Mastopathy – a Common Breast Condition

Although it is a common occurrence and not always dangerous, mastopathy requires attention and timely monitoring. Learn all about the different forms and treatment of mastopathy!

Mastopathy (breast dysplasia) is a term that denotes the simultaneous presence of progressive and regressive changes in breast tissue, which to varying degrees show signs of atrophy, hyperplasia, and metaplasia of different tissue components of the mammary gland, and which share a common pathogenic feature of hormonal dependence. As a rule, mastopathy occurs bilaterally and manifests through various structural changes that are individually specific. It occurs throughout the entire reproductive period and primarily affects the upper outer quadrants of the breasts.

Mastopathy is most commonly divided into three stages:

• Mastopathy grade I: simple mastopathy or mild breast dysplasia, mastopathy without epithelial proliferation

• Mastopathy grade II: simple proliferative mastopathy or moderately severe dysplasia, mastopathy with epithelial proliferation but without cellular atypia

• Mastopathy grade III: mastopathy with atypical epithelial proliferation, severe breast dysplasia

Mastopathy grade I (simple mastopathy)
The largest proportion, about 70%, consists of breast tissue changes classified as fibrocystic mastopathy. These are benign structural changes in breast tissue that occur in two forms:

• Fibrous form – characterized primarily by proliferation of connective tissue between glandular lobules or intralobularly, with sclerosis and hyalinization of the stroma, as well as atrophy of the acini

• Fibrocystic form – in addition to connective tissue proliferation, smaller or larger cysts are present within the glandular parenchyma

A common structural change in grade I mastopathy is also adenosis (sclerosing adenosis, adenomatosis), which accounts for approximately 9% of benign breast tissue changes. In this form, epithelial hyperplasia of the acini, small ducts, and myoepithelium predominates. Formation of cystic structures is usually absent.

Mastopathy grade II
In addition to the above changes, this form includes the presence of intraductal epithelial growth, which occurs optionally (about 20%) in fibrocystic mastopathy. The intraductal epithelium is thickened, often multilayered, or forms solid adenoid or papillary structures. The cellular appearance is uniform, mitoses are only sporadically present, and cellular atypia is absent.

Mastopathy grade III (severe breast dysplasia)
Atypical proliferative mastopathy indicates the presence of epithelial proliferation intraductally, intra-acinar, or intrapapillary, accompanied by signs of mitosis and cellular atypia such as polymorphism and hyperchromasia of cell nuclei. Atypical foci are found in about 10% of fibrocystic mastopathies. It is very important to recognize severe breast dysplasia for both preventive and prognostic reasons, as atypical mastopathy must be clearly differentiated from preinvasive intraductal breast cancer.

Simple mastopathy is not a precancerous condition. The presence of non-proliferative forms of mastopathy does not represent an increased risk for the development of breast cancer. Even with a positive family history, the risk of breast cancer arising from grade I mastopathy is 0.5% and does not exceed the usual incidence of breast cancer. In cases of moderately severe mastopathy with proliferative changes without atypia, the relative risk of developing breast cancer later is increased 1.9 times, and with a positive family history 2.7 times. According to statistical data, within 15 years of diagnosis of mastopathy, 2% of women with non-proliferative mastopathy and 4% of women with proliferative mastopathy develop breast cancer. In severe mastopathy with atypical proliferative changes (severe dysplasia), the risk of breast cancer is increased 2 to 4 times compared to the general population.

One third to one half of all benign breast changes are mastopathic changes, and fibrocystic changes are found in as many as 90% of women. In the etiology of mastopathy, ovarian dysfunction with quantitative or synchronous imbalance in the production of follicular phase hormones and corpus luteum hormones, resulting in estrogen dominance, plays the most significant role. The resulting dysregulation of cyclic changes in the mammary gland, with premenstrual hyperemia, tissue tension, and dilation of milk ducts, under increased estrogen stimulation or in the absence of postmenstrual regression of changes, easily progresses into a pathological state. Reduction of symptoms during menopause and the absence of mastopathy, as well as breast involution in postmenopause, support this sequence of events. Non-proliferative forms account for 70%, proliferative forms 27%, and atypical proliferative forms 3.5–4% of all mastopathy types. The incidence of mastopathy increases after the third decade of life and is most common during perimenopause, between the ages of 45 and 50.

The clinical presentation of mastopathy primarily includes three symptoms:

• Presence of thickening and nodules in the breasts (mastopathic “plaques”), most often located in the upper outer quadrants, more commonly diffusely distributed and bilaterally

• Breast pain (mastodynia, mastalgia), which is cyclical in nature and typically occurs before menstruation, in the second half of the cycle, and subsides with the onset of menstrual bleeding

• Presence of nipple discharge, usually watery or milky, less commonly bloody or brownish; in 50–60% of cases, the presence of blood in the discharge indicates papillomatous proliferations within the milk ducts

The diagnosis of mastopathy is established based on breast examination, ultrasound findings, and mammography, and in cases of discharge, galactography and cytological analysis. In all suspicious findings, diagnostics must be supplemented with fine-needle aspiration or biopsy of suspicious lesions, that is, histological analysis of tissue changes. Given the different forms of mastopathy and the variability of subjective symptoms, treatment is individualized. In simple mastopathy, the primary goal is to correct estrogen dominance. Treatment includes local application of progesterone creams (with about 10% absorption of the applied dose), as well as gestagen supplementation during the second phase of the cycle. Low-dose oral contraception may also be used for this purpose.

A higher amount of body fat and dietary fat, especially saturated fatty acids combined with refined carbohydrates, increases estrogen production. In contrast, soluble dietary fiber of plant origin helps eliminate estrogen. An equally important role is played by indole-3-carbinol (found in green leafy vegetables such as cabbage, kale, Brussels sprouts, broccoli, and turnips), which has been shown to reduce the ability of estrogen to bind to breast tissue. The same applies to soy-based foods. About 80% of women with cyclical breast pain respond very well to dietary changes: reduced intake of saturated fatty acids and refined carbohydrates, increased intake of green leafy vegetables and fiber-rich foods, as well as soy. Research shows that many women suffering from breast pain benefit from the intake of antioxidant vitamins: beta-carotene (A), vitamin E, selenium, and vitamin C, which reduce serum levels of pituitary hormones (LH and FSH) in women who take them for breast pain.

Among herbal and homeopathic remedies, the beneficial effect of chaste tree (Agnus castus) should be mentioned. Breast tension, especially when inflammatory processes are involved, is successfully reduced by evening primrose oil, gamma-linolenic acid, and omega-3 fatty acids.