Pink Papule on the Lower Eyelid

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Pink Papule on the Lower Eyelid

THE DIAGNOSIS: Poroma

Poromas are benign adnexal neoplasms that often are classified into the broader category of acrospiromas. They most commonly affect areas with a high density of eccrine sweat glands, such as the palms and soles, but also can appear in any area of the body with sweat glands.1 Poromas may have cuboidal eccrine cells with ovoid nuclei and a delicate vascularized stroma on histology or may show apocrinelike features with sebaceous cells.2,3 Immunohistochemically, poromas stain positively for carcinoembryonic antigen, epithelial membrane antigen, and periodic acid–Schiff (PAS) with diastase sensitivity.1,4 Cytokeratin (CK) 1 and CK-10 are expressed in the tumor nests.1

Poromas are the benign counterpart of porocarcinomas, which can recur and may become invasive and metastasize. Porocarcinomas have been shown to undergo malignant transformation from poromas as well as develop de novo.5 Histologic differentiation between the 2 conditions is key in determining excisional margins for treatment and follow-up. Poromas are histologically similar to porocarcinomas, but the latter show invasion into the dermis, nuclear and cytoplasmic pleomorphism, nuclear hyperchromatism, and increased mitotic activity.6 S-100 protein can be positive in porocarcinoma.7 Both poromas and porocarcinomas are associated with Yes-associated protein 1 (YAP1), Mastermind-like protein 2 (MAML2), and NUT midline carcinoma family member 1 (NUTM1) gene fusions.5

Basal cell carcinoma (BCC) is the most common cutaneous malignancy. It rarely metastasizes but can be locally destructive.8 Basal cell carcinomas typically occur on sun-exposed skin in middle-aged and elderly patients and classically manifest as pink or flesh-colored pearly papules with rolled borders and overlying telangiectasia.9 Risk factors for BCC include a chronic sun exposure, lighter skin phenotypes, immunosuppression, and a family history of skin cancer. The 2 most common subtypes of BCC are nodular and superficial, which comprise around 85% of BCCs.10 Histologically, nodular BCCs demonstrate nests of malignant basaloid cells with central disorganization, peripheral palisading, tumor-stroma clefting, and a mucoid stroma with spindle cells (Figure 1). Superficial BCC manifests with small islands of malignant basaloid cells with peripheral palisading that connect with the epidermis, often with a lichenoid inflammatory infiltrate.9 Basal cell carcinomas stain positively for Ber-EP4 and are associated with patched 1 (PTCH1), patched 2 (PTCH2), and tumor protein 53 (TP53) gene mutations.9,11

Filley-1
FIGURE 1. Basal cell carcinoma characterized by basaloid tumor islands with peripheral palisading and tumor-stromal retraction (H&E, original magnification ×20).

Spiradenomas are benign adnexal tumors manifesting as painful, usually singular, 1- to 3-cm nodules in younger adults.12 Histologically, spiradenomas have large clusters of small irregularly shaped aggregations of small basaloid and large polygonal cells with surrounding hyalinized basement membrane material and intratumoral lymphocytes (Figure 2).4 Spiradenomas stain positive for p63, D2-40, and CK7 and are associated with cylindromatosis lysine 63 deubiquitinase (CYLD) and alpha-protein kinase 1 (ALPK1) gene mutations.5

Filley-2
FIGURE 2. Well-circumscribed dermal basophilic tumor with ductal structures, basement membrane material arranged in trabeculae, and scattered lymphocytes throughout in the setting of spiradenoma (H&E, original magnification ×50).

Squamous cell carcinoma (SCC) is the second most common nonmelanoma skin cancer worldwide.13 Lesions typically develop on sun-exposed skin and manifest as red, hyperkeratotic, and sometimes ulcerated plaques or nodules.14 Risk factors for SCC include chronic sun exposure, lighter skin phenotypes, increased age, and immunosuppression. Histologically, there are several variants of SCC: low-risk variants include keratoacanthomas, verrucous carcinomas, and clear cell SCC, and high-risk variants include acantholytic SCC, spindle cell SCC, and adenosquamous carcinoma.14 Generally, low-grade SCC will have well-differentiated or moderately differentiated intercellular bridges or keratin pearls with tumor cells in a solid or sheetlike pattern (Figure 3). High-grade SCC will be poorly differentiated with the presence of infiltrating individual tumor cells.15 Immunohistochemically, SCC stains positive for p63, p40, AE1/AE3, CK5/6, and MNF116 while Ber-Ep4 is negative.14,15 Poorly differentiated SCCs have high rates of mutation, commonly in the tumor protein 53 (TP53), Cyclin-dependent kinase inhibitor 2A (CDKN2A), Ras pathway, and notch receptor 1 (NOTCH-1) genes.13

Filley-3
FIGURE 3. Squamous cell carcinoma manifesting with proliferation of atypical keratinocytes with abundant eosinophilic cytoplasm extending into the dermis and forming keratin pearls (H&E, original magnification ×50).

Syringomas are benign adnexal tumors that manifest as multiple soft, yellow to flesh-colored, 1- to 2-mm papules typically located on the lower eyelids, most commonly in women of reproductive age.16 Syringomas are described on histology as small comma-shaped nests with cords of eosinophilic to clear cells with central ducts surrounded by a sclerotic stroma (Figure 4). They stain positively for carcinoembryonic antigen, epithelial membrane antigen, and CK-5 and are associated with genetic mutations in phosphatidylinositol-4, 5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) and AKT serine/threonine kinase 1 (ATK1).4

Filley-4
FIGURE 4. Syringoma with well-circumscribed proliferation of basaloid, cuboidal, and double-layered epithelial cells forming comma-shaped ducts as well as nests, cysts, and cords located primarily in the papillary dermis (H&E, original magnification ×50).

Due to its regular exposure to sunlight, the eyelid accounts for 5% to 10% of all skin malignancies. Common eyelid lesions include squamous papilloma, seborrheic keratosis, epidermal inclusion cyst, hidrocystoma, intradermal nevus, BCC, SCC, and sebaceous carcinoma.17 Aside from syringomas, benign sweat gland tumors like poromas, hidradenomas, and spiradenomas usually do not manifest on the eyelids but should be included in the differential diagnosis of an unidentifiable lesion due to the small risk for malignant transformation. Eyelid poromas manifest polymorphically, most commonly being clinically diagnosed as BCC, making the histologic examination key for proper diagnosis and management.18

References
  1. Patterson J. Weedon’s Skin Pathology. 5th ed. Elsevier Limited; 2021.
  2. Aoki K, Baba S, Nohara T, et al. Eccrine poroma. J Dermatol. 1980; 7:263-269. doi:10.1111/j.1346-8138.1980.tb01967.x
  3. Harvell JD, Kerschmann RL, LeBoit PE. Eccrine or apocrine poroma? six poromas with divergent adnexal differentiation. Am J Dermatopathol. 1996;18:1-9. doi:10.1097/00000372-199602000-00001
  4. Miller AC, Adjei S, Temiz LA, et al. Dermal duct tumor: a diagnostic dilemma. Dermatopathology. 2022;9:36-47. doi:10.3390
  5. Macagno N, Sohier P, Kervarrec T, et al. Recent advances on immunohistochemistry and molecular biology for the diagnosis of adnexal sweat gland tumors. Cancers. 2022;14:476. doi:10.3390/cancers14030476
  6. Robson A, Greene J, Ansari N, et al. Eccrine porocarcinoma (malignant eccrine poroma): a clinicopathologic study of 69 cases. Am J Surg Pathol. 2001;25:710-720. doi:10.1097/00000478-200106000-00002 /dermatopathology9010007
  7. Kurisu Y, Tsuji M, Yasuda E, et al. A case of eccrine porocarcinoma: usefulness of immunostain for S-100 protein in the diagnoses of recurrent and metastatic dedifferentiated lesions. Ann Dermatol. 2013;25:348-351. doi:10.5021/ad.2013.25.3.348
  8. Stanoszek LM, Wang GY, Harms PW. Histologic mimics of basal cell carcinoma. Arch Pathol Lab Med. 2017;141:1490-1502. doi:10.5858 /arpa.2017-0222-RA
  9. Niculet E, Craescu M, Rebegea L, et al. Basal cell carcinoma: comprehensive clinical and histopathological aspects, novel imaging tools and therapeutic approaches (review). Exp Ther Med. 2022;23:60. doi:10.3892/etm.2021.10982
  10. Pelucchi C, Di Landro A, Naldi L, et al. Risk factors for histological types and anatomic sites of cutaneous basal-cell carcinoma: an Italian case-control study. J Invest Dermatol. 2007;127:935-944. doi:10.1038/sj.jid.5700598
  11. Sunjaya AP, Sunjaya AF, Tan ST. The use of BEREP4 immunohistochemistry staining for detection of basal cell carcinoma. J Skin Cancer. 2017;2017:2692604. doi:10.1155/2017/2692604
  12. Kim J, Yang HJ, Pyo JS. Eccrine spiradenoma of the scalp. Arch Craniofacial Surg. 2017;18:211-213. doi:10.7181/acfs.2017.18.3.211
  13. Que SKT, Zwald FO, Schmults CD. Cutaneous squamous cell carcinoma: incidence, risk factors, diagnosis, and staging. J Am Acad Dermatol. 2018;78:237-247. doi:10.1016/j.jaad.2017.08.059
  14. Waldman A, Schmults C. Cutaneous squamous cell carcinoma. Hematol Oncol Clin North Am. 2019;33:1-12. doi:10.1016/j.hoc.2018.08.001
  15. Yanofsky VR, Mercer SE, Phelps RG. Histopathological variants of cutaneous squamous cell carcinoma: a review. J Skin Cancer. 2011;2011:210813. doi:10.1155/2011/210813
  16. Lee JH, Chang JY, Lee KH. Syringoma: a clinicopathologic and immunohistologic study and results of treatment. Yonsei Med J. 2007;48:35-40. doi:10.3349/ymj.2007.48.1.35
  17. Adamski WZ, Maciejewski J, Adamska K, et al. The prevalence of various eyelid skin lesions in a single-centre observation study. Adv Dermatol Allergol Dermatol Alergol. 2021;38:804-807. doi:10.5114 /ada.2020.95652
  18. Mencía-Gutiérrez E, Navarro-Perea C, Gutiérrez-Díaz E, et al. Eyelid eccrine poroma: a case report and review of literature. Cureus. 202:12:E8906. doi:10.7759/cureus.8906
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Dr. Filley is from the Department of Medical Education, Texas A&M University College of Medicine, Dallas. Drs. Preston and Parekh are from Baylor Scott and White Medical Center Dermatology, Temple, Texas.

The authors have no relevant financial disclosures to report.

Correspondence: Aidan Filley, MD, Texas A&M College of Medicine, Department of Medical Education, 3500 Gaston Ave, 6-Roberts, Dallas, TX 75246 (aidanfilley@tamu.edu).

Cutis. 2025 March;115(3):94, 100-101. doi:10.12788/cutis.1175

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Dr. Filley is from the Department of Medical Education, Texas A&M University College of Medicine, Dallas. Drs. Preston and Parekh are from Baylor Scott and White Medical Center Dermatology, Temple, Texas.

The authors have no relevant financial disclosures to report.

Correspondence: Aidan Filley, MD, Texas A&M College of Medicine, Department of Medical Education, 3500 Gaston Ave, 6-Roberts, Dallas, TX 75246 (aidanfilley@tamu.edu).

Cutis. 2025 March;115(3):94, 100-101. doi:10.12788/cutis.1175

Author and Disclosure Information

Dr. Filley is from the Department of Medical Education, Texas A&M University College of Medicine, Dallas. Drs. Preston and Parekh are from Baylor Scott and White Medical Center Dermatology, Temple, Texas.

The authors have no relevant financial disclosures to report.

Correspondence: Aidan Filley, MD, Texas A&M College of Medicine, Department of Medical Education, 3500 Gaston Ave, 6-Roberts, Dallas, TX 75246 (aidanfilley@tamu.edu).

Cutis. 2025 March;115(3):94, 100-101. doi:10.12788/cutis.1175

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THE DIAGNOSIS: Poroma

Poromas are benign adnexal neoplasms that often are classified into the broader category of acrospiromas. They most commonly affect areas with a high density of eccrine sweat glands, such as the palms and soles, but also can appear in any area of the body with sweat glands.1 Poromas may have cuboidal eccrine cells with ovoid nuclei and a delicate vascularized stroma on histology or may show apocrinelike features with sebaceous cells.2,3 Immunohistochemically, poromas stain positively for carcinoembryonic antigen, epithelial membrane antigen, and periodic acid–Schiff (PAS) with diastase sensitivity.1,4 Cytokeratin (CK) 1 and CK-10 are expressed in the tumor nests.1

Poromas are the benign counterpart of porocarcinomas, which can recur and may become invasive and metastasize. Porocarcinomas have been shown to undergo malignant transformation from poromas as well as develop de novo.5 Histologic differentiation between the 2 conditions is key in determining excisional margins for treatment and follow-up. Poromas are histologically similar to porocarcinomas, but the latter show invasion into the dermis, nuclear and cytoplasmic pleomorphism, nuclear hyperchromatism, and increased mitotic activity.6 S-100 protein can be positive in porocarcinoma.7 Both poromas and porocarcinomas are associated with Yes-associated protein 1 (YAP1), Mastermind-like protein 2 (MAML2), and NUT midline carcinoma family member 1 (NUTM1) gene fusions.5

Basal cell carcinoma (BCC) is the most common cutaneous malignancy. It rarely metastasizes but can be locally destructive.8 Basal cell carcinomas typically occur on sun-exposed skin in middle-aged and elderly patients and classically manifest as pink or flesh-colored pearly papules with rolled borders and overlying telangiectasia.9 Risk factors for BCC include a chronic sun exposure, lighter skin phenotypes, immunosuppression, and a family history of skin cancer. The 2 most common subtypes of BCC are nodular and superficial, which comprise around 85% of BCCs.10 Histologically, nodular BCCs demonstrate nests of malignant basaloid cells with central disorganization, peripheral palisading, tumor-stroma clefting, and a mucoid stroma with spindle cells (Figure 1). Superficial BCC manifests with small islands of malignant basaloid cells with peripheral palisading that connect with the epidermis, often with a lichenoid inflammatory infiltrate.9 Basal cell carcinomas stain positively for Ber-EP4 and are associated with patched 1 (PTCH1), patched 2 (PTCH2), and tumor protein 53 (TP53) gene mutations.9,11

Filley-1
FIGURE 1. Basal cell carcinoma characterized by basaloid tumor islands with peripheral palisading and tumor-stromal retraction (H&E, original magnification ×20).

Spiradenomas are benign adnexal tumors manifesting as painful, usually singular, 1- to 3-cm nodules in younger adults.12 Histologically, spiradenomas have large clusters of small irregularly shaped aggregations of small basaloid and large polygonal cells with surrounding hyalinized basement membrane material and intratumoral lymphocytes (Figure 2).4 Spiradenomas stain positive for p63, D2-40, and CK7 and are associated with cylindromatosis lysine 63 deubiquitinase (CYLD) and alpha-protein kinase 1 (ALPK1) gene mutations.5

Filley-2
FIGURE 2. Well-circumscribed dermal basophilic tumor with ductal structures, basement membrane material arranged in trabeculae, and scattered lymphocytes throughout in the setting of spiradenoma (H&E, original magnification ×50).

Squamous cell carcinoma (SCC) is the second most common nonmelanoma skin cancer worldwide.13 Lesions typically develop on sun-exposed skin and manifest as red, hyperkeratotic, and sometimes ulcerated plaques or nodules.14 Risk factors for SCC include chronic sun exposure, lighter skin phenotypes, increased age, and immunosuppression. Histologically, there are several variants of SCC: low-risk variants include keratoacanthomas, verrucous carcinomas, and clear cell SCC, and high-risk variants include acantholytic SCC, spindle cell SCC, and adenosquamous carcinoma.14 Generally, low-grade SCC will have well-differentiated or moderately differentiated intercellular bridges or keratin pearls with tumor cells in a solid or sheetlike pattern (Figure 3). High-grade SCC will be poorly differentiated with the presence of infiltrating individual tumor cells.15 Immunohistochemically, SCC stains positive for p63, p40, AE1/AE3, CK5/6, and MNF116 while Ber-Ep4 is negative.14,15 Poorly differentiated SCCs have high rates of mutation, commonly in the tumor protein 53 (TP53), Cyclin-dependent kinase inhibitor 2A (CDKN2A), Ras pathway, and notch receptor 1 (NOTCH-1) genes.13

Filley-3
FIGURE 3. Squamous cell carcinoma manifesting with proliferation of atypical keratinocytes with abundant eosinophilic cytoplasm extending into the dermis and forming keratin pearls (H&E, original magnification ×50).

Syringomas are benign adnexal tumors that manifest as multiple soft, yellow to flesh-colored, 1- to 2-mm papules typically located on the lower eyelids, most commonly in women of reproductive age.16 Syringomas are described on histology as small comma-shaped nests with cords of eosinophilic to clear cells with central ducts surrounded by a sclerotic stroma (Figure 4). They stain positively for carcinoembryonic antigen, epithelial membrane antigen, and CK-5 and are associated with genetic mutations in phosphatidylinositol-4, 5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) and AKT serine/threonine kinase 1 (ATK1).4

Filley-4
FIGURE 4. Syringoma with well-circumscribed proliferation of basaloid, cuboidal, and double-layered epithelial cells forming comma-shaped ducts as well as nests, cysts, and cords located primarily in the papillary dermis (H&E, original magnification ×50).

Due to its regular exposure to sunlight, the eyelid accounts for 5% to 10% of all skin malignancies. Common eyelid lesions include squamous papilloma, seborrheic keratosis, epidermal inclusion cyst, hidrocystoma, intradermal nevus, BCC, SCC, and sebaceous carcinoma.17 Aside from syringomas, benign sweat gland tumors like poromas, hidradenomas, and spiradenomas usually do not manifest on the eyelids but should be included in the differential diagnosis of an unidentifiable lesion due to the small risk for malignant transformation. Eyelid poromas manifest polymorphically, most commonly being clinically diagnosed as BCC, making the histologic examination key for proper diagnosis and management.18

THE DIAGNOSIS: Poroma

Poromas are benign adnexal neoplasms that often are classified into the broader category of acrospiromas. They most commonly affect areas with a high density of eccrine sweat glands, such as the palms and soles, but also can appear in any area of the body with sweat glands.1 Poromas may have cuboidal eccrine cells with ovoid nuclei and a delicate vascularized stroma on histology or may show apocrinelike features with sebaceous cells.2,3 Immunohistochemically, poromas stain positively for carcinoembryonic antigen, epithelial membrane antigen, and periodic acid–Schiff (PAS) with diastase sensitivity.1,4 Cytokeratin (CK) 1 and CK-10 are expressed in the tumor nests.1

Poromas are the benign counterpart of porocarcinomas, which can recur and may become invasive and metastasize. Porocarcinomas have been shown to undergo malignant transformation from poromas as well as develop de novo.5 Histologic differentiation between the 2 conditions is key in determining excisional margins for treatment and follow-up. Poromas are histologically similar to porocarcinomas, but the latter show invasion into the dermis, nuclear and cytoplasmic pleomorphism, nuclear hyperchromatism, and increased mitotic activity.6 S-100 protein can be positive in porocarcinoma.7 Both poromas and porocarcinomas are associated with Yes-associated protein 1 (YAP1), Mastermind-like protein 2 (MAML2), and NUT midline carcinoma family member 1 (NUTM1) gene fusions.5

Basal cell carcinoma (BCC) is the most common cutaneous malignancy. It rarely metastasizes but can be locally destructive.8 Basal cell carcinomas typically occur on sun-exposed skin in middle-aged and elderly patients and classically manifest as pink or flesh-colored pearly papules with rolled borders and overlying telangiectasia.9 Risk factors for BCC include a chronic sun exposure, lighter skin phenotypes, immunosuppression, and a family history of skin cancer. The 2 most common subtypes of BCC are nodular and superficial, which comprise around 85% of BCCs.10 Histologically, nodular BCCs demonstrate nests of malignant basaloid cells with central disorganization, peripheral palisading, tumor-stroma clefting, and a mucoid stroma with spindle cells (Figure 1). Superficial BCC manifests with small islands of malignant basaloid cells with peripheral palisading that connect with the epidermis, often with a lichenoid inflammatory infiltrate.9 Basal cell carcinomas stain positively for Ber-EP4 and are associated with patched 1 (PTCH1), patched 2 (PTCH2), and tumor protein 53 (TP53) gene mutations.9,11

Filley-1
FIGURE 1. Basal cell carcinoma characterized by basaloid tumor islands with peripheral palisading and tumor-stromal retraction (H&E, original magnification ×20).

Spiradenomas are benign adnexal tumors manifesting as painful, usually singular, 1- to 3-cm nodules in younger adults.12 Histologically, spiradenomas have large clusters of small irregularly shaped aggregations of small basaloid and large polygonal cells with surrounding hyalinized basement membrane material and intratumoral lymphocytes (Figure 2).4 Spiradenomas stain positive for p63, D2-40, and CK7 and are associated with cylindromatosis lysine 63 deubiquitinase (CYLD) and alpha-protein kinase 1 (ALPK1) gene mutations.5

Filley-2
FIGURE 2. Well-circumscribed dermal basophilic tumor with ductal structures, basement membrane material arranged in trabeculae, and scattered lymphocytes throughout in the setting of spiradenoma (H&E, original magnification ×50).

Squamous cell carcinoma (SCC) is the second most common nonmelanoma skin cancer worldwide.13 Lesions typically develop on sun-exposed skin and manifest as red, hyperkeratotic, and sometimes ulcerated plaques or nodules.14 Risk factors for SCC include chronic sun exposure, lighter skin phenotypes, increased age, and immunosuppression. Histologically, there are several variants of SCC: low-risk variants include keratoacanthomas, verrucous carcinomas, and clear cell SCC, and high-risk variants include acantholytic SCC, spindle cell SCC, and adenosquamous carcinoma.14 Generally, low-grade SCC will have well-differentiated or moderately differentiated intercellular bridges or keratin pearls with tumor cells in a solid or sheetlike pattern (Figure 3). High-grade SCC will be poorly differentiated with the presence of infiltrating individual tumor cells.15 Immunohistochemically, SCC stains positive for p63, p40, AE1/AE3, CK5/6, and MNF116 while Ber-Ep4 is negative.14,15 Poorly differentiated SCCs have high rates of mutation, commonly in the tumor protein 53 (TP53), Cyclin-dependent kinase inhibitor 2A (CDKN2A), Ras pathway, and notch receptor 1 (NOTCH-1) genes.13

Filley-3
FIGURE 3. Squamous cell carcinoma manifesting with proliferation of atypical keratinocytes with abundant eosinophilic cytoplasm extending into the dermis and forming keratin pearls (H&E, original magnification ×50).

Syringomas are benign adnexal tumors that manifest as multiple soft, yellow to flesh-colored, 1- to 2-mm papules typically located on the lower eyelids, most commonly in women of reproductive age.16 Syringomas are described on histology as small comma-shaped nests with cords of eosinophilic to clear cells with central ducts surrounded by a sclerotic stroma (Figure 4). They stain positively for carcinoembryonic antigen, epithelial membrane antigen, and CK-5 and are associated with genetic mutations in phosphatidylinositol-4, 5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) and AKT serine/threonine kinase 1 (ATK1).4

Filley-4
FIGURE 4. Syringoma with well-circumscribed proliferation of basaloid, cuboidal, and double-layered epithelial cells forming comma-shaped ducts as well as nests, cysts, and cords located primarily in the papillary dermis (H&E, original magnification ×50).

Due to its regular exposure to sunlight, the eyelid accounts for 5% to 10% of all skin malignancies. Common eyelid lesions include squamous papilloma, seborrheic keratosis, epidermal inclusion cyst, hidrocystoma, intradermal nevus, BCC, SCC, and sebaceous carcinoma.17 Aside from syringomas, benign sweat gland tumors like poromas, hidradenomas, and spiradenomas usually do not manifest on the eyelids but should be included in the differential diagnosis of an unidentifiable lesion due to the small risk for malignant transformation. Eyelid poromas manifest polymorphically, most commonly being clinically diagnosed as BCC, making the histologic examination key for proper diagnosis and management.18

References
  1. Patterson J. Weedon’s Skin Pathology. 5th ed. Elsevier Limited; 2021.
  2. Aoki K, Baba S, Nohara T, et al. Eccrine poroma. J Dermatol. 1980; 7:263-269. doi:10.1111/j.1346-8138.1980.tb01967.x
  3. Harvell JD, Kerschmann RL, LeBoit PE. Eccrine or apocrine poroma? six poromas with divergent adnexal differentiation. Am J Dermatopathol. 1996;18:1-9. doi:10.1097/00000372-199602000-00001
  4. Miller AC, Adjei S, Temiz LA, et al. Dermal duct tumor: a diagnostic dilemma. Dermatopathology. 2022;9:36-47. doi:10.3390
  5. Macagno N, Sohier P, Kervarrec T, et al. Recent advances on immunohistochemistry and molecular biology for the diagnosis of adnexal sweat gland tumors. Cancers. 2022;14:476. doi:10.3390/cancers14030476
  6. Robson A, Greene J, Ansari N, et al. Eccrine porocarcinoma (malignant eccrine poroma): a clinicopathologic study of 69 cases. Am J Surg Pathol. 2001;25:710-720. doi:10.1097/00000478-200106000-00002 /dermatopathology9010007
  7. Kurisu Y, Tsuji M, Yasuda E, et al. A case of eccrine porocarcinoma: usefulness of immunostain for S-100 protein in the diagnoses of recurrent and metastatic dedifferentiated lesions. Ann Dermatol. 2013;25:348-351. doi:10.5021/ad.2013.25.3.348
  8. Stanoszek LM, Wang GY, Harms PW. Histologic mimics of basal cell carcinoma. Arch Pathol Lab Med. 2017;141:1490-1502. doi:10.5858 /arpa.2017-0222-RA
  9. Niculet E, Craescu M, Rebegea L, et al. Basal cell carcinoma: comprehensive clinical and histopathological aspects, novel imaging tools and therapeutic approaches (review). Exp Ther Med. 2022;23:60. doi:10.3892/etm.2021.10982
  10. Pelucchi C, Di Landro A, Naldi L, et al. Risk factors for histological types and anatomic sites of cutaneous basal-cell carcinoma: an Italian case-control study. J Invest Dermatol. 2007;127:935-944. doi:10.1038/sj.jid.5700598
  11. Sunjaya AP, Sunjaya AF, Tan ST. The use of BEREP4 immunohistochemistry staining for detection of basal cell carcinoma. J Skin Cancer. 2017;2017:2692604. doi:10.1155/2017/2692604
  12. Kim J, Yang HJ, Pyo JS. Eccrine spiradenoma of the scalp. Arch Craniofacial Surg. 2017;18:211-213. doi:10.7181/acfs.2017.18.3.211
  13. Que SKT, Zwald FO, Schmults CD. Cutaneous squamous cell carcinoma: incidence, risk factors, diagnosis, and staging. J Am Acad Dermatol. 2018;78:237-247. doi:10.1016/j.jaad.2017.08.059
  14. Waldman A, Schmults C. Cutaneous squamous cell carcinoma. Hematol Oncol Clin North Am. 2019;33:1-12. doi:10.1016/j.hoc.2018.08.001
  15. Yanofsky VR, Mercer SE, Phelps RG. Histopathological variants of cutaneous squamous cell carcinoma: a review. J Skin Cancer. 2011;2011:210813. doi:10.1155/2011/210813
  16. Lee JH, Chang JY, Lee KH. Syringoma: a clinicopathologic and immunohistologic study and results of treatment. Yonsei Med J. 2007;48:35-40. doi:10.3349/ymj.2007.48.1.35
  17. Adamski WZ, Maciejewski J, Adamska K, et al. The prevalence of various eyelid skin lesions in a single-centre observation study. Adv Dermatol Allergol Dermatol Alergol. 2021;38:804-807. doi:10.5114 /ada.2020.95652
  18. Mencía-Gutiérrez E, Navarro-Perea C, Gutiérrez-Díaz E, et al. Eyelid eccrine poroma: a case report and review of literature. Cureus. 202:12:E8906. doi:10.7759/cureus.8906
References
  1. Patterson J. Weedon’s Skin Pathology. 5th ed. Elsevier Limited; 2021.
  2. Aoki K, Baba S, Nohara T, et al. Eccrine poroma. J Dermatol. 1980; 7:263-269. doi:10.1111/j.1346-8138.1980.tb01967.x
  3. Harvell JD, Kerschmann RL, LeBoit PE. Eccrine or apocrine poroma? six poromas with divergent adnexal differentiation. Am J Dermatopathol. 1996;18:1-9. doi:10.1097/00000372-199602000-00001
  4. Miller AC, Adjei S, Temiz LA, et al. Dermal duct tumor: a diagnostic dilemma. Dermatopathology. 2022;9:36-47. doi:10.3390
  5. Macagno N, Sohier P, Kervarrec T, et al. Recent advances on immunohistochemistry and molecular biology for the diagnosis of adnexal sweat gland tumors. Cancers. 2022;14:476. doi:10.3390/cancers14030476
  6. Robson A, Greene J, Ansari N, et al. Eccrine porocarcinoma (malignant eccrine poroma): a clinicopathologic study of 69 cases. Am J Surg Pathol. 2001;25:710-720. doi:10.1097/00000478-200106000-00002 /dermatopathology9010007
  7. Kurisu Y, Tsuji M, Yasuda E, et al. A case of eccrine porocarcinoma: usefulness of immunostain for S-100 protein in the diagnoses of recurrent and metastatic dedifferentiated lesions. Ann Dermatol. 2013;25:348-351. doi:10.5021/ad.2013.25.3.348
  8. Stanoszek LM, Wang GY, Harms PW. Histologic mimics of basal cell carcinoma. Arch Pathol Lab Med. 2017;141:1490-1502. doi:10.5858 /arpa.2017-0222-RA
  9. Niculet E, Craescu M, Rebegea L, et al. Basal cell carcinoma: comprehensive clinical and histopathological aspects, novel imaging tools and therapeutic approaches (review). Exp Ther Med. 2022;23:60. doi:10.3892/etm.2021.10982
  10. Pelucchi C, Di Landro A, Naldi L, et al. Risk factors for histological types and anatomic sites of cutaneous basal-cell carcinoma: an Italian case-control study. J Invest Dermatol. 2007;127:935-944. doi:10.1038/sj.jid.5700598
  11. Sunjaya AP, Sunjaya AF, Tan ST. The use of BEREP4 immunohistochemistry staining for detection of basal cell carcinoma. J Skin Cancer. 2017;2017:2692604. doi:10.1155/2017/2692604
  12. Kim J, Yang HJ, Pyo JS. Eccrine spiradenoma of the scalp. Arch Craniofacial Surg. 2017;18:211-213. doi:10.7181/acfs.2017.18.3.211
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Issue
Cutis - 115(3)
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Cutis - 115(3)
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94, 100-101
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94, 100-101
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Pink Papule on the Lower Eyelid

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Pink Papule on the Lower Eyelid

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A 57-year-old man with no notable medical history presented to the dermatology clinic for evaluation of an asymptomatic papule on the left lower eyelid. The patient reported that the lesion seemed to wax and wane in size over time. Physical examination revealed a small, pink, verrucous papule on the left lower eyelid. A shave biopsy of the lesion revealed a well-circumscribed collection of small, monomorphic, cuboidal cells with basophilic round nuclei, inconspicuous nucleoli, and compact eosinophilic cytoplasm (top) with focal areas of duct formation (bottom) that was sharply demarcated from normal keratinocytes.

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