Abstract

The pathogenesis of the duct ectasia/periductal mastitis complex remains unclear.’ The classic theory states that duct dilatation (ectasia) is the primary event and that stagnant secretion leaks from the dilated ducts producing a chemical inflammation, which presents as periductal mastitis. Duct dilatation occurs during breast involution which begins around the age of 35, which conforms to the age distribution of duct dilatation seen in postmortem studies’ and of clinically presenting duct ectasia.3 However, the clinical manifestations of periductal mastitis, subareolar abscess and mammary duct fistula are more frequently seen in women under the age of 35. This has led to the suggestion that the classical sequence of events may be incorrect and that periductal mastitis may be a separate condition. The aetiology of periductal mastitis in these young women is unknown, although two recent studies suggest that cigarette smoking may be important4,’ A further study” has shown a propensity for smokers to develop heavy oral colonisation of the same range of bacteria which can be cultured from the lesions of periductal mastitis.’ The clinical details are presented in the Table. None of the patients had any past or family history of breast disease. One patient was taking the oral contraceptive pill, she was 20 months postpartum and had not breast fed, the other 5 patients were nulliparous. Case 6 was referred with a subareolar mass and nipple discharge which spontaneously resolved, unilateral transverse nipple retraction was noted and a diagnosis of periductal mastitis made. She represented 7 months later with a subareolar abscess and a mammary duct fistula on the same side. None of the other patients have developed further breast problems. Nipple retraction was present in the three patients who required surgical treatment (cases 2, 5 and 6), and was bilateral in case 2. Staphylococcus epidermidis and Bacteroides species were cultured from cases 2 and 5 respectively; case 6 had received prior antibiotic treatment and the abscess was sterile. All these patients were regularly exposed to tobacco smoke. Two smoked themselves and the others were passive smokers as members of their household smoked. The two active smokers developed the most aggressive

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