Effects of hormone replacement therapy regimens on mammographic breast density: The role of progestins

Topal, Naile Bolca; Ayhan, Serdal; Topal, Uğur; Bilgin, Tufan

doi:10.1111/j.1447-0756.2006.00402.x

Cited by 26 publications

(24 citation statements)

References 23 publications

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“…These observations are in line with numerous earlier studies showing similar significant increases in breast density with treatment with continuously combined estrogen plus progestin [18][19][20][21][22][23][24] . Increases in breast density cannot be related to one particular combination or progestin per se, because similar observations were reported from trials testing combinations with norethisterone acetate, medroxyprogesterone acetate or micronized progestin 18,23,25 .…”

Section: Clinical Aspectssupporting

confidence: 93%

Parallel assessment of the impact of different hormone replacement therapies on breast density by radiologist- and computer-based analyses of mammograms

et al. 2008

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Section: Clinical Aspectssupporting

confidence: 93%

Parallel assessment of the impact of different hormone replacement therapies on breast density by radiologist- and computer-based analyses of mammograms

et al. 2008

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“…Breast cancer is a multifactorial disease which is believed to be related to a number of risk factors such as age, nulliparity or first pregnancy at older age, genetic predisposition (BRCA1, BRCA2), personal and family history of breast cancer, previous abnormal biopsy results, mammographic density, obesity, radiation, early onset of menarche, alcohol, smoking, and hormone therapy [22,35,39,46,72]. After age and BRCA1/2 genetic predisposition, high mammographic density is the third largest population risk factor for subsequent development of in situ or invasive carcinoma ( [8,9,49].…”

Section: Possible Relationship Of Ccls To Mammographic Densitymentioning

confidence: 99%

Are columnar cell lesions the earliest histologically detectable non-obligate precursor of breast cancer?

Turashvili¹,

Hayes

Watson³

et al. 2008

Virchows Arch

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Columnar cell lesions (CCLs) are one of the most common abnormalities in the adult female human breast, characterized by the presence of columnar-shaped epithelial cells lining enlarged terminal-duct lobular units. CCLs are being seen increasingly in core biopsies taken for the non-palpable calcifications. The increased incidence may reflect improved delineation and recognition of CCLs by pathologists or a true increase in incidence related to biological and/or environmental factors. Columnar cell-like lesions have been described under a variety of names such as blunt duct adenosis, flat epithelial atypia, and ductal intraepithelial neoplasia type DIN1a. The current histologic classification used by some pathologists divides them into simple columnar cell change and columnar cell hyperplasia, both of which can occur with or without atypia. Columnar cells lack mature luminal or basal/myoepithelial phenotype markers, but they are usually positive for estrogen receptor-alpha. The cellular origin of CCLs and their possible relationship to either expansion or metaplasia of a preexisting normal cell phenotype remains unclear. CCLs are frequently associated with lobular and ductal in situ tumors and invasive lobular and tubular carcinomas. The relationship and natural history of CCLs to invasive ductal carcinoma is enigmatic, but they may prove of clinical relevance when detected by screening mammography.

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“…111 Interestingly, there also seems to be a dose dependency for HRT as shown in a study where increased risk was observed in 60% of those receiving higher doses of progestin compared with 16.7% in those receiving a lower dose. 3 Increased risk has also been reported to be dependent on regimens, i.e. higher in those using cc HRT (39%) compared with those using cyclic HRT (15%) or unopposed oestrogen (<5%).…”

Section: Breast Cancermentioning

confidence: 96%

“…increased risk for coronary heart disease (CHD), breast cancer, venous thromboembolism (VTE) and stroke. 2 Interestingly, some literature indicate at least for some of the caveats, a dose dependency for HRT, [3][4][5][6][7][8] as well as a dependency of the particular type of hormone used. 6,[8][9][10] We review the literature on these issues and the rationale behind recommendations from authorities 11,12 and menopause societies 13,14 that women deemed in need of HRT should receive the lowest possible dose of oestrogen and progestogen.…”

Section: Introductionmentioning

confidence: 98%

Rationale for low-dose systemic hormone replacement therapy and review of estradiol 0.5 mg/NETA 0.1 mg

Johansen

Qvigstad

2008

Adv Therapy

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The menopausal transition is associated with several symptoms, for which both non-pharmacological and pharmacological measures are available to provide relief. However, present knowledge indicates that the former is not highly effective, and that the latter, in terms of systemic oestrogen and progestogen-based hormone replacement therapy (HRT), although being effective (e.g. on vasomotor symptoms, bleeding control, bone mineral density, vaginal atrophy and quality of life), can be associated with some caveats. Amongst these are an increased risk for coronary heart disease, breast cancer, venous thromboembolism and stroke. In recent years, literature has indicated a dose dependency for HRT on some of the caveats, hence authorities (Food and Drug Administration, and the European Medicines Agency) and menopause societies (International Menopause Society and North American Menopause Society) now recommend that women deemed in need of HRT should receive the lowest possible dose without compromising the effect of symptom relief. Estradiol 0.5 mg/norethisterone acetate (NETA) 0.1 mg, despite being a lower dose than conventional hormones, is a compound, among a few other low-dose options, that can be used in such therapy. As a first-line oral option, it has demonstrated its effectiveness (which seems comparable to other compounds), with high tolerability and, apparently, no safety concerns, in a 6-month study. Further long-term clinical trials and observational studies are mandatory in order to capture any potential harm as well as to elucidate this compound's full potential. Following a thorough literature search using PubMed and MEDLINE from the earliest publication dates through to January 2008, including results from various types of clinical trials and statements on HRT, we review the rationale for these recommendations. We also review the effects and safety of a novel 'ultra-low-dose' oral continuous combined HRT tablet, estradiol 0.5 mg/NETA 0.1 mg.

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Effects of hormone replacement therapy regimens on mammographic breast density: The role of progestins

Abstract: Postmenopausal HRT may increase mammographic breast density. Breast density appears to be mostly affected by higher doses and continuous administration of progestin.

Cited by 26 publications

References 23 publications

Parallel assessment of the impact of different hormone replacement therapies on breast density by radiologist- and computer-based analyses of mammograms

Parallel assessment of the impact of different hormone replacement therapies on breast density by radiologist- and computer-based analyses of mammograms

Are columnar cell lesions the earliest histologically detectable non-obligate precursor of breast cancer?

Rationale for low-dose systemic hormone replacement therapy and review of estradiol 0.5 mg/NETA 0.1 mg

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