title: [Genetic factors of predisposition to endometriosis and response to its treatment].
abstract: The relative frequencies of the normal (+) and null (0) alleles of the glutathione-S-transferase M1 (GSTM1) gene, as well as those of the rapid (R) and slow (S) forms of N-acetyl transferase 2 (NAT-2), were studied in the Russian and French populations and in endometriosis (EM) patients. In the total Russian and French populations, the proportions of homozygotes for deletion in gene GstM1 (0/0) were 42.2 and 45.8%, respectively, whereas in Russian and French EM patients, these values were 58.6 and 76.9%, respectively. The differences in these proportions between the total population and subjects with EM were significant at the confidence levels of 0.98 (chi 2 = 5.45; P < 0.02) and 0.90 (chi 2 = 3.01; P < 0.1) for the French and Russian populations, respectively. The frequencies of allele S of the Nat-2 gene were also similar in the Russian and French populations (60 and 63.1%, respectively), with these frequencies being somewhat higher in EM patients (71.2 and 77.7%, respectively). In Russians, the proportion of EM patients who were homozygous for the R form of NAT-2 (R/R) was significantly lower (chi 2 = 5.1). Forty-three of the patients with external genital EM received complex treatment with the use of the interferon inducer Cyclopheron. In 17 patients, a pronounced positive dynamics was observed, and 29 patients exhibited an increased resistance to the immunomodulating therapy. These groups comprised 1 and 25 GstM1 0/0 homozygotes, respectively; the number of patients with the slow NAT-2 form was 13 (7 S/S and 6 S/R genotypes) and 29 (20 S/S and 9 S/R genotypes), respectively. The obtained data indicate that the GstM1 and Nat-2 genes are involved in the EM pathogenesis. Therefore, molecular screening for the GstM1 0 and Nat-2 S alleles would be a good prognostic test when prescribing the postoperative treatment for EM and predicting its effectiveness.
authors.affiliation: Ott Institute of Obstetrics and Gynecology, Russian Academy of Medical Sciences, St. Petersburg, Russia.
authors.forename: V S
authors.initials: VS
authors.lastname: Baranov
authors.forename: T E
authors.initials: TE
authors.lastname: Ivashchenko
authors.forename: N Iu
authors.initials: NIu
authors.lastname: Shved
authors.forename: M I
authors.initials: MI
authors.lastname: Iarmolinskata
authors.forename: S A
authors.initials: SA
authors.lastname: Sel'kov
authors.forename: S M
authors.initials: SM
authors.lastname: Gorbushin
authors.forename: G A
authors.initials: GA
authors.lastname: Savitskiĭ
authors.forename: P
authors.initials: P
authors.lastname: Malet
authors.forename: M
authors.initials: M
authors.lastname: Kanis
authors.forename: M
authors.initials: M
authors.lastname: Bruhat
authors.forename: E
authors.initials: E
authors.lastname: Baranova
mesh_terms: D000166:Acridines / Q000627:therapeutic use*; D000483:Alleles; D001191:Arylamine N-Acetyltransferase / Q000235:genetics*; D004715:Endometriosis / Q000188:drug therapy* / Q000453:epidemiology / Q000235:genetics* / Q000276:immunology; D005260:Female; D005602:France / Q000453:epidemiology; D020022:Genetic Predisposition to Disease; D005982:Glutathione Transferase / Q000235:genetics*; D006720:Homozygote; D006801:Humans; D007369:Interferon Inducers / Q000627:therapeutic use*; D007372:Interferons / Q000276:immunology; D007527:Isoenzymes / Q000235:genetics; D012426:Russia / Q000453:epidemiology
chemical_list: D000166:Acridines; D001191:Arylamine N-Acetyltransferase; D005982:Glutathione Transferase; D007369:Interferon Inducers; D007372:Interferons; D007527:Isoenzymes; C026430:10-carboxymethyl-9-acridanone