Progestagen supplementation of exogenous oestrogens and risk of endometrial cancer

Voigt, Lynda F.; Weiss, Noel S.; Chu, Joseph; Daling, Janet R.; McKnight, Barbara; Belle, Gerald van

doi:10.1016/0140-6736(91)90417-n

Cited by 258 publications

(51 citation statements)

References 15 publications

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“…The commonly used estrogen preparations are conjugated equine estrogen and natural estradiol in micronized form, and the most commonly used progesterone is medroxyprogesterone acetate (MPA). Combined estrogen/progesterone HRT is widely prescribed to millions of women (17)(18)(19). It is used in either cyclic or continuous fashion.…”

Section: Hormone Replacement Therapymentioning

confidence: 99%

Hormonal Pathology of the Endometrium

2000

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The endometrial tissue is a sensitive target for steroid sex hormones and is able to modify its structural characteristics with promptness and versatility. This article discusses briefly endogenous hormonal effects (cyclic changes, luteal phase defect, unopposed estrogen effect) and describes the histologic patterns encountered in the most commonly used hormone therapies: oral contraceptives, ovulation stimulation, hormone replacement therapy, and antitumoral hormone therapy.Oral contraceptives exert a predominant progestational effect on the endometriun, inducing an arrest of glandular proliferation, pseudosecretion, and stromal edema followed by decidualized stroma with granulocytes and thin sinusoidal blood vessels. Prolonged use results in progressive endometrial atrophy.Ovulation induction therapy accelerates the maturation of the stroma and is often associated with a discrepancy between early secretory glands and an edematous or decidualized stroma with spiral arterioles.Hormone replacement therapy with estrogen alone may result in continuous endometrial proliferation, hyperplasia, and neoplasia. The use of both estrogen and progesterone elicits a wide range of histologic patterns, seen in various combinations: proliferative and secretory changes, often mixed in the same tissue sample; glandular hyperplasia (in polyps or diffuse) ranging from simple to complex atypical; stromal hyperplasia and/or decidual transformation; epithelial metaplasia (eosinophilic, ciliated, mucinous); and inactive and atrophic endometrium.Progesterone therapy for endometrial hyperplasia and neoplasia induces glandular secretory changes, decidual reaction, and spiral arterioles. Glandular proliferation is usually arrested, but neoplastic changes may persist and coexist with secretory changes.Lupron therapy produces a shrinking of uterine leiomyomas by accelerating their hyaline degeneration, similar to that in postmenopausal involution. It generally produces endometrial atrophy.Tamoxifen for breast carcinoma has an estrogenagonist effect on the uterus in approximately 20% of patients, who develop endometrial polyps, glandular hyperplasia, adenomyosis, and/or leiomyomata. Both endometrioid and nonendometrioid carcinomas are seen, often in polyps. Their causal relationship to tamoxifen therapy is debatable. Mod Pathol 2000;13(3):285-294Hormone therapy is widely used throughout the world by women of all ages for a variety of reasons, ranging from oral contraception and ovulation stimulation for family planning to hormone replacement therapy in menopause, to adjuvant therapy of tumors of the breast and uterus. The histopathologic changes of the uterus, and particularly of the endometrium, associated with these therapies encompass a variety of morphologic features that are often difficult to interpret. The endometrium is a sensitive target tissue for steroid sex hormones and is able to modify its structural characteristics with promptness and versatility. The physiologic changes of the endometrium during reproductive life and after men...

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Section: Hormone Replacement Therapymentioning

confidence: 99%

Hormonal Pathology of the Endometrium

2000

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“…Neste estudo, o uso de estrógenos sem oposição por progestínico aumentou o risco de carcinoma do endométrio em 2,2 (IC95%: 1,2-4,4) vezes, enquanto a combinação com progesterona exibia risco similar aos controles: 0,9 (IC95%: 0,4-2,0) 12 . Em 1991, Voight et al 13 publicaram um estudo caso-controle avaliando o efeito de progestí-nicos exógenos sobre a incidência de câncer de endométrio entre usuários de estrógenos para reposição hormonal. O grupo caso foi composto por 158 mulheres entre 40 e 64 anos com diagnóstico de câncer de endométrio identificados nos anos de 1985 a 1987 residentes do Estado de Washington.…”

Section: Esquemas Usados Para Reposição Hormonalunclassified

Terapia de reposição hormonal e o câncer do endométrio

Júnior

Athanazio

2007

Cad. Saúde Pública

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A reposição hormonal para alívio dos sintomas menopausais é amplamente utilizada em todo o mundo. A evolução do conhecimento sobre os riscos deste tratamento sempre foi mais lenta do que sua aplicação na prática clínica. Na década de 70, um aumento de incidência de câncer do endométrio ocorreu nos países desenvolvidos sendo que a terapia de estrógenos exógenos na menopausa foi o principal fator relacionado. Nas décadas de 80 e 90, a combinação entre estrógenos e progestínicos passou a ser largamente utilizada com base na premissa de que apresentava efeitos benéficos sobre os sistemas cardiovascular e osteoarticular, sem aumento no risco de câncer uterino. Entretanto, relatos recentes novamente questionam a segurança da reposição hormonal e, desta vez, apontam para o risco maior de câncer total e doença cardiovascular nos esquemas combinados. Concluímos neste trabalho que os riscos recentemente relacionados à terapia combinada têm grande potencial de impacto na Saúde Pública, e este esquema não é indicado para proteção do risco de carcinoma endometrial uma vez que seus riscos superam os benefícios.

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“…EPT does not increase the risk of endometrial cancer, with a relative risk of 0.71 (95% CI: 0.56-0.90) compared to non-HRT patients (46). Therefore, the preferred regimen in these patients is EPT, comprising 0.625 mg of conjugated estrogen daily and 5-10 mg of medroxyprogesterone acetate for ≥10 days over 28 days (47). However, EPT may increase the risk of breast cancer and HRT in patients with breast cancer may induce tumor cell proliferation; therefore, its use is contraindicated (24).…”

Section: Complications and Surveillance Following Rrsmentioning

confidence: 99%

Risk-reducing surgery in hereditary gynecological cancer: Clinical applications in Lynch syndrome and hereditary breast and ovarian cancer

Adachi

Banno

Yanokura

et al. 2014

Molecular and Clinical Oncology

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Abstract. Risk-reducing surgery (RRS) is defined as a prophylactic approach with removal of organs at high risk of developing cancer, which is performed in cases without lesions or absence of clinically significant lesions. Hereditary gynecological cancers for which RRS is performed include hereditary breast and ovarian cancer (HBOC) and Lynch syndrome. For HBOC, RRS in the United States (US) is recommended for women with mutations in the breast cancer susceptibility (BRCA)1 and BRCA2 genes and bilateral salpingo-oophorectomy (BSO) is generally performed. This procedure may reduce the risk of breast, ovarian, Fallopian tube and primary peritoneal cancer, although ovarian deficiency symptoms occur postoperatively. For Lynch syndrome, RRS in the US is considered for postmenopausal women or for women who do not desire to bear children and BSO and hysterectomy are usually performed. This approach may reduce the risk of endometrial and ovarian cancer, although ovarian deficiency symptoms also occur. For RRS, there are several issues that must be addressed to reduce the risk of cancer development in patients with HBOC or Lynch syndrome. To the best of our knowledge, this is the first review to discuss RRS with a focus on hereditary gynecological cancer. IntroductionHereditary gynecological cancers include ovarian cancer associated with hereditary breast and ovarian cancer (HBOC); endometrial and ovarian cancer associated with Lynch syndrome; endometrial, cervical and ovarian cancer associated with Peutz-Jeghers syndrome; and ovarian cancer associated with Cowden disease. HBOC is an autosomal dominant hereditary disease that may cause breast, ovarian, Fallopian tube and peritoneal cancer.Mutations of the breast cancer susceptibility (BRCA)1 and BRCA2 genes have been identified in ~8-13% of patients with ovarian cancer (1,2). By the age of 70 years, the estimated risks of developing ovarian cancer are 35-60 and 10-27% in BRCA1 and BRCA2 mutation carriers, respectively (2). The mean ages at diagnosis of ovarian cancer are 54, 62 and 63 years for BRCA1 and BRCA2 mutation carriers and non-carriers, respectively, indicating that BRCA1 mutation carriers are more likely to be affected by ovarian cancer at a younger age (3). Clinicopathologically, the majority of ovarian cancers that are BRCA1/2 mutation-positive are of serous histology and are poorly differentiated (grade 3) stage III-IV tumors, according to the International Federation of Gynecology and Obstetrics (FIGO) staging criteria, as defined in 1988 (4,5). In BRCA1/2 mutation-positive and -negative cases, the rates of serous adenocarcinoma are 63-86 and 57-58%, those of poorly differentiated tumors 68-87 and 48-58% and those of stage III-IV tumors 72-88 and 62-70%, respectively.Lynch syndrome, also referred to as hereditary non-polyposis colorectal cancer, is an autosomal dominant hereditary disease that may lead to colorectal, endometrial, gastric and ovarian cancer. Lynch syndrome is caused by germline mutations in DNA mismatch repair (MMR) genes, which include mu...

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Progestagen supplementation of exogenous oestrogens and risk of endometrial cancer

Cited by 258 publications

References 15 publications

Hormonal Pathology of the Endometrium

Hormonal Pathology of the Endometrium

Terapia de reposição hormonal e o câncer do endométrio

Risk-reducing surgery in hereditary gynecological cancer: Clinical applications in Lynch syndrome and hereditary breast and ovarian cancer

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