Abstract

Pseudoangiomatous stromal hyperplasia (PASH) was first described by Vuitch et al. in 1986. The authors described the tumorous, histological and ultrastructural features of PASH in nine premenopausal women. The women presented with unilateral breast masses. PASH is a benign proliferative lesion of the stroma whose aetiology and pathogenesis are ill-understood (Virk and Khan 2010). Leon et al. (2002) believed the proliferation originated from mammary fibroblasts and proposed the term nodular myofibroblast hyperplasia of the mammary stroma which indicates its true histogenesis. The stromal hyperplasia in PASH is due to exaggerated, aberrant responsiveness of the mammary myofibroblasts to hormonal stimuli, either endogenous or exogenous. The main hormone implicated is progesterone. The nuclei in PASH are progesterone receptor (PR) positive, whereas expression of oestrogen receptors (ER) is variable (Anderson et al. 1991). Powell et al. (1995) also reported expression of PR in 36 % (5/14) and ER in 12 % (2/14) cases of PASH. Further hormonal basis for this lesion is supported by the fact that half of postmenopausal women with tumorous PASH were on hormone replacement therapy (HRT) and occurred in men with gynaecomastia (Powell et al. 1995; Anderson 1991). The origin of the slit-like spaces is unknown but on electron microscopy the spaces are lined by an incomplete layer of spindle cells joined through cell junctions or occasionally by tight junctions (Vuitch et al. 1986).

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