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Xerographic manifestations of male breast disease.
Male breast disease, although overshadowed by its female counterpart, is still a problem which often comes to the attention of the radiologist. The major importance of mammography is differentiating unilateral gynecomastia from cancer. We now recognize four xeroradiographic patterns of gynecomastia: (1) increased ducts only; (2) ductal hyperplasia mimicking adenosis; (3) small ducts with stromal proliferation; and (4) fatty replacement only. These reflect the duration of the process. Gynecomastic masses are central, smooth, and most important, extend from the nipple outward, usually bisecting the midplane. Ducts may be visible. Carcinoma is usually central, dense, with irregular spiculated margins and, unlike gynecomastia is rarely in the midplane of the nipple, although it can be retroareolar in location. There may be concomitant skin changes or lymphadenopathy seen on the xerogram and these never occur in gynecomastia. There are numerous etiologies for gynecomastia, and these have been discussed in detail. It is thought that the radiologist should be aware of the pathophysiology of male breast disease and understand its significance.
Fine needle aspiration biopsy of proliferative breast disease.
Proliferative breast disease (PBD) is a well-recognized histologic entity that has received increasing attention in the cytologic literature. We have attempted to prospectively identify and subclassify PBD by fine needle aspiration biopsy since 1987 using criteria we developed through our experience. Over 2800 breast FNABs were performed on breast lesions from 1987 to mid-1992; 257 were cytologically diagnosed as PBD with or without atypia. Eighty-four were significantly worrisome clinically to warrant surgical excision. Forty of these were designated PBD without atypia by cytology; 23 (58%) were in agreement with histology; three (8%) were PBD with atypia by histology; five (13%) were cancers; and nine (22%) were nonproliferative. Forty-four cases were designated PBD with atypia; 24 (55%) were in agreement with the histologic diagnosis; 12 (27%) proved to be PBD without atypia; six (13%) were carcinoma; and two (5%) were nonproliferative. After 1991 we employed stricter criteria for PBD, improving on the results from 1991-1992. During this period, there were 53 diagnoses of PBD with or without atypia and 34 were excised. Nine of the 10 (90%) aspirates designated as PBD without atypia were in agreement with histologic findings. The other case was nonproliferative. Fifteen of the 24 cases diagnosed as PBD with atypia were in concordance with histologic findings (63%), one was nonproliferative, seven were PBD without atypia (29%), and one (4%) proved to be carcinoma.(ABSTRACT TRUNCATED AT 250 WORDS)
Early life factors and incidence of proliferative benign breast disease.
Proliferative benign breast disease is a marker of increased breast cancer risk, yet little is known about its etiology. Most studies of benign breast disease have focused only on risk factors in adulthood, despite growing evidence that factors in early life influence breast cancer risk. We explored the relations of several early life factors with incidence of proliferative benign breast disease among 71,896 premenopausal women in the Nurses' Health Study II who recalled their body fatness at young ages, physical activity in adolescence, birthweight, and history of being breastfed. Between 1991 and 1997, 901 of these women were identified as having proliferative benign breast disease from a centralized pathology review. Relative risks (RR) and 95% confidence intervals (95% CI) were estimated from Cox proportional hazards models. Greater childhood body fatness (ages 5-10) was associated with decreased risk of proliferative benign breast disease; the multivariate RR (95% CI) for the most overweight compared with the most lean was 0.61 (0.44-0.86; P(trend) < 0.0001) and remained significant after adjustment for current body mass index. Body mass index at age 18 was also inversely associated with incidence of proliferative benign breast disease, with a multivariate RR (95% CI) of 0.67 (0.52-0.88) for those who were > or =25 kg/m(2) compared with those who were <19 kg/m(2) (P(trend) = 0.001). There were no clear associations for physical activity in adolescence, birthweight, or being breastfed. These results indicate that premenopausal women who were heavier at young ages have lower incidence of proliferative benign breast disease, consistent with previous findings for breast cancer.
Benign breast disease and the risk of breast cancer.
BACKGROUND: Benign breast disease is an important risk factor for breast cancer. We studied a large group of women with benign breast disease to obtain reliable estimates of this risk. METHODS: We identified all women who received a diagnosis of benign breast disease at the Mayo Clinic between 1967 and 1991. Breast-cancer events were obtained from medical records and questionnaires. To estimate relative risks, we compared the number of observed breast cancers with the number expected on the basis of the rates of breast cancer in the Iowa Surveillance, Epidemiology, and End Results registry. RESULTS: We followed 9087 women for a median of 15 years. The histologic findings were nonproliferative lesions in 67 percent of women, proliferative lesions without atypia in 30 percent, and atypical hyperplasia in 4 percent. To date, 707 breast cancers have developed. The relative risk of breast cancer for the cohort was 1.56 (95 percent confidence interval, 1.45 to 1.68), and this increased risk persisted for at least 25 years after biopsy. The relative risk associated with atypia was 4.24 (95 percent confidence interval, 3.26 to 5.41), as compared with a relative risk of 1.88 (95 percent confidence interval, 1.66 to 2.12) for proliferative changes without atypia and of 1.27 (95 percent confidence interval, 1.15 to 1.41) for nonproliferative lesions. The strength of the family history of breast cancer, available for 4808 women, was a risk factor that was independent of histologic findings. No increased risk was found among women with no family history and nonproliferative findings. In the first 10 years after the initial biopsy, an excess of cancers occurred in the same breast, especially in women with atypia. CONCLUSIONS: Risk factors for breast cancer after the diagnosis of benign breast disease include the histologic classification of a benign breast lesion and a family history of breast cancer.
Training obstetrics-and-gynecology residents to manage breast disease. Incorporation into a breast care clinic.
The American Board of Obstetricians and Gynecologists recently issued a directive that education in breast disease be incorporated into all residency training programs. At the University of Michigan Medical Center, the Comprehensive Breast Care Center (BCC) provides the vehicle for the education and training of residents in the area of breast disease. The department of obstetrics and gynecology is fully integrated and participates actively in the care of patients in the BCC.
Nonassociation of caffeine and fibrocystic breast disease.
Fibrocystic breast disease (FBD) is common in women. Caffeine-containing foods and beverages have been implicated as a cause of FBD or as an important factor in its progression. Relationships of causation are difficult to demonstrate. Only rigorous investigational methods can show true association between cause and effect. Our critical review of the medical literature indicated that there is weak evidence for an association between caffeine and FBD. We conclude that physicians need not recommend the avoidance of caffeine in otherwise healthy women who have FBD.
The role of the gynecologist in the management of breast disease.
The breast is an organ of reproduction. The diagnosis and treatment of most benign breast conditions and a knowledge of the contemporary treatment of breast cancer are essential components of the current practice of obstetrics and gynecology.
The prognostic significance of previous benign breast disease for women with carcinoma of the breast.
BACKGROUND: Risk factors for carcinoma of the breast may also have prognostic influence. Because benign breast disease is a risk factor for carcinoma of the breast, we compared the outcomes of patients with carcinoma of the breast with a history of benign breast disease to patients with carcinoma of the breast without a history of benign breast disease. STUDY DESIGN: Patients with benign breast disease and subsequent carcinoma of the breast were matched by age and ethnicity to patients with carcinoma of the breast with no prior history of benign breast disease. Risk factors, pathologic findings, and disease-free survival rates were compared. RESULTS: Patients with previous benign breast disease had a significantly greater family history of carcinoma of the breast (35 percent compared with 22 percent, p = 0.015) and used postmenopausal hormones significantly more frequently (16 percent compared with 5 percent; p < 0.001) than women without benign breast disease. In patients with benign breast disease, their subsequent carcinomas were smaller (T1, 53 percent compared with 43 percent), with significantly fewer nodes involved (1.8 compared with 2.7, p = 0.031), and were significantly more likely to contain an infiltrating lobular component (9 percent compared with 3 percent, p = 0.023). Significantly fewer patients with previous benign breast disease had metastatic disease (18 percent compared with 31 percent; p = 0.001). The ten-year cumulative disease-free survival rate for patients with benign breast disease was 68 percent compared with 59 percent for women without a history of benign breast disease. CONCLUSIONS: This study indicates that women with benign breast disease who have carcinoma of the breast develop may have a better outcome than women without a history of benign breast disease.
Medical radiation, family history of cancer, and benign breast disease in relation to breast cancer risk in young women, USA.
OBJECTIVE: In previous studies breast cancer risk has been increased among women who received high doses (above 100-200 cGy) of ionizing radiation or those exposed to lower doses prior to age 20. Some evidence suggests that such risk may be distinctly elevated among women with a family history of breast or ovarian cancer (probably only carriers of specific gene mutations) and women with benign breast disease (BBD). METHODS: A population-based case-control study in Los Angeles County obtained interview data from 744 women who were aged 40 or younger and diagnosed with breast cancer during 1983-1988, and from 744 matched controls. Women with a positive family history of breast or ovarian cancer reported cancer in a mother, sister, or grandmother. Women with BBD reported a physician diagnosis. Radiation exposure was defined as a history of either radiation therapy or moderate exposure to medical radiography. RESULTS: Breast cancer risk was elevated among women exposed to medical radiation prior to age 20 years (odds ratio (OR) = 1.4, 95% confidence interval (CI) = 1.2-1.8), relative to unexposed women. This increased risk was observed only among women with a history of BBD (OR = 2.4, 95% CI = 1.6-3.7). Overall, risk was not associated with exposure to medical radiation after age 20 years, although among women with a positive family history of breast or ovarian cancer, exposed women had an increased risk (OR= 1.8, 95% CI = 1.0-3.1). Breast cancer risk was not increased among women with a family history of breast/ovarian cancer exposed to medical radiation before age 20 years or those with BBD exposed to medical radiation after age 20 years. DISCUSSION: Study participants may have received radiation doses that are no longer common, hampering study generalizability. Although differences in recall between cases and controls cannot be completely excluded, women with BBD or a family history of breast cancer appear to have greater breast cancer risk following relatively low ionizing radiation exposure than other women in this study.
Benign breast disease: indicators of increased breast cancer risk.
Assessment of cancer risk, particularly with a view toward targeting strategies for prevention, is a recent development. The future will see the garnering of more specific information about determinants of risk and their interaction with screening prevention and therapeutic modalities. We are not a full professional generation removed from a time when the question of malignancy in the breast was absolute, yes or no. Now special types of breast cancer are recognized that pose little threat to life, while some benign conditions indicate greatly increased risk of death from cancer. Comparisons of premalignant determinants in other organ systems indicate that cytologic, histologic, and metaplastic features may be more or less important in different organs. Their separate and combined analysis as predictors give a complex measure of tissue organization, which is often predictive of concurrent cancer and/or future cancer development. In proliferative breast disease, the markers of cancer risk may be classified into histologic categories of slightly, moderately, and markedly increased risk. In cases of slightly increased risk, the probability for cancer development is 1.5 to 2 times that of the general population; a moderately increased risk denotes that the likelihood of cancer development may be 4 to 5 times greater; a markedly increased risk has a predictive value of 9 to 10 times that of the general population.
Historical and epidemiologic background of human premalignant breast disease.
Premalignant breast disease in humans is a concept that admits to a broad range of elements and possible determinants predicting the likelihood of developing breast cancer. Most of these elements are relative, such as the risk of breast cancer for women that is 130 times that of men and peaks at a younger age by about 10 years. Breast cancer is clearly a stochastic, multifactorial process that evolves over many years in which we must make predictions by likelihood. This review will present the most specially defined and reliably proven of these elements, highlighting anatomic and molecular factors.
A comparison of serum and breast duct fluid-immunoassayable prolactin and growth hormone with bioassayable lactogenic hormones in healthy women and patients with cystic breast disease.
Serum and breast fluid obtained by nipple aspiration were collected from 46 healthy premenopausal women, and 36 patients with cystic breast disease and cyclical mastalgia of similar age. Serum prolactin and growth hormone levels determined by radioimmunoassay were similar in the two groups, but the patients showed a significant elevation in bioactive lactogenic hormones (prolactin plus growth hormone) as determined by the Nb2 rat lymphoma cell bioassay (P less than 0.001). The radioimmunoassayable prolactin levels in breast fluid were extremely variable; there was a trend towards higher concentrations in the cystic breast disease patients, but this just failed to achieve statistical significance (P = 0.06). Immunoreactive growth hormone was rarely detected in nipple aspirates obtained from either the patient or control groups. The mean breast fluid bioactive lactogenic hormone level was significantly higher in the cystic breast disease patients than in the normal controls (P less than 0.001); also ten of 46 (22%) controls, but only two of 36 (6%) patients had no detectable bioactivity. It is concluded that lactogenic hormone bioactivity, when assessed by the Nb2 cell assay, is indicative of an endocrine abnormality which is associated with benign breast disease, and is reflected in breast duct fluid, but is not identified by the conventional radioimmunoassays.
Benign breast disease.
Benign breast disorders (BBD), classified by the ANDI system (aberrations of normal development and involution), constitute the major workload in breast clinics. Breast pain (mastalgia) is classified as cyclical, and non-cyclical extramammary causes such as ribircage pain have to be identified. Most patients need reassurance alone but those with moderate/severe pain present for > 6 months may need treatment: randomised trials have shown danazol, bromocriptine and tamoxifen to be effective. Fibroadenoma is the commonest benign solid lump in women aged 15-30 years. The diagnosis must be confirmed by triple assessment. Cysts occur usually in women of middle to late reproductive life. After ultrasound has confirmed the lump as cystic, it can be aspirated. Nipple discharge should be tested for the presence of haemoglobin (Hb). Those with HB+ discharge may require microdochectomy for treatment and diagnosis, common causes being duct papilloma and duct ectasia. Breast abscesses may occur during lactation or in women with duct ectasia and are treated by incision or aspiration together with antibiotics.
[The importance of hormone receptors in benign breast diseases].
Benign breast lesions are usually divided with regard to the proliferative activity into three categories. These lesions, depending on their histopathological characteristics and correlation with epidemiological studies differ as to the risk of breast cancer. 1. The concentration of hormonal receptors in the breast tissue in our group correlated with the proliferative activity of the lesion. 2. A major proliferative lesion and atypical hyperplasia of the ductal epithelium are a typical precancerous condition. 3. The hormonal receptor concentration defines, in addition to the histological classification, the biological activity more accurately. The prevalence of the oestrogen receptor or its trend to predominate over the progesterone receptor is a serious marker of imminent cancerogenesis. 4. Based on the prevalence of hormonal receptors it is possible to select suitable hormonal treatment to suppress the proliferative potential of the breast lesion. 5. A high level of the oestrogen receptor in non-malignant formations of the breast can be considered a manifestation of increased sensitivity of this target tissue to circulating oestrogens. It is a question whether it is the manifestation of mutation of the oestrogen receptor or the consequence of long-term exposure to uncovered levels of bioavailable oestrogens.
Tamoxifen for benign breast disease.
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A prospective study of benign breast disease and the risk of breast cancer.
OBJECTIVE: To examine the relation between proliferative benign breast disease with and without atypical hyperplasia and the subsequent risk of breast cancer. DESIGN: Case-control study nested within a prospective cohort study. Median follow-up after breast biopsy was 8 years (25th to 75th percentile, 5 to 14 years). PARTICIPANTS: Selected from a prospective cohort of 121,700 US registered nurses followed up from 1976 to 1986. Cases were women with breast cancer who had a prior biopsy for benign breast disease. Controls were randomly selected and matched on year of biopsy and year of birth from among women in the cohort who had a benign breast biopsy but who did not develop breast cancer. Included in the analysis were 121 cases and 488 controls. MAIN OUTCOME MEASURE: Development of breast cancer. RESULTS: Slides from the first benign breast biopsy were reviewed by two breast pathologists blinded to the outcome. The multiply adjusted relative risks (RRs) for breast cancer, relative to women with no proliferative disease, were 1.6 for proliferative disease without atypia (95% confidence interval [Cl], 1.0 to 2.5) and 3.7 for atypical hyperplasia (95% Cl, 2.1 to 6.8). Breast cancer risk was more strongly associated with atypical hyperplasia among premenopausal women (RR = 5.9; 95% Cl, 2.9 to 13.2) than postmenopausal women (RR = 2.3; 95% Cl, 0.9 to 5.9), but the association of breast cancer risk with proliferative disease without atypia did not differ across menopausal status. CONCLUSION: These results confirm the marked increase in breast cancer risk among women with atypical hyperplasia, particularly in premenopausal women, and suggest that these women should be encouraged to undergo frequent breast cancer screening.