Ovarian cyst formation in patients using tamoxifen for breast cancer

OBJECTIVE: The purpose of this study was to evaluate patient-related parameters that determine ovarian cyst formation in women using tamoxifen for breast cancer. METHODS: A retrospective review of tamoxifen-treated women with breast cancer who were followed up in the outpatient clinic at Ankara Oncology Hospital between January 2002 and December 2004 was performed. Tamoxifen doses and duration, post-treatment menstrual function, adjuvant therapy, ultrasonographic and hormonal [follicle-stimulating hormone and serum estradiol (E(2))] data, details of gynecologic surgical procedure and histopathology were recorded. RESULTS: Twenty-nine of 150 tamoxifen-treated patients (19.3%) had ovarian cysts. Cysts were detected in 28 of 57 pre-menopausal women (49.1%) and 1 of 93 post-menopausal women (1.1%). Patients with ovarian cysts had higher serum E(2) levels compared with patients without cysts (24 versus 345 pg/ml; P < 0.001). Patients with ovarian cysts had <1 year amenorrhoea duration (P < 0.001) compared with the patients without cysts. Adjuvant standard chemotherapy did not have relationship between the development of ovarian cysts. Multivariant analysis showed that cyst development is related to high E(2) levels (P < 0.05). CONCLUSIONS: Patients still having a menstrual cycle during tamoxifen had high risk (58.33%) of developing ovarian cysts. We have described an association between pre-menopausal patients using tamoxifen with high E(2) level and ovarian cyst enlargement.     

Ovarian failure after adjuvant chemotherapy is associated with rapid bone loss in women with early-stage breast cancer.

PURPOSE: We sought to evaluate the effects of chemotherapy-induced ovarian failure on bone loss and markers of skeletal turnover in a prospective longitudinal study of young women with breast cancer receiving adjuvant chemotherapy. PATIENTS AND METHODS: Forty-nine premenopausal women with stage I/II breast cancers receiving adjuvant chemotherapy were evaluated within 4 weeks of starting chemotherapy (baseline), and 6 and 12 months after starting chemotherapy with dual-energy absorptiometry and markers of skeletal turnover osteocalcin and bone-specific alkaline phosphatase. Chemotherapy-induced ovarian failure was defined as a negative pregnancy test, greater than 3 months of amenorrhea, and a follicle-stimulating hormone > or = 30 MIU/mL at the 12-month evaluation. RESULTS: Among the 35 women who were defined as having ovarian failure, highly significant bone loss was observed in the lumbar spine by 6 months and increased further at 12 months. The median percentage decrease of bone mineral density in the spine from 0 to 6 months and 6 to 12 months was -4.0 (range, -10.4 to +1.0; P =.0001) and -3.7 (range, -10.1 to 9.2; P =.0001), respectively. In contrast, there were no significant decreases in bone mineral density in the 14 patients who retained ovarian function. Serum osteocalcin and bone specific alkaline phosphatase, markers of skeletal turnover, increased significantly in the women who developed ovarian failure. CONCLUSION: Chemotherapy-induced ovarian failure causes rapid and highly significant bone loss in the spine. This may have implications for long-term breast cancer survivors who may be at higher risk for osteopenia, and subsequently osteoporosis. Women with breast cancer who develop chemotherapy-induced ovarian failure should have their bone density monitored and treatments to attenuate bone loss should be evaluated.     

Successful co-treatment with LHRH-agonist for ovarian over-stimulation and cystic formation in premenopausal tamoxifen exposure.

The present study evaluates the potential beneficial effect of co-treatment with LHRH-agonist in resolving premenopausal tamoxifen's induced supraphysiological serum 17beta estradiol levels and persistent ovarian cysts. Ultrasonographic and serum hormonal evaluations were performed before, during, and following three consecutive injections of long acting LHRH-agonist administered to 14 premenopausal breast cancer patients treated with tamoxifen, who had supraphysiological serum 17beta estradiol levels and simultaneous persistent ovarian cysts. Within 3 weeks of the first LHRH-agonist injection, all patients had menopausal serum estradiol levels. Ovarian cysts completely disappeared within 2 months following the first injection. Following the discontinuation of LHRH-agonist co-treatment, serum estradiol levels remained in physiological levels and the ovaries remained a normal size in 64.3% of the patients for 13.3 +/- 11.5 months. 28.6% of the patients had a gradual reappearance of high serum estradiol levels and of ovarian cysts, and were, therefore, treated with a second course of LHRH-agonist. Following the second course, serum estradiol levels remained in physiological levels and the ovaries remained a normal size for 8-15 months. It is concluded that short duration of co-treatment with long acting LHRH-agonist administered to premenopausal breast cancer patients treated with tamoxifen, successfully resolved the tamoxifen-induced supraphysiological serum 17beta estradiol levels and the ovarian cysts.     

Ovarian cysts in women receiving tamoxifen for breast cancer

Tamoxifen is a nonsteroidal anti-oestrogen with gynaecological side-effects. Only recently, ovarian cyst formation during tamoxifen treatment has been reported. The present study aimed to evaluate patient-related parameters that determine ovarian cyst formation in women using tamoxifen for breast cancer. A cross-sectional study was performed in 142 breast cancer patients using tamoxifen. Forty-five patients were also examined prior to tamoxifen treatment. Gynaecological assessment, transvaginal ultrasonography (TVU) and serum oestradiol (E2) and follicle stimulating hormone (FSH) analysis were performed. Follow-up assessments were performed twice a year. Uni- or bilateral ovarian cysts were detected by TVU in 24 tamoxifen-using patients and in one patient before tamoxifen treatment. Multiple regression analysis showed that cyst development is related (multiple R = 0.73) to high E2 (P < 0.001), younger age (P < 0.001) and absence of high-dose chemotherapy (P = 0.007). Patients with ovarian cysts had higher serum E2 levels compared to patients without cysts (1.95 vs 0.05 nmol l(-1); P < 0.001). All patients after high-dose chemotherapy or older than 50 years had E2 < 0.10 nmol l(-1) and/or amenorrhoea > 1 year and did not develop ovarian cysts. Patients still having a menstrual cycle during tamoxifen had a high chance (81%) of developing ovarian cysts. Breast cancer patients receiving tamoxifen only develop ovarian cysts if their ovaries are able to respond to FSH stimulation as shown by E2 production.     

Ovarian ablation for premenopausal breast cancer: A review of treatment considerations and the impact of premature menopause

Historically, ovarian ablation (OA) was used as therapy for women with recurrent hormone-receptor-positive (HRP) premenopausal breast cancer. With the publication of the SOFT (Suppression of Ovarian Function Trial) and TEXT (Tamoxifen and Exemestane Trial) randomized trials, there is considerable interest in OA as an adjuvant treatment, either in combination with tamoxifen or an aromatase inhibitor (AI). Thus, we have reviewed current guidelines and key studies on this important topic and have highlighted the relevant biological and pharmacological aspects of the various endocrine therapies. The results of two key randomized trials addressing the use and controversies of OA in premenopausal breast cancer are discussed and recent research emphasizing the detrimental consequences of premature menopause and the cost-effectiveness of OA is presented. In low-risk patients with HRP premenopausal breast cancer, OA is not beneficial and tamoxifen remains the anti-hormone treatment of choice. In high-risk women (previous chemotherapy or women younger than 35), OA in combination with AI is more effective but is arguably not cost-effective, particularly when OA is achieved medically using a GnRH agonist/antagonist. Compared to tamoxifen alone, the SOFT trial showed a 4.5–7.7% reduction in breast cancer relapse using OA (in combination with either tamoxifen or AI) in high-risk women, though the 5-year overall survival benefit was limited (1.4–3.6%). Premature menopause is associated with long-term mortality risks and women often experience significant menopausal symptoms that impact on quality of life. These considerations should play a role in the treatment selection of those patients who may benefit from adjuvant OA.     

Alteration of endocrine parameters in premenopausal women with breast cancer during long-term adjuvant therapy with tamoxifen as the single agent

Tamoxifen is used to treat selected patients at each stage of breast cancer. Although most clinical experience has been obtained with postmenopausal women, increasing numbers of premenopausal women will be treated with 5 or more years of adjuvant tamoxifen therapy following surgery. Indeed, the proposed use of tamoxifen to prevent breast cancer in high-risk women could result in its extended use during the childbearing years. We have monitored the changes in circulating hormone levels from the ovary and pituitary gland in premenopausal (41-47 years old) women with stage I or II breast cancer during adjuvant therapy with tamoxifen as the single agent for 4-72 months following a mastectomy. Each patient (total eight) continued to menstruate, and ovulation occurred. Circulating levels of luteinizing hormone and follicle-stimulating hormone (except in one woman) remained in the normal range (determined in 12 regularly menstruating women in a control group). The levels of estradiol, estrone, and progesterone were elevated onefold to threefold. Prolactin levels decreased by 30%-40%, but the levels of sex hormone binding-globulin were unaffected. These data demonstrate that premenopausal women taking tamoxifen are potentially at risk for pregnancy and must be counseled about barrier contraception. Furthermore, the impact of many years of ovarian stimulation by tamoxifen must be evaluated, especially in women with node-negative disease or in healthy women in whom tamoxifen is used to prevent breast cancer.     

Ovarian cancer risk in premenopausal and perimenopausal women treated with Tamoxifen: a case-control study

As tamoxifen stimulates ovarian steroidogenesis in premenopausal women, induces ovulation and increases the incidence of benign ovarian cysts, there has been concern that it might also increase ovarian cancer risk in women treated premenopausally. In a national case-control study in Britain, treatment histories were collected for 158 cases of ovarian cancer after breast cancer diagnosed at ages under 55 years and 464 controls who had breast cancer at these ages without subsequent ovarian cancer. Risk of ovarian cancer was not raised for women overall who had taken tamoxifen (odds ratio (OR)=0.9, 95% confidence interval (CI) 0.6-1.3) or for those treated when premenopausal (OR=1.0, 95% CI 0.6-1.6) or perimenopausal (OR=0.7, 95% CI 0.2-2.4). There was also no relation of risk to daily dose, duration or cumulative dose of tamoxifen, or time since last use. There was, however, a significantly raised risk in relation to non-hormonal chemotherapy. The results suggest that tamoxifen treatment of premenopausal or perimenopausal women does not materially affect ovarian cancer risk, but that non-hormonal chemotherapy might increase risk.     

Duration of tamoxifen effect on lipidemic profile of postmenopausal breast cancer patients following deprivation of treatment

OBJECTIVE: It was the aim of this study to investigate the effect of tamoxifen withdrawal on markers of lipid metabolism in postmenopausal women with breast cancer who completed tamoxifen therapy and received no further treatment. METHODS: Lipidemic profile changes were studied in 190 postmenopausal patients with operable breast cancer, following cessation of 5-7 years of tamoxifen treatment. Assessments of total cholesterol, high-density lipoprotein, low-density lipoprotein and total serum triglycerides were performed at baseline, 6 months and 12 months. RESULTS: By 6 months, both total cholesterol and low-density lipoprotein levels were significantly increased, and total triglyceride levels were significantly reduced compared with baseline values and maintained to 12 months. There was no significant alteration observed for high-density lipoprotein levels over the study period. CONCLUSION: The beneficial effect of tamoxifen on the lipidemic profile of postmenopausal breast cancer patients seems to be lost in less than 12 months time following cessation of 5-7 years of tamoxifen treatment. A 'rebound effect' on the lipidemic parameters should be expected and those patients should be monitored carefully.     

Third generation aromatase inhibitors may prevent endometrial growth and reverse tamoxifen-induced uterine changes in postmenopausal breast cancer patients.

BACKGROUND: Tamoxifen may induce uterine abnormalities of clinical concern. Our aim was to compare early uterine changes occurring in postmenopausal breast cancer patients treated in first-line with tamoxifen or third generation aromatase inhibitors. We also assessed the effect of aromatase inhibitors on tamoxifen-induced uterine changes. PATIENTS AND METHODS: Seventy-seven consecutive postmenopausal breast cancer patients scheduled to start endocrine treatment were included in this prospective study. Transvaginal ultrasonography (TVUS) was carried out before and after 3 months of therapy. No interventions were done on pre-existing asymptomatic uterine abnormalities seen on baseline sonography. RESULTS: After 3 months of therapy, tamoxifen significantly increased endometrial thickness and uterine volume. Additionally, tamoxifen induced endometrial cysts and polyps, and increased the size of pre-existing fibroids. In contrast, aromatase inhibitors did not stimulate endometrial growth and were not associated with endometrial pathologies seen under tamoxifen. Furthermore, aromatase inhibitors decreased endometrial thickness and uterine volume in patients previously treated with tamoxifen. CONCLUSIONS: Our study demonstrates that tamoxifen induces uterine abnormalities from as early as 3 months of therapy. In contrast, these abnormalities are not seen in patients on aromatase inhibitors. Furthermore, our data indicate that tamoxifen therapy followed by an aromatase inhibitor may lead to a reduction in endometrial pathologies associated with tamoxifen.     

A comparison of survival outcomes and side effects of toremifene or tamoxifen therapy in premenopausal estrogen and progesterone receptor positive breast cancer patients: a retrospective cohort study

ABSTRACT: INTRODUCTION: In premenopausal women, endocrine adjuvant therapy for breast cancer primarily consists of tamoxifen alone or with ovarian suppressive strategies. Toremifene is a chlorinated derivative of tamoxifen, but with a superior risk-benefit profile. In this retrospective study, we sought to establish the role of toremifene as an endocrine therapy for premenopausal patients with estrogen and/or progesterone receptor positive breast cancer besides tamoxifen. METHODS: Patients with early invasive breast cancer were selected from the breast tumor registries at the Sun Yat-Sen Memorial Hospital (China). Premenopausal patients with endocrine responsive breast cancer who underwent standard therapy and adjuvant therapy with toremifene or tamoxifen were considered eligible. Patients with breast sarcoma, carcinosarcoma, concurrent contralateral primary breast cancer, or with distant metastases at diagnosis, or those who had not undergone surgery and endocrine therapy were ineligible. Overall survival and recurrence-free survival were the primary outcomes measured. Toxicity data was also collected and compared between the two groups. RESULTS: Of the 810 patients reviewed, 452 patients were analyzed in the study: 240 received tamoxifen and 212 received toremifene. The median and mean follow up times were 50.8 and 57.3 months, respectively. Toremifene and tamoxifen yielded similar overall survival values, with 5-year overall survival rates of 100% and 98.4%, respectively (p = 0.087). However, recurrence-free survival was significantly better in the toremifene group than in the tamoxifen group (p = 0.022). Multivariate analysis showed that recurrence-free survival improved independently with toremifene (HR = 0.385, 95% CI = 0.154-0.961; p = 0.041). Toxicity was similar in the two treatment groups with no women experiencing severe complications, other than hot flashes, which was more frequent in the toremifene patients (p = 0.049). No patients developed endometrial cancer. CONCLUSION: Toremifene may be a valid and safe alternative to tamoxifen in premenopausal women with endocrine-responsive breast cancer.     

Measuring Ovarian Escape in Premenopausal Estrogen Receptor-Positive Breast Cancer Patients on Ovarian Suppression Therapy

PurposeThis study evaluated the proportion of premenopausal women who experience persistent ovarian escape (OE) while receiving ovarian suppression (OS) therapy for estrogen receptor‐positive (ER+) breast cancer treatment. The study also examined clinical factors that may predispose to higher risk of persistent OE.Materials and MethodsThis was a retrospective, “real‐world” study to evaluate premenopausal women receiving adjuvant endocrine OS therapy. The primary objective was to measure the percentage of persistent OE within the first 3 months of OS injections (using either leuprolide or goserelin). The secondary objective was to associate baseline clinical data (age, body mass index [BMI], and previous chemotherapy) with the probability of OE.ResultsOf the 46 patients included in this analysis, 11 (23.9%) women did not achieve OS within 3 months. Three women (6.5%) remained in OE at 12 months. Older age (odds ratio, 0.86; confidence interval, 0.76–0.98, p = .024) was associated with lower chance of developing OE. BMI, previous chemotherapy, and drug used (tamoxifen versus aromatase inhibitor) did not correlate with the likelihood of OE in this patient cohort.ConclusionAmong the premenopausal women who did not attain complete ovarian suppression, young age was a significant risk factor for likelihood of OE. Although the clinical relevance of this finding is not yet known, it should prompt further studies to determine whether inadequate OS is associated with higher recurrence risk for patients with ER+ breast cancer.Implications for PracticeBecause up to a quarter of premenopausal women do not attain adequate ovarian suppression within the first 3 months of gonadotropin‐releasing hormone (GnRH) agonist therapy, bloodwork should be checked to ascertain hormone levels prior to starting aromatase inhibitor therapy, and at regular intervals, for these women.     

Breastfeeding and Ovarian Cancer Risk: a Systematic Review and Meta-analysis of 40 Epidemiological Studies

The present systematic review and meta-analysis was conducted to assess any association between breastfeeding and the risk of ovarian cancer. A systematic search of published studies was performed in PUBMED and EMBASE and by reviewing reference lists from retrieved articles through March 2013. Data extraction was conducted independently by two authors. Pooled relative risk ratios were calculated using random-effect models. Totals of 5 cohort studies and 35 case-control studies including 17,139 women with ovarian cancer showed a30% reduced risk of ovarian cancer when comparing the women who had breastfed with those who had never breastfed (pooled RR = 0.70, 95% CI: 0.64-0.76; p = 0.00), with significant heterogeneity in the studies (p = 0.00;I2 = 76.29%). A significant decreasd in risk of epithelial ovarian cancer was also observed (pooled RR = 0.68, 95% CI: 0.61-0.76). When the participants were restricted to only parous women, there was a slightly attenuated but still significant risk reduction of ovarian cancer (pooled RR = 0.76, 95% CI: 0.69-0.83). For total breastfeeding duration, the pooled RRs in the < 6 months, 6-12 months and > 12 months of breastfeeding subgroups were 0.85 (95% CI: 0.77-0.93), 0.73 (95% CI: 0.65-0.82) and 0.64 (95%CI: 0.56-0.73), respectively. Meta-regressionof total breastfeeding duration indicated an increasing linear trend of risk reduction of ovarian cancer with the increasing total breastfeeding duration (p = 0.00). Breastfeeding was inversely associated with the risk of ovarian cancer, especially long-term breastfeeding duration that demonstrated a stronger protective effect.     

Tamoxifen and Cataracts: A Null Association

BACKGROUND: Previous studies have reported an increased risk of cataract for breast cancer patients treated with tamoxifen. We assessed whether breast cancer patients treated with tamoxifen were at increased risk of developing cataracts compared to women not prescribed tamoxifen. METHODS: We used a nested, matched case-control study design and data collected in the General Practice Research Database. We identified all women 30-79 years old who were diagnosed with breast cancer and treated with tamoxifen within 6 months, or with bladder cancer, colorectal cancer or non-melanoma skin cancer between January 1991 and December 1999. From this population, we identified all newly diagnosed cases of cataract. We matched four female controls to each case on age (+/- 1 year), index date and study entry date (+/- 6 months). We assessed the risk of cataracts for current, past and ever users of tamoxifen and according to cumulative use of tamoxifen. We calculated adjusted odds ratios (AOR) and 95% confidence intervals (CI) controlling the matching factors and adjusting for important cataract risk factors. FINDINGS: Current tamoxifen users were at no increased risk of cataract (AOR = 1.0, 95% CI: 0.7, 1.4). There was no evidence of an increased risk with increasing cumulative dose. INTERPRETATION: We detected no increased risk of cataract among breast cancer patients who were treated with tamoxifen compared to women with other cancers who were not prescribed tamoxifen.     

Treatment of breast cancer in elderly women: retrospective analysis of 111 wide lumpectomies performed in a day hospital regimen between 1982 and 1988.

Between 1982 and 1988, 111 elderly women with breast cancer but without clinical involvement of the axillary lymph nodes underwent wide lumpectomy in a Day Hospital regimen at the National Cancer Institute of Milan. The patients ranged in age from 70 to 92 years (median, 79). An adjuvant treatment was carried out in all but 9 cases: tamoxifen only in 84 cases, tamoxifen plus radiotherapy in 6 cases, radiotherapy alone in 12 cases. The median duration of follow-up was 44 months (range, 30-109 months). Four patients (3.6%) were lost to follow-up. In the remaining 107 patients, 10 local-regional relapses (9.1%) and 7 distant metastases (6.5%) occurred. Six patients died from the disease, 14 from unrelated conditions. This retrospective study showed that selected elderly patients with breast cancers can be treated successfully under local anesthesia on an outpatient basis. The treatment guarantees local control of the disease, meets the favor of elderly women and consequently improves their quality of life.     

青年女性乳腺癌155例临床分析

目的研究青年女性乳腺癌患者的临床特点、生存期及预后影响因素。方法回顾性分析155例35岁以下女性乳腺癌患者的临床资料,并进行随访和统计分析。结果155例患者中激素受体阳性占61．6％（77／125）,激素受体阳性和阴性患者的中位生存时间分别是119．0和51．3个月（P〈0．01）,其5年生存率分别为68％和33％。辅助他莫昔芬（TAM）治疗占47．1％（73／155）,中位生存时间182个月,较未辅助TAM者显著延长生存期（P〈0．05）。全组患者的中位无瘤生存期24个月,中位生存时间91个月,3、5、10年生存率分别为79％、60％和5．1％。COX多因素分析显示影响预后的主要因素有肿瘤大小、腋淋巴结转移、辅助内分泌治疗和Her-2过表达。激素受体阳性可能是预后的参考因素。结论≤35岁女性乳腺癌患者的预后影响因素是肿瘤大小、腋淋巴结转移、辅助内分泌治疗和Her-2表达情况。青年乳腺癌患者只要经过系统的综合治疗预后不差,仍可获得长期生存。     

Tamoxifen alone versus adjuvant tamoxifen for operable breast cancer of the elderly: long-term results of the phase III randomized controlled multicenter GRETA trial.

BACKGROUND: To evaluate the efficacy of tamoxifen as primary treatment in women aged over 70 years with operable breast cancer versus surgery followed by adjuvant tamoxifen. PATIENTS AND METHODS: Patients randomly received tamoxifen alone (160 mg day 1, then 20 mg/day) for 5 years or surgery followed by tamoxifen (20 mg/day) for 5 years. Overall survival was the main study end point; secondary objectives included breast cancer survival and local control of the disease. RESULTS: Between 1987 and 1992, 239 patients were assigned to surgery plus tamoxifen and 235 to tamoxifen alone. Treatment arms were comparable for tumor size, clinical nodal status and performance status. At a median follow-up of 80 months 274 patients had died. No difference between groups had emerged in overall and breast cancer survival. There were 27 local progressions in the surgery plus tamoxifen group and 106 in the tamoxifen-alone group (P = 0.0001). In the surgery plus tamoxifen group, no difference in overall survival had emerged according to the extension of operation. CONCLUSIONS: The long-term results of the study confirm the 3-year interim analysis already reported. Surgery (radical or minimal) followed by adjuvant tamoxifen does not modify overall and breast cancer survival as compared with tamoxifen alone in early breast cancer of older women. Because of the high rate of local progressions with tamoxifen alone, minimal surgery followed by tamoxifen appears to be the appropriate treatment in such patients. More extensive surgery is not useful. Tamoxifen alone is an adequate alternative treatment in very old or frail patients.     

The efficacy of tamoxifen in patients with advanced epithelial ovarian cancer

Background: Activity of tamoxifen as a salvage therapy in patients with advanced epithelial ovarian cancer was evaluated by a number of studies. In this study, we evaluated efficacy of tamoxifen in our patients with platinum-resistant epithelial ovarian carcinoma. Patients and Methods: A retrospective analysis was conducted of patients who received tamoxifen at a dose 20 mg twice daily for the treatment of advanced epithelial ovarian cancer. Results: Twenty-nine eligible patients were included to the study. There were 1 (3%) complete response, 2 (7%) partial response, 6 (21%) stable disease, and 20 (69%) progressive disease. All patients were progressed after initiation of tamoxifen. Median progression-free survival was 4 mo (95% CI: 2.98–5.02). Disease progression of 19 (65%) patients were shown within the first 6 mo after initiation of tamoxifen. Progression-free survival was between 6 and 12 mo for 7 (24%) patients and ≥ 12 mo for 3 (10%) patients. The median survival after initiation of tamoxifen was 15 mo (95% CI: 7.2–22.8). No toxicity attributable to tamoxifen was seen in any of the patients. The only independent prognostic factor that had a significant predictive value for progression-free survival was the response to tamoxifen treatment (p=0.043, hazard ratio: 0.12, 95% CI: 0.01–0.94). Conclusion: Considering minimal side effects and ability to cause objective responses, there is a place for tamoxifen in treatment of patients with platinum-resistant ovarian cancer. A phase III trial is required to confirm the value of the drug in patients presenting these clinical settings.     

CLINICAL DIAGNOSIS AND TREATMENT OF SMALL OVARIAN TUMOR IN POSTMENOPAUSAL WOMEN

Objective： To investigate the clinical symptom, ultrasonographic scan finding, serum CA125 value, histopathological type and treatment of small ovarian tumor （〈5 cm） in postmenopausal women. Methods： Retrospective analysis was carried out for 52 clinical materials of ovarian tumor cases in women more than one year after menopausal between Jan 1997 and Dec 2004. The largest diameter of the ovarian mass is less than 5 cm. Results： There were 11 ovarian cancers and 1 borderline ovarian tumor among 52 small ovarian tumors （23.1%）. 10 ovarian cancers were epithelial neoplasms and 2 were sex cord-stromal tumors, and 8 cases were in late stage according to FIGO staging system （33.3%）. Compared with benign tumor, there is no significant difference in the onset age, interval after menopausal and duration of history. The main clinical feature is abdominal symptoms, such as abdominal pain and distension in the malignant cases. The patients with benign tumors often showed the ovarian mass during the annual screening or admitted into hospital for other causes. The ultrasonography finding and serum CA125 level showed much difference between benign and malignant cases. Unilocular smooth-walled ovarian cysts mostly were found in benign tumor and the CA125 values were always less than 35 U/ml; but the solid or complex sonographic structures （multilocular, or with a papillary projections on the wall） often indicated a high risk of cancer, especially there was ascites in the pelvic cavity. Serum CA125 level in many cancer cases was elevated （〉35 U/ml）, over 300 U/ml in more than half of the patients. Surgery is still the first choice to treat ovarian cancer, and chemotherapy would be an auxiliary method. Till now, 3 ovarian cancer patients died of complications of cancer and 2 cases had recurrence. Conclusion： Small ovarian tumor in postmenopausal women has a comparatively low malignant occurrence but more in later stage. Many are epithelial carcinoma. If there is complex or parenchymal sonographic structure accompanied with a high serum CA125 level, operation should be considered, while it can be followed up when the ultrasound shows a smooth cyst with normal CA125 value.     

Medical adrenalectomy in patients with advanced breast cancer resistant to anti-oestrogen treatment

Summary Fifty-three women with actively progressing advanced breast cancer, who had all previously received tamoxifen, were treated with aminoglutethimide to induce medical adrenalectomy. Sixty-nine percent of the patients who had previously responded to tamoxifen subsequently responded to aminoglutethimide, while thirty-five percent of the nonresponders to tamoxifen subsequently responded to aminoglutethimide. The median duration of remission to aminoglutethimide was 12 months with a range from 4 to 22 + months. The drug was well tolerated and would appear to be the treatment of choice in tamoxifen responsive cases of advanced breast cancer. Address for repints: Robin M.L. Murray, M.D., Head, Endocrine Clinic, Cancer Institute, Melbourne 3000, Australia.