Epithelial Proliferative Lesions, Usual and Atypical Ductal Hyperplasia

2.1 FLORID HYPERPLASIA VS. CRIBRIFORM-PATTERN ATYPICAL DUCTAL HYPERPLASIA

	Florid Hyperplasia without Atypia	Cribriform-Pattern Atypical Ductal Hyperplasia (ADH)
Age	Adult women	Adult women
Imaging findings	Calcifications, rarely mass, often incidental	Calcifications, often incidental
Etiology	Unknown	Unknown
Histology	Affects terminal duct lobular unit (Fig. 2.1.1) Nuclear variability and overlap (Figs. 2.1.1, 2.1.2, 2.1.3, 2.1.4, 2.1.5) Irregular secondary spaces (Figs. 2.1.2, 2.1.3, 2.1.4, 2.1.5) Indistinct cell borders (Figs. 2.1.4 and 2.1.5)	Affects terminal duct lobular unit (Figs. 2.1.6 and 2.1.7) Uniform cell population with even cell placement (Figs. 2.1.8 and 2.1.9) Distinct cell borders; solid pattern of ADH shows microrosette formation with cells evenly arranged around small lumens (Figs. 2.1.8 and 2.1.9)
Special studies	None; CK5/6 is variably expressed	None; CK5/6 is usually not expressed
Genetic abnormalities	None	Loss of 16q, 17p
Treatment	None	Excision if detected in core biopsy specimen; mammographic follow-up ± antiestrogen therapy
Clinical implication	Slightly increased risk of later cancer development (1.5×); risk level insufficient to affect patient management	Moderately increased risk of later cancer development (4-5×); risk is bilateral

Figure 2.1.1 Florid hyperplasia without atypia: A terminal duct lobular unit is expanded by proliferating epithelial cells; the proliferation is confined to the lobular unit without involving an adjacent true duct.

Figure 2.1.6 ADH: Several lobular units have dilated acini that show epithelial hyperplasia.

Figure 2.1.2 The secondary spaces created by the epithelial hyperplasia have an irregular shape.

Figure 2.1.3 Secondary spaces are fenestrated and not sharply defined in florid hyperplasia without atypia.

Figure 2.1.4 The irregular secondary spaces are a manifestation of uneven cell placement; note nuclear variability and overlap in this example of florid hyperplasia without atypia.

Figure 2.1.7 The two acini in the center contain a proliferation of epithelial cells; secondary spaces are peripheral but uniform in this example of ADH. Microcalcifications are present in one of the involved acini.

Figure 2.1.8 Nuclear uniformity and even cell placement characterize ADH.

Figure 2.1.9 The uniform cells of ADH form small microrosettes. Cell borders are evident.

Figure 2.1.5 Fewer secondary spaces are present in this solid, compact focus of florid hyperplasia without atypia, recognized by nuclear variability and overlap.

2.2 COMPACT FLORID HYPERPLASIA VS. SOLID-PATTERN ATYPICAL DUCTAL HYPERPLASIA

	Compact Florid Hyperplasia	Solid-Pattern ADH
Age	Adult women	Adult women
Imaging findings	Calcifications or incidental finding	Calcifications or incidental finding
Etiology	Unknown	Unknown
Histology	Expansion of terminal duct lobular unit (Fig. 2.2.1) Solid growth pattern with few residual secondary lumens (Figs. 2.2.2, 2.2.3, 2.2.4) Nuclear variability (Figs. 2.2.3 and 2.2.4) Jumbled cellular arrangement with nuclear overlap, indistinct cell borders, and few, if any, secondary spaces (Figs. 2.2.3 and 2.2.4)	Affects terminal duct lobular unit (Fig. 2.2.5) Solid proliferation of uniform cells partially occupying the involved spaces (Figs. 2.2.5, 2.2.6, 2.2.7, 2.2.8) Cells are evenly placed and have distinct cell borders (Figs. 2.2.7 and 2.2.8)
Special studies	None; CK5/6 may be expressed in a patchy distribution	None; CK5/6 is usually not expressed
Genetic abnormalities	None	Loss of 16q, 17p
Treatment	Excision not required if detected in a core biopsy specimen	Excision if detected in core biopsy specimen; mammographic follow-up ± antiestrogen therapy
Clinical implication	Slightly increased risk of later cancer development (1.5×); risk level insufficient to affect patient management	Moderately increased risk of later cancer development (4-5×); risk is bilateral