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Biomedical subjects

D Ouzan

Publications and source records attributed to D Ouzan.

At least 55 records · Page 3Linked to original sources
PubMed1994

Recurrence of hepatitis C virus after liver transplantation.

The hepatitis C virus is a common cause of chronic hepatitis after orthotopic liver transplantation (OLT). We evaluated 95 consecutive patients who underwent OLT at our institute between March 1988 and November 1992 and who had a follow-up period longer than 3 months. All patients had a second-generation test (ELISA + RIBA) for HCV antibodies (HCV Ab) before and monthly after OLT; all had a polymerase chain reaction (PCR) test for detection of viral RNA after the operation. Whenever biochemical abnormalities (hypertransaminasemia 2 times the normal range) were seen, a percutaneous liver biopsy was performed. Forty-two HCV Ab+ patients before OLT remained positive after OLT. In this group the PCR test was positive in 32 cases (78.5%). In 13/42 (30.9%) cases (all PCR+) with hypertransaminasemia histological examination showed signs of viral C hepatitis (score of Knodell minimum 3, maximum 12, median 5.5). Of 53 HCV Ab patients before OLT, only 1 became HCV Ab+ and PCR+ 15 months after OLT. In the remaining 52 patients 15 were PCR+. Twenty of 53 patients (37.7%) had a liver biopsy because of hypertransaminasemia: in no case did histology show any signs of hepatitis C. In conclusion, viral C recurs often after OLT for post-hepatitic C cirrhosis. The histological graft lesions are in most cases moderate. We did not observe any deaths related to viral C infection in grafted patients. According to our results post-hepatic C cirrhosis remains a good indication for OLT.

Adult↗
PubMed1992

[Liver transplantation for hepatocellular carcinoma. Mid-term results].

The results of liver transplantation for hepatocellular carcinoma are disappointing. Thus, in 11 patients transplanted for hepatocellular carcinoma on cirrhosis, the actuarial survival rate at 3 years was 20 percent, with a postoperative mortality of 27 percent and 4 deaths caused by recurrence of the malignancy. These poor results contrast with those we obtained after liver transplantation for cirrhosis and finding of incidental hepatocellular carcinoma in the resected part of the liver. Out of 6 patients with incidental carcinoma only 1 died postoperatively (16.6 percent), and no case of recurrent malignancy was observed. These results confirm that the malignancy recurrence rate is high after transplantation for large carcinoma. On the other hand, the absence of recurrence after transplantation for incidental hepatocellular carcinoma encourages us to look for small carcinomas on cirrhosis.

Actuarial Analysis↗
PubMed1992

[Recurrence of virus B hepatitis after liver transplantation].

Thirty-three HBs antigen positive patients without signs of viral replication underwent orthotopic liver transplantation and received long term passive immunoprophylaxis with anti-HBs immunoglobulins at high doses perioperatively and then at a dose of 10,000 IU every month. All patients became negative during the first 6 months following surgery. At 34 months the survival rate was 67 percent and the actuarial recurrence rate of serum HBs antigen was 7.1 percent. Reappearance of HBs antigen was associated with evidence of HBV replication and histological alterations of the graft. In our experience, long term passive immunoprophylaxis reduces HBV reinfection of the grafted liver.

Adult↗
PubMed1991

Comparison of 1 or 3 MU of interferon alfa-2b and placebo in patients with chronic non-A, non-B hepatitis.

Ninety patients with histologically documented chronic non-A, non-B hepatitis were randomly allocated to receive SC injections of placebo or of 1 or 3 MU of recombinant interferon alfa-2b three times weekly for 24 weeks. Complete normalization of alanine aminotransferase levels occurred posttreatment in 43.3% of patients receiving 3 MU, in 20% of those receiving 1 MU, and in 6.7% of untreated patients (P less than 0.0005 vs. those treated with 3 MU). Alanine aminotransferase normalization was sustained for 6 months after therapy in 13.3% of the patients treated with 3 MU and in 3.3% of those given 1 MU or placebo. The decline of alanine aminotransferase levels following interferon therapy showed independent, positive correlations with female sex (P less than 0.03) and younger age (P less than 0.05). The Knodell's fibrosis score was strongly positively correlated with age (P less than 0.0001). It is concluded that 3 MU of interferon is a more effective dose than 1 MU for controlling disease activity in non-A, non-B chronic hepatitis patients. Women and younger and noncirrhotic patients are more likely to respond.

Adult↗
PubMed1991

Protective effects of prostaglandin E1 on normothermic liver ischemia.

Effects of treatment with prostaglandin E1 (PgE1) on normothermic liver ischemia were studied in male Lewis rats. Animals were subjected to 90 min of warm liver ischemia. Two groups of rats were constituted: group A (no treatment) and group B (PgE1 treatment). PgE1 (100 micrograms/kg) was given as a bolus 2 min before induction of ischemia and 2 min before the end of ischemia. Survival rates were assessed and, 6 h after the end of ischemia, serum transaminases, histology of the liver, Kupffer cell activity were evaluated. PgE1 treatment significantly improved survival rate (80%) in comparison with the nontreated group (40%). A significant reduction in transaminase levels was observed after PgE1 The extent of necrosis and congestion was improved by PgE1 treatment. Sheep red blood cell 51Cr liver uptake was deeply depressed 6 h after the end of ischemia in group A (6 +/- 2.3%/g tissue), and was significantly higher (p less than 0.001) after PgE1 administration in group B (32.98 +/- 11.7%/g tissue). Our results demonstrate that PgE1 is able to protect the liver from ischemic insult. The mechanism by which prostaglandins exert this beneficial effect on normothermic liver ischemia may be related to their action on hepatic macrophages.

Alprostadil↗
PubMed1990

[The medical interview motivated by the discovery of markers of viral hepatitis permits the identification, in blood donors, of behavior at risk for HIV infection].

From December 1988 to September 1989, 973 blood donors, deferred for anti-HBc reactivity, Ag-HBs positivity, elevated ALT, isolated or associated, but negative for anti-HIV, were interviewed in our blood center in the weeks after donation. Among these 973 donors, 53 (5.4%, 46 males, 7 females) were found at risk for HIV infection: intravenous drug abuse: 24 cases; heterosexuality with multiple partners: 17 cases; homosexuality: 8 cases; sexual relations with persons at risk: 4 cases. These 53 donors did not recognize their risk behaviour during the medical talk before donation. 25 out of these 53 donors were seen afterwards and one of them, homosexual man, seroconverted for anti-HIV seven months after the anti HIV negative but anti-HBc positive blood donation. We conclude that, in our experience, director surrogate viral hepatitis markers help to identify donors at risk for HIV infection, and, in one case, earlier in the course of demonstrated HIV infection than the enzyme immunoassays currently licensed.

Alanine Transaminase↗
PubMed1989

Randomized controlled trial of adenine arabinoside 5'-monophosphate in chronic active hepatitis B: comparison of the efficacy in heterosexual and homosexual patients.

Twenty-two heterosexuals and 21 homosexuals with chronic active hepatitis B and who had HBsAg, HBeAg and hepatitis B virus DNA in serum were randomized separately to receive adenine arabinoside monophosphate or placebo. In the 10 heterosexuals and nine homosexuals who received placebo, no change in hepatitis B virus DNA level and HBeAg was observed. Among the patients who received adenine arabinoside monophosphate, seven of the 12 heterosexuals and five of the 12 homosexuals lost hepatitis B virus DNA; five heterosexuals and three homosexuals also lost HBeAg; one homosexual lost HBsAg. There was no significant differences in response between heterosexual and homosexual patients. When results were pooled, there was a significant effect of adenine arabinoside monophosphate on hepatitis B virus replication. None of the 19 patients who received placebo but 50% of the 24 patients who received adenine arabinoside monophosphate were negative for serum hepatitis B virus DNA at 10 months after treatment (p less than 0.001) and none of the 19 patients who received placebo and 33% of the 24 patients who received adenine arabinoside monophosphate were negative for HBeAg in serum (p less than 0.005). Retrospective analysis showed that disappearance of hepatitis B virus DNA after administration of adenine arabinoside monophosphate was more common (i) in patients with a low pretreatment hepatitis B virus DNA level than in patients with a high pretreatment hepatitis B virus DNA level (8/11 vs. 4/13, p less than 0.05); (ii) in patients with a high pretreatment ALT level than in patients with a low pretreatment ALT level (10/14 vs. 2/10, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Detection of HBs antigen, DNA polymerase activity, and hepatitis B virus DNA in tears: relevance to hepatitis B transmission by tears.

Hepatitis B surface antigen, DNA polymerase, and hepatitis B virus DNA have been sought in the tears of 72 patients. These markers were detected in a high percentage of hepatitis B carriers, which proves the presence of hepatitis B virus in the tears and raises the question of its eventual transmission in this way. The severity and extreme contagiousness of hepatitis B together with the increasing number of virus carriers justify systematic sanitary rules among ophthalmic clinicians and staff, but vaccination remains the best mean of limiting the spread of the disease.

DNA, Viral↗
PubMed1988

[Superiority of a new etiopathogenic treatment curing periarteritis nodosa caused by hepatitis B virus, using a combination of brief corticotherapy, vidarabine and plasma exchange].

A new physiopathological treatment of HBV-related polyarteritis inspired by advances in the treatment of chronic active hepatitis B was tested in 7 patients. The new protocol included short term corticosteroid therapy, a course of antiviral chemotherapy with vidarabine and repeated plasma exchanges enabling steroids to be discontinued after 2 weeks. This treatment was well tolerated, and 6 of the 7 patients treated were clinically, biologically and virologically cured. The eradication of HBV among the patients who were cured was confirmed by clearance of HBs Ag and its replacement by anti HBs. None of the 6 patients relapsed during a 2 to 7 years' follow-up. The seventh patient died. In contrast, no patient had been cured in a similar group of 7 polyarteritis patients previously treated with the conventional symptomatic therapy using corticosteroids (6/7), plasma exchanges (4/7) and immunosuppressants (2/7). The outcome in this older series followed up for 3 years was altogether unfavourable, with 3 deaths, 3 chronic forms with multiple relapses and 1 spontaneous stabilisation. All patients remained chronic carriers of HBV. These results suggest that the new aetiopathogenic treatment capable of curing polyarteritis patients should replace the classical symptomatic treatment as soon as these preliminary results are confirmed by those of a multicentre study in progress.

Adolescent↗