PubMed Health⌕ Search

Biomedical subjects

S Pol

Publications and source records attributed to S Pol.

At least 145 records · Page 8Linked to original sources
PubMed1992

Hepatitis C viremia and anti-HCV antibodies in alcoholics.

We determined serum hepatitis C status using a RIBA2 kit and a sensitive PCR procedure in 62 chronic alcoholics, 36 of whom had anti-HCV antibodies (Ab) detectable in an ELISA1 assay. Anti-HCV antibodies were detected in 22 patients using RIBA2. HCV RNA was detected by means of PCR in 18 patients who were RIBA2 positive and in none who were RIBA2 negative. Liver biopsies, available for 12 HCV RNA-positive patients, revealed histological features of purely alcohol-related lesions in seven and mixed alcohol-viral lesions in five. These results indicate that HCV replication is maintained in most alcoholics who score positive for anti-HCV Ab in the RIBA2 test, and that HCV viremia can be associated with histological features typical of alcoholic liver disease.

Adult↗
PubMed1992

Serum hepatitis C virus RNA and hepatitis B virus DNA in non-A, non-B post-transfusional and sporadic chronic hepatitis.

The sera of 36 French patients with post-transfusional and sporadic non-A, non-B chronic hepatitis were investigated, for HBV and HCV infections using a combination of serological and polymerase chain reaction (PCR) assays. Anti-HCV was detected in 75% (27/36) of the patients by ELISA1 and/or RIBA2 tests. HCV-RNA sequences were found in 75% (27/36) of the sera by a single step PCR, using a set of primers located in the 5' non-coding region. Altogether, 89% (32/36) of the patients were found positive with serological and/or molecular tests. Among the positive patients, 68% (22/32) were found positive for both anti-HCV and HCV-RNA, 16% (5/32) and 16% (5/32) were found positive for either anti-HCV or HCV-RNA, respectively. HBV-DNA sequences were detected in two patients associated to the HCV viraemia. This study confirms the extremely high prevalence of HCV infection in NANB chronic hepatitis in France. It also shows possible co-infection by HCV and HBV in hepatitis.

Base Sequence↗
PubMed1992

Absence of hepatitis delta virus infection in chronic hemodialysis and kidney transplant patients in france.

Hemodialyzed patients and kidney recipients are frequently multiply-transfused and infected by hepatitis B virus (HBV). Hepatitis delta virus (HDV) has a symbiotic association with HBV. The prevalence of HDV infection has, surprisingly, not been assessed in patients in hemodialysis or renal transplantation setting. We retrospectively studied the prevalence of serum delta antigen and antidelta antibodies by a microenzyme-linked immunosorbent assay in 77 of the 80 HBsAg-positive patients who underwent a kidney transplantation over a 10-year period. Of these patients, 73% had active HBV replication as assessed by the presence of serum HBV DNA and 65% had a biopsy-proved chronic active hepatitis, including cirrhosis. None of our patients had any marker of HDV infection at the end of the hemodialysis period or at the end of follow-up in transplantation. These results establish that HDV superinfection has indeed been extremely rare during end-stage renal failure and kidney transplantation in France, in contrast to HBV reactivation or hepatitis C virus infection.

DNA, Viral↗
PubMed1992

Herpesvirus infection of the respiratory tract in patients with alcoholic hepatitis.

Respiratory herpesvirus infections have rarely been described in alcoholics. We report four cases of severe respiratory herpesvirus infections in patients with alcoholic liver disease. Two were related to Herpes Simplex Virus and two to Cytomegalovirus. Both chronic alcoholism and severe liver disease induce immunosuppression, which might account for these unusual herpesvirus infections of the respiratory tract. These cases suggest that infections with herpesviruses should be considered in patients with alcoholic liver disease and pulmonary or tracheobronchial disease unresponsive to standard antibiotic therapy. Bronchoscopy, viral culture, and serological tests appear warranted, particularly given the existence of specific therapy.

Adult↗
PubMed1991

[Hepatitis C in kidney recipients. Epidemiology and impact on kidney transplantation].

In an attempt to evaluate the prevalence, the kinetics and the impact of HCV infection in renal transplantation, we analyzed 140 kidney recipients according to hepatic histology: 33 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 test. The overall prevalence of anti-HCV antibodies was 24.3 percent: anti-HCV were more frequently present in HBsAg negative patients with chronic active hepatitis (57.5 percent) than in HBsAg negative patients with normal liver (8.2 percent) (P less than 0.0001) or minimal changes (33.3 percent, NS) and HBsAg positive patients with cirrhosis (15.4 percent) (P = 0.02). Among the 30 anti-HCV positive kidney recipients with serological follow up, 13 (43.3 percent) had anti-HCV antibodies at the time of transplantation and kept anti-HCV during follow up, 11 (36.7 percent) acquired anti-HCV after renal transplantation in a mean time-lag of 95 months while 6 (20 percent), who had anti-HCV prior to transplantation, exhibited negativation of anti-HCV antibodies in a mean time-lag of 111 months after transplantation. The kinetics of anti-HCV antibodies was the same irrespective of the liver status. Patients and grafts survivals were not different in anti-HCV positive and anti-HCV negative kidney recipients, whatever the hepatic histology. Our data suggest that, in kidney transplantation, a) the prevalence of anti-HCV antibodies is around 24 percent in kidney recipients and varies greatly according to hepatic histology; b) anti-HCV antibodies are not systematically associated with the development of chronic liver disease; c) post-transfusion hepatitis as well as so called community acquired hepatitis may occur in transplantation follow up; d) HCV infection does not clearly influence the survival of allograft or that of kidney recipients.

Adult↗
PubMed1991

Association between HCV and HBV infection in hepatocellular carcinoma and alcoholic liver disease.

We conducted a retrospective study in 229 patients to determine the prevalence of hepatitis C virus (HCV) according to the type of liver disease and also the serum hepatitis B virus (HBV) status. There were 55 cases of hepatocellular carcinoma (HCC), 78 cases of alcoholic cirrhosis (AC) and 96 cases of non-cirrhotic alcohol liver disease (NCA). Half the AC and NCA groups were constituted of patients with or without serum HBV markers. The prevalence of anti-HCV antibodies in HCC (58.2%) was significantly higher than in the other groups (AC, 35.9%; NCA, 17.7%). Combining the two AC and NCA groups gave a 25.8% anti-HCV prevalence in the alcoholics. Altogether anti-HCV antibodies were more frequently present in HBV-positive than in HBV-negative patients (42.2 vs. 26.1%, p less than 0.01), although the difference was not significant when the HCC group was separately analysed. The S/N ratio of anti-HCV-positive samples varied according to the type of the disease (tumorous vs. non-tumorous) and to the serum HBV status. Indeed, 65.6% of HCC had a S/N greater than 4 compared to only 32.2 and 23.5% in AC and NCA, respectively (p less than 0.01). On the other hand more than half of the AC and NCA had a S/N less than 2, indicating possible artefacts in certain cases. The 15 HBsAg and anti-HCV-positive patients had a significantly lower mean S/N than patients displaying only antibodies against HBV, even in the HCC group.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Hepatic activity and mRNA expression of aspartate aminotransferase isoenzymes in alcoholic and nonalcoholic liver disease.

In liver and serum, AST activity is dependent on two isoenzymes, which are mitochondrial and cytosolic in nature. In an attempt to explain the well-known increase of serum mitochondrial AST-to-total AST ratio in chronic alcoholism (which is due to a specific increase of the mitochondrial isoenzyme), we analyzed: (a) liver and serum AST, ALT and glutamate dehydrogenase activities in 23 active drinkers with minimal liver changes, 11 alcoholic patients with cirrhosis who had stopped drinking, 18 nonalcoholic patients with viral chronic hepatitis and 11 subjects with normal livers; and (b) the expression of messenger RNAs for AST isoenzymes in the corresponding liver samples. Enzymatic activities were decreased in the liver irrespective of the origin of the liver disease. In patients with viral chronic hepatitis (or in those with alcoholic cirrhosis when abstinent), variations in liver proteins and messenger RNAs paralleled significant decreases in mitochondrial AST, ALT and glutamate dehydrogenase and a nonsignificant decrease of cytosolic AST. In alcoholic patients with minimal liver changes, the significant decrease of hepatic cytosolic AST, ALT and glutamate dehydrogenase activities contrasted with a close-to-normal liver mitochondrial AST activity; the increased amounts of mitochondrial AST messenger RNA give evidence for a pretranslational mechanism of regulation, indicating a possible increase in the total production of mitochondrial AST in the liver. The decrease of hepatic cytosolic AST activity was statistically significant only in alcoholic patients without cirrhosis who had a normal cytosolic AST mRNA level, thus suggesting a contributory role of translational or posttranslational regulation. In conclusion, regulation of AST isozymes during liver disease is complex, including differential, pretranslational and translational or posttranslational mechanisms.

Aspartate Aminotransferases↗
PubMed1991

[Mechanism of action of adenosine on intracellular calcium and platelet aggregation].

Adenosine inhibits platelet aggregation and elevates the levels of cytoplasmic Ca2+ induced by thrombin, 0.3 U/ml). When given at the maximal (100 microM) concentration, adenosine completely inhibits the aggregation, but only partially (by 55%) suppresses the growth of Ca2+, blocking both its entry and intracellular depot mobilization. Adenosine is likely to affect intracellular Ca2+, by activating adenylate cyclase, since 2',5'-didesoxyadenosine (1 mM) prevents the effect of adenosine, by inhibiting the enzyme, whereas the phosphodiesterase inhibitor papaverine (1 microM) potentiates its effect. When stimulated with adrenaline, 1 microM, adenosine and dibutyryl-cAMP are also able to inhibit platelet aggregation in the absence of cytoplasmic Ca2+ growth.

Adenosine↗
PubMed1990

Is hepatitis C virus involved in hepatitis-associated aplastic anemia?

OBJECTIVE: To determine whether hepatitis C virus is involved in hepatitis-associated aplastic anemia. DESIGN: Retrospective analysis. SETTING: Bone marrow transplantation unit. PATIENTS: One hundred and eighteen patients with severe aplastic anemia, including 19 with hepatitis-associated aplasia, 61 with aplastic anemia of undetermined cause, and 38 with aplastic anemia related to an inherited syndrome or an acquired etiology. MEASUREMENTS AND MAIN RESULTS: There was no statistically significant difference in antihepatitis C virus antibodies between hepatitis-related aplastic anemia (15.8%; 95% CI, 4% to 36%) and aplasia of unknown (9.8%; CI, 5% to 22%) or known (7.9%; CI, 2% to 22%) cause. The antihepatitis C virus levels did not differ according to the cause of aplastic anemia. There was no relation between hepatitis C and hepatitis B virus serologies, regardless of cause. CONCLUSIONS: Hepatitis C virus is not a frequent cause of non-A, non-B hepatitis-associated aplastic anemia. Either a non-A, non-B, non-C hepatitis virus is involved in non-A, non-B hepatitis-related aplasia or hepatitis C virus prevalence is underestimated in patients with hepatitis-related aplasia, possibly as a result of immunologic defects.

Anemia, Aplastic↗
PubMed1990

Properties of human liver cytosolic aspartate aminotransferase mRNAs generated by alternative polyadenylation site selection.

Human cytosolic aspartate aminotransferase (cAspAT) cDNA clones have been isolated from an adult human liver cDNA library. Among the clones, two cDNAs of 1550 and 1950 base pairs, respectively, have been characterized. These two cDNAs differ only in the lengths of their 3' noncoding regions and by the presence of one or two putative polyadenylation signals AATAAA. Northern blot analysis revealed two different mRNAs of 2.1 and 1.8 kbp in several human tissues, whereas Southern blot analysis suggested the existence of a single gene for the human cAspAT. The two mRNA species result from the alternative use of two polyadenylation signals. In the liver, the relative ratio of these mRNAs varies among different species and, in humans at least, during development. The properties of the two mRNAs were compared. The half-lives of the 2.1 and 1.8 kbp mRNAs, in the HepG2 cell line, are 8 and 12 h, respectively. The two mRNAs have similar and rather short poly(A) tracts of 20-50 nucleotides. Both mRNAs are capable of directing the in vitro synthesis of the cAspAT protein. We conclude that both the 2.1 and 1.8 kbp cAspAT mRNAs are functional and exhibit similar properties.

Amino Acid Sequence↗
PubMed1990

Chronic hepatitis in kidney allograft recipients.

98 HBsAg-positive and 31 HBsAg-negative kidney recipients were compared to assess the effect of renal transplantation on chronic liver disease and vice versa. Diagnosis was based on analysis of liver biopsy specimens including semiquantitative evaluation of histological features of chronic hepatitis. Serial specimens were examined: chronic liver disease occurred in 88% of HBsAg-positive patients and 4% of HBsAg-negative patients with normal liver at the time of transplantation. Liver abnormalities in the former were chronic persistent hepatitis (32%), chronic active hepatitis (51%), and cirrhosis (17%). Actuarial patient survival was similar in HBsAg-positive (78%) and HBsAg-negative (87%) patients, as was allograft survival (64% and 71%, respectively). In both HBsAg-positive and HBsAg-negative patients chronic alcohol consumption was more frequent in those with chronic liver disease than those without. These data suggest that renal transplantation may be appropriate for haemodialysis patients with chronic hepatitis whatever their HBV status.

Actuarial Analysis↗
PubMed1990

Genetic basis of nonresponse to hepatitis B vaccine in hemodialyzed patients.

Genetic factors are implicated in the response of normal subjects to hepatitis B vaccine. The aim of our study was to investigate if HLA Class I and II proteins could participate in a nonresponse to this vaccine in immunocompromised, namely hemodialyzed, patients. One hundred and seven hemodialyzed patients (68 men and 39 women, mean age 35 years) were vaccinated with Pasteur Hevac B vaccine, with a mean delay of 2 months following the onset of chronic hemodialysis. Patients were considered nonresponders when their serum antiHBs remained less than 10 mUI/ml on at least two occasions within the 12 months following the vaccination. HLA-A, B and DR antigens were determined by complement-dependent microlymphotoxicity. Ninety patients (84%) were responders and 17 (16%) nonresponders. The HLA-A1, B8 and DR3 frequency was higher in nonresponders (35, 35 and 44%, respectively) than in responders (18, 4 and 14%, respectively). The extended haplotype HLA-A1, B8, DR3 was more frequent in the former (19%) than in the latter (2%) (p less than 0.03). There was only one female within the nonresponders (6%) as compared to 37 (41%) in the responders (p less than 0.05). We conclude that genetic determinants (sex and HLA markers) play a critical role in the induction of an antiHBs immune response in both immunoincompetent hemodialyzed patients and normal immunocompetent hosts.

Adolescent↗
PubMed1990

Diagnostic value of serum gamma-glutamyl-transferase activity and mean corpuscular volume in alcoholic patients with or without cirrhosis.

In an attempt to assess the diagnostic values of serum gamma-glutamyltransferase (GGT) and mean corpuscular volume (MCV) variations as markers of liver disease and of abstinence in alcoholic patients, we compared 174 patients with alcoholic cirrhosis, 175 with noncirrhotic alcoholic liver disease and 67 patients with nonalcoholic cirrhosis. GGT and MCV values were checked three times, the day of admission, 7 days later, and on the last sample available during follow-up (1 to 12 months), and were compared according to the liver disease and abstinence. A decrease of GGT activity during the 1st week of hospitalization was noted in alcoholics with (-9 IU/liter) or without (-13 IU/liter) cirrhosis and not in nonalcoholic cirrhosis (+8 IU/liter), without MCV variations. During follow-up, median GGT activity was strikingly different in abstinent patients with (27 IU/liter) or without (21 IU/liter) cirrhosis and in nonabstinent patients (99 IU/liter and 123 IU/liter, respectively) (p less than 0.001). MCV decrease was noted in alcoholics whatever their abstinence or not, contrasting with the absence of decrease in nonalcoholic patients. For the diagnosis of alcoholism in cirrhotic patients, the positive predictive value (PPV) of a GGT or a MCV decrease during the 1st week of hospitalization was 0.82 and 0.78, respectively, and the negative predictive value (NPV) was 0.33 and 0.70, respectively. For abstinence during follow-up, the PPV of a GGT activity less than 50 IU/liter was 0.92 and the NPV was 0.65.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗
PubMed1989

Regulation of cytosolic aspartate aminotransferase mRNAs in the Fao rat hepatoma cell line by dexamethasone, insulin and cyclic AMP.

Glucocorticoid hormones increase the activity of cytosolic aspartate aminotransferase (cAspAT) in the Fao rat hepatoma cell line. Maximal increase (6-10-fold) was observed 48 h following the addition of the glucocorticoid agonist dexamethasone at a concentration of 0.1 microM. The effect of dexamethasone was specific since it was not mimicked by sex steroids and was inhibited by the glucocorticoid antagonist RU 486. Insulin (0.1 microM) inhibited by more than 50% the induction of cAspAT by glucocorticoids. The cAMP analog, 8-bromoadenosine 3',5'-monophosphate (Br8cAMP, 0.5 mM), potentiated the effect of dexamethasone (2-3-fold) and partially relieved the inhibitory effect of insulin on the induction by dexamethasone. Both insulin and Br8-cAMP had no significant effect on basal activity. The mitochondrial isoenzyme was insensitive to the various hormonal treatments. Northern blot analysis revealed the presence of two major (2.1-kb and 1.8-kb) and one minor (4-kb) mRNA species hybridizing with a rat cAspAT probe. The regulation of these mRNAs by glucocorticoids, insulin and cAMP correlated with the variation of the cAspAT activity, suggesting that these hormones act at the pretranslational level. We compared the regulation of cAspAT mRNAs with those of tyrosine aminotransferase mRNA. Both were similarly increased by dexamethasone but the latter was also increased by cAMP even in the absence of the glucocorticoid agonist. In addition, the increase in tyrosine aminotransferase mRNA was inhibited by cycloheximide whereas the increase in cAspAT mRNAs was not. These results show that there are significant differences in the regulation of cAspAT and tyrosine aminotransferase by glucocorticoids and other hormones, although both enzymes probably contribute to the same metabolic pathway.

Animals↗