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J Nataf

Publications and source records attributed to J Nataf.

15 recordsLinked to original sources

[Prostate-specific antigen. Interpretation of the results in relation to the sampling method].

The authors compare the two prostate specific antigen assay methods most widely used in France. The first method (RIA Baxter) uses an isotope marker (Iodine 125), the other (EIA Biotrol) uses an enzymatic marker (alkaline phosphatase). Prostate specific antigen was assayed by means of these two techniques in two groups of patients: one group of 49 men considered to be free of any prostatic disease, recruited from blood donors; another group of 89 male patients in whom a prostate specific antigen assay was performed prospectively at the first urology outpatients visit. The two prostate specific antigen assay techniques gave different results, but the values obtained by these two methods were not discordant. It is therefore possible to define a coefficient of proportionality of 1.45 regardless of the prostate specific antigen concentration or the urological disease considered (EIA Biotrol x 1.47 = RIA Baxter).

Adult

[Prostatic specific antigen (PSA). Interpretation of results as a function of the assay method].

The authors compare the two PSA assay methods most widely used in France. The first method (RIA Baxter) uses an isotope marker (Iodine 125), the other (EIA Biotrol) uses an enzymatic marker (alkaline phosphatase). PSA was assayed by means of these two techniques in 2 groups of patients: one group of 49 men considered to be free of any prostatic disease, recruited from blood donors; another group of 87 male patients in whom a PSA assay was performed prospectively at the first urology outpatients visit. The two PSA assay techniques gave different results, but the values obtained by these two methods were not discordant. It is therefore possible to define a coefficient of proportionality of 1.47 regardless of the PSA concentration or the urological disease considered (EIA Biotrol x 1.47 = RIA Baxter).

Adult

Clinical course of spontaneous reactivation of hepatitis B virus infection in patients with chronic hepatitis B.

The purposes of this study were (a) to describe the clinical and biochemical manifestations associated with spontaneous reactivation of hepatitis B virus as defined by the reappearance of hepatitis B virus DNA in serum using dot-blot hybridization and (b) to determine whether the clinical and biochemical manifestations associated with hepatitis B virus reactivation were different in patients with and without human immunodeficiency virus-1 infection. During 1 yr, 110 French patients were admitted to Hôpital Beaujon for chronic hepatitis B. Fourteen were found to have hepatitis B virus reactivation; of these, three were anti-human immunodeficiency virus-1-positive. These 14 patients were HBsAg-positive for 60 mo (range = 6 to 180 mo). Clinical manifestations related to reappearance of hepatitis B virus DNA were present in 11 patients. HBeAg/anti-HBe status did not change in nine patients in whom hepatitis B virus reactivation would not have been recognized without hepatitis B virus DNA testing. Cirrhosis was present in nine patients. Four patients, of whom two were anti-human immunodeficiency virus-1-positive, had fulminant liver failure. Two patients died; one was anti-human immunodeficiency virus-1-positive. One patient was given an emergency transplant.

Adult

Anti-liver endoplasmic reticulum autoantibodies are directed against human cytochrome P-450IA2. A specific marker of dihydralazine-induced hepatitis.

Sera from patients with dihydralazine-induced hepatitis were shown to contain anti-liver microsomal autoantibodies (anti-LM) by indirect immunofluorescence. These anti-LM antibodies were different from anti-liver/kidney microsomes (anti-LKM) 1 or 2 autoantibodies which have been previously described. Sera recognized a single 53,000 = Mr polypeptide in human liver microsomes as judged by immunoblotting, and the target antigen was identified as cytochrome P-450IA2 (P-450IA2) by (a) comparison of immunoblotting patterns with anti-human P-450IA2 and anti-rat P-450IA2 and with five anti-LM sera, and (b) specific immunoinhibition of microsomal ethoxyresorufin and phenacetin O-deethylation activities (both P-450IA2 supported reactions) by anti-LM antibodies. Finally, purified human P-450IA2 was recognized by these anti-LM sera. The anti-LM antibodies are specific for the disease because none of the other antisera tested behaved in the same manner as anti-LM, even those from patients treated with dihydralazine and without hepatic disease. A possible role of P-450IA2 in the metabolism of dihydralazine was suggested by competitive inhibition of ethoxyresorufin-O-deethylase observed in microsomal incubations. Thus, a new example is presented in which a cytochrome P-450 may be a target for autoantibodies in drug-induced hepatitis.

Autoantibodies