Surgical follow-up results for apocrine adenosis and atypical apocrine adenosis diagnosed on breast core biopsy

Surgical follow-up results for apocrine adenosis and atypical apocrine adenosis diagnosed on breast core biopsy

Annals of Diagnostic Pathology 24 (2016) 4–6 Contents lists available at ScienceDirect Annals of Diagnostic Pathology Surgical follow-up results fo...

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Annals of Diagnostic Pathology 24 (2016) 4–6

Contents lists available at ScienceDirect

Annals of Diagnostic Pathology

Surgical follow-up results for apocrine adenosis and atypical apocrine adenosis diagnosed on breast core biopsy☆ Yanjun Hou a, Shweta Chaudhary a, Faye F. Gao b, Zaibo Li a,⁎ a b

Department of Pathology, Ohio State University Wexner Medical Center, Columbus, OH Department of Pathology, Medstar Washington Hospital Center, Washington, DC, 20010

a r t i c l e

i n f o

Keywords: Apocrine adenosis Atypical apocrine adenosis Core needle biopsy Follow-up excision Breast carcinoma

a b s t r a c t Apocrine adenosis (AA) and atypical apocrine adenosis (AAA) are uncommon findings in breast biopsies that may be misinterpreted as carcinoma. The clinical significance and risk implications of AAA diagnosed on core biopsy are not well established. This study aimed to determine the frequency of carcinoma on follow-up excision in patients with a diagnosis of AA or AAA on core biopsy. Forty-one breast core biopsies of AA (n = 29) and AAA (n = 12) were identified during a study period of 12 years. Of the 41 core biopsies with AA or AAA, 10 biopsies showed coexisting/concurrent atypical hyperplasia or carcinoma. In the absence of coexisting/concurrent atypical hyperplasia or carcinoma in core biopsy, none of the follow-up excision specimens after a diagnosis of AA or AAA showed ductal carcinoma in situ or invasive carcinoma. In conclusion, AA or AAA by itself is an uncommon core biopsy diagnosis that may not require surgical excision. © 2016 Elsevier Inc. All rights reserved.

1. Introduction Apocrine adenosis (AA) and atypical apocrine adenosis (AAA) are parts of the spectrum of apocrine lesions in the breast, ranging from benign apocrine change to apocrine ductal carcinoma in situ (DCIS) and invasive apocrine carcinoma. Apocrine adenosis and AAA can mimic patterns of DCIS and invasive carcinoma, causing misdiagnosis of carcinoma [1,2]. Apocrine adenosis is a finding with the combination of apocrine change and sclerosing adenosis (SA). Both apocrine change and SA are considered as benign changes in breast and are associated with very low risk for breast carcinoma. It has been reported that apocrine change is associated with a relative risk (RR) of 1.2 for invasive carcinoma [3] and SA is associated with an RR of 1.7 [4]. However, little is known about the RR of AA. Atypical apocrine adenosis is defined as AA with cytological atypia and the absence of necrosis or architectural atypia. Although the cytological atypia of AAA generally refers to a 3-fold variation in nuclear size and prominent nucleoli, the diagnostic criteria are variable in literature and have not been well validated [5-8]. A study from the Mayo Clinic showed that only 2.7% (1/37) of patients with AAA developed invasive carcinoma, indicating that AAA may not be a highrisk lesion for breast carcinoma [9]. Currently, both breast mammogram screening and core needle biopsy are widely implemented in diagnosing breast lesions; therefore, it is ☆ Disclosure: All authors have no potential conflict of interest. ⁎ Corresponding author at: Department of Pathology, Ohio State University Wexner Medical Center, 410 W 10th Ave, Columbus, OH, 43210. Tel.: +1 614 366 4859; fax: +1 614 293 4715. E-mail address: [email protected] (Z. Li). http://dx.doi.org/10.1016/j.anndiagpath.2016.07.001 1092-9134/© 2016 Elsevier Inc. All rights reserved.

important to know the frequency of carcinoma identified in excision following a diagnosis of AA or AAA on core needle biopsy. However, the data regarding follow-up excision (FUE) results after a diagnosis of AA or AAA are very limited, with only 1 recent study from the Cleveland Clinic available [10]. In this study, no DCIS or invasive carcinoma was identified in the surgical excision specimens after a pure diagnosis of AA (2 cases) or AAA (7 cases) on core needle biopsy [10]. Because of the limited data in the literature, our study aimed to further investigate the frequency of carcinoma in FUE after a diagnosis of AA or AAA on core needle biopsy.

2. Methods and materials After institutional review board approval at the Ohio State University, a pathology archive database search was performed for a period of 12 years (January 2003-December 2014). Biopsy specimens were received in 10% formalin and embedded in paraffin. Four levels of sections for each tissue block were obtained and stained with standard hematoxylin and eosin (H&E). Surgical excision specimens were also fixed in 10% formalin and embedded in paraffin. Most excisional specimens were submitted entirely for histologic examination. Apocrine adenosis was diagnosed based on the following criteria: a whorled lobulocentric pattern of sclerosis adenosis composed of cells with apocrine change (granular eosinophilic cytoplasm) (Fig. 1A and B). Atypical apocrine adenosis was diagnosed based on similar overall architecture with cytologic atypia (3-fold variation in nuclear size and prominent nucleoli) (Fig. 2A and B). No necrosis or architectural atypia was present within either AA or AAA.

Y. Hou et al. / Annals of Diagnostic Pathology 24 (2016) 4–6

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Fig. 1. Representative images of apocrine adenosis and atypical apocrine adenosis. (A) Apocrine adenosis without atypia; H&E staining, 100×. (B) Apocrine adenosis without atypia; H&E staining, 200×. (C) Atypical apocrine adenosis; H&E staining, 100×. (D) Atypical apocrine adenosis with marked variation in nuclear size and prominent nucleoli; H&E staining, 200×.

A total of 41 cases were interpreted as AA (n = 29) and AAA (n = 12) with or without other benign or malignant lesions. Ten cases with a diagnosis of AA (n = 5) or AAA (n = 5) were excluded from this study because of coexisting/concurrent diagnosis of atypical hyperplasia ([atypical ductal hyperplasia [ADH] or atypical lobular hyperplasia [ALH]) or carcinoma (DCIS or invasive carcinoma). The details were summarized in Table. The remaining 31 cases of pure AA (n = 24) and AAA (n = 7) were included in this study. Medical records were reviewed for patient age, radiologic findings (calcification, mass, asymmetric density), and biopsy methods. FUEs with the histologic findings were also reviewed and recorded when available.

3. Results The mean age at diagnosis was 59.7 years (range, 31-85). The indications for core biopsy include calcifications (n = 17), a mass/asymmetric density (n = 22), and a mass/asymmetric density with calcifications (n = 2). The biopsy methods include stereotactic-guided biopsy (n = 17), ultrasound-guided biopsy (n = 14), and unknown image-guided biopsy (n = 10). The detailed characteristics for each case were summarized in Table. Of the 29 core biopsies with AA, 1 contained ALH and 4 contained DCIS or invasive carcinoma. FUE was performed in 3 of 24 pure AA cases, and no significant lesion (DCIS or invasive carcinoma) was

Fig. 2. Diagram of all core needle biopsies with either AA or AAA and their FUE results. Abbreviation: IDP, intraductal papilloma.

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Table Apocrine adenosis and AAA on breast core biopsy Case # Diagnosis Age (y) Indication for biopsy

Biopsy type

Atypical hyperplasia/carcinoma

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41

Ultrasound Stereotactic Unknown Ultrasound Stereotactic Ultrasound Unknown Ultrasound Ultrasound Stereotactic Stereotactic Stereotactic Ultrasound Unknown Ultrasound Stereotactic Stereotactic Ultrasound Ultrasound Unknown Ultrasound Stereotactic Ultrasound Stereotactic Ultrasound Unknown Ultrasound Stereotactic Unknown Stereotactic Stereotactic Unknown Stereotactic Stereotactic Unknown Unknown Ultrasound Stereotactic Stereotactic Stereotactic Unknown

IDC DCIS DCIS ALH ADH/ALH

AAA AAA AAA AAA AAA AAA AAA AAA AAA AAA AAA AAA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA AA

79 69 71 49 54 58 77 63 74 47 55 70 66 73 75 72 85 52 47 31 75 55 51 49 67 31 43 52 74 46 63 45 69 53 45 64 61 75 63 66 35

Mass Calcification Mass Mass Calcification Mass Mass Mass Mass Calcification Calcification Calcification Mass + calcification Mass + calcification Mass Calcification Calcification Mass Asymmetric density Mass Mass Calcification Mass Calcification Mass Asymmetric density Mass Calcification Mass Calcification Calcification Mass Calcification Calcification Mass Mass Asymmetric density Calcification Calcification Calcification Mass

IDC IDC IDC DCIS ALH

identified (1 case with AA and 2 cases with small intraductal papilloma on FUE) (Fig. 2). Of 12 core biopsies with AAA, 1 contained ADH, 1 contained ALH, and 3 contained DCIS or invasive carcinoma. FUE was performed in all 7 pure AAA cases, and no significant lesion (DCIS or invasive carcinoma) was identified (3 cases with AAA, 2 with ALH, and 2 with only benign findings) (Fig. 2). 4. Discussion Apocrine adenosis and AAA are uncommon findings in breast that may be interpreted as carcinoma. They are parts of the spectrum of apocrine lesions in the breast, ranging from benign apocrine change to apocrine DCIS and invasive apocrine carcinoma. The expected frequency of AA and AAA on core biopsies specifically is not well established. Based on previous study, less than 1% of patients with breast biopsies had AAA and approximately 3% had AA [9]. In a series of approximately 5000 consultation cases, 1.2% of biopsies contained AAA [2]. One recent study from the Cleveland Clinic identified 34 cases of AA and AAA on core biopsy from a study period of 18 years [10]. Our study confirmed the rarity of AA or AAA, with only 41 cases identified from a study period of 12 years. The mean age at diagnosis in our cohort was 59.7 years, very similar to the average age of 58-60 years reported in previous studies

[2,9,10]. The Cleveland Clinic study showed that 20.6% (7/34) of cases of AA or AAA were associated with coexisting/concurrent ipsilateral atypical hyperplasia (ADH or ALH) and that 15% (5/34) of cases were associated with coexisting/concurrent ipsilateral DCIS or invasive carcinoma [10]. In our series, 10 of 41 (24.4%) cases were associated with atypical hyperplasia (AD/ALH), DCIS, or invasive carcinoma. The majority of previous studies included cases of AA or AAA identified in either biopsy or excision specimens and investigated the relative risk of AA or AAA for breast carcinoma during a certain follow-up period [2,8,9]. In the Mayo cohort, 5.4% (2/37) of patients with AAA but without any atypical hyperplasia developed DCIS or invasive carcinoma [9]. Carter and Rosen [2] studied 51 patients with AAA, and none of them developed carcinoma after an average of 35 months of follow-up. In contrast, Seidman et al [8] reported that 4 of 37 cases with AAA developed carcinoma after a mean of 5.6 years of follow-up; however, 1 case had ADH when AAA was diagnosed. Apocrine adenosis was considered as a benign lesion with a very low risk for developing carcinoma. The management for patients with AA diagnosed on core needle biopsy is usually just follow-up; no excision is necessary. However, the routine management for patients with AAA diagnosed on core needle biopsy is usually excision due to the presence of atypia and concerns about a more significant lesion in adjacent tissue which might not be sampled. To our knowledge, this is the second study to evaluate excisional findings on patients with AA or AAA identified on CNB besides the recent study from the Cleveland Clinic. In the Cleveland Clinic study, no DCIS or invasive carcinoma was found on excision in 9 of 34 cases with pure AA (n = 2) or AAA (n = 7) and FUE [10]. Consistent with the findings from this study, our data also demonstrated that no DCIS or invasive carcinoma was identified on the FUE specimens from patients with AA or AAA on CNB. Together with the data from the Cleveland Clinic, our findings suggest that surgical excision may not be necessary for patients with a diagnosis of AA or AAA without atypical hyperplasia (ADH/ALH) on core biopsy. However, our data were limited by the small cohort size due to the rarity of AA or AAA. Future multi-institutional studies are warranted to further examine the immediate upgrade risk and determine whether an excision will be necessary for these patients. In conclusion, our data suggest that an excision may not be required for patients with a diagnosis of AA or AAA on core needle biopsy. However, case-by-case examination with pathologic-radiologic correlation would be necessary for patients with a diagnosis of AAA on core needle biopsy because of the limited data available in literature.

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