The distinction between DCIS and ADH is based on evidence derived from many series, including studies by David Page and co-workers [3
]. These have been supported by other studies, such as the Nurses' Health Study [4
]. Clearly, ADH is a rare condition [6
], being seen in 4% of symptomatic benign biopsies [7
], although it is more common in association with screen-detected benign microcalcifications (31%) and is seen most commonly as an incidental finding [7
The significance of the diagnosis of ADH lies in the increased risk of invasive breast carcinoma, which is about four to five times that of the general population [8
] and may be even greater for premenopausal women (approaching a sixfold risk) [12
]. This risk is further increased if the patient has a first-degree relative with breast cancer (10-fold risk) [8
The diagnostic criteria used to define ADH are imperfect. ADH was described initially based on exclusion rather than positive criteria, i.e. the recognition of some but not all of the features of DCIS (as well as the lack of the characteristics of usual-type epithelial hyperplasia) [8
]. This definition of ADH has been updated and, while the diagnosis stills rests on an absence of all the features of DCIS, additional supporting features have been described [15
]. The view of Page and colleagues that the cellular changes of DCIS are present but occupy fewer than two separate duct spaces is widely accepted. Others use a 2-mm cutoff; a lesion less than 2 mm in maximum dimension being classified as ADH and a larger one as DCIS [17
]. These criteria recognise essentially the same lesions. In essence, ADH is usually small and focal, measuring less than 2 to 3 mm. Larger foci are accepted if associated with a radial scar/complex sclerosing lesion or a papilloma.
There are three components to the diagnosis of ADH, namely the architectural pattern, cytology, and disease extent. ADH is formed from a uniform population of small or medium-sized, round, cuboidal or polygonal hyperchromatic cells, which are regularly arranged. The nuclei are evenly distributed and may form a rosette-like pattern. Single small nucleoli only are present. Mitoses, particularly abnormal forms, are infrequently seen. Geometric spaces are present and, in the cribriform type, the cells are arranged at right angles to the bridges formed. Micropapillary ADH is also recognised and a solid pattern may very rarely be seen. Small foci of necrosis may rarely be identified in ADH and do not indicate that the process should be classified as DCIS.
At present, it is recommended that the diagnosis of ADH should be restricted to lesions that show the features described by Page and colleagues [8
], to which the quantified risk of developing breast carcinoma is linked. Even then, the diagnosis of ADH should be made with caution and only if low-grade DCIS has been seriously considered in the differential diagnosis. Lesser changes for which the possible classification lies between florid usual epithelial hyperplasia and ADH are less relevant with regard to a risk of developing breast carcinoma and should not be classified as ADH. However, it should also always be borne in mind that a proliferation at the edge of a biopsy may represent the periphery of a more established lesion of DCIS and further excision of the adjacent tissue may be warranted.
The major problem of ADH is the difficulty in achieving acceptable levels of concordance or consistency in diagnosis. Various strategies have been used to try to improve its recognition, including revision of the criteria, providing a more positive basis for recognition, and education and emphasis on the use of one system by all for diagnosis [15
]. Despite the adoption of such principles, the reliable classification around the boundaries of ADH and the 'borderline' epithelial intraductal proliferations in the breast remained elusive in several [18
], although not all [20