scholarly journals Intraductal cystadenopapillomas of the mammary glands: diagnosis and treatment

Author(s):  
Diana Danilov ◽  
◽  
Veronica Svet ◽  
Ion Mereuta ◽  
◽  
...  

About one in two women has symptoms of breast formation. According to various data, the frequency of detection of benign pathologies of the mammary gland is much higher compared to the frequency of referring women to the doctor with these pathologies. Benign tumors of the mammary gland are characterized by a slow, expansive growth (compresses the neighboring tissue), are well encapsulated, most are the result of hormonal changes (hyperestrogenemia, hyperprolactinemia), after excision rarely recur, do not invade local tissues and do not metastasize to others. organs. The basic treatment is surgery – excision of the breast formations. Recurrences rarely occur, do not invade adjacent tissues and do not metastasize to other organs.

Author(s):  
Natalia Cara ◽  
◽  
Veronica Svet ◽  
Ion Mereuta ◽  
◽  
...  

Steatonecrosis of the mammary gland is necrosis of its adipose tissue, followed by replacement with scar tissue. Lipogranuloma is known as a benign inflammatory process, necrosis of breast fat occurs due to iatrogenic breast trauma. Most often, fatty necrosis is seen in women with large breasts – in women with small breasts, it develops much less often. It is important to diagnose lipogranulomas because it can often mimic breast cancer. Fat necrosis of the breast is a common pathological condition, with a wide variety of presentations on mammography, ultrasound and MRI. The incidence of fatty necrosis of the breast is estimated at 0.6%, representing 2.75% of all breast lesions.


2021 ◽  
Vol 11 ◽  
Author(s):  
Zeyu Li ◽  
Min Lu

BackgroundPresacral tumors are a group of rare and heterogeneous tumors that arise from the potential presacral space between the rectum and sacrum. The low occurrence and diverse origins make the diagnosis and treatment of these tumors a challenge. The aim of the study was to retrospectively review patient demographics and to identify advantages and disadvantages in the diagnosis and treatment of these tumors.MethodsRetrospectively collected and reviewed data from patients who received treatment of presacral tumors at the First Affiliated Hospital of China Medical University between August 2009 and June 2019.ResultsThe data from forty-four patients (33 females) with a median age of 50 years who were diagnosed with a presacral/retrorectal tumor were analyzed. The majority of tumors were congenital (61.4%) and benign tumors are more common (59.1%). The median age of patients with benign tumor was significantly higher than that of malignant tumor. The most common symptoms were sacrococcygeal/perianal pain (56.8%) and mass (36.4%), and 8 out of 9 patients having lower limb symptoms diagnosed with malignant tumor. The tumor detection rate of digital rectal examination was 75% and more than 90% of all patients underwent one or more radiology imaging exams for tumor diagnosis. Every patient had a biopsy result. The most common type of tumor was presacral cyst (40.9%) with overall tumor median size of 5.6 cm. Thirty-one (70.5%) patients underwent surgery, most often via the posterior route (83.9%). Posterior route surgery had significantly shorter operation time and tumors operated via posterior route were significantly smaller. The survival rate after surgery was 100%. The median course of disease was 6 months and median follow-up was 25 months.ConclusionsPresacral tumors have low occurrence and are more frequently observed in females in their 30s and 50s indicating a possible link between tumor occurrence and hormonal changes. Patients with lower limb symptoms were more likely to have a malignant presacral tumor. Posterior route was the most commonly utilized surgical approach. Supplementary iodine tincture treatment of cysts ruptured in operation could potentially be helpful in reducing the chance of recurrence.


2019 ◽  
Vol 23 (4) ◽  
pp. 733-739
Author(s):  
O.Yu. Kruk

Annotation. This article highlights the urgent problem of combined diseases of women's reproductive system. On the basis of theoretical analysis, generalized statistics for recent years are presented. The modern concepts of pathogenesis of diseases of the uterus and mammary glands, their correlation, as well as models of diagnosis and treatment are considered. Indeed, a more in-depth understanding of the problems of the combined pathology of the woman’s reproductive system (diseases of the uterus, ovaries, mammary gland), namely etiopathogenesis, diagnostic and treatment algorithms, will reduce the incidence of women of reproductive and perimenopausal age, as well as improve their quality of life. Only having the fullness of information about the state of the reproductive system of women, the doctor is able to prescribe thoughtful and effective treatment.


2006 ◽  
Vol 190 (2) ◽  
pp. 271-285 ◽  
Author(s):  
Caroline Manhès ◽  
Christine Kayser ◽  
Philippe Bertheau ◽  
Bruce Kelder ◽  
John J Kopchick ◽  
...  

Experimental, clinical, and epidemiological data support the growth-promoting role of endocrine prolactin (PRL) in mammary tumors. PRL is also produced by the breast, where it is now recognized to act as a growth/survival factor via autocrine/paracrine mechanisms. Recent transgenic (Tg) mouse models have revealed the pro-oncogenic effect of PRL over-expression in virgin mammary glands. To address the question whether PRL tumorigenicity was maintained on differentiated mammary glands, we generated mammary-specific Tg mice expressing human (h)PRL under the control of the milk whey acidic protein promoter, which directs autocrine hPRL over-expression in late gestation throughout lactation. Minimal levels of transgene expression were detected in the mammary glands of virgin animals, which at best induced partial ductal branching and lobulo-alveolar structures in older nulliparous females. As expected, expression of mammary hPRL dramatically increased at the end of first pregnancy, and from this point it never returned to baseline, although it peaked at each gestation/lactation cycle. Over-expression of hPRL that starts when the gland is already well into the differentiation process led to various morphological mammary alterations, including abnormally differentiated epithelium, atropy of the myoepithelial layer, dilated ducts, cysts, and lymphocytic infiltrates. These phenotypes tended to worsen with successive pregnancies, also reflecting cumulative damage of failure of involution. Although some older, multiparous females developed benign tumors (papillomas and metaplasias), none of the animals studied developed mammary carcinomas. In addition, we noticed that half of the Tg females exhibited lactation defects, leading to significantly increased pup mortality. This phenotype was due neither to failure of milk production nor to modification of its protein content, but rather it was correlated to lipid enrichment of the milk, which, in combination with profoundly altered morphology of the gland, led to impaired milk extrusion through the nipple. In summary, these data show that over-expression of autocrine hPRL in a differentiating mammary gland induces dramatic functional and morphological defects, but not carcinoma. This deserves further investigations on the emerging concept that autocrine PRL may have different effects on pathological development of the mammary gland depending on the differentiation state of the latter.


1956 ◽  
Vol 104 (4) ◽  
pp. 525-538 ◽  
Author(s):  
Charles Huggins ◽  
Yolanda Torralba ◽  
Klaus Mainzer

A transplanted mammary fibroadenoma was found to grow in 95 per cent of intact adult female rats and the increment of tumor weights was progressive and logarithmic. The growth of the tumor was retarded by ovariectomy and still more when this was combined with adrenalectomy. In ovariectomized rats the growth of the tumor was stimulated by phenolic estrogens, this increase being enhanced when progesterone was added. In these responses to hormonal changes the mammary gland and the tumor resembled each other. Yet there are many differences between the growth of the fibroadenoma and that of the mammary gland. In contrast to the progressive growth which occurred in intact adult females there was a prolonged period of indolent growth of transplants in hypophysectomized rats; but after many weeks active growth began and the tumors eventually reached large size. During the period of quiescent growth the tumor was cytologically atrophic but after the growth spurt had started the microscopic appearance of the fibroadenoma resembled that of tumors growing in normal adult females. The mammary gland remained atrophic during both the slow and the accelerated phases of tumor growth, and so too with the other secondary sex expressions. In hypophysectomized rats estrone and progesterone, when combined, stimulated the growth of the tumor, and this growth was accelerated by the additional administration of lactogenic or growth hormones. None of these hormones, separately, stimulated the growth of the tumor. In ovariectomized rats other differences were demonstrated between the growth of the mammary gland and the fibroadenoma. Progesterone, injected alone, accelerated the growth of the tumor but not that of the mammary glands. The administration of phenolic estrogens exerted a biphasic effect on the growth of the tumor whilst that on the breast of its hosts was monophasic. With progressively increasing doses of these phenols there occurred primarily an augmentation of the rate of growth of the tumor until a peak was achieved; an increase of the dose above the optimal amount depressed the growth of the tumor. The stage of depression of growth was not observed in the mammary glands of these tumor-bearing rats. Many steroids which induced gestational changes in the mammary gland accelerated the growth of the tumor. Among these were estrone and progesterone in combination and 17α-ethinyl-19-nor-testosterone administered alone. But gestational changes developed in the mammary gland of rats treated with 4-androstene-3α,17ß-diol, without growth of the tumor. The evidence which we have presented proves that the mammary fibroadenoma tested had some of the functional properties of a normal mammary gland, and neoplastic traits as well. In its response to hormones it had characteristics which set it apart from all other endocrine targets of the rat.


Author(s):  
I.C. Murray

In women, hyperprolactinemia is often due to a prolactin (PRL)-secreting adenoma or PRL cell hyperplasia. RRL excess stimulates the mammary glands and causes proliferation of the alveolar epithelium. Bromocriptine, a dopamine agonist, inhibits PRL secretion and is given to women to treat nonpuerperal galactorrhea. Old female rats have been reported to have PRL cell hyperplasia or adenoma leading to PRL hypersecretion and breast stimulation. Herein, we describe the effect of bromocriptine and consequently the reduction in serum PRL levels on the ultrastructure of rat mammary glands.Female Long-Evans rats, 23 months of age, were divided into control and bromocriptine-treated groups. The control animals were injected subcutaneously once daily with a 10% ethanol vehicle and were later divided into a normoprolactinemic control group with serum PRL levels under 30 ng/ml and a hyperprolactinemic control group with serum PRL levels above 30 ng/ml.


1961 ◽  
Vol 36 (1) ◽  
pp. 141-156 ◽  
Author(s):  
B. Bengtsson ◽  
A. Norgren

ABSTRACT The effect of testosterone and oestrone on the mammary glands of castrated male rabbits was studied. Testosterone propionate was used in daily doses from 0.5 to 80 mg. The doses of oestrone ranged from 0.05 to 25 μg per day. Mammary glands were examined after 14, 28 or 56 days of injections. 1) Testosterone in doses below 20 mg failed to affect the mammary glands. With 40 or 80 mg a distinct, though abnormal growth reaction was consistently obtained. 2) Oestrone in doses lower than 0.5 μg did not stimulate mammary growth. With 0.5 μg and higher doses extensive growth of the mammary glands occurred. Stunted growth and secretion were found in the mammary glands of rabbits injected with 12.5 or 25 μg oestrone. 3) Testosterone in doses of 1 or 5 to 10 mg depressed or abolished the response of the mammary glands to 0.5 μg oestrone. When testosterone, in doses ineffective when given alone, was added to at least 3.125 μg oestrone, the mammary glands developed alveoli. The abnormalities produced by the highest doses of oestrone studied were exaggerated by the addition of testosterone. 4) The observations indicate a complicated interplay between the actions of testosterone and oestrone on the mammary gland of the rabbit. The interactions between testosterone and oestrone are presumably different from those observed between progesterone and oestrone.


1973 ◽  
Vol 73 (4) ◽  
pp. 700-712 ◽  
Author(s):  
J. D. Bruce ◽  
X. Cofre ◽  
V. D. Ramirez

ABSTRACT On the day following delivery (day 1 of lactation) one abdominal mammary gland was implanted with oestrogen and the contralateral gland received an empty needle. At 2, 5 or 10 days of lactation the rats were anaesthetized with pentobarbital and the nipples of both abdominal glands were cannulated and their pressures recorded by means of transducers coupled to an amplifier and recording system. The normal mammary glands of 5-day lactating rats responded to very low doses of oxytocin (Syntocinon®, Sandoz) (5× 10−8 mU) with a rhythmic elevation in pressure. However, saline infusion also evoked a small rise in intra-mammary pressure. Earlier (2 days) and later (10 days) in lactation the responses were smaller. Oestrogen decreases significantly the milk ejection response to oxytocin, and the effect was maximal at day 10 of lactation. Histological observations confirmed the diminished reaction of the gland to oxytocin, since the milk was retained in the alveoli of rats bearing a mammary-oestrogen implant. A paradoxical rise in pressure was detected in normal as well as in oestrogen-implanted glands when the lowest dose of oxytocin was injected in lactating rats which had previously received a high dose of oxytocin (50 mU or 500 mU). These results reinforce the hypothesis that oestrogen alters the milk ejection response to oxytocin and that the mechanism is probably related to changes in the contractility of the myoepithelial cells.


1982 ◽  
Vol 208 (3) ◽  
pp. 611-618 ◽  
Author(s):  
M R Grigor ◽  
A Geursen ◽  
M J Sneyd ◽  
S M Warren

1. The rate of mammary-gland lipogenesis measured in vivo from 3H2O was suppressed after decreasing the milk demand by decreasing the number of pups from ten to two or three, as well as by giving diets containing lipid [Grigor & Warren (1980) Biochem. J. 188, 61-65]. 2. The specific activities of the lipogenic enzymes fatty acid synthase, glucose 6-phosphate dehydrogenase and ‘malic’ enzyme increased between 6- and 10-fold in the mammary gland and between 2- and 3-fold in the livers during the first 10 days of lactation. The increases in specific activity coupled with the doubling of liver mass which occurred during pregnancy and lactation resulted in considerable differences in total liver activities when compared with virgin animals. 3. Although consumption of a diet containing 20% peanut oil suppressed the activities of the three lipogenic enzymes in the livers, only the ‘malic’ enzyme was affected in the mammary glands. 4. In contrast, decreased milk demand did not affect the specific activities of any of the liver enzymes, whereas it resulted in suppression of all three lipogenic enzymes of the mammary glands. There was no effect on either the cytoplasmic malate dehydrogenase or the lactate dehydrogenase of the mammary gland. 5. In all the experiments performed, the activity of the fatty acid synthase correlated with the amount of material precipitated by the rabbit antibody raised against rat fatty acid synthase.


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