During pregnancy and lactation, the breast is subjected to a variety of morphological changes. These range from hyperplastic lobules filled with milk containing ducts and acini to destruction of these acini when the job is done. The latter process is known as involution and is accomplished by means of increased apoptosis of epithelial cells and phagocytosis of the residual milk and cell debris. This is followed by stromal regenerative changes. All of these changes prepare the breast for the next pregnancy [4
]. Any delay in involution of lactation may lead to troublesome symptoms.
Delayed involution is characterized by a peculiar morphology. The breast shows a mixed picture comprising both hyperplastic and involuting lobules along with infiltration by inflammatory cells. The polymorphs and macrophages are involved in phagocytosis and clearance of unwanted acini. The lymphocytes are probably involved in the transfer of immunological agents from mother to offspring via the milk during lactation but their role in involution is not known. Focal calcification may be seen [5
], however this was absent in our patient.
The condition may clinically or morphologically mimic many other diseases which occur during lactation such as mastitis, galactocele, lactating adenoma and rarely inflammatory carcinoma. Lactation mastitis is characterized by a heavy polymorphonuclear infiltrate due to infection acquired during feeding of the baby. A galactocele is a cystic dilatation of a breast duct as a result of obstruction by inspissated secretions. Another lesion which may simulate the delayed involution is a nodular lactating adenoma. This neoplastic lesion can be easily differentiated by its gross circumscription, lack of inflammation and scanty stroma [6
]. Inflammatory carcinoma is a close differential clinically, but does not pose any difficulty in diagnosis on microscopy.
The pathophysiology of lactational involution has been extensively studied in animals. The process is presumably controlled by lowered milk demand, decreased milk removal and slow changes in the circulating hormones and insulin-like growth factors (GF-I, IGFBP-3) [7
]. Several molecular factors including AKT1/Protein kinase Bα, P53, and stat3 have also been implicated in mammary involution [8
]. It is possible that abnormal expression of one or more genes regulating these chemical substances may be responsible for delayed involution. Further studies on cases like ours may provide a definite causal link between these factors and delayed involution.
Studies in the past have demonstrated the protective role of breast feeding in mammary carcinoma [10
]. One mechanism postulated for this effect is the apoptosis of abnormal cells at early stages of involution [11
]. Some of the more recent studies have shown the importance of components of the fatty stroma of involuting breast in metastasis [12
]. In this patient, the delay in involution was accompanied by a low apoptotic activity and lack of fatty stroma. The significance of these findings, if any, in pathogenesis of breast cancer should be studied further in larger series of patients. Therefore, more cases like ours need to be reported.
The treatment protocol in symptomatic delayed involution of lactation is not well characterized. However, in our patient, surgical excision provided symptomatic relief.