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THE DIAGNOSIS: Apocrine Hidrocystoma

Histology for all 3 lesions demonstrated similar cystic structures lined by a dual layer of epithelial cells, with the outermost layer composed of flattened myoepithelial cells and the inner layer composed of cells with apocrine features (Figure 1). Based on these findings, a diagnosis of apocrine hidrocystoma was made. The patient underwent successful surgical excision shortly thereafter without recurrence at follow-up 1 year later. 

Apocrine hidrocystomas are rare benign cystic lesions that are considered to be adenomatous proliferations of apocrine glands. They typically manifest as solitary asymptomatic lesions measuring 3 to 15 mm.1 They tend to appear on the face, usually in the periorbital region, but also have been described on the neck, scalp, trunk, arms, and legs.2-4 Multiple apocrine hidrocystomas can be a marker of 2 rare inherited disorders: Gorlin-Goltz syndrome and Schopf-Schulz-Passarge syndrome.5 Apocrine hidrocystomas may be flesh colored or may have a blue, black, or brown appearance due to the Tyndall effect, in which light with shorter wavelengths is scattered by the contents of the lesions.2 Histologically, apocrine hidrocystomas are cysts lined by a dual layer of epithelial cells. The inner layer is composed of cells with apocrine features, and the outer layer is composed of flattened myoepithelial cells. Due to their range of colors and predilection for sun-exposed surfaces, apocrine hidrocystomas may be mistaken for various malignant neoplasms, including melanoma.6,7

FIGURE 1. Apocrine hidrocystoma. Cystic space lined by a dual layer of epithelial cells with the outermost layer composed of flattened myoepithelial cells and the inner layer of cells with apocrine features (H&E, original magnification ×10).

The differential diagnosis for our patient included agminated blue nevi, melanoma, pigmented basal cell carcinoma (BCC), and seborrheic keratosis. A blue nevus is a dermal melanocytic lesion that manifests as a well-demarcated, blue to blue-black papule that typically appears on the face, scalp, arms, legs, lower back, and buttocks. Although there are several histologic subtypes, the common blue nevus usually manifests as a solitary lesion measuring less than 1 cm, often developing during childhood to young adulthood.8 Histologically, common blue nevi are characterized by a dermal proliferation of deeply pigmented bipolar spindled melanocytes embedded in thickened collagen bundles, often with scattered epithelioid melanophages, and no conspicuous mitotic activity (Figure 2).9 There are other types of blue nevi, including cellular blue nevi, which tend to be larger and manifest commonly on the buttocks and sacrococcygeal region in early adulthood.9 Histologically, cellular blue nevi contain oval to spindled melanocytes with scattered melanophages forming a well-demarcated nodule typically in the reticular dermis. There may be bulbous extension into the subcutaneous adipose tissue. Occasional mitoses may be seen.9,10 Melanoma can arise from common or cellular blue nevi, though it more frequently occurs with cellular blue nevi. Other subtypes of blue nevi have been described, including the sclerosing, plaque-type, combined, hypomelanotic/amelanotic, and pigmented epithelioid melanocytoma.11 However, they typically have features of the common blue nevus or cellular blue nevus, such as oval/spindle cell morphology, some degree of melanin, and biphasic architecture, but are classified according to their dominant histologic characteristics. 

FIGURE 2. Common blue nevus. Deeply pigmented dermal spindle cell proliferation separated from the overlying epidermis by a Grenz zone (H&E, original magnification ×10).

Given the location of our patient’s lesions on the scalp and his extensive history of sun exposure, malignancy was high in the differential. Multiple synchronous primary melanomas including nodular melanoma, blue nevus–like metastatic melanoma, and metastatic melanoma were considered. The leg and the scalp have the highest reported incidence of cutaneous metastases of melanoma, with many cases presenting as dermal or subcutaneous nodules and eruptive blue nevus–like papules, similar to our patient’s clinical presentation.12,13 Nodular melanoma (NM) is one of 4 major types of melanoma, accounting for approximately 15% to 30% of cases in the United States.14 Nodular melanoma typically manifests as a smooth, raised, symmetric, well-circumscribed lesion with variable pigmentation, from very dark to amelanotic. Histologically, NM is defined as a dermal mass, either in isolation or with an epidermal component, not to exceed 3 rete ridges beyond the dermal component.15 Tumor cells have a high cell density with pleomorphism, usually with atypical epithelioid cells with vesicular nuclei and irregular cytoplasm, and occasionally spindle cells (Figure 2).16 Mitoses and necrosis are frequent. Scalp location independently is responsible for worse survival, both overall and melanoma specific.17 Nodular melanoma tends to have greater Breslow thickness at diagnosis than other melanoma subtypes and often carries a worse prognosis. 

FIGURE 3. Nodular melanoma. Prominent vertical growth into the dermis with cytoplasmic melanin present (H&E, original magnification ×10).

Malignant melanomas that develop from or in conjunction with or bear histologic resemblance to blue nevi are termed blue nevus–like melanoma or blue nevus–associated melanoma. These malignancies are exceedingly rare, accounting for only 0.3% of melanomas in one Turkey-based multicenter study.18 The histologic criteria for diagnosing blue nevus–like melanoma are poorly defined, and terminology of these lesions has led to some debate in naming conventions.19 Nevertheless, unlike blue nevus, blue nevus–like melanoma demonstrates histologic features of malignancy, including pleomorphism, prominent nucleoli, mitotic activity, vascular invasion, and potential necrosis.10 The lack of an inflammatory infiltrate, surrounding fibrosis, junctional activity, and pre-existing nevus can help distinguish cutaneous melanoma metastases from primary nodular melanoma. Immunohistochemical stains such as S100, Melan-A/MART1, or SOX-10 can help confirm melanocytic lineage.12 

Pigmented BCC is a clinical and histologic variant of BCC characterized by increased melanin pigmentation due to melanocytes admixed with tumor cells. Dermoscopically, the pigment can have a maple leaf–like appearance with spoke-wheel areas, in-focus dots, and concentric structures at the dermoepidermal junction, which is more characteristic of superficial and infiltrating BCC.20 In nodular BCC, the pigment occurs as blue-gray ovoid nests and globules in deeper layers of the dermis.20 

Seborrheic keratoses (SKs) can vary widely in clinical appearance, with pigmentation ranging from flesh colored to yellow to brown to black. Melanoacanthomas are acanthotic SKs that are highly pigmented due to intermixed epidermal melanocytes and subepidermal melanophages.21 Dermoscopy can help distinguish cutaneous malignancies from SKs, which often demonstrate fissures and ridges, comedolike openings, and milialike cysts. Biopsy sometimes is required to assess for malignancy, as was the case in our patient. The classic histologic features of SKs include acanthosis, papillomatosis, and hyperkeratosis.22 

This case highlights the need to consider apocrine hidrocystoma, along with malignancy, in the differential diagnosis of pigmented cystic masses of the face and scalp. Because apocrine hidrocystomas are benign, they do not need to be treated but often are surgically excised for cosmesis or complete histopathologic examination. Destruction via electrodessication, carbon dioxide ablation, trichloroacetic acid chemical ablation, botulinum toxin injection, and anticholinergic creams sometimes is used, especially for cosmetic treatment of multiple small lesions.5 Our patient was treated with surgical excision with no evidence of recurrence on follow-up 1 year later. 

References
  1. Ioannidis DG, Drivas EI, Papadakis CE, et al. Hidrocystoma of the external auditory canal: a case report. Cases J. 2009;2:79. doi:10.1186/1757- 1626-2-79 
  2. Nguyen HP, Barker HS, Bloomquist L, et al. Giant pigmented apocrine hidrocystoma of the scalp. Dermatol Online J. 2020;26. doi:10.5070/D3268049895 
  3. Mendoza-Cembranos MD, Haro R, Requena L, et al. Digital apocrine hidrocystoma: the exception confirms the rule. Am J Dermatopathol. 2019;41:79. doi:10.1097/DAD.0000000000001044 
  4. May C, Chang O, Compton N. A giant apocrine hidrocystoma of the trunk. Dermatol Online J. 2017;23. doi:10.5070/D3239036497 
  5. Sarabi K, Khachemoune A. Hidrocystomas—a brief review. Medscape Gen Med. 2006;8:57. 
  6. Kruse ALD, Zwahlen R, Bredell MG, et al. Apocrine hidrocystoma of the cheek. J Craniofac Surg. 2010;21:594-596. doi:10.1097 /SCS.0b013e3181d08c77 
  7. Zaballos P, Bañuls J, Medina C, et al. Dermoscopy of apocrine hidrocystomas: a morphological study. J Eur Acad Dermatol Venereol. 2014;28:378-381. doi:10.1111/jdv.12044 
  8. Rodriguez HA, Ackerman LV. Cellular blue nevus. clinicopathologic study of forty-five cases. Cancer. 1968;21:393-405. doi:10.1002 /1097-0142(196803)21:3<393::aid-cncr2820210309>3.0.co;2-k 
  9. Murali R, McCarthy SW, Scolyer RA. Blue nevi and related lesions: a review highlighting atypical and newly described variants, distinguishing features and diagnostic pitfalls. Adv Anat Pathol. 2009;16:365. doi:10.1097/PAP.0b013e3181bb6b53 
  10. Borgenvik TL, Karlsvik TM, Ray S, et al. Blue nevus-like and blue nevusassociated melanoma: a comprehensive review of the literature. ANZ J Surg. 2017;87:345-349. doi:10.1111/ans.13946 
  11. de la Fouchardiere A. Blue naevi and the blue tumour spectrum. Pathology. 2023;55:187-195. doi:10.1016/j.pathol.2022.12.342 
  12. Lowe L. Metastatic melanoma and rare melanoma variants: a review. Pathology (Phila). 2023;55:236-244. doi:10.1016/j.pathol.2022.11.006 
  13. Plaza JA, Torres-Cabala C, Evans H, et al. Cutaneous metastases of malignant melanoma: a clinicopathologic study of 192 cases with emphasis on the morphologic spectrum. Am J Dermatopathol. 2010;32:129-136. doi:10.1097/DAD.0b013e3181b34a19 
  14. Shaikh WR, Xiong M, Weinstock MA. The contribution of nodular subtype to melanoma mortality in the United States, 1978 to 2007. Archives of Dermatology. 2012;148:30-36. doi:10.1001/archdermatol.2011.264 
  15. Clark WH, From L, Bernardino EA, et al. The histogenesis and biologic behavior of primary human malignant melanomas of the skin. Cancer Res. 1969;29:705-727. 
  16. Bobos M. Histopathologic classification and prognostic factors of melanoma: a 2021 update. Ital J Dermatol Venereol. 2021;156:300-321. doi:10.23736/S2784-8671.21.06958-3 
  17. Ozao-Choy J, Nelson DW, Hiles J, et al. The prognostic importance of scalp location in primary head and neck melanoma. J Surg Oncol. 2017;116:337-343. doi:10.1002/jso.24679 
  18. Gamsizkan M, Yilmaz I, Buyukbabani N, et al. A retrospective multicenter evaluation of cutaneous melanomas in Turkey. Asian Pac J Cancer Prev APJCP. 2014;15:10451-10456. doi:10.7314 /apjcp.2014.15.23.10451 
  19. Mones JM, Ackerman AB. “Atypical” blue nevus, “malignant” blue nevus, and “metastasizing” blue nevus: a critique in historical perspective of three concepts flawed fatally. Am J Dermatopathol. 2004;26:407-430. doi:10.1097/00000372-200410000-00012 
  20. Tanese K. Diagnosis and management of basal cell carcinoma Curr Treat Options Oncol. 2019;20:13. doi:10.1007/s11864 -019-0610-0
  21. Barthelmann S, Butsch F, Lang BM, et al. Seborrheic keratosis. JDDG J Dtsch Dermatol Ges. 2023;21:265-277. doi:10.1111/ddg.14984
  22. Taylor S. Advancing the understanding of seborrheic keratosis. J Drugs Dermatol. 2017;16:419-424.
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From the Dell Medical School, University of Texas at Austin. Drs. Tabata, Keeling, and Brown are from the Division of Dermatology. 

Georgia E. Williams and Drs. Keeling and Brown have no relevant financial disclosures to report. Dr. Tabata has received a research grant from the Seton Educational Research Fund. 

Correspondence: Georgia E. Williams, BA, MArch, 1501 Red River St, Austin, TX 78712 ([email protected]). 

Cutis. 2025 May;115(5):E3-E6. doi:10.12788/cutis.1221

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From the Dell Medical School, University of Texas at Austin. Drs. Tabata, Keeling, and Brown are from the Division of Dermatology. 

Georgia E. Williams and Drs. Keeling and Brown have no relevant financial disclosures to report. Dr. Tabata has received a research grant from the Seton Educational Research Fund. 

Correspondence: Georgia E. Williams, BA, MArch, 1501 Red River St, Austin, TX 78712 ([email protected]). 

Cutis. 2025 May;115(5):E3-E6. doi:10.12788/cutis.1221

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From the Dell Medical School, University of Texas at Austin. Drs. Tabata, Keeling, and Brown are from the Division of Dermatology. 

Georgia E. Williams and Drs. Keeling and Brown have no relevant financial disclosures to report. Dr. Tabata has received a research grant from the Seton Educational Research Fund. 

Correspondence: Georgia E. Williams, BA, MArch, 1501 Red River St, Austin, TX 78712 ([email protected]). 

Cutis. 2025 May;115(5):E3-E6. doi:10.12788/cutis.1221

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THE DIAGNOSIS: Apocrine Hidrocystoma

Histology for all 3 lesions demonstrated similar cystic structures lined by a dual layer of epithelial cells, with the outermost layer composed of flattened myoepithelial cells and the inner layer composed of cells with apocrine features (Figure 1). Based on these findings, a diagnosis of apocrine hidrocystoma was made. The patient underwent successful surgical excision shortly thereafter without recurrence at follow-up 1 year later. 

Apocrine hidrocystomas are rare benign cystic lesions that are considered to be adenomatous proliferations of apocrine glands. They typically manifest as solitary asymptomatic lesions measuring 3 to 15 mm.1 They tend to appear on the face, usually in the periorbital region, but also have been described on the neck, scalp, trunk, arms, and legs.2-4 Multiple apocrine hidrocystomas can be a marker of 2 rare inherited disorders: Gorlin-Goltz syndrome and Schopf-Schulz-Passarge syndrome.5 Apocrine hidrocystomas may be flesh colored or may have a blue, black, or brown appearance due to the Tyndall effect, in which light with shorter wavelengths is scattered by the contents of the lesions.2 Histologically, apocrine hidrocystomas are cysts lined by a dual layer of epithelial cells. The inner layer is composed of cells with apocrine features, and the outer layer is composed of flattened myoepithelial cells. Due to their range of colors and predilection for sun-exposed surfaces, apocrine hidrocystomas may be mistaken for various malignant neoplasms, including melanoma.6,7

FIGURE 1. Apocrine hidrocystoma. Cystic space lined by a dual layer of epithelial cells with the outermost layer composed of flattened myoepithelial cells and the inner layer of cells with apocrine features (H&E, original magnification ×10).

The differential diagnosis for our patient included agminated blue nevi, melanoma, pigmented basal cell carcinoma (BCC), and seborrheic keratosis. A blue nevus is a dermal melanocytic lesion that manifests as a well-demarcated, blue to blue-black papule that typically appears on the face, scalp, arms, legs, lower back, and buttocks. Although there are several histologic subtypes, the common blue nevus usually manifests as a solitary lesion measuring less than 1 cm, often developing during childhood to young adulthood.8 Histologically, common blue nevi are characterized by a dermal proliferation of deeply pigmented bipolar spindled melanocytes embedded in thickened collagen bundles, often with scattered epithelioid melanophages, and no conspicuous mitotic activity (Figure 2).9 There are other types of blue nevi, including cellular blue nevi, which tend to be larger and manifest commonly on the buttocks and sacrococcygeal region in early adulthood.9 Histologically, cellular blue nevi contain oval to spindled melanocytes with scattered melanophages forming a well-demarcated nodule typically in the reticular dermis. There may be bulbous extension into the subcutaneous adipose tissue. Occasional mitoses may be seen.9,10 Melanoma can arise from common or cellular blue nevi, though it more frequently occurs with cellular blue nevi. Other subtypes of blue nevi have been described, including the sclerosing, plaque-type, combined, hypomelanotic/amelanotic, and pigmented epithelioid melanocytoma.11 However, they typically have features of the common blue nevus or cellular blue nevus, such as oval/spindle cell morphology, some degree of melanin, and biphasic architecture, but are classified according to their dominant histologic characteristics. 

FIGURE 2. Common blue nevus. Deeply pigmented dermal spindle cell proliferation separated from the overlying epidermis by a Grenz zone (H&E, original magnification ×10).

Given the location of our patient’s lesions on the scalp and his extensive history of sun exposure, malignancy was high in the differential. Multiple synchronous primary melanomas including nodular melanoma, blue nevus–like metastatic melanoma, and metastatic melanoma were considered. The leg and the scalp have the highest reported incidence of cutaneous metastases of melanoma, with many cases presenting as dermal or subcutaneous nodules and eruptive blue nevus–like papules, similar to our patient’s clinical presentation.12,13 Nodular melanoma (NM) is one of 4 major types of melanoma, accounting for approximately 15% to 30% of cases in the United States.14 Nodular melanoma typically manifests as a smooth, raised, symmetric, well-circumscribed lesion with variable pigmentation, from very dark to amelanotic. Histologically, NM is defined as a dermal mass, either in isolation or with an epidermal component, not to exceed 3 rete ridges beyond the dermal component.15 Tumor cells have a high cell density with pleomorphism, usually with atypical epithelioid cells with vesicular nuclei and irregular cytoplasm, and occasionally spindle cells (Figure 2).16 Mitoses and necrosis are frequent. Scalp location independently is responsible for worse survival, both overall and melanoma specific.17 Nodular melanoma tends to have greater Breslow thickness at diagnosis than other melanoma subtypes and often carries a worse prognosis. 

FIGURE 3. Nodular melanoma. Prominent vertical growth into the dermis with cytoplasmic melanin present (H&E, original magnification ×10).

Malignant melanomas that develop from or in conjunction with or bear histologic resemblance to blue nevi are termed blue nevus–like melanoma or blue nevus–associated melanoma. These malignancies are exceedingly rare, accounting for only 0.3% of melanomas in one Turkey-based multicenter study.18 The histologic criteria for diagnosing blue nevus–like melanoma are poorly defined, and terminology of these lesions has led to some debate in naming conventions.19 Nevertheless, unlike blue nevus, blue nevus–like melanoma demonstrates histologic features of malignancy, including pleomorphism, prominent nucleoli, mitotic activity, vascular invasion, and potential necrosis.10 The lack of an inflammatory infiltrate, surrounding fibrosis, junctional activity, and pre-existing nevus can help distinguish cutaneous melanoma metastases from primary nodular melanoma. Immunohistochemical stains such as S100, Melan-A/MART1, or SOX-10 can help confirm melanocytic lineage.12 

Pigmented BCC is a clinical and histologic variant of BCC characterized by increased melanin pigmentation due to melanocytes admixed with tumor cells. Dermoscopically, the pigment can have a maple leaf–like appearance with spoke-wheel areas, in-focus dots, and concentric structures at the dermoepidermal junction, which is more characteristic of superficial and infiltrating BCC.20 In nodular BCC, the pigment occurs as blue-gray ovoid nests and globules in deeper layers of the dermis.20 

Seborrheic keratoses (SKs) can vary widely in clinical appearance, with pigmentation ranging from flesh colored to yellow to brown to black. Melanoacanthomas are acanthotic SKs that are highly pigmented due to intermixed epidermal melanocytes and subepidermal melanophages.21 Dermoscopy can help distinguish cutaneous malignancies from SKs, which often demonstrate fissures and ridges, comedolike openings, and milialike cysts. Biopsy sometimes is required to assess for malignancy, as was the case in our patient. The classic histologic features of SKs include acanthosis, papillomatosis, and hyperkeratosis.22 

This case highlights the need to consider apocrine hidrocystoma, along with malignancy, in the differential diagnosis of pigmented cystic masses of the face and scalp. Because apocrine hidrocystomas are benign, they do not need to be treated but often are surgically excised for cosmesis or complete histopathologic examination. Destruction via electrodessication, carbon dioxide ablation, trichloroacetic acid chemical ablation, botulinum toxin injection, and anticholinergic creams sometimes is used, especially for cosmetic treatment of multiple small lesions.5 Our patient was treated with surgical excision with no evidence of recurrence on follow-up 1 year later. 

THE DIAGNOSIS: Apocrine Hidrocystoma

Histology for all 3 lesions demonstrated similar cystic structures lined by a dual layer of epithelial cells, with the outermost layer composed of flattened myoepithelial cells and the inner layer composed of cells with apocrine features (Figure 1). Based on these findings, a diagnosis of apocrine hidrocystoma was made. The patient underwent successful surgical excision shortly thereafter without recurrence at follow-up 1 year later. 

Apocrine hidrocystomas are rare benign cystic lesions that are considered to be adenomatous proliferations of apocrine glands. They typically manifest as solitary asymptomatic lesions measuring 3 to 15 mm.1 They tend to appear on the face, usually in the periorbital region, but also have been described on the neck, scalp, trunk, arms, and legs.2-4 Multiple apocrine hidrocystomas can be a marker of 2 rare inherited disorders: Gorlin-Goltz syndrome and Schopf-Schulz-Passarge syndrome.5 Apocrine hidrocystomas may be flesh colored or may have a blue, black, or brown appearance due to the Tyndall effect, in which light with shorter wavelengths is scattered by the contents of the lesions.2 Histologically, apocrine hidrocystomas are cysts lined by a dual layer of epithelial cells. The inner layer is composed of cells with apocrine features, and the outer layer is composed of flattened myoepithelial cells. Due to their range of colors and predilection for sun-exposed surfaces, apocrine hidrocystomas may be mistaken for various malignant neoplasms, including melanoma.6,7

FIGURE 1. Apocrine hidrocystoma. Cystic space lined by a dual layer of epithelial cells with the outermost layer composed of flattened myoepithelial cells and the inner layer of cells with apocrine features (H&E, original magnification ×10).

The differential diagnosis for our patient included agminated blue nevi, melanoma, pigmented basal cell carcinoma (BCC), and seborrheic keratosis. A blue nevus is a dermal melanocytic lesion that manifests as a well-demarcated, blue to blue-black papule that typically appears on the face, scalp, arms, legs, lower back, and buttocks. Although there are several histologic subtypes, the common blue nevus usually manifests as a solitary lesion measuring less than 1 cm, often developing during childhood to young adulthood.8 Histologically, common blue nevi are characterized by a dermal proliferation of deeply pigmented bipolar spindled melanocytes embedded in thickened collagen bundles, often with scattered epithelioid melanophages, and no conspicuous mitotic activity (Figure 2).9 There are other types of blue nevi, including cellular blue nevi, which tend to be larger and manifest commonly on the buttocks and sacrococcygeal region in early adulthood.9 Histologically, cellular blue nevi contain oval to spindled melanocytes with scattered melanophages forming a well-demarcated nodule typically in the reticular dermis. There may be bulbous extension into the subcutaneous adipose tissue. Occasional mitoses may be seen.9,10 Melanoma can arise from common or cellular blue nevi, though it more frequently occurs with cellular blue nevi. Other subtypes of blue nevi have been described, including the sclerosing, plaque-type, combined, hypomelanotic/amelanotic, and pigmented epithelioid melanocytoma.11 However, they typically have features of the common blue nevus or cellular blue nevus, such as oval/spindle cell morphology, some degree of melanin, and biphasic architecture, but are classified according to their dominant histologic characteristics. 

FIGURE 2. Common blue nevus. Deeply pigmented dermal spindle cell proliferation separated from the overlying epidermis by a Grenz zone (H&E, original magnification ×10).

Given the location of our patient’s lesions on the scalp and his extensive history of sun exposure, malignancy was high in the differential. Multiple synchronous primary melanomas including nodular melanoma, blue nevus–like metastatic melanoma, and metastatic melanoma were considered. The leg and the scalp have the highest reported incidence of cutaneous metastases of melanoma, with many cases presenting as dermal or subcutaneous nodules and eruptive blue nevus–like papules, similar to our patient’s clinical presentation.12,13 Nodular melanoma (NM) is one of 4 major types of melanoma, accounting for approximately 15% to 30% of cases in the United States.14 Nodular melanoma typically manifests as a smooth, raised, symmetric, well-circumscribed lesion with variable pigmentation, from very dark to amelanotic. Histologically, NM is defined as a dermal mass, either in isolation or with an epidermal component, not to exceed 3 rete ridges beyond the dermal component.15 Tumor cells have a high cell density with pleomorphism, usually with atypical epithelioid cells with vesicular nuclei and irregular cytoplasm, and occasionally spindle cells (Figure 2).16 Mitoses and necrosis are frequent. Scalp location independently is responsible for worse survival, both overall and melanoma specific.17 Nodular melanoma tends to have greater Breslow thickness at diagnosis than other melanoma subtypes and often carries a worse prognosis. 

FIGURE 3. Nodular melanoma. Prominent vertical growth into the dermis with cytoplasmic melanin present (H&E, original magnification ×10).

Malignant melanomas that develop from or in conjunction with or bear histologic resemblance to blue nevi are termed blue nevus–like melanoma or blue nevus–associated melanoma. These malignancies are exceedingly rare, accounting for only 0.3% of melanomas in one Turkey-based multicenter study.18 The histologic criteria for diagnosing blue nevus–like melanoma are poorly defined, and terminology of these lesions has led to some debate in naming conventions.19 Nevertheless, unlike blue nevus, blue nevus–like melanoma demonstrates histologic features of malignancy, including pleomorphism, prominent nucleoli, mitotic activity, vascular invasion, and potential necrosis.10 The lack of an inflammatory infiltrate, surrounding fibrosis, junctional activity, and pre-existing nevus can help distinguish cutaneous melanoma metastases from primary nodular melanoma. Immunohistochemical stains such as S100, Melan-A/MART1, or SOX-10 can help confirm melanocytic lineage.12 

Pigmented BCC is a clinical and histologic variant of BCC characterized by increased melanin pigmentation due to melanocytes admixed with tumor cells. Dermoscopically, the pigment can have a maple leaf–like appearance with spoke-wheel areas, in-focus dots, and concentric structures at the dermoepidermal junction, which is more characteristic of superficial and infiltrating BCC.20 In nodular BCC, the pigment occurs as blue-gray ovoid nests and globules in deeper layers of the dermis.20 

Seborrheic keratoses (SKs) can vary widely in clinical appearance, with pigmentation ranging from flesh colored to yellow to brown to black. Melanoacanthomas are acanthotic SKs that are highly pigmented due to intermixed epidermal melanocytes and subepidermal melanophages.21 Dermoscopy can help distinguish cutaneous malignancies from SKs, which often demonstrate fissures and ridges, comedolike openings, and milialike cysts. Biopsy sometimes is required to assess for malignancy, as was the case in our patient. The classic histologic features of SKs include acanthosis, papillomatosis, and hyperkeratosis.22 

This case highlights the need to consider apocrine hidrocystoma, along with malignancy, in the differential diagnosis of pigmented cystic masses of the face and scalp. Because apocrine hidrocystomas are benign, they do not need to be treated but often are surgically excised for cosmesis or complete histopathologic examination. Destruction via electrodessication, carbon dioxide ablation, trichloroacetic acid chemical ablation, botulinum toxin injection, and anticholinergic creams sometimes is used, especially for cosmetic treatment of multiple small lesions.5 Our patient was treated with surgical excision with no evidence of recurrence on follow-up 1 year later. 

References
  1. Ioannidis DG, Drivas EI, Papadakis CE, et al. Hidrocystoma of the external auditory canal: a case report. Cases J. 2009;2:79. doi:10.1186/1757- 1626-2-79 
  2. Nguyen HP, Barker HS, Bloomquist L, et al. Giant pigmented apocrine hidrocystoma of the scalp. Dermatol Online J. 2020;26. doi:10.5070/D3268049895 
  3. Mendoza-Cembranos MD, Haro R, Requena L, et al. Digital apocrine hidrocystoma: the exception confirms the rule. Am J Dermatopathol. 2019;41:79. doi:10.1097/DAD.0000000000001044 
  4. May C, Chang O, Compton N. A giant apocrine hidrocystoma of the trunk. Dermatol Online J. 2017;23. doi:10.5070/D3239036497 
  5. Sarabi K, Khachemoune A. Hidrocystomas—a brief review. Medscape Gen Med. 2006;8:57. 
  6. Kruse ALD, Zwahlen R, Bredell MG, et al. Apocrine hidrocystoma of the cheek. J Craniofac Surg. 2010;21:594-596. doi:10.1097 /SCS.0b013e3181d08c77 
  7. Zaballos P, Bañuls J, Medina C, et al. Dermoscopy of apocrine hidrocystomas: a morphological study. J Eur Acad Dermatol Venereol. 2014;28:378-381. doi:10.1111/jdv.12044 
  8. Rodriguez HA, Ackerman LV. Cellular blue nevus. clinicopathologic study of forty-five cases. Cancer. 1968;21:393-405. doi:10.1002 /1097-0142(196803)21:3<393::aid-cncr2820210309>3.0.co;2-k 
  9. Murali R, McCarthy SW, Scolyer RA. Blue nevi and related lesions: a review highlighting atypical and newly described variants, distinguishing features and diagnostic pitfalls. Adv Anat Pathol. 2009;16:365. doi:10.1097/PAP.0b013e3181bb6b53 
  10. Borgenvik TL, Karlsvik TM, Ray S, et al. Blue nevus-like and blue nevusassociated melanoma: a comprehensive review of the literature. ANZ J Surg. 2017;87:345-349. doi:10.1111/ans.13946 
  11. de la Fouchardiere A. Blue naevi and the blue tumour spectrum. Pathology. 2023;55:187-195. doi:10.1016/j.pathol.2022.12.342 
  12. Lowe L. Metastatic melanoma and rare melanoma variants: a review. Pathology (Phila). 2023;55:236-244. doi:10.1016/j.pathol.2022.11.006 
  13. Plaza JA, Torres-Cabala C, Evans H, et al. Cutaneous metastases of malignant melanoma: a clinicopathologic study of 192 cases with emphasis on the morphologic spectrum. Am J Dermatopathol. 2010;32:129-136. doi:10.1097/DAD.0b013e3181b34a19 
  14. Shaikh WR, Xiong M, Weinstock MA. The contribution of nodular subtype to melanoma mortality in the United States, 1978 to 2007. Archives of Dermatology. 2012;148:30-36. doi:10.1001/archdermatol.2011.264 
  15. Clark WH, From L, Bernardino EA, et al. The histogenesis and biologic behavior of primary human malignant melanomas of the skin. Cancer Res. 1969;29:705-727. 
  16. Bobos M. Histopathologic classification and prognostic factors of melanoma: a 2021 update. Ital J Dermatol Venereol. 2021;156:300-321. doi:10.23736/S2784-8671.21.06958-3 
  17. Ozao-Choy J, Nelson DW, Hiles J, et al. The prognostic importance of scalp location in primary head and neck melanoma. J Surg Oncol. 2017;116:337-343. doi:10.1002/jso.24679 
  18. Gamsizkan M, Yilmaz I, Buyukbabani N, et al. A retrospective multicenter evaluation of cutaneous melanomas in Turkey. Asian Pac J Cancer Prev APJCP. 2014;15:10451-10456. doi:10.7314 /apjcp.2014.15.23.10451 
  19. Mones JM, Ackerman AB. “Atypical” blue nevus, “malignant” blue nevus, and “metastasizing” blue nevus: a critique in historical perspective of three concepts flawed fatally. Am J Dermatopathol. 2004;26:407-430. doi:10.1097/00000372-200410000-00012 
  20. Tanese K. Diagnosis and management of basal cell carcinoma Curr Treat Options Oncol. 2019;20:13. doi:10.1007/s11864 -019-0610-0
  21. Barthelmann S, Butsch F, Lang BM, et al. Seborrheic keratosis. JDDG J Dtsch Dermatol Ges. 2023;21:265-277. doi:10.1111/ddg.14984
  22. Taylor S. Advancing the understanding of seborrheic keratosis. J Drugs Dermatol. 2017;16:419-424.
References
  1. Ioannidis DG, Drivas EI, Papadakis CE, et al. Hidrocystoma of the external auditory canal: a case report. Cases J. 2009;2:79. doi:10.1186/1757- 1626-2-79 
  2. Nguyen HP, Barker HS, Bloomquist L, et al. Giant pigmented apocrine hidrocystoma of the scalp. Dermatol Online J. 2020;26. doi:10.5070/D3268049895 
  3. Mendoza-Cembranos MD, Haro R, Requena L, et al. Digital apocrine hidrocystoma: the exception confirms the rule. Am J Dermatopathol. 2019;41:79. doi:10.1097/DAD.0000000000001044 
  4. May C, Chang O, Compton N. A giant apocrine hidrocystoma of the trunk. Dermatol Online J. 2017;23. doi:10.5070/D3239036497 
  5. Sarabi K, Khachemoune A. Hidrocystomas—a brief review. Medscape Gen Med. 2006;8:57. 
  6. Kruse ALD, Zwahlen R, Bredell MG, et al. Apocrine hidrocystoma of the cheek. J Craniofac Surg. 2010;21:594-596. doi:10.1097 /SCS.0b013e3181d08c77 
  7. Zaballos P, Bañuls J, Medina C, et al. Dermoscopy of apocrine hidrocystomas: a morphological study. J Eur Acad Dermatol Venereol. 2014;28:378-381. doi:10.1111/jdv.12044 
  8. Rodriguez HA, Ackerman LV. Cellular blue nevus. clinicopathologic study of forty-five cases. Cancer. 1968;21:393-405. doi:10.1002 /1097-0142(196803)21:3<393::aid-cncr2820210309>3.0.co;2-k 
  9. Murali R, McCarthy SW, Scolyer RA. Blue nevi and related lesions: a review highlighting atypical and newly described variants, distinguishing features and diagnostic pitfalls. Adv Anat Pathol. 2009;16:365. doi:10.1097/PAP.0b013e3181bb6b53 
  10. Borgenvik TL, Karlsvik TM, Ray S, et al. Blue nevus-like and blue nevusassociated melanoma: a comprehensive review of the literature. ANZ J Surg. 2017;87:345-349. doi:10.1111/ans.13946 
  11. de la Fouchardiere A. Blue naevi and the blue tumour spectrum. Pathology. 2023;55:187-195. doi:10.1016/j.pathol.2022.12.342 
  12. Lowe L. Metastatic melanoma and rare melanoma variants: a review. Pathology (Phila). 2023;55:236-244. doi:10.1016/j.pathol.2022.11.006 
  13. Plaza JA, Torres-Cabala C, Evans H, et al. Cutaneous metastases of malignant melanoma: a clinicopathologic study of 192 cases with emphasis on the morphologic spectrum. Am J Dermatopathol. 2010;32:129-136. doi:10.1097/DAD.0b013e3181b34a19 
  14. Shaikh WR, Xiong M, Weinstock MA. The contribution of nodular subtype to melanoma mortality in the United States, 1978 to 2007. Archives of Dermatology. 2012;148:30-36. doi:10.1001/archdermatol.2011.264 
  15. Clark WH, From L, Bernardino EA, et al. The histogenesis and biologic behavior of primary human malignant melanomas of the skin. Cancer Res. 1969;29:705-727. 
  16. Bobos M. Histopathologic classification and prognostic factors of melanoma: a 2021 update. Ital J Dermatol Venereol. 2021;156:300-321. doi:10.23736/S2784-8671.21.06958-3 
  17. Ozao-Choy J, Nelson DW, Hiles J, et al. The prognostic importance of scalp location in primary head and neck melanoma. J Surg Oncol. 2017;116:337-343. doi:10.1002/jso.24679 
  18. Gamsizkan M, Yilmaz I, Buyukbabani N, et al. A retrospective multicenter evaluation of cutaneous melanomas in Turkey. Asian Pac J Cancer Prev APJCP. 2014;15:10451-10456. doi:10.7314 /apjcp.2014.15.23.10451 
  19. Mones JM, Ackerman AB. “Atypical” blue nevus, “malignant” blue nevus, and “metastasizing” blue nevus: a critique in historical perspective of three concepts flawed fatally. Am J Dermatopathol. 2004;26:407-430. doi:10.1097/00000372-200410000-00012 
  20. Tanese K. Diagnosis and management of basal cell carcinoma Curr Treat Options Oncol. 2019;20:13. doi:10.1007/s11864 -019-0610-0
  21. Barthelmann S, Butsch F, Lang BM, et al. Seborrheic keratosis. JDDG J Dtsch Dermatol Ges. 2023;21:265-277. doi:10.1111/ddg.14984
  22. Taylor S. Advancing the understanding of seborrheic keratosis. J Drugs Dermatol. 2017;16:419-424.
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A 67-year-old man presented to the dermatology clinic with 3 asymptomatic pigmented papules on the scalp. The patient reported that he was unaware of the lesions until they were pointed out weeks earlier by his primary care physician during a routine visit. He then was referred to dermatology for follow-up. Physical examination at the current presentation revealed clustered firm, smooth, well-circumscribed, pigmented papules on the scalp measuring 5 to 8 mm. The patient reported no personal or family history of skin cancer but stated that he spent a lot of time outdoors and had a history of 6 blistering sunburns in his life. A punch biopsy of each lesion was performed.

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