliary microsporidosis. Intraepithelial E. bieneusi spores (1 to 2 microns) and supranuclear plasmodia (3 to 8 microns) were identified in the six duodenal-biopsy specimens. May-Grünwald-Giemsa staining of bile samples revealed free forms of microsporidia in all eight patients, and the presence of E. bieneusi was confirmed by electron microscopy. E. bieneusi was also identified in ductal biliary cells on a liver biopsy, in one common-bile-duct smear, and in gallbladder epithelium (in two patients). Four patients were found to have associated but previously undetected biliary or duodenal cryptosporidiosis, whereas another had biliary infection associated with cytomegalovirus. CONCLUSIONS: Infection of the biliary tract with E. bieneusi is associated with and may be a cause of AIDS-related cholangitis.

AIDS-Related Opportunistic Infections↗
PubMed1993

Hepatitis C virus RNA in anti-HCV positive hemodialyzed patients: significance and therapeutic implications.

About 25% of French hemodialysis patients have antibodies against the hepatitis C virus (HCV), which may reflect either past or active HCV infection. It is important to evaluate the significance of these antibodies, as most hemodialysis patients are candidates for kidney transplantation and have normal transaminase activities despite biopsy-proven chronic hepatitis. We prospectively assayed HCV viremia with the nested polymerase chain reaction in 61 patients on maintenance hemodialysis who had anti-HCV antibodies detectable in second generation tests (ELISA2 or RIBA2). HCV RNA was repeatedly detected in the serum of 52 (85.2%) patients. Liver biopsy, which was performed in 17 cases, revealed chronic hepatitis in 16 cases (including 2 of cirrhosis) and steatosis in one. Hypertransaminasemia was observed in only 31.3% and 30.8% of patients with chronic hepatitis and HCV viremia, respectively. Anti-HCV antibodies are frequently associated with HCV viremia, resulting usually in chronic hepatitis, although hypertransaminasemia is uncommon. HCV viremia reflects both post-transfusional and community-acquired HCV infection. These findings suggest a need for liver biopsy and antiviral treatment before kidney transplantation. The isolation of anti-HCV positive subjects in the dialysis setting should be evaluated to reduce patient-to-patient transmission of HCV.

Base Sequence↗
PubMed1993

Lack of evidence for a role of HCV in hepatitis-associated aplastic anaemia.

Hepatitis-associated aplastic anaemia (HAAA) is usually related to non-A, non-B hepatitis agents but the prevalence of anti-hepatitis C virus (HCV) antibodies is similar in HAAA and aplasia of other origins according to the results of the ELISA 1 assay. This fact could reflect either that HCV is not involved in HAAA or that HAAA-associated defective immune function could yield false negative assays despite on-going HCV infection. To test these hypotheses, we compared 19 patients with HAAA, including three ELISA 1-positive, to 23 patients with aplasia of known and unknown origin, including eight ELISA 1-positive, who were matched for age, sex and blood transfusion units. HCV infection was searched for by the second-generation recombinant-immunoblot assay (RIBA2), and by the polymerase chain reaction which detects HCV viraemia. HCV viraemia was detected in four among the 19 patients with HAAA and in six among the 23 patients with aplasia of other causes. HCV does not clearly appear responsible for hepatitis-associated aplastic anaemia which could be due to non-A, non-B, non-C hepatitis virus. HCV viraemia is frequent in severe aplastic anaemia, even without detectable anti-HCV antibodies, and reflects mainly transfusion-associated HCV infection.

Anemia, Aplastic↗
PubMed1993

Secondary immune response to hepatitis B virus vaccine in alcoholics.

The efficacy of full vaccination against hepatitis B virus (i.e., including the 1-year booster injection) was evaluated in 28 alcoholic patients with minimal liver disease. Although such patients are reportedly poor responders, the proportion of those protected (anti-HBs titer > = 10 mlU/ml) rose from 42.8% after primary immunization to 82% after the booster. The mean anti-HBs titer, which remained low in the overall group, was significantly lower in the subjects who resumed drinking during the follow-up period than in those who did not. This suggests a direct influence of alcohol itself on the response, because none of our patients had cirrhosis and none were clearly malnourished. Among the 17 patients for whom the 2-year post-booster anti-HBs titer could be determined, all those with a 1-month postbooster titer above 1000 mlU/ml still had a high anti-HBs level (> 100), whereas 80% of those with a 1-month postbooster titer < 1000 had 2 years later only a low (< 100) or even an unprotective anti-HBs level; this means that only the latter should be considered for a new booster injection. Our data indicate that protection against hepatitis B virus can be achieved in a good proportion of alcoholics with a full vaccination protocol. We suggest that efficacy should be evaluated 1 month after the booster, and that patients with low postbooster anti-HBs titers should be tested at regular intervals, because they can also be protected provided an adapted schedule of further injections is conducted.

Adult↗
PubMed1993

[Efficacy of immunotherapy with vaccination against hepatitis B virus on virus B multiplication].

In a prospective, non-randomized, pilot study, we evaluated the efficacy of hepatitis B virus (HBV) vaccination in inhibiting HBV replication of chronic hepatitis B. Fourteen consecutive chronic HBs antigen carriers received standard vaccination with three injections of the GenHevac B vaccine, one month apart. All the patients had active HBV replication with chronic hepatitis but not cirrhosis. They were compared to a historical group of 34 patients who fulfilled the same inclusion criteria. Over the 6-month follow-up period after the first injection, serum HBV DNA became undetectable in 3 patients (21.4%). Four additional patients (28.6%) showed a significant decrease in HBV replication. In 4 cases, the disappearance of or decrease in HBV DNA was preceded by an increase in transaminase activities, which was also observed in one patient who did not modify his viral replication. Vaccination was otherwise uneventful. By contrast, during a mean follow-up of 40 months, only 3 (9%) of the 34 unvaccinated patients who served as controls lost serum HBV DNA, giving a 6-month HBV DNA disappearance rate of 1%. In sum, vaccination appeared able to reduce or stop HBV replication in half of the chronic HBsAg carriers with chronic hepatitis. This additional therapeutic tool may enhance the rate of response to interferon-alpha therapy, which is dependent on the level of HBV replication. Thus, immunotherapy should be considered of potential importance for the treatment of HBV infection.

Adult↗
PubMed1992

Interactions between human immunodeficiency virus-1, hepatitis delta virus and hepatitis B virus infections in 260 chronic carriers of hepatitis B virus.

To evaluate the factors determining the severity of chronic hepatitis B virus infection and the interactions of human immunodeficiency virus and hepatitis delta virus infections, we retrospectively analyzed 260 patients, 146 of whom were followed for a mean of 31.4 +/- 1.8 mo. Human immunodeficiency virus, hepatitis B virus, and hepatitis delta virus status and aminotransferase activities, histological activity index, alcohol consumption and the prevalence of cirrhosis were investigated. The patients included 54 homosexuals, 19 parenteral drug abusers and 187 subjects with other or unidentified risk factors for exposure to hepatitis B virus. Thirty-five patients (13%) were positive for antibody to human immunodeficiency virus; 27 were homosexual and 8 were drug abusers. The mean aminotransferase activities, histological activity index and the prevalence of cirrhosis were similar in the human immunodeficiency virus-positive and human immunodeficiency virus-negative subgroups. Actuarial survival was significantly lower in the human immunodeficiency virus-negative subgroups. Actuarial survival was significantly lower in the human immunodeficiency virus-positive group than in the human immunodeficiency virus-negative subjects (p = 0.004); the cause of death was clearly related to liver failure in four of the five human immunodeficiency virus-positive patients and two of the six human immunodeficiency virus-negative subjects who died. To evaluate the factors determining the severity of liver disease, we compared homogeneous subgroups of subjects. Among the homosexual patients, the prevalence of HBeAg and hepatitis B virus DNA, aminotransferase activities and the histological activity index did not differ according to human immunodeficiency virus antibody status.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1992

Enterocytozoon bieneusi infection in acquired immunodeficiency syndrome-related sclerosing cholangitis.

Acalculous cholecystitis and sclerosing cholangitis due to Cryptosporidium sp, and cytomegalovirus have been described in patients with the acquired immunodeficiency syndrome (AIDS). However, in about 40% of cases of AIDS-related biliary disease, no opportunistic pathogen is identified. The current case report describes the first case, to the best of the authors' knowledge, of AIDS-related sclerosing cholangitis associated with microsporidiosis. Enterocytozoon bieneusi was detected in the duodenum and bile by means of light microscopy and confirmed by electron microscopy. Microsporidian infection should be suspected in patients with AIDS-related sclerosing cholangitis as well as in cases of diarrhea in which none of the usual pathogens are found.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Hepatitis C virus in kidney recipients. Epidemiology and impact on renal transplantation.

In an attempt to evaluate the prevalence, kinetics and impact of HCV infection in renal transplantation, we analyzed 140 kidney recipients according to the histopathological status of the liver. Thirty-three HBsAg-negative patients had chronic active hepatitis, 73 HBsAg-negative patients had a normal liver, 21 HBsAg-negative kidney recipients had minimal pathological changes and 13 patients had HBsAg-positive cirrhosis. Serum antibodies to HCV were detected using the ELISA from Ortho Diagnostic and confirmatory tests using the Ortho recombinant-based immunoblot assays. The overall prevalence of antiHCV antibodies was 23.6%. AntiHCV were more frequently present in HBsAg-negative patients with chronic active hepatitis (60.6%) than in HBsAg-negative patients with normal livers (8.2%) (p less than 0.0001) or minimal liver changes (33.3%) (NS) or in HBsAg-positive patients with cirrhosis (0%) (p less than 0.001). The recombinant-based immunoblot assays confirmed antiHCV-positive ELISA results in 86.7% of patients. Among the 27 antiHCV-positive kidney recipients who had serial serological follow-up, 10 (37.0%) were already positive at transplantation and remained antiHCV-positive during follow-up. Eleven patients (40.8%) acquired antiHCV an average of 95 months after renal transplantation, while antiHCV disappeared an average of 111 months after transplantation in six (22.2%), who had antiHCV prior to transplantation. The kinetics of antiHCV antibodies did not differ according to liver histology. Patient and graft survival were not different in antiHCV-positive and antiHCV-negative kidney recipients irrespective of liver histology, and there was no difference in survival between antiHCV-positive and antiHCV-negative patients with chronic hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗