Department of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
Eur J Obstet Gynecol Reprod Biol. 2013 Jul;169(1):60-3. doi: 10.1016/j.ejogrb.2013.01.014. Epub 2013 Feb 28.
To investigate the possible effect of clinical and genetic variables on the association between PTPN22 and endometriosis.
PTPN22, ACP₁ and p53 codon 72 genetic polymorphisms and duration of previous pharmacological treatment were studied. The study sample consisted of 132 women hospitalized for endometriosis diagnosed by laparoscopic intervention and histologically confirmed: 359 healthy blood donors were studied as controls. PTPN22, ACP1 and p53 codon 72 genotypes were determined by DNA analysis. Discriminant statistical analysis, logistic regression analysis, chi square of independence, power test and linear correlation were performed using SPSS programs.
A significant increase of PTPN22 T allele in endometriosis is observed in women carrying ACP1C allele, in women carrying p53 codon 72 *Pro allele and in women with prolonged pharmacological treatment.
PTPN22 may not be a primary factor in the etiology of endometriosis but may cooperate with clinical and genetic factors influencing susceptibility and clinical course of disease. These new observations point to a multifactorial origin of endometriosis and help to explain the reported differences between human populations concerning the association between PTPN22 and endometriosis.
探讨临床和遗传变量对 PTPN22 与子宫内膜异位症之间关联的可能影响。
研究了 PTPN22、ACP₁和 p53 密码子 72 基因多态性以及先前药物治疗的持续时间。研究样本包括 132 名因腹腔镜干预和组织学证实的子宫内膜异位症住院的女性：研究了 359 名健康献血者作为对照。通过 DNA 分析确定 PTPN22、ACP1 和 p53 密码子 72 基因型。使用 SPSS 程序进行判别统计分析、逻辑回归分析、独立性卡方检验、功效检验和线性相关分析。
在携带 ACP1C 等位基因的女性、携带 p53 密码子 72Pro 等位基因的女性和接受延长药物治疗的女性中，观察到子宫内膜异位症中 PTPN22*T 等位基因的显著增加。
PTPN22 可能不是子宫内膜异位症病因的主要因素，但可能与影响疾病易感性和临床过程的临床和遗传因素合作。这些新的观察结果表明子宫内膜异位症的多因素起源，并有助于解释关于 PTPN22 与子宫内膜异位症之间关联的报道在不同人群之间的差异。
