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Prospective, randomized, assessor-blind comparative trial of the effects of menopausal hormone therapy with levonorgestrel-releasing intrauterine systems and other regimens on mammographic density.


In prescribing a postmenopausal hormone therapy (HT) in women with intact uterus, progestins are essential to protect the endometrium from the development of unopposed estrogen effects. Recently, supplying the progestagenic component of therapy by intrauterine systems was introduced in clinical practice. Levonorgestrel intrauterine system (LNG-IUS) (Mirena[R], Schering, Turku, Finland) has been widely used for hormonal contraception; recently its role was expanded in continuous combined HT(CCHT). (1-3) Intrauterine progestin administration ensures lower blood levels of progestins in comparison with levels measured in oral administration. (1-3) Up to date, mammographic density changes that may occur during CCHT with LNG-IUS have not been extensively studied.

This is a prospective, randomized, assessor--blind comparative trial of CCHT with LNG-IUS and other regimens in women receiving postmenopausal HT, based on mammographic density measurements.

Material and methods

Study design

For the trial of the compared methods 77 postmenopausal women with intact uterus and climacteric symptoms were tracked; all of them were registered patients in the Menopause Clinic of Reproductive Endocrinology Department of Obstetric and Gynecology Department, Cerrahpasa Medical School, Istanbul University, between June 2003 and February 2004. The study protocol was approved by the ethical committee of the medical school before the study was initiated, and the informed consents of the patients were obtained. The study was conducted in accordance with the basic principles of the Declaration of Helsinki. The trial was registered and approved by the Hospital Scientific Committee.

Eligibility criteria

Inclusion criteria of the study were: presence of climacteric complaints, intact uterus, amenorrhea for more than 6 months, no postmenopausal HT in the last 6 months, and absence of known HT contraindications (undiagnosed vaginal bleeding, history of tromboembolic disease, active liver disease, genital cancer, migrain headache, hypersensitivity to steroid hormones).

Study protocol

The patients enrolled in the study were randomly allocated into three treatment groups: Group 1 (n:23), daily oral 0.625 mg conjugated equine estrogen (CEE) plus oral 2.5 medroxyprogesterone acetate (MPA) therapy (Premelle 2.5[R]--Wyeth, Newbridge, Ireland); Group 2 (n:30), daily oral 0.625 mg CEE (Premarin[R]--Wyeth, Newbridge, Ireland) in conjunction with LNG-IUS (Mirena[R]--Schering, Turku, Finland); and Group 3 (n:24), daily oral 2.5 mg tibolone (Livial[R]--Organon, Amsterdam, Netherland). At the beginning of the study, LNG-IUS was applied in the patients of Group 1.

I. Evaluation of Climacteric Complaints

Climacteric complaints reported by the patients were evaluated and compared either at baseline or in the 6th month of treatment according to the modified Kupperman index (4).

II. Evaluation of Mammographic Density

A baseline mammogram was performed at baseline and after 6 months of treatment at the Radiology Department of Cerrahpasa Medical School using the same medical equipment (Siemens Mammomat-3). The mammographies were obtained in standard bilateral craniocaudal and mediolateral oblique views. The mammographic density changes were evaluated and compared by an expert radiologist who was blinded to the treatment groups. The evaluations were performed according to Breast Imaging Report or Data System (BI-RADS) or on clinical evaluation system that was based on the percentage of increase in mammographic density, as explained in section III. (5)

III. Classification of Mammographic Density Increase
BI-RADS Clinical Evaluation
 (Mammographic density increase %)

1. Breast parenchyma is almost completely
replaced by fatty tissue 0-25%

2. Breast parenchyma is characterized with
increase of messy fibroglandular tissue 26-50%

3. Breast parenchyma is heterogeneous and contains
large amounts of fibroglandular tissue 51-75%

4. Breast parenchyma is dense with
fibroglandular tissue 76-100%

Endometrial Biopsies

Endometrial biopsies were obtained from all the subjects to determine the local endometrial protective effect(s) of LNG-IUS. The Pipelle (Laboratoire CCD, Paris, France) endometrial sampling method was used before any treatment and in the 6th month visit. The biopsies were studied by an expert pathologist, who was blinded to the treatment groups, from the Pathology Department of Cerrahpasa Medical School, University of Istanbul, Turkey.

Evaluation of treatment related adverse effects

Known side effects of HT on each treatment group (6) were evaluated with a questionnaire form in the 6th month visit.

Statistical analysis

The Statistical Package for Social Sciences (SPSS version 11.5) was used for the statistical analysis. Chi-square test, Fisher's exact test, and one-way ANOVA test were performed. Statistical significance was set at 0.05.


The baseline characteristics of the study population are presented in Table 1. The demographic parameters and baseline hormonal status of the study groups were similar. No significant differences were found between the baseline mammographic findings of the subjects (Table 2).

After 6 months of treatment, the baseline mammographic findings of 12 patients (52.2%) in Group1, 21 patients (70%) in Group 2, and 19 patients (79.2%) in Group 3 did not change. The breast density of 6 patients (26.1%) in Group 1, 5 patients (16.7%) in Group 2, 4 patients (16.7%) in Group 3 were higher, which was secondary to HT. There was no significant difference between the groups regarding the increase in breast parenchyma on the 6th month mammography. The changes in mammographic findings over the 6-months-study period are shown in Table 3.

Density increases observed in mammographies performed the 6th month were reevaluated according to the BI-RADS classification (Table 4). The BI-RADS categories of 6 patients (26.1%) in Group 1, 2 patients (6.7%) in Group 2, 3 patients (12.5%) in Group 3 increased. The breast densities of 3 patients (10%) in Group 2 and 1 patient (4.2%) in Group 3 minimally increased; however, BI-RADS categories of these patients did not change. The BI-RADS categories of the patients whose breast densities increased on the 6th month mammography are shown in Table 5.

Endometrial effects of the treatment were evaluated via biopsy specimens obtained at the baseline and after 6-month treatment. After 6 months of treatment, a strong endometrial suppression was found in 56% of the patients who had received oral CEE with LNG-IUS. The most relevant result of the biopsies of the patients in Group1 and Group 3 was atrophic endometrium. Endometrial hyperplasia was not observed in any of the treatment groups. The patients were asked about any adverse events after 6 months of the treatment.

HT related adverse events were recorded and compared. After 6 months of treatment, 81% of patients in Group 1; 70% of patients in Group 2; 90% of patients in Group 3 were free of any treatment related adverse events. The most frequent adverse event in each group was irregular vaginal bleeding. Two patients (8.1%) in Group1, 9 patients (30%) in Group 2, 1 patient (45%) in Group 3 had irregular vaginal bleeding in the 6th month visit. However, total compliance to treatment was achieved in 21 patients (91.3%) in Group 1, 28 patients (93.3%) in Group 2, 17 patients (73.9%) in Group 3 at the end of 6 months. There were no significant differences between the groups for the parameters of treatment related to adverse events and compliance to the treatment regimens.


After menopause, breast tissue density is normally decreased due to decreased sex hormone production from the ovaries. However, fibroglandular breast tissue is known to proliferate under HT, which is considered a risk factor for breast cancer. (7,8,9,10) Conner reported increased epithelial proliferation in the breasts of women on HT in comparison with women without any HT. (8) Yilmaz et al had previously reported increased mammographic density in 60% of women who were eventually diagnosed with breast cancer. (9) On the other hand, most of the epidemiological and observational studies have concluded that increased breast density is an undesired effect of the treatment. (11,12,13,14)

Under HT, expected involution in breast tissue due to menopause is delayed, and the breast is found to be denser in mammographic examination. (11) Diagnosis of breast tumours with high density in mammographic imaging is more difficult. (12,13) This undesired effect of HT is considered to be a risk factor for breast cancer. (12,13) To the best of our knowledge, literature reveals no studies comparing the the effects of menopausal HT in combination with LNG-IUS and classical CCHT on mammographic density. Although numerous studies have shown an apparent relationship between the menopausal HT and increased breast density, some authors have found no increase in breast density in women under HT. (15,16)

The intensity of the increase in the breast density of women under HT is mainly related to the type, route, and duration of the treatment. However, it may change depending on the age, duration of the menopause, baseline breast density, and hormonal status specific to every individual. (11,16,17) Sterns and Zee found no significant differences between the women under HT and the control group, consisted of women under the age of 55 years. (16) However, the authors reported a significant increase in the breast density of the women under HT who were over the age of 55 compared to the control group. (16) In our study, the mean duration of menopause in Group 2 was shorter than that of the other groups, but the difference was not statistically significant. The other baseline characteristics of each group were not significantly different based on baseline mammographies.

One of the factors that influence breast density in Mammographies is type of HT. Estrogen treatment (ET) alone has been suggested as having minimal effect on mamographic density than other HT regimens. (15) In two different studies conducted in 1999 and 2001, Lundstrom and Magnusson suggested that ET applied either by oral or transdermal route influenced the mammographic density by the minimal increase of 2%. (15,18) Persson et al reported a 4.2 % increase in mammographic density in women taking either oral or transdermal ET. (17)

Continuous combined HT (CCHT) is the most commonly used type of HT for menopause, and it has been suggested to show the strongest effect on mammographic density. (19,20,21) Lundstrom et al reported 33% increase in mammographic density of women taking CCHT of 0.625 mg CEE plus 2.5 mg MPA daily. (15) Similarly, Laya et al reported 24% increase in mammographic density with the same treatment. (22) Greendale et al reported 19.4% increase in mammographic density of women taking daily combination of 0.625 mg CEE plus 2.5 mg MPA in PEPI trial. (23)

Different options have been studied to avoid the problem of increase in mammographic density in women taking CCHT. Greendale et al compared different progestagenic agents used in CCHT to show their effects on mammographic density and found no significant differences in the effects of different progestagenic agents on mammographic density. (23) However, Persson et al determined that NETA, as an agent used in CCHT, affected mammographic density more than other progestagenic agents did. (17) Sendag et al reported 34.1% increase in mamographic density of women taking transdermal estrogen plus 1 mg NETA daily and 23.5% increase in women taking 0.625 mg oral CEE plus 2.5 mg MPA daily. (24) The effect of different Progestagens as a component of CCHT on mammographic density is still debated.

In this study, even though the rate of mammographic density increase was higher in the patients taking CCHT, there were no significant differences between the groups. This finding is compatible with the findings of previous studies. (17,25,26) Tibolone, which has estrogenic, progestagenic and androgenic features, (27) was suggested to be the least effective agent according to mammographic density, which has been established as risk biomarker for developing breast cancer. (21,25,28) Likewise, in our study, tibolone was determined to be less effective regarding mammographic density effects than other regimens. In agreement with our study it was shown by Kutlu et al, a 15% increase in mammographic density of women taking tibolone was determined after 1-year follow up compared to low breast density on the baseline mammograms. (29)

Increase in systemic progesterone level has been shown to induce epithelial proliferation in the breast tissue. (30) Recently, LNG-IUS was introduced as a part of CCHT. Lower systemic progestagen levels in women taking ET in conjunction with LNG-IUS have been shown. (1,2) Lundstrom et al first reported increase on mammographic density in 15% of patients under estrogen therapy combination with LNG-IUS after 18-month follow-up. (31,32)

In our study, similarly, a lower rate of increase in mammographic density was determined in the patients under HT with LNG-IUS than in the patients under CCHT; however, the difference was not statistically significant. This finding is important because it suggests that HT with LNG-IUS can be an alternative to other HT regimens to avoid the mammographic density increase, which is commonly encountered in CCHT. Limitations of our study is that we did not make a placebo-controlled trial and that we should have tracked larger series with long-term follow up.

The endometrial response to LNG-IUS had been reported as gestagen induced endometrium or atrophic endometrium. (2,3) Compatible with literature information, the endometrial biopsy results of patients in our study were strong gestagenic effect in stroma (56%) and atrophic endometrium (26%) in Group 2.

We evaluated the effectiveness of the treatment regimens regarding the climacteric complaints at the baseline and in the 6th month of the treatment measured by Modified Kupperman Index. A decrease in the Kupperman Index scores of each group was noted in the 6th month visit; however, there were no statistically significant differences between the groups. Similar to our findings, the menopause symptoms subside in HT with LNG-IUS with. (1)

Treatment related adverse effects and compliance to treatment were evaluated using a questionnaire form in the 6th month of the treatment. In general, 80% of the patients were free of any serious adverse effects in the 6th month visit. Unexpected irregular vaginal bleeding was encountered in 9 patients (30%) in Group 2, 2 patients (8.7%) in Group 1, and 1 patient (4.5%) in Group 3. The most common side effect of HT with LNG-IUS has been reported to be irregular spotting, which was found to be the most common cause of discontinuation. (1,2) The rate of irregular spotting related to the HT with LNG-IUS has been reported to be 32% after 6 months of treatment. (1) However, this adverse event did not seem to affect the patient compliance, even in Group 2. There were no differences between the groups with respect to the patient compliance to the treatment.

In conclusion, in our study we found an insignificant tendency towards a lower increase rate in mammographic density of patients under HT with LNG-IUS than those under CCHT. On the other hand, HT with LNG-IUS is effective, tolerable and appears safe for the endometrium as conventional treatment methods do. However, randomized, prospective placebo-controlled trials with larger series are needed to confirm the findings of our study.


The authors of the article would like to thank Safak Ugur for offering linguistic services for this article.

Conflict of interest: None declared.


(1.) Raudaskoski T, Tapanainen J, Tomas E, Luotola H, Pekonen F, Ronni-Sivula H, et al. Intrauterine 10 and 20 Mg levonorgestrel systems in postmenopausal women receiving oral oestrogen replacement therapy: clinical, endometrial and metabolic response. Br J Obstet Gynecol 2002;109: 136-44.

(2.) Suhonen SP, Holmstrom T, Allonen HO, Lahteenmaki P. Intrauterine and subdermal progestin administration in postmenopausal hormone replacement therapy. Fertil Steril 1995; 63:336-342.

(3.) Gunay T, Tufekci C, Ilter E, Akyol H, Ocal A. [Effectiveness of levonorgestrel-releasing intrauterin system (Mirena[R]) on the treatment of menorrhagia and simple endometrial hyperplasia without atypia]. Turkish Clinics Journal of Gynecol Obst 2007;17:7-13 [Article in Turkish].

(4.) Hauser GA, Huber IC, Keller PJ, Lauritzen C, Schneider HP. [Evaluation of climacteric symptoms (Menopause Rating Scale)]. Zentralbl Gynakol. 1994;116(1):16-23 [Article in German].

(5.) Lehman C, Holt S, Peacock S, White E, Urban N. Use of the American College of Radiology BI-RADS guidelines by community radiologists: concordance of assessments and recom-mendations assigned to screening mammograms. AJR Am J Roentgenol 2002;179(1):15-20.

(6.) Graser T, Robner P, SchubET K, Muler A, Bonisch U, Oettel MA. A comparative study of two levonorgestrel-containing hormone replacement therapy regimens on efficacy and tolerability variables. Maturitas 1997;28:169-179.

(7.) Banks E. Hormone replacement therapy and the sensitivity and specificity of breast cancer screening: a review. J Med Screen 2001;8:29-35.

(8.) Conner P, Christow A. A comparative study of breast cell proliferation during hormone replacement therapy: effects of tibolon and continuous combined estrogen-progestogen treatment. Climacteric 2004: 7(1): 50-8.

(9.) Yilmaz E, Lebe B, BalcI P, Sal S, Canda T. Comparison of mammographic and sonographic findings in typical and atypical medullary carcinomas of the breast. Clinical Radiology: 2002;57 640-45.

(10.) Conner P. Breast response to menopausal hormone therapy - aspects on proliferation, apoptosis and mammographic density. Ann Med. 2007; 39(1): 28-41.

(11.) Writing group for the Women's Health Initiative Investigators. Risks and benefits of estrogen plus progestin in healthy postmenopausal women. Principal results from the Women's Health initiative randomized controlled trial. JAMA 2002;288:321-33.

(12.) Leung W, Goldberg F, Zee B, Sterns F. Mammographic density in women on postmenopausal hormone replacement therapy. Surgery 1997; 122(4):669-74.

(13.) Laya MB, Larson EB, Taplin SH, White E. Effect of estrogen replacement therapy on the specificity and sensitivity of screening mammography. J Natl Cancer Inst 1996;88(10):643-9.

(14.) Bremnes Y, Ursin G, Bjurstam N, Lund E, Gram IT. Different types of postmenopausal hormone therapy and mammographic density in Norwegian women. Int J Cancer. 2007 ; 15; 120 (4): 880-4.

(15.) Lundstrom E, Wilczek B, von Palffy Z, Soderquist G, Von Schoultz B. Mammographic breast density during hormone replacement therapy: effects of continuous combina-tion, unopposed transdermal and low-potency estrogen regimens. Climacteric 2001;4:42-8.

(16.) Sterns EE, Zee B. Mammographic density changes in perimenopausal and postmenopausal women: is effect of hormone replacement therapy predictable. Breast Cancer Res Treat 2000;59:125-32.

(17.) Persson I, Thurfjell E, Holmberg L. Effect of estrogen and estrogen-progestin replacement regimens on mammographic breast parenchymal density. J Clin Oncol 1997;15(10):3201-7.

(18.) Magnusson C, Baron JA, Correira N. Breast cancer risk following long term oestrogen and oestrogen-progestin replacement therapy. Int J Cancer 1999;31:339-44.

(19.) Sendag F, Ozsener S, Oztekin K, Bilgin O. Continuous combined hormone replacement therapy regimens and mammographic density changes . Turkish Clinics Journal of Gynecol Obst 2003;13:199-204 [Article in Turkish].

20. Persson I, Thurfjell E, Holmberg L. Effect of estrogen and estrogen-progestin replacement regimens on mammographic breast parenchymal density. J Clin Oncol 1997;15(10):3201-7.

(21.) Marchesoni D, Driul L, Ianni A, Fabiani G, Della Martina M, Zuiani C, Bazzocchi M. Postmenopausal hormone therapy and mammographic breast density. Maturitas 2006;53 (1): 59-64.

(22.) Laya MB, Gallagher JC, Schreiman JS, Larson EB, Watson P, Weinstein L. Effect of postmenopausal replace-ment therapy on mammographic density and parenchymal pattern. Radiology 1995;196:433-7.

(23.) Greendale GA, Reboussin BA, Sie A, Singh R, Olson LK, Gatewood O, et al. Effects of estrogen and estrogen-progestin on mammographic parenchymal density. Ann Intern Med 1999:130:262-9.

(24.) Sendag F, Terek MC, Ozsener S, Oztekin K, Bilgin O, Bilgen I, et al. Mammographic density changes during different postmenopausal hormone replacement therapies. Fertil Steril 2001;76:445-50.

(25.) Erel CT, Elter K, Akman C, Ersavasti G, Altug A, Seyisoglu H, et al. Mammographic changes in women receiving tibolone therapy. Fertil Steril 1998;69:970-875.

(26.) Marugg RC, van der Mooren MJ, Hendriks JHCL, Rolland R, Ruijs SHJ. Mammographic changes in post-menopausal women on hormonal replacement therapy. Eur Radiol 1997;7:749-55.

(27.) Moore RA. Livial: a review of clinical studies. Br J Obstet Gynaecol 1999; 106 (Suppl.19) : 1-21.

(28.) Erel C.T, Esen G, Seyisoglu H, Elter K, Uras C,Ertungealp E et al. Mammographic density increase in women receiving different hormone replacement regimens. Maturitas 2001; 40:2:151-57.

(29.) Kutlu T, Ficicioglu C, Basaran T, Basaran E, Topaloglu T. Mammographic breast density changes after 1 year of tibolon use. Maturitas 2004; 48 :133- 36

(30.) Soderqvist G, Isaksson E, von Schoultz B, Carlstrom K, Tani E, Skoog. Proliferation of breast epithelial cells in healthy women during the menstrual cycle. Am J Obstet Gynecol 1997;176:123-8.

(31.) Wollter-Svensson LO, Stadberg E, Andersson K, Andersson K, Mattsson LA, Odlind V, et al. Intrauterine administration of levonorgestrel 5 and10 microg/24 hours in perimenopausal hormone replacement therapy. A randomized clinical study during one year. Acta Obstetricia et Gynecologica Scandinavica 1997; 76: 449-454.

(32.) Lundstrom E, Soderqvist G, Svane G, Azavedo E, Olovsson M, Skoog L, et al. Digitized assessment of mammographic breast density in patients who received low-dose intrauterine levonorgestrel in continuous combination with oral estradiol valerate: a pilot study. Fertil Steril. 2006;85(4):989-95.

Yavuz Simsek [1], Altay Gezer [2], Levent Senturk [2], Seyfettin Uludag [2]

[1] Dr.Zekai Tahir Burak Women's Health Training and Research Hospital, Ankara,Turkey

[2] University of Istanbul Cerrahpasa Medical Faculty, Department of Obstetrics and Gynecology, Cerrahpasa, Istanbul, Turkey

Corresponding Author:

Yavuz Simsek, M.D.

Specialist in Obstetrics and Gynecology

Dr.Zekai Tahir Burak

Training and Research Hospital, Ankara, Turkey

Hospital phone: 0090 312 306 51 48

Fax: 0090 312 306 50 00

Table 1. The Baseline characteristics and variable measurements
of subjects

 Group-1 n=23 Group-2 n=30
 mean [+ or -] SD mean [+ or -] SD

 Age 49 [+ or -] 4.7 48 [+ or -] 4.9
 (40-58) (34-58)

Duration of 26 [+ or -] 33.8 15 [+ or -] 26.3
 Menopause (6-120) (6-120)

Pregnancies 4 [+ or -] 2.1 4 [+ or -] 2.4
 (0-8) (1-12)

 Births 3 [+ or -] 1.6 3 [+ or -] 1.3
 (0-7) (0-7)

 Kupperman 25 [+ or -] 7.0 22 [+ or -] 7.7
 Menopausal (11-35) (8-39)

BMI (kg/m2) 28 [+ or -] 5.1 30 [+ or -] 4.8
 (20-38) (23-44)

 FSH 66 [+ or -] 22.8 58 [+ or -] 23.9
 (28-106) (8-110)

 LH 28 [+ or -] 11.5 25 [+ or -] 15.9
 (10-51) (2-61)

 Estradiol 19 [+ or -] 12.4 39 [+ or -] 81.8
 (10-69) (9-464)

Progesterone 0.5 [+ or -] 0.1 0.5 [+ or -] 0.1
 (0.1-0.84) (0.1-0.9)

 Group-3 n=24 Whole subjects
 mean [+ or -] SD mean [+ or -] SD

 Age 50 [+ or -] 5.2 49 [+ or -] 4.9

Duration of 43 [+ or -] 52.8 28 [+ or -] 39.5
 Menopause (6-216)

Pregnancies 4 [+ or -] 2.4 4 [+ or -] 2.2

 Births 3 [+ or -] 1.7 3 [+ or -] 1.5

 Kupperman 25 [+ or -] 6.9
 Menopausal (11-35) 24 [+ or -] 7.3

BMI (kg/m2) 28 [+ or -] 5.1 29 [+ or -] 5.0

 FSH 63 [+ or -] 27.0 58 [+ or -] 25.6

 LH 26 [+ or -] 12.9 27 [+ or -] 13.7

 Estradiol 13 [+ or -] 5.3 25 [+ or -] 52.4

Progesterone 0.5 [+ or -] 0.1 0.5 [+ or -] 0.1


 Age 0.365

Duration of 0.052

Pregnancies 0.939

 Births 0.933

 Menopausal 0.233

BMI (kg/m2) 0.222


 LH 0.727

 Estradiol 0.154

Progesterone 0.415

(BMI: Body mass index)

Table 2. Baseline mammographic findings

 Group I

 MAMOGRAPHIC Replaced with fatty N 15
 FINDINGS tissue % 65.2

 Dense breast N 3
 parenchyma % 13.0

 Macrocalcificetion N 0
 % 0

 Microcelcificetion N 1
 % 4.3

 Benign nodule N 0
 % 0

 Fibrocystic pattern N 2
 % 8.7

 Asymmetrical N 1
 density increase % 4.3

 Punctate calcrfica- N 1
 don % 4.3

 Whole N 23
 subjects % 100.0

 Group II Group III

 Replaced with fatty N 18 14
 tissue % 60.0 58.3

 Dense breast N 6 3
 parenchyma % 20.0 12.5

 Macrocalcificetion N 0 1
 % 0 42

 Microcelcificetion N 0 1
 % 0 4.2

 Benign nodule N 1 2
 % 3.3 8.3

 Fibrocystic pattern N 3 3
 % 10.0 12.5

 Asymmetrical N 2 0
 density increase % 6.7 0

 Punctate calcrfica- N 0 0
 don % 0 0

 N 30 24
 % 100.0 100.0

 Whole Subjects

 Replaced with fatty N 47
 tissue % 61.0

 Dense breast N 12
 parenchyma % 15.6

 Macrocalcificetion N 1
 % 1.3

 Microcelcificetion N 2
 % 2.6

 Benign nodule N 3
 % 3.9

 Fibrocystic pattern N 8
 % 10.4

 Asymmetrical N 3
 density increase % 3.9

 Punctate calcrfica- N 1
 don % 1.3

 N 77
 % 100.0

p = 0,73

Table 3. Mammographic findings at the 6th month of treatment

 Group I Group II
 n=23 n=30

Mamogrophy No difference N 12 21
 % 52.2 70.0

 Increased breast
 N 6 5
 density % 26.1 16.7

 Distordon N 1 0
 % 4.3 0

 Nodule N 1 2
 % 4.3 6.7

 Asymmetric density N 1 0
 % 4.3 0

 Dense parenchyma N 2 2
 % 8.7 6.7

Total N 23 30
 % 100.0 100.0

 Group III Total

 No difference N 19 52
 % 79.2 67.5

Increased breast
 density N 4 15
 % 16.7 19.5

 Distordon N 0 1
 % 0 1.3

 Nodule N 0 3
 % 0 3.9

Asymmetric N 0 1
density % 0 1.3

Dense parenchyma N 1 5
 % 42 6.5

 N 24 77
 % 100.0 100.0

p = 0,565

Table 4. Distribution of the increased breast densities according
to the BI-RADS system

BI-RADS Group I Group II
 n=23 n=30
 Increased density
 which made N 6 2
 BI-RADS categories % 26.1 6.7

 Minimally increased N 0 3
 denstity % 0 10

Total N 6 5
 % 26,1 16,7

 Group III Total
 Increased density
 which made N 3 11
 BI-RADS categories % 12.5 14.3

 Minimally increased N 1 4
 denstity % 4.2 5.1

 N 4 15
 % 16,7 19,5

p = 0,260

Table 5. The baseline and 6th month BIRADS categories of the patients
with increased density on the 6th month mammography

BIRDS category Group 1 (n=6) Group 2 (n=5)

 N n n n
 Baseline 6th month Baseline 6th month
BIRDS 1 1 1
BIRDS 2 6 4 2
BIRDS 3 6 2

BIRDS category Group 3 (n=4)

 N N
 Baseline 6th month
BIRDS 2 2 3
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Title Annotation:Original Article--Clinical Trial
Author:Simsek, Yavuz; Gezer, Altay; Senturk, Levent; Uludag, Seyfettin
Publication:Experimental Medicine
Article Type:Report
Geographic Code:7TURK
Date:Jan 1, 2009
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