Pseudoangiomatous Stromal Hyperplasia Research Articles

Hamartoma of the breast: a clinicopathological review

Aims: To review 25 cases of breast hamartoma and discuss the pathological criteria, and the usefulness of imaging modalities, fine needle aspiration cytology (FNAC), and needle core biopsy in the...

Malignant neoplasms infiltrating pseudoangiomatous' stromal hyperplasia of the breast: an unrecognized pathway of tumour spread.

To describe five malignant tumours in the breast (two invasive carcinomas and three non-Hodgkin's lymphomas) showing an unusual pattern of spread within anastomosing spaces consistent with those described in pseudoangiomatous stromal hyperplasia. The histological and immunohistochemical features of the cases are presented. In all cases, the neoplasms consisted of non-cohesive E-cadherin-negative cells located within anastomosing vascular-like channels. These channels showed morphological and immunohistochemical features consistent with those seen in pseudoangiomatous stromal hyperplasia: they were lined by flattened cells that expressed CD34, bcl2 and smooth muscle actin, while CD31 was consistently negative. The open channels of pseudoangiomatous stromal hyperplasia have been regarded as spaces due to loss of cohesiveness between stromal fibroblasts if not artefacts. The fact that neoplastic cells spread through these spaces suggests that the spaces are true open channels that may represent part of a complex network of stromal channels (pre-lymphatics) connected to the main lymphatic system of the breast. This finding opens new insights into the routes of tumour spread.

Pseudoangiomatous Stromal Hyperplasia

This report describes five cases of pseudoangiomatous stromal hyperplasia of the breast. The lesion manifested as a discrete palpable slowly growing lumps. The patients ranged in age from 30 to 71 years. The clinical diagnosis was that of fibroadenoma in most cases. Pathologic examination revealed complex vascular like lesions closely resemble mimic well-differentiated angiosarcoma. The accurate diagnosis was established following the application of appropriate immunohistochemical markers.

Developing asymmetric breast tissue.

To show that benign asymmetric breast tissue detected mammographically may increase over time. Serial mammograms obtained in 21 women with negative physical examination results and mammographically detected developing asymmetric breast tissue were reviewed, and findings were correlated with results of biopsy (n = 16), ultrasonography (US) (n = 8), and contrast material-enhanced magnetic resonance (MR) imaging (n = 3). Five patients who did not undergo biopsy were followed up for 13-84 months. Thirteen of 16 biopsy specimens were reviewed. At the time of mammographic change, 12 patients without baseline asymmetric tissue had a mean age of 41.7 years and a mean size of asymmetric tissue of 2.4 cm. The mean age of nine patients with baseline asymmetric tissue was 46.9 years. In eight patients, the mean size increase was 2.5 cm. One patient showed increased tissue density but stable size. All US and MR images were negative. Pseudoangiomatous stromal hyperplasia was present in all 13 biopsy specimens reviewed and extensive in 12. No malignancies have been reported in five of the followed-up patients, and two have had continued enlargement of asymmetric tissue. Pseudoangiomatous stromal hyperplasia is a common histopathologic finding in developing asymmetric breast tissue. Follow-up, rather than biopsy, is a management option if benign imaging and clinical criteria are met.

Pseudoangiomatous stromal hyperplasia: mammographic and sonographic appearances.

Pseudoangiomatous stromal hyperplasia is a benign, localized form of stromal overgrowth with a probable hormonal etiology. Our purpose is to describe the mammographic, sonographic, and clinical features of this entity. A retrospective review of breast imaging studies and demographic information for seven patients identified as having pseudoangiomatous stromal hyperplasia was performed. The patients were chosen from a 1-year period during which 1661 breast biopsies were performed. The patients were 36-61 years old. Six were premenopausal, and the one postmenopausal woman was on hormone replacement therapy. Three patients wee evaluated palpable breast lumps, and four were asymptomatic. All seven women had noncalcified masses that measured 1.1-11 cm and that were visible by mammography. The border characteristics were as follows: three masses were well circumscribed, two were partly circumscribed, and two were indistinct, probably because they were obscured by overlying parenchyma. Sonography was performed for five patients; lesions were visible in four. All four of these lesions were solid and circumscribed. Five of the masses had increased in size since earlier studies, and one palpable mass was found by physical examination to have grown over time. Two patients had a local recurrence of pseudoangiomatous stromal hyperplasia. Surgical excision was performed for three patients, large-core biopsy was performed for three patients, and both surgery and large-core biopsy were performed for one patient. Pseudoangiomatous stromal hyperplasia should be included in the differential diagnosis of a circumscribed or partially circumscribed mass, especially in the premenopausal population. These masses often grow over time and can recur locally. Pathologic diagnosis of the lesion may be difficult unless the pathologist is aware of the presence of a mass lesion and appreciates the stromal changes characteristic of such a lesion.

Pseudoangiomatous stromal hyperplasia: mammographic, sonographic, and clinical patterns.

To analyze the mammographic, ultrasonographic (US), and clinical patterns of pseudoangiomatous stromal hyperplasia (PASH). Preoperative mammographic and US images, clinical records, and histologic assessments were reviewed in seven cases of PASH as the sole component or dominant stromal component of a clinically or mammographically defined mass lesion. In five, a PASH tumor was diagnosed at image-guided 14-gauge core-needle biopsy; in two, it was diagnosed at surgical excisional biopsy. Four women were premenopausal, two were postmenopausal, and one 40-year-old patient had iatrogenic primary amenorrhea. Four of seven masses were palpable; three were discovered at mammography. Four masses enlarged over 6 months to 5 years. At mammography, all masses lacked calcifications; six were well defined, and one was spiculated. One was inapparent at US; the remaining six were well defined and hypoechoic. The diagnosis of this rare lesion with image-guided breast biopsy or surgical biopsy is consistent with a well-defined uncalcified mass at mammography and a solid hypoechoic mass at US, usually in a premenopausal woman.

Pseudoangiomatous Stromal Hyperplasia (PASH)

Pseudoangiomatous stromal hyperplasia (PASH) is frequently a microscopic incidental finding in breast biopsies performed for benign or malignant disease. However, it may also produce a mass lesion. We reviewed PASH seen first as a tumor in 40 women aged 14 to 67 years (mean, 37 years). All but one lesion were clinically palpable. The exceptional tumor was found by mammography. The mass, typically unilateral, was usually diagnosed clinically as a fibroadenoma. Most specimens contained a well-circumscribed tumor with a firm white-gray cut surface. In six cases, there was no discrete gross lesion in the surgical specimen. Microscopically, there was a spectrum of pathological stromal changes ranging from classical PASH with anastomosing slit-shaped spaces outlined by flat, bland spindle cells to more proliferative lesions composed of bundles of plump spindle cells that obscured the underlying pseudoangiomatous architecture in the most florid lesions. The spindle cells were vimentin and CD34 positive and factor VIII negative. In more cellular fascicular lesions, the stromal cells acquired desmin and actin positivity. These immunohistochemical features were consistent with myofibroblastic histogenesis of PASH. Reactivity for progesterone receptor (PR) typically exceeded estrogen receptor (ER) in the nuclei of stromal and glandular cells. In most lesions, the nuclei of stromal spindle cells were ER negative. The majority of the patients were treated by excisional biopsy. One lesion, incompletely excised, spontaneously regressed. One patient had bilateral mastectomies. Follow-up was 0.6-11 years (mean, 4.5 years). Five patients had ipsilateral recurrences, and two had subsequent contralateral PASH. The morphological spectrum of cellular proliferation and staining qualities indicates that the myofibroblast plays a major role in the histogenesis of PASH. The pathogenesis of PASH remains uncertain, but aberrant reactivity of myofibroblasts to endogenous or exogenous hormones is likely to be an important factor. Simple excision is adequate treatment initially and for infrequent recurrences, Diffuse PASH occasionally presents a difficult management problem that may necessitate mastectomy.