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IPEH presents as a less than 2 cm solitary purple-red nodule in middle-aged adults, with a slight predilection for females.4 However, clinical findings are nonspecific and diagnosis depends on histological evaluation. Histological differential diagnosis includes angiosarcoma. Both entities exhibit papillated proliferations of endothelial cells sometimes associated with sclerosis within vascular lumina. Unlike angiosarcoma, IPEH is usually sharply circumscribed, lacks pleomorphism and mitotic figures, and does not form a network of vascular spaces dissecting through tissue.2 The pathogenesis of IPEH is uncertain but hypothesized to be due to endothelial cell proliferation, triggered with the release of basic fibroblast growth factor (bFGF) by macrophages at the site of a thrombus. Endothelial cells release more bFGF during proliferation, creating a positive feedback loop.5 Treatment of IPEH is surgical excision. Recurrences are rare when there is no associated vascular tumor.4 Intravascular papillary endothelial hyperplasia has not been reported previously in a Mohs surgical scar and may have developed from thrombosis of a superficial artery. Although certainly rare, IPEH can be added to the differential diagnosis of new nodules that develop in the postoperative setting. References 1. North PE, Kincannon J. Vascular neoplasms and neoplastic-like proliferations. In: Bolognia JL, Jorizzo JL, Rapini RP, Callen JP, eds. Dermatology. Spain: Elsevier; 2008. 2. Requena L, Sangueza OP. Cutaneous vascular proliferations. Part II. Hyperplasias and benign neoplasms. J Am Acad Dermatol 1997;37: 887–919.

3. Sartore L, Voltan A, Tomat V, Bassetto F. Masson’s disease in hand surgery: a clinicopathologic study of four cases. J Hand Surg Eur 2011; 36:694–7. 4. Inaloz HS, Patel G, Knight AG. Recurrent intravascular papillary endothelial hyperplasia developing from a pyogenic granuloma. J Eur Acad Dermatol Venerol 2001;15:156–8. 5. Moriyama S, Kunitomo R, Sakaguchi H, Okamoto K, et al. Intravascular papillary endothelial hyperplasia in an aneurysm of the superficial temporal artery: report of a case. Surg Today 2011;41:1450–4.

Nicole F. Vélez, MD Dermatology Professionals, Inc East Greenwich Rhode Island Susan M. Sweeney, MD Dermatology Professionals, Inc East Greenwich, Rhode Island Division of Dermatology University of Massachusetts Medical School Worcester, Massachusetts Erin O’Leary, MD New England Tissue Issue Fall River, Massachusetts Nathaniel J. Jellinek, MD Dermatology Professionals, Inc East Greenwich, Rhode Island Division of Dermatology University of Massachusetts Medical School Worcester, Massachusetts Department of Dermatology Warren Alpert Medical School of Brown University Providence Rhode Island

Unique Basaloid Findings During Mohs Surgery for Basal Cell Carcinoma: A Dermatopathology Challenge A 67-year-old white male presented with an asymptomatic primary 0.5 · 0.6 cm biopsy-proven nodular and infiltrative basal cell carcinoma (BCC) of the right medial eyebrow of unknown duration that was detected by his dermatologist on routine skin examination. His pertinent medical history included atrial

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fibrillation requiring a defibrillator and anticoagulation (warfarin) and 1 BCC previously treated by his dermatologist. Because of the location and histology, Mohs micrographic surgery (MMS) was performed for this high-risk

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Figure 1. (A) Frozen section, Mohs stage I2 (H&E, original magnification ·2), (B) Frozen section, Mohs stage I2 (H&E, original magnification ·4)

BCC. Frozen sections of initial stages showed classic BCC with nodular basaloid islands with peripheral palisading and clefting. In addition, unique cribriform basaloid islands were noted (Figure 1). Subsequent Mohs surgical layers displayed less classic BCC with residual mixed histology of extensive basaloid proliferations with features of both benign trichoblastoma (Figure 2A) and spiradenomatous nodules (Figure 2B), some in association with the same follicular unit. The patient underwent a total of 5 stages of MMS with the fifth layer showing no evidence of frank BCC, and residual lesions did not meet criteria for carcinoma and seemed representative of his background skin that included trichoblastic proliferations and spiradenomatous nodules. Because of these unusual findings, an intraoperative consultation with dermatopathology was sought to review the final Mohs

layer. The dermatopathologist agreed with these benign findings, and no further MMS was pursued. The resulting defect measured 2.5 by 2.4 cm. Of note, on physical examination, patient had additional pink ill-defined papules on his right medial upper eyelid and left mid-forehead (Figure 3) that were subsequently biopsied and found to be spiradenomas or trichoblastic basaloid proliferations with several small spiradenomatous nodules suggestive of his background skin and potentially a unique syndrome. A mid-nasal root lesion, however, proved to be a BCC that similarly was treated with MMS and also had the unique benign basaloid/trichoblastic proliferations at margins. Mohs surgery was limited to the removal of frank BCC only.

Figure 2. (A) Frozen section, Mohs stage V1 with benign trichoblastic proliferation associated with same follicular unit and lack of mucinous stroma, clefting, and cytologic atypia (H&E, original magnification 4·). (B) Frozen section, Mohs stage V4 with sharply circumscribed lobules of highly cellular basophilic nuclei and hyalinized eosinophilic material that lack epidermal connection (H&E, original magnification ·4).

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distinguish from BCC though clefting, stroma characteristics, and atypia are all differentiating features (Table 1).1–3 Histologic interpretation of these diagnostic dilemmas can be even more challenging on frozen section. Additional surgery would have unnecessarily enlarged the defect size, led to a more complex reconstruction, and posed increased risk to the patient given his medical comorbidities.

Figure 3. Clinical photograph. (A) Trichoblastic basaloid proliferations with several small spiradenomatous nodules, (B) initial presenting BCC, (C) BCC with trichoblastic proliferations at margins, and (D) spiradenoma.

Discussion Margin assessment of most BCCs is usually straightforward; however, this case proved to be challenging given the unique rare findings of a classic BCC within an unusual background of benign trichoblastic and spiradenomatous proliferations. Benign trichoblastic proliferations can be difficult to

TABLE 1. Histologic Challenges of Differentiating BCC, Trichoblastoma, and Spiradenoma Histologic Differences of BCC Versus Trichoblastoma BCC

Trichoblastoma

Between tumor Absent or between epithelium and tumoral stroma and dermis dermis

Clefts

Papillary Usually absent mesenchymal bodies

Usually present

Cytologic atypia

Absent

Present

Mitotic figures Common

Rare

Fibromucinous Common stroma

Absent

Histologic Features of Spiradenoma Sharply circumscribed lobule of basophilic nuclei Hyalinized eosinophillic material within lobule

There are few published reports regarding benign histologic mimickers of BCC in Mohs micrographic surgery. Two case series describe subclinical folliculocentric basaloid proliferations (FBPs) at the periphery of BCCs.4,5 Folliculocentric basaloid proliferations usually lack single-cell necrosis and mitotic figures and have a normal stroma and mostly preserved prominent hyaline basement membrane at the periphery of the basaloid aggregates.4,5 There are additional lesions in the histologic differential diagnosis of BCC to be aware of including trichoepithelioma, basaloid follicular hamartoma, trichodiscoma, and trichofolliculoma.5 Our patient was educated extensively regarding these rare findings in case additional lesions were to develop or be biopsied with the goal of limiting unnecessary risk of surgery given his multiple comorbidities. Our management goal is to limit surgery only to aggressive BCCs and clinically monitor any other benign basaloid proliferations. Of note, the long-term clinical course of these proliferations is unclear. The patient may potentially have a genetic syndrome such as a variant of Brooke–Spiegler syndrome, although a genetic work-up was deferred per patient preference. Other instances in which unique basaloid findings may occur include in association with nevus sebaceous or in other genetic syndromes such as Birt–Hogg–Dube syndrome. Mohs surgeons and dermatopathologists should be aware of the rare potential for benign basaloid proliferations to occur at the periphery of classic BCCs.

No epidermal connection Hypercellular High vascularity

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Acknowledgments The authors acknowledge the Memorial Sloan Kettering Cancer Center

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histotechnicians William Phillips, Barbara Strippoli, and Marie Tudisco for their contribution to this patient’s management.

References 1. Helm KF, Cowen EW, Billingsley EM, Ackerman AB. Trichoblastoma or trichoblastic carcinoma? J Am Acad Dermatol 2001;44:547. 2. LeBoit PE. Trichoblastoma, basal cell carcinoma, and follicular differentiation: what should we trust? Am J Dermatopathol 2003;25: 260–3. 3. Yamamoto O, Asahi M. Cytokeratin expression in trichoblastic fibroma (small nodular type trichoblastoma), trichoepithelioma and basal cell carcinoma. Br J Dermatol 1999;140:8–16. 4. Leshin B, White WL. Folliculocentric basaloid proliferation. The bulge (der Wulst) revisited. Arch Dermatol 1990;126:900–6.

5. Patel NS, Johnston RB, Messina JL, Cherpelis BS. A unique basaloid proliferation encountered during Mohs surgery: potential pitfall for overdiagnosis of basal cell carcinoma. Dermatol Surg 2011;37:1180–8.

Rajiv I. Nijhawan, MD Kishwer S. Nehal, MD Department of Medicine, Dermatology Service Memorial Sloan Kettering Cancer Center New York, NY Klaus J. Busam, MD Department of Pathology, Dermatopathology Service Memorial Sloan Kettering Cancer Center New York, NY

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Unique basaloid findings during Mohs surgery for basal cell carcinoma: a dermatopathology challenge.

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