Sclerosing adenosis clinically feigning as carcinoma breast: A case report.

Sclerosing Adenosis (SA) is a lobulocentric proliferative process that involves both the epithelial and the mesenchymal component of the breast suggesting benignity. The disease has an increased incidence among reproductive-age and perimenopausal women, especially between 35 and 50 years of age. The clinical, radiological, and histopathological properties of sclerosing adenosis may resemble malignancy, which is the factor responsible for the clinical significance of the disease. Early diagnosis of sclerosing adenosis (SA) is very important as it is associated with a doubling of the risk of developing breast carcinoma, even though its role in carcinogenesis remains to be controversial and unclear. The main histopathological alterations of the terminal ductal lobular unit (TDLU) present as a widening and distortion of lobules with an increased number of acini and stromal fibrosis. The lesion is also called an “adenosis tumor of the breast” or “nodular sclerosing adenosis” if it presents as a palpable mass. Sclerosing adenosis is present in 12% of benign proliferative lesions and 20-25% of malignant lesions on histopathological examination. On mammography (MG), it can present as opacity, focal asymmetry, architectural distortion, or micro calcifications, mimicking a carcinoma. We have presented a case of 42 year old female who was diagnosed as carcinoma breast clinically and on radiology. Mammography showed a fibrosed lesion of size 4.5x3 cm with focal specks of microcalcification and irregular borders. But repeated fine needle aspiration cytology (FNAC) smears revealed small and large clusters of ductal epithelial cells with minimal anisonucleosis with background showing amorphous crystalline material and stromal fragments. Basing on FNAC, plan of surgery changed and a wide local excision with 2 cm normal margins was done and the specimen sent for histopathological examination (HPE), which revealed the lesion as sclerosing adenosis (SA).

CD56 and High Molecular Weight Cytokeratin as Diagnostic Markers of Papillary Thyroid Carcinoma

BACKGROUND: The incidence of papillary thyroid carcinoma (PTC) has been increasing recently and a precise diagnosis is essential for optimal treatment. Ancillary immunohistochemical stains are important for diagnosing some difficult cases. METHODS: The dignostic value of CD56, high molecular weight cytokeratin (HMCK), galectin-3 (GAL3), and cytokeratin 19 (CK19) were evaluated to distinguish PTC from other benign thyroid lesions (BTL). We studied 23 cases of papillary thyroid overt carcinomas, 57 papillary thyroid microcarcinomas, five follicular adenomas, five cases of Hashimoto's thyroiditis, and 12 nodular hyperplasias. RESULTS: The statistical analysis showed significantly different expressions of CD56, HMCK, GAL3, and CK19 in PTC vs other BTL. The diagnostic specificity of HMCK and CD56 (90.9% and 72.7%, respectively) was higher than that of GAL3 and CK19 (50.0% and 36.4%, respectively). However, the sensitivity of HMCK and CD56 detection (92.5% and 95.0%, respectively) was lower than that of GAL3 and CK19 (98.8% and 100.0%, respectively). The combined use of CD56, HMCK, GAL3, and CK19 showed 87.5% sensitivity, 100.0% specificity, and 100.0% positive predictive value in differentiating PTC from other BTL. CONCLUSIONS: Although the differential diagnosis of thyroid follicular lesions are based on histological and cytomorphological criteria, CD56 and HMCK might be useful markers for diagnosing PTC.

The Utility of HMW-CK and CK5/6 Immunohistochemical Stains for Differentiating Ductal Proliferative Lesions and Ducal Carcinoma of the Breast

BACKGROUND: Basal-type cytokeratins may help to distinguish benign from malignant intraductal proliferative lesions. The basal-type cytokeratins expression is markedly decreased or absent in atypical ductal hyperplasia (ADH), ductal carcinoma in situ (DCIS) and invasive ductal carcinomas (IDC). However, the expression patterns vary according to the antibodies that are used for staining. METHODS: HMW-CK (clone 34 E12) was applied to 175 lesions, and CK5/6 (clone D5/16B4) was applied to 145 lesions. The specimens were IDC (n=165), DCIS (n=35), ADH (n=37), florid ductal hyperplasia (FDH) (n=38) and columnar cell lesion (CCL) (n=45). The expression patterns of HMW-CK and CK5/6 were categorized as negative, focal positive and positive. RESULTS: Loss of the HMW-CK expression was noted in 76% (66/87) of the IDC, 78% (21/27) of the DCIS, 78% (21/28) of the ADH, and 55% (10/18) of the FDH. Loss of the CK5/6 expression was found in 96% (75/78) of the IDC, in all the DCIS (n=8) and ADH (n=9), and in none of the FDH (n=20). Loss of the CK5/6 expression is more reliable than that of the HMW-CK expression for differentiating FDH, ADH and malignant intraductal proliferatve lesions. Eleven (73%) of 15 CCLs revealed the loss of the HMW-CK expression, but all the CCLs (n=30) were negative for CK5/6 (p=0.0161). CONCLUSION: CK5/6 antibody is more reliable than HMW-CK antibody for differentiating FDH from ADH or DCIS, and for discriminating CCL.

A Case of Trichilemmal Carcinoma

Trichilemmal carcinoma is a rare tumor that is located predominantly on sun-exposed skin of the elderly. It is thought to be related to the external root sheath of the hair follicle and the malignant counterpart of a trichilemmoma. We report a case of trichilemmal carcinoma in a 88-year-old woman who had a 10 year history of a single, dark brown tumor on the right preauricular region. In her past medical history, it had been excised twice at a private clinic without a histopathological evaluation and recurred 2 years later. Histopathological findings showed atypical clear cells resembling those of the outer root sheath. Tumor cells showed PAS-positive cytoplasm. Immunohistochemistry revealed positive high molecular weight cytokeratin expression. To our knowledge, this is the second case of trichilemmal carcinoma in the Korean literature. (Ann Dermatol 100) 175178, 1998).