Patrícia Rangel Sobral Dantas1, Izildinha Maestá2, Jorge Rezende Filho3, Joffre Amin Junior3, Kevin M Elias4, Neil Howoritz4, Antonio Braga5, Ross S Berkowitz4. 1. Department of Gynecology and Obstetrics, Botucatu Medical School, Postgraduate Program of Gynecology, Obstetrics and Mastology of São Paulo State University. Rubião Júnior District, Botucatu, São Paulo, Brazil; Rio de Janeiro Trophoblastic Disease Center, Brazilian Association of Gestational Trophoblastic Disease, 180 Laranjeiras St, Laranjeiras, Rio de Janeiro, RJ, Brazil. 2. Department of Gynecology and Obstetrics, Botucatu Medical School, Postgraduate Program of Gynecology, Obstetrics and Mastology of São Paulo State University. Rubião Júnior District, Botucatu, São Paulo, Brazil. 3. Rio de Janeiro Trophoblastic Disease Center, Brazilian Association of Gestational Trophoblastic Disease, 180 Laranjeiras St, Laranjeiras, Rio de Janeiro, RJ, Brazil; Department of Gynecology and Obstetrics, Maternity School, Postgraduate Program of Perinatal Health of Rio de Janeiro Federal University, 180 Laranjeiras St, Laranjeiras, Rio de Janeiro, RJ, Brazil. 4. Department of Obstetrics and Gynecology and Reproductive Biology, Division of Gynecologic Oncology, New England Trophoblastic Disease Center, Donald P. Goldstein MD Trophoblastic Tumor Registry, Brigham and Women's Hospital, Dana-Farber Cancer Institute, Harvard Medical School, 75 Francis St, Boston, MA, USA. 5. Rio de Janeiro Trophoblastic Disease Center, Brazilian Association of Gestational Trophoblastic Disease, 180 Laranjeiras St, Laranjeiras, Rio de Janeiro, RJ, Brazil; Department of Gynecology and Obstetrics, Maternity School, Postgraduate Program of Perinatal Health of Rio de Janeiro Federal University, 180 Laranjeiras St, Laranjeiras, Rio de Janeiro, RJ, Brazil; Department of Maternal-Child, Antonio Pedro University Hospital, Postgraduate Program of Medical Sciences of Fluminense Federal University, 303 Marquês do Paraná St, Centro, Niterói, Rio de Janeiro, Brazil. Electronic address: bragamed@yahoo.com.br.
Abstract
OBJECTIVE: To evaluate the influence of hormonal contraception (HC) on the development and clinical aggressiveness of gestational trophoblastic neoplasia (GTN) and the time for normalization of human chorionic gonadotropin (hCG) levels. METHODS: A retrospective cohort study was conducted with women diagnosed with molar pregnancy, followed at the Rio de Janeiro Trophoblastic Disease Center, between January 2005 and January 2015. The occurrence of postmolar GTN and the time for hCG normalization between users of HC or barrier methods (BM) during the postmolar follow-up or GTN treatment were evaluated. RESULTS: Among 2828 patients included in this study, 2680 (95%) used HC and 148 (5%) used BM. The use of HC did not significantly influence the occurrence of GTN (ORa: 0.66, 95% CI: 0.24-1.12, p=0.060), despite different formulations: progesterone-only (ORa: 0.54, 95% CI: 0.29-1.01, p=0.060) or combined oral contraception (COC) (ORa: 0.50, 95% CI: 0.27-1.01, p=0.60) or with different dosages of ethinyl estradiol: 15mcg (ORa, 1.33, 95% CI 0.79-2.24, p=0.288), 20mcg (ORa: 1.02, 95% CI: 0.64-1.65, p=0.901), 30mcg (ORa: 1.17, 95% CI: 0.78-1.75, p=0.437) or 35mcg (ORa: 0.77, 95% CI: 0.42-1.39, p=0.386). Time to hCG normalization ≥10weeks (ORa: 0.58, 95% CI: 0.43-1.08, p=0.071) or time to remission with chemotherapy≥14weeks (ORa: 0.60, 95% CI: 0.43-1.09, p=0.067) did not significantly differ among HC users when compared to patients using BM, when controlling for other risk factors using multivariate logistic regression. CONCLUSIONS: The use of HC during postmolar follow-up or GTN treatment does not seem to increase the risk of GTN or its severity and does not postpone the normalization of hCG levels.
OBJECTIVE: To evaluate the influence of hormonal contraception (HC) on the development and clinical aggressiveness of gestational trophoblastic neoplasia (GTN) and the time for normalization of humanchorionic gonadotropin (hCG) levels. METHODS: A retrospective cohort study was conducted with women diagnosed with molar pregnancy, followed at the Rio de Janeiro Trophoblastic Disease Center, between January 2005 and January 2015. The occurrence of postmolar GTN and the time for hCG normalization between users of HC or barrier methods (BM) during the postmolar follow-up or GTN treatment were evaluated. RESULTS: Among 2828 patients included in this study, 2680 (95%) used HC and 148 (5%) used BM. The use of HC did not significantly influence the occurrence of GTN (ORa: 0.66, 95% CI: 0.24-1.12, p=0.060), despite different formulations: progesterone-only (ORa: 0.54, 95% CI: 0.29-1.01, p=0.060) or combined oral contraception (COC) (ORa: 0.50, 95% CI: 0.27-1.01, p=0.60) or with different dosages of ethinyl estradiol: 15mcg (ORa, 1.33, 95% CI 0.79-2.24, p=0.288), 20mcg (ORa: 1.02, 95% CI: 0.64-1.65, p=0.901), 30mcg (ORa: 1.17, 95% CI: 0.78-1.75, p=0.437) or 35mcg (ORa: 0.77, 95% CI: 0.42-1.39, p=0.386). Time to hCG normalization ≥10weeks (ORa: 0.58, 95% CI: 0.43-1.08, p=0.071) or time to remission with chemotherapy≥14weeks (ORa: 0.60, 95% CI: 0.43-1.09, p=0.067) did not significantly differ among HC users when compared to patients using BM, when controlling for other risk factors using multivariate logistic regression. CONCLUSIONS: The use of HC during postmolar follow-up or GTN treatment does not seem to increase the risk of GTN or its severity and does not postpone the normalization of hCG levels.
Authors: Allison A Gockley; Lawrence H Lin; Michelle Davis; Alexander Melamed; Anthony Rizzo; Sue Yazaki Sun; Kevin Elias; Donald P Goldstein; Ross S Berkowitz; Neil S Horowitz Journal: Clinics (Sao Paulo) Date: 2021-08-27 Impact factor: 2.365
Authors: Marisa Victoria Diniz; Sue Y Sun; Claudia Barsottini; Mauricio Viggiano; Roney C Signorini Filho; Bruna Sanches Ozane Pimenta; Kevin M Elias; Neil S Horowitz; Antonio Braga; Ross S Berkowitz Journal: J Med Internet Res Date: 2018-09-24 Impact factor: 5.428