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Background Medical management of atypical endometrial hyperplasia (AEH) includes oral or intrauterine progestins. This study aims to evaluate the oncological and reproductive outcomes of these patients and the predictive factors for disease regression, as well as to compare the treatment efficacy of different forms of progestins. Methodology This retrospective study was conducted at KK Women's and Children's Hospital, Singapore. Women diagnosed with AEH on endometrial biopsy between January 2015 to October 2017 and treated with at least eight weeks of the same progestin were included for analysis. Results Of the 42 patients who met the inclusion criteria, 37 were treated with oral progestins and five with the levonorgestrel intrauterine device (LNG-IUS). In total, 28 (66.6%) patients achieved complete regression (CR), but eight recurred with AEH or endometrial carcinoma. Four (9.5%) progressed to grade 1 endometrioid adenocarcinoma. Patients under 39 years old were 9.75 times more likely (95% confidence interval (CI) = 1.12-85.16, p = 0.04) to achieve CR compared to those who were 40 years old and above. In multivariate analysis, older age and higher mean body mass index had a significantly lower chance of CR. The probability of CR plateaued at nine months at 0.63 (95% CI = 0.47-0.79). There was no significant difference in time to regression, chance of regression, and risk of recurrence between oral progestin and LNG-IUS. Nine patients were trying to conceive. The clinical pregnancy rate was 44.4% (n = 4), and the live birth rate was 22.2% (n = 2). Conclusions Younger patients, especially those below 39 years old, are more likely to achieve CR. The value of medical treatment beyond nine months needs to be re-evaluated. There was no difference in treatment outcomes between oral progestins and LNG-IUS.
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Methods: A retrospective single-centre cohort study of patients with early-stage endometrioid endometrial cancer undergoing staging surgery (total hysterectomy, bilateral salpingo-oophorectomy with/without pelvic lymph node, and/or para-aortic lymph node dissection (PLND)) with either SLN mapping or routine lymphadenectomy between July 2017 and December 2018. Results: 203 cases with clinical and radiological International Federation of Gynaecology and Obstetrics (FIGO) stage I endometrioid endometrial cancer were included, out of which 109 cases underwent SLN mapping and 94 cases complete lymphadenectomy. Compared to the PLND group, the SLN group had shorter operative time (129 vs. 162 minutes), less blood loss (100 vs. 300 ml), and decreased length of postoperative hospital stay (3 vs. 4 days) (p < 0.001). The lymph node metastases detection rate was 4.6% and 7.4% for the SLN and PLND groups, respectively (p = 0.389). With a median follow-up of 14 months for the SLN and 15 months for the PLND group, the disease-free (DFS) and overall survival (OS) were comparable for both at 13 months (p = 0.538 and p = 0.333, respectively). Conclusion: SLN mapping has been shown to be an acceptable alternative to routine lymphadenectomy in the surgical staging of early-stage endometrial cancer in our centre, with a comparable lymph node metastases detection rate, DFS and OS, and reduction in operative morbidity. Our results with SLN mapping reproduce comparable outcomes to those reported in the literature.
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Neurofibromatosis type 1 (NF1) is a multisystem disorder caused by germline heterozygous NF1 loss-of-function variants. The NF1 gene encodes neurofibromin, a RAS GTPase-activating protein, which functions by down-regulating RAS/RAF/MAPK-signalling pathways. Somatic NF1 aberrations frequently occur in sporadic ovarian cancer (OC), but the incidence of OC in NF1 patients is rare. Here we report the germline and somatic findings for two unrelated patients with NF1 and high-grade serous OC. Germline testing revealed a heterozygous NF1 pathogenic variant in each patient, c.7096_7101del (p.Asn2366_Phe2367del) and c.964delA (p.Ile322Leufs*54), respectively. No germline variants in well-established OC predisposition genes were detected, including BRCA1 and BRCA2. Tumor loss-of-heterozygosity analysis demonstrated loss of the wild type NF1 allele for both patients. Biallelic NF1 inactivation occurs as part of OC pathogenesis in NF1 patients. Although the penetrance of NF1-associated OC is insufficient to warrant risk-reducing interventions, our findings highlight the potential for therapies targeting the RAS/RAF/MAPK-signalling pathway for these cases.