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Microcystic Adnexal Carcinoma Workup

  • Author: Nektarios I Lountzis, MD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Jun 27, 2016
 

Imaging Studies

MRI or CT scanning may be used to assess tumor extent and map out local invasion into nerves, muscle, cartilage, or bone.[26, 28, 17, 18, 37] Lesions on MRI tend to have a low T2-signal intensity, given its low cellularity and fibrosing nature.[37] Imaging may also be used to help define metastatic disease, if suspected. However, imaging is not necessary in most cases of microcystic adnexal carcinoma (MAC).

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Other Tests

Dermoscopy can be used but known specific features are limited and are rarely described in the literature. Some notable dermatoscopic features include dense, white, structureless areas centrally with white clods of variable diameter peripherally; white clods may represent keratin retention cysts also common to other mimicking tumors, such as trichoepithelioma.[38]

Optical coherence tomography is a biomedical tissue-imaging technique used to obtain high-resolution subsurface images similar to a low-power microscope. The process is similar to confocal microscopy. In one instance, this technique was used to diagnose microcystic adnexal carcinoma (MAC) that was subsequently confirmed by histologic evaluation.[39] Similarly, reflectance confocal microscopy can be used in defining MAC in vivo.[40] The availability of these devices is limited, but their potential use as a noninvasive means of diagnosing subtle tumors and outlining ill-defined malignancies (eg, MAC) could prove to be an invaluable tool, particularly on cosmetically sensitive areas.

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Procedures

A deep incisional or excisional biopsy is required. Superficial biopsies lead to misdiagnosis because deep extension and perineural invasion are key features of the tumor. Fine-needle aspiration has been attempted,[41] but its use is not standardized.

Ensuring that the biopsy specimen is adequate for diagnosis and that the histopathologist is aware of this entity is important because as many as 30-85% of cases of microcystic adnexal carcinoma are misdiagnosed.[29, 42]

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Histologic Findings

Note the images below.

A low-power view of microcystic adnexal carcinoma A low-power view of microcystic adnexal carcinoma demonstrates superficially located keratocysts and variably sized tumor nests and ducts. Note the diminution in size of the nests and cysts with the depth of dermal invasion. Courtesy of Dirk M. Elston, MD
Small ductular structures lined by 2-3 cell layers Small ductular structures lined by 2-3 cell layers of small eosinophilic cells showing little pleomorphism set in a dense fibrous stroma. Courtesy of Dirk M. Elston, MD.
A high-power view of small, irregularly shaped nes A high-power view of small, irregularly shaped nests and strands of small tumor cells without obvious ductal formation. Courtesy of Dirk M. Elston, MD.

Hematoxylin and eosin

Hematoxylin and eosin of deep biopsy specimens (preferably to subcutaneous fat) still remains the criterion standard in diagnosing microcystic adnexal carcinoma. Overall, microcystic adnexal carcinoma is a poorly circumscribed, deeply infiltrative, asymmetric tumor composed of variable proportions of keratocysts, squamoid or basaloid nests, infiltrating cords, and ductular structures set in a variably hyalinized but usually paucicellular desmoplastic stroma. In a minority of cases, microcystic adnexal carcinoma shows attachment to the epidermis or the follicles, but generally, a striking zonal separation is noted between the tumor and the epidermis.

In the superficial aspects of the tumor, small-to-medium keratinizing cysts lined by squamous epithelium can be seen. Atypia and mitoses are sparse. Nests of small basaloid or squamoid cells, sometimes showing a whorled-appearing infiltrate between the cysts with depth, are present. These may be solid, show central keratinization, can rarely be calcified or demonstrate central lumen formation, and have a tadpole or paisley-tie appearance.

In deeper sections, variable numbers of small ducts lined by 1-2 layers of cuboidal cells are present throughout the tumor. Narrow cords of cuboidal cells usually characterize the deepest portion of the tumor. Some of the nests and ducts show tail-like cellular extensions reminiscent of syringoma. Glycogen-rich, clear-cell change, foci of decapitation secretion, and sebaceous cell or duct differentiation may be present. The nuclei of all the components are mainly small, slightly irregular, and hyperchromatic, but little pleomorphism or mitotic activity occurs. Perineural infiltration is common (80%).[43] Presence of eosinophils, particularly with the presence of lesional clear cell change, can be seen.[44, 45] Lymphoid aggregates are common, particularly at the dermal-subcutaneous junction.

With regard to histologic subtype, tumors displaying the architectural features of microcystic adnexal carcinoma but with increased nuclear pleomorphism, hyperchromasia, vascular invasion, and necrosis may be suggestive of a more aggressive subtype.[43, 31] Clinically, these can demonstrate rapid growth, carcinosarcomatous metaplastic transformation with relapse, and suspected metastases.[31] Sebaceous[45] and trichoepitheliomatous[46] differentiation has been reported, which is of no prognostic significance. Monophasic eccrine variants are also seen (see Histologic differential diagnosis below).

Toluidine blue

Special staining with toluidine blue has been shown to highlight infiltrating tumor strands with a distinctive pink halo and perineural invasion with a maroon tint.[47] This stain may be of benefit in Mohs micrographic surgery (MMS).

Immunohistochemistry

Definitive immunostaining to differentiate microcystic adnexal carcinoma from other sclerosing neoplasms, especially in superficial samples, is lacking. However, a few stains can be of some assistance.

p63, a member of the p53 gene family highly expressed in the basal cells and adnexa of human epithelial tissues, was compared with microcystic adnexal carcinoma, sclerosing basal cell carcinoma (SBCC), and desmoplastic trichoepithelioma (DTE) in one study. All tumors were stained with p63, but the nuclear staining pattern was more complete and diffuse in SBCC (20 of 20 cases) and DTE (10 of 10 cases). Individual microcystic adnexal carcinoma tumor islands had selective "scattered" positivity mostly confined to the periphery (5 of 5 cases) and even extinguished with tumor depth. The disadvantage is that the scattered pattern was most obvious in deeper portions of microcystic adnexal carcinoma and may not be of help in superficial biopsies.[48]

p75 neurotrophin receptor has been found to play a role in hair follicle biology, and one study[49] extrapolated its use in differentiating morpheaform basal cell carcinoma (14% positive with < 30% cells staining) and desmoplastic trichoepitheliomas (100% positive with >80% cells staining). Microcystic adnexal carcinoma was not used in the study, but it was used in another study in which 4 (44%) of 9 microcystic adnexal carcinomas stained for p75 neurotrophin receptor.[50] Desmoplastic trichoepitheliomas and infiltrative basal cell carcinoma stained 94% and 36%, respectively, in this particular study.

CK (cytokeratin)–15 was found in a study using a battery of immunomarkers (ie, CK15, CK7, CK20, CK903, carcinoembryonic antigen [CEA], CD10, CD15, BerEP4) to stain microcystic adnexal carcinoma (92% of 13 cases) and DTE (100% of 8 cases), but not infiltrative basal carcinomas (10 cases) or squamous cell carcinomas (8 cases, 5 with ductal differentiation). Although the other stains were not reliably distinguishing, CK15 may be of help to exclude microcystic adnexal carcinoma and DTE from the latter 2 entities.[51]

BerEP4, a basal cell marker, was reported to differentiate basal cell carcinoma from microcystic adnexal carcinoma,[52] but reappraisal found that 38% of microcystic adnexal carcinomas revealed positivity.[51]

CD5, a lymphoid tumor marker, was found to stain microcystic adnexal carcinomas 71% of the time, particularly in deeper portions of the tumor, which may help differentiate them from desmoplastic trichoepitheliomas and morpheaform basal cell carcinomas.[53] This, again, may not facilitate diagnosis in superficial samples.

CK20 staining for the presence of Merkel cells in the tumor was negative in one case report.[52] Its utility was suggested to help differentiate microcystic adnexal carcinoma from other benign adnexal tumors that typically carry scattered Merkel cells throughout. Some studies appear to support this concept,[51, 54] but the variable presence of Merkel cells within sections makes its use less predictable.[49]

Other stains of interest but of little utility in diagnostic distinction include pancytokeratin, AE1/AE3, and cytokeratin-1; these all positively highlight tumor cells. Reactivity to hard keratin subclasses AE13 and AE14 has been demonstrated and suggests pilar differentiation.[55] Epithelial membrane antigen and CEA highlight ductal structures or intracytoplasmic lumen formation and suggest a sudoriferous origin, but ductal differentiation can be seen in other mimicking tumors. At times, microcystic adnexal carcinoma can also be negative for CEA.[51] Additionally, Leu-M1 is positive and S-100 is negative.[55]

A suggested immunohistochemistry panel may include the following:

  • Superficial biopsies: p63 may be of assistance if the peripheral pattern is seen, but this is best visualized in deeper portions of the dermis. CK15 may help exclude other malignancies, such as basal cell and squamous cell carcinomas, but DTE remains in the differential. Presence of tumoral CK20 cells may support a benign process, but lack of CK20 cells may not exclude a malignant process. Multiple sections should be considered.
  • Deep (midreticular dermis or deeper) biopsies: p63 with a scattered peripheral pattern within in each tumor island, or extinction with depth, may help confirm a diagnosis of microcystic adnexal carcinoma. CK15 and CK20 can be used, as above. CD5 could also be used to verify microcystic adnexal carcinoma but may be less reliable.

Histologic differential diagnosis

With hematoxylin and eosin staining, attention to the infiltrative growth pattern and, if present, perineural invasion, usually easily discriminates microcystic adnexal carcinoma from the other tumors in suitable biopsy specimens. Rendering a definitive diagnosis from a shave or superficial punch biopsy specimen is often impossible. In this context, duct formation, if present, would favor microcystic adnexal carcinoma over DTE, but perineural invasion can be seen in both. DTE tends to be more circumscribed and contain stromal calcification and rudimentary papillary mesenchymal bodies, but an eosinophilic infiltrate, particularly with lesional clear cell change, has been postulated to favor MAC.[44, 45] In the case of syringoma, the presence of keratocysts, slight atypia, and few mitoses would favor microcystic adnexal carcinoma.

Distinction from a morpheaform basal cell carcinoma can be made by the demonstration of duct and intracytoplasmic lumen formation and with zonation of the tumor from the epidermis, which is typically seen with microcystic adnexal carcinoma. Ductal formation is rare in basal cell carcinoma. If seen, it is usually in nodular subtypes. Subtle features, if seen, consistent with basal cell carcinoma (retraction artifact, fibromyxoid stroma, necrosis en mass) in basaloid islands may be supportive. CD5 positivity, CK15 positivity, or distinct p63 staining in deeper sections would also favor microcystic adnexal carcinoma over morpheaform basal cell carcinoma, whereas Ber-EP4 positivity favors basal cell carcinoma.

Desmoplastic squamous cell carcinoma or adenosquamous carcinoma generally lacks zonation from the epidermis, ductal structures, or intracytoplasmic lumen formation. CK15 positivity would favor microcystic adnexal carcinoma.

Desmoplastic melanoma also typically lacks zonation, ductal structures, and keratocyst formation, and it is reliably S-100 positive. Lymphoid aggregates are usually situated throughout the tumor, as opposed to the dermal-subcutaneous junction, as is seen in microcystic adnexal carcinoma.

Trichoadenomas tend to be more well-defined tumors with larger keratin cysts surrounded by a fibrovascular stroma. Typically, they lack deep invasion and do not show perineural invasion.

Metastatic adenocarcinomas (most commonly breast and colon) demonstrate more pleomorphism and cytologic atypia, and they lack keratocyst formation. p63 positivity may help in differentiating a primary adnexal tumor over metastatic adenocarcinoma.[56] Furthermore, an immunoprofile of CK5, C14, CK17, and p63 positivity and Mammaglobin negativity may favor a primary adnexal carcinoma, such as MAC, over metastatic breast carcinoma to the skin.[57] Moreover, newly described microcystic squamous cell carcinoma of the lung has distinct features similar to MAC. Although none has metastasized to the skin, the potential is there and could be discerned from MAC via thyroid transcription factor 1 expression.

Unusual presentation of childhood onset diffuse atrophoderma vermiculata of the head and neck with histologic features of small keratocysts in the superficial dermis and sclerotic syringomatous proliferations in the mid dermis to subcutaneous fascia may mimic MAC.[36] The proliferations differed from MAC in that they lacked obvious perineural involvement, were diffuse across body surface areas, and did not progress over time. Ductal epithelial strands were also embedded in concentric fibrotic rings, and distinct ball-like papillary dermal elastin aggregates were present. These patients were thought to have possible syndromic relationship to Nicolau-Balus syndrome, Rombo syndrome, and the so-called multiple eccrine-pilar hamartoma syndrome.

Most authorities distinguish microcystic adnexal carcinoma from similar low-grade sweat gland carcinomas that have previously been termed syringomatous carcinoma, eccrine epithelioma, or group 2 sclerosing sweat duct carcinoma, largely based on the presence of biphasic differentiation evidenced by keratocysts or other signs of follicular differentiation typically seen in MAC.[2, 43] They may also lack the sclerosing stroma of MAC. However, some have suggested that these tumors could be variations of the same entity. Of note, these subtypes tend to occur in younger patients.[2, 55]

Likewise, squamoid eccrine ductal carcinoma, a sweat gland carcinoma consisting of stranded epithelium with ductal differentiation and prominent squamoid features, is considered by some authorities to be a monophasic eccrine version of microcystic adnexal carcinoma (lacking follicular differentiation), similar to eccrine epithelioma. Although one case report described follicular features in a squamoid eccrine ductal carcinoma, this tends to be minimal, if present, and differs from eccrine carcinoma (and microcystic adnexal carcinoma) due to its conspicuous squamoid or syringosquamous metaplasialike qualities.[58]

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Contributor Information and Disclosures
Author

Nektarios I Lountzis, MD Consulting Staff, Advanced Dermatology Associates, Ltd, Lehigh Valley Health Network

Nektarios I Lountzis, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, American Contact Dermatitis Society, International Society of Dermatopathology

Disclosure: Nothing to disclose.

Coauthor(s)

Mary Grace Petrick, MD Consulting Staff, Department of Dermatology, Geisinger Medical Center

Mary Grace Petrick, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Mohs Surgery, American Society for Dermatologic Surgery

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael J Wells, MD, FAAD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD, FAAD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Texas Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Kelly M Cordoro, MD Assistant Professor of Clinical Dermatology and Pediatrics, Department of Dermatology, University of California, San Francisco School of Medicine

Kelly M Cordoro, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Medical Society of Virginia, Society for Pediatric Dermatology, Women's Dermatologic Society, Association of Professors of Dermatology, National Psoriasis Foundation, Dermatology Foundation

Disclosure: Nothing to disclose.

Acknowledgements

Mary Farley, MD Dermatologic Surgeon/Mohs Surgeon, Anne Arundel Surgery Center

Disclosure: Nothing to disclose.

Bruce C Gee, MBBCh, MRCP Specialist Registrar, Department of Dermatology, Queen's Medical Centre, UK

Bruce C Gee, MBBCh, MRCP is a member of the following medical societies: Royal College of Physicians

Disclosure: Nothing to disclose.

Kevin Hollowood, MD, MBBS, MRCP, FRCPath Consulting Staff, Department of Pathology, John Radcliffe Hospital of Oxford, UK

Disclosure: Nothing to disclose.

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Clinical photo of a microcystic adnexal carcinoma on the left upper lip of an elderly woman. Note the close clinical resemblance to basal cell carcinoma. Courtesy of Dirk M. Elston, MD.
A low-power view of microcystic adnexal carcinoma demonstrates superficially located keratocysts and variably sized tumor nests and ducts. Note the diminution in size of the nests and cysts with the depth of dermal invasion. Courtesy of Dirk M. Elston, MD
Small ductular structures lined by 2-3 cell layers of small eosinophilic cells showing little pleomorphism set in a dense fibrous stroma. Courtesy of Dirk M. Elston, MD.
A high-power view of small, irregularly shaped nests and strands of small tumor cells without obvious ductal formation. Courtesy of Dirk M. Elston, MD.
 
 
 
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