Effects of progestogens used in menopause hormone therapy on the normal breast and benign breast disease in postmenopausal women.

Hormone replacement therapy in menopause is used to improve climacteric syndrome in women whose quality of life is affected. However, given the wide variety of progestogens available, it is important to evaluate their differential benign changes (radiological, cellular, and clinical) on the breast. This review aimed to determine the different benign changes of progestogens used in postmenopausal combined hormone therapy on the breast (radiological, cellular, and clinical), in women without mammary pathology, in order to establish their safety profile. A systematic review of the literature was carried out with a balanced search strategy for the identification of relevant references in the MEDLINE, BVSalud, EMBASE, ProQuest, and Cochrane databases until November 2019. The search terms used were 'menopause' or 'hormonal replacement therapy' or 'progestins' or 'estrogen' or 'mastodynia' or 'benign breast disease' or 'mammography'. Data were collected from the 'eligible' articles by two researchers (ARF and SHA), and possible discrepancies in inclusion were resolved by consensus. A total of 1886 articles were identified; 60 full-text articles were reviewed, and 17 articles that met the inclusion criteria were included for the qualitative analysis. In conclusion, combined hormone replacement therapy is associated with benign effects on the breast, such as mastodynia and increased mammographic density.

Testosterone therapy and breast histopathological features in transgender individuals.

Testosterone therapy (TT) is administered to enhance masculinization in transgender individuals. The long-term effect of exogenous testosterone on breast tissues remains unclear. Our study evaluated the modulation of breast morphology by TT in transgender individuals with special attention to duration of TT. We reviewed 447 breast surgical specimens from gender affirming chest-contouring surgery, and compared histopathological findings including degree of lobular atrophy, and atypical and non-atypical proliferations between subjects who did (n = 367) and did not (n = 79) receive TT. TT for one patient was unknown. TT for >12 months was associated with seven histopathological features. Longer duration of TT was significantly associated with higher degrees of lobular atrophy (p < 0.001). This relationship remained significant after accounting for age at surgery, ethnicity, body mass index, and presurgical oophorectomy (adjusted p < 0.001). Four types of lesions were more likely to be absent in breast tissues exposed to longer durations of TT: cysts (median = 16.2 months; p < 0.01; adjusted p = 0.01), fibroadenoma (median = 14.8 months; p = 0.02; adjusted p = 0.07), pseudoangiomatous stromal hyperplasia (median = 17.0 months; p < 0.001; adjusted p < 0.001), and papillomas (median = 14.7 months; p = 0.04; adjusted p = 0.20). Columnar cell change and mild inflammation were also less likely to occur in subjects receiving TT (p < 0.05), but were not linked to the duration of TT. Atypia and ductal carcinoma in situ were detected in 11 subjects (2.5%) all of whom received TT ranging from 10.1 to 64.1 months. The incidental findings of high-risk lesions and carcinoma as well as the risk of cancer in residual breast tissue after chest-contouring surgery warrant the consideration of culturally sensitive routine breast cancer screening protocols for transgender men and masculine-centered gender nonconforming individuals. Long-term follow-up studies and molecular investigations are needed to understand the breast cancer risk of transgender individuals who receive TT.

Association of Mondor's disease with oral contraceptive pills.

Mondor's disease (MD) is a rare disease characterised by thrombophlebitis of superficial veins in the body. We describe a case of a 28-year-old woman with a painful cord-like lesion of the right breast (3 cm) overlying the right upper quadrant. The patient was recently prescribed metformin and oral contraceptive pills for symptomatic polycystic ovarian syndrome. Right breast ultrasound showed a tubular anechoic structure with several areas of narrowing, resembling a beaded appearance. The patient was diagnosed with MD associated with use of oral contraceptive pills. We recommended the patient to discontinue oral contraceptive because discontinuation of the causative drug is important. The patient was started on topical non-steroidal anti-inflammatory drugs and a therapeutic dose of enoxaparin. The patient showed significant clinical improvement after 5 days. At 6-week outpatient follow-up, complete resolution of the disease was noted.

Analysis of Data From Breast Diseases Treated With 5-Alpha Reductase Inhibitors for Benign Prostatic Hyperplasia.

OBJECTIVE: 5-alpha reductase inhibitors (5ARIs) decrease the androgen levels in vivo and are currently used for the treatment of benign prostatic hyperplasia (BPH) in men. However, these inhibitors can also increase the risk of gynecomastia, breast tenderness, and breast cancer. Hence, we did a systematic review and meta-analysis to evaluate the rate of breast-related diseases in men treated with 5ARIs. MATERIALS AND METHODS: PubMed, Embase, Cochrane, and CNKI databases were searched for randomized controlled trials using 5ARIs in patients with BPH. Data were analyzed by using Cochrane Collaboration review manager program and Stata 12.0 software. RESULTS: In total, 14 studies were included in the meta-analysis. Gynecomastia was significantly more common with 5ARIs treatment when compared with placebo (3.30% vs. 1.84%; P < .00001) or alpha blockers (ABs) monotherapy (2.33% vs. 1.00%; P = .0009). Both dutasteride (2.03% vs. 0.90%; P < .00001) and finasteride (4.08% vs. 2.43%; P < .00001) are associated with significantly higher risk of gynecomastia than placebo. Risk for breast tenderness was elevated in 5ARIs users (0.83% vs. 0.25%; P = .01) or in users having combination therapy with ABs (2.48% vs. 0.58%; P < .0001). Finasteride is associated with significantly higher risk of breast tenderness than placebo (0.80% vs. 0.25%; P = .02). CONCLUSION: In male patients with BPH, 5ARIs have significantly increased the risk of gynecomastia and breast tenderness but may be not to the breast cancer. In addition, combination therapy is significantly associated with higher risk of breast tenderness compared to single ABs monotherapy.

The tributyltin leads to obesogenic mammary gland abnormalities in adult female rats.

Tributyltin chloride (TBT) is an obesogen associated with several complications. However, few investigations have evaluated TBT effects on adult mammary glands (MG). In this investigation, we assessed whether TBT's obesogenic effects resulted in abnormal MG fat pad expansion and other irregularities. TBT was administered to female rats (100 ng/kg/day for 15 days via gavage), and their MG morphophysiological development was assessed. We further assessed the MG fat pad for PPARγ, ERα, and aromatase protein expression, as well as inflammation, oxidative stress (OS), apoptosis and fibrosis. Irregular MG morphological development such as lower TEB number, alveolar (AB), lobule and differentiation (DF) score were observed in TBT rats. TBT rats had abnormal MG fat accumulation as evidenced by increased numbers of hypertrophic adipocytes, triglyceride (TG) levels and PPARγ expression. A strong negative correlation between the MG obesogenic makers and TEB number, AB and DF score were observed in TBT rats. MG inflammation was observed in TBT rats. A positive correlation between the MG obesogenic markers and inflammation were observed. High ERα and aromatase expression were observed in MG of TBT rats. MG OS, apoptosis and fibrosis were present in the TBT rats. Additionally, a positive correlation between the MG obesogenic markers and OS were observed in TBT rats. Thus, these data suggest that obesogenic TBT effects led to MG irregularities in the adult female rats.

Breast abscess after intravenous methamphetamine injection into the breast.

Intravenous drug use is a problem plaguing our society. We present a case of a young female who injected methamphetamine into her mammary vein, resulting in the formation of a breast abscess. This case demonstrates a rare but dangerous complication of intravenous drug use and a possible differential diagnosis in a patient presenting with a breast abscess.

A MOUSE MODEL OF MAMMARY HYPERPLASIA INDUCED BY ORAL HORMONE ADMINISTRATION.

BACKGROUND: Mammary hyperplasia is one of the most common benign breast disorders. Although traditional Chinese medicine has a vast experience in the treatment of mammary hyperplasia, it is not accepted widely due to its unclear mechanism. METHODS AND MATERIALS: To address the mechanism, we developed a mouse model of mammary hyperplasia. We gave mice estradiol valerate tablets and progesterone capsules sequentially for one month by intragastric administration. RESULTS: Mice treated by this method had a series of pathological changes which are similar to those detected in women with mammary hyperplasia, including ectopic level of estradiol and progesterone in serum, hyperplasia of mammary glands and increased expression of ERα and PR. CONCLUSION: This model will facilitate the mechanical study of traditional medicine on mammary hyperplasia.

Lesiones destructivas mamarias / Destructive Lesions of the Breast

No disponible

Necrosis mamaria completa por acenocumarol / Complete mammary necrosis due to acenocoumarol

No disponible

Increased vascular calcification in patients receiving warfarin.

OBJECTIVE: Matrix gla protein is a vitamin K-dependent inhibitor of medial arterial calcification whose synthesis and activity are blocked by warfarin. Warfarin induces arterial calcification in experimental models, but whether this occurs in humans is unclear. This was addressed by examining breast arterial calcification, which is exclusively medial and easily identified on mammograms. APPROACH AND RESULTS: Screening mammograms from women with current, past, or future warfarin use were examined for the presence of arterial calcification and compared with mammograms obtained in untreated women matched for age and diabetes mellitus. Women with a serum creatinine >2.0 mg/dL or a history of end-stage renal disease were excluded. In 451 women with mammograms performed after ≥1 month of warfarin therapy, the prevalence of arterial calcification was 50% greater than in 451 untreated women (39.0% versus 25.9%; P<0.0001). However, in 159 mammograms performed before warfarin therapy, the prevalence of arterial calcification was not increased (26.4% versus 25.8%). The increased prevalence varied with duration of treatment, from 25.0% for <1 year to 74.4% for >5 years. In a multivariable logistic model, only age and duration of warfarin, but not the period of time after stopping warfarin, were significant determinants of arterial calcification in women with current or past warfarin use. CONCLUSIONS: The prevalence of breast arterial calcification is increased in women with current or past warfarin use independent of other risk factors and conditions predating warfarin use. This effect appears to be cumulative and may be irreversible.

Tocopherols inhibit oxidative and nitrosative stress in estrogen-induced early mammary hyperplasia in ACI rats.

Oxidative stress is known to play a key role in estrogen-induced breast cancer. This study assessed the chemopreventive activity of the naturally occurring γ-tocopherol-rich mixture of tocopherols (γ-TmT) in early stages of estrogen-induced mammary hyperplasia in ACI rats. ACI rats provide an established model of rodent mammary carcinogenesis due to their high sensitivity to estrogen. Female rats were implanted with 9 mg of 17ß-estradiol (E2) in silastic tubings and fed with control or 0.3% γ-TmT diet for 1, 3, 7, and 14 d. γ-TmT increased the levels of tocopherols and their metabolites in the serum and mammary glands of the rats. Histological analysis revealed mammary hyperplasia in the E2 treated rats fed with control or γ-TmT diet. γ-TmT decreased the levels of E2-induced nitrosative and oxidative stress markers, nitrotyrosine, and 8-oxo-dG, respectively, in the hyperplastic mammary tissues. 8-Isoprostane, a marker of oxidative stress in the serum, was also reduced by γ-TmT. Noticeably, γ-TmT stimulated Nrf2-dependent antioxidant response in the mammary glands of E2 treated rats, evident from the induced mRNA levels of Nrf2 and its downstream antioxidant enzymes, superoxide dismutase, catalase, and glutathione peroxidase. Therefore, inhibition of nitrosative/oxidative stress through induction of antioxidant response is the primary effect of γ-TmT in early stages of E2-induced mammary hyperplasia. Due to its cytoprotective activity, γ-TmT could be a potential natural agent for the chemoprevention of estrogen-induced breast cancer.