Objective: The aim of this study was to investigate the influence on fertility and pregnancy outcome in cervical intraepithelial neoplasia (CIN) patients after a loop electrosurgical excision procedure (LEEP) or cold-knife conization (CKC). Methods: 269 patients with CIN-II-III who wanted to conceive were prospectively enrolled in this randomized clinical trial to receive either the LEEP or CKC procedure. Fertility, neonatal and maternal outcomes were observed and compared. Results: 244 evaluable patients were divided into two groups. There were 124 in the LEEP group and 120 in the CKC group. The preterm premature rupture of membranes (16 vs. 8%; p = 0.03), preterm delivery rate (11 vs. 5%; p = 0.04) and low birth weight infants rate (<2,500 g) (10 vs. 6%; p = 0.04) were higher in the CKC group than in the LEEP group, but there was no difference in mean birth weight, cesarean delivery, labor induction, or neonatal intensive care unit admission. There was no case of neonatal mortality. Conclusions: In a prospective evaluation the findings of this study demonstrate that LEEP is safer for future pregnancies when compared to CKC. LEEP should be an appropriate choice for patients with CIN who want to become pregnant later in life.

Perfluorotetradecanoic acid (PFTeDA) is a long‐chain perfluoroalkyl compound with increased applications. Its effect on Leydig cell function and its underlying mechanism remain unclear. Male Sprague–Dawley rats (60 days old) were gavaged with PFTeDA at doses of 0, 1, 5, and 10 mg/kg/day from 60 to 87 days after birth. PFTeDA significantly reduced serum testosterone levels at 1 mg/kg and higher doses, while markedly increasing serum luteinizing hormone level at 10 mg/kg and follicle‐stimulating hormone at ≥1 mg/kg. PFTeDA significantly reduced the sperm number at the cauda of epididymis at ≥1 mg/kg. PFTeDA also reduced the number of CYP11A1‐positive Leydig cells due to increased apoptosis shown by the terminal deoxynucleotidyl transferase‐mediated dUTP nick end labeling (TUNEL) assay. PFTeDA significantly repressed the expression of Cyp17a1 and Star and their proteins at 1–10 mg/kg, while it increased the expression of Srd5a1 and its protein (an immature Leydig cell biomarker) at 10 mg/kg. PFTeDA markedly increased testicular malondialdehyde level, while inhibiting antioxidants (SOD1, SOD2, and CAT), triggering oxidative stress, thereby further inducing BAX and CASP3 while inhibiting BCL2, which led to cell apoptosis. PFTeDA also reduced DHH level secreted by Sertoli cells, which indirectly affected Leydig cell function. PFTeDA inhibited testosterone secretion in primary Leydig cells in vitro by increasing reactive oxygen species and inducing apoptosis at 50 μM. In conclusion, PFTeDA inhibits the function of Leydig cells by inducing oxidative stress and subsequently stimulating cell apoptosis.

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