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7.3 High-Yield Dermatopathology Differential Diagnoses
COMMON LOCALIZATION OF AUTOANTIBODIES IN INDIRECT
IMMUNOFLOURESCENCE MICROSCOPY STUDIES OF SALT-SPLIT SKIN
Basal keratinocytes
Bullous pemphigoid
Lamina lucida
Lamina densa
Sublamina densa
Fig. 7.15 Common localization of autoantibodies in indirect immunouorescence microscopy studies of salt-split skin. Subregions of salt-split skin commonly bound
by circulating autoantibodies in patients with subepidermal immunobullous diseases. (From Yancey KB. The biology of the basement membrane. In: Bolognia JL,
Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Philadelphia: Elsevier; 2018:483–493.)
Pemphigoid gestationis
Linear IgA bullous dermatosis
Cicatricial pemphigoid
Anti-epiligrin
cicatricial pemphigoid
Epidermolysis bullosa acquisita
The bullous eruption of
systemic lupus
erythematosus
7.2 HIGH-YIELD DERMATOPATHOLOGY DIAGNOSES AT A GLANCE
• Herein, we present an abbreviated summary of the 226
most testable dermpath diagnoses, including their most
essential histopathologic features, as well as their mimics
(Table 7.11). Because of space constraints, we are unable to
include microscopic images of all entities. We encourage
the reader to refer to one of the many excellent Elsevier
Dermatopathology titles.
7.3 HIGH-YIELD DERMATOPATHOLOGY
DIFFERENTIAL DIAGNOSES
• See Tables 7.12 to 7.38
Table 7.12 “Normal Skin” DDx
Macular amyloid Light pink deposits papillary dermis; pigment
TMEP
Tinea corporis Pale-staining hyphae in lower stratum corneum,
Tinea versicolor Basaloid spores and hyphae (“spaghetti and
Argyria Small black granules in sweat glands
Ichthyosis vulgaris Compact orthohyperkeratosis w/ paradoxically
Erythrasma Organisms one-fifth the size of hyphae; vertical
incontinence/melanophages
Superficial dermal telangiectasias 1 sparse
proliferation of spindled mast cells; may need
CD117 immunostain or other mast cell stain (Leder,
Tryptase, or Giemsa) to confirm (Fig. 7.16)
brisk dermal inflammation, 1/– subcorneal pustule
meatballs”) in upper stratum corneum, much
easier to see than tinea corporis on H&E, and
minimal to no dermal inflammation
↓ granular layer (almost all other diseases w/
orthohyperkeratosis have ↑ granular layer)
filaments in stratum corneum
Fig. 7.16 Telangiectasia macularis eruptiva perstans. Microscopic changes are
subtle, with a sparse perivascular inltrate of mast cells that often require demonstration by immunohistochemistry.
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CHAPTER 7 • Dermatopathology
Table 7.13 Busy Dermis DDx (Mnemonic: Busy Dermis Can Kill Grandma’s Sweet Niece Lucy)
Blue nevus Paucicellular dendritic melanocyte proliferation within sclerotic stroma , melanophages, and HMB-45 diffusely positive
Dermatofibroma Interstitial spindle cell proliferation in “curlicue pattern,” collagen trapping, epidermal/follicular induction, hemosiderin-laden
Cutaneous metastasis Most commonly tested: metastatic breast cancer (“single-cell filing,” small ducts), RCC (clear cells, highly vascular), colon
Kaposi sarcoma (plaque
stage)
GA (interstitial)
Scleromyxedema
Neurofibroma
Leukemia cutis Interstitial infiltrate of atypical cells w/ “ blast” morphology (fine chromatin, prominent nucleoli, and larger than normal inflammatory
(vs. gradient staining in conventional nevi) (Fig. 7.17)
1
histiocytes/Touton-like GCs, Factor XIIIa
cancer (“dirty necrosis”); although not always true, a rule of thumb to help determine primary tumor location is: CK71 (above
diaphragm), versus CK201 (below diaphragm) (Figs. 7.19–7.21 )
Relatively bland interstitial spindle cell proliferation , “promontory sign ,” vascular wrapping, thin slit-like vascular
spaces, extravasated RBCs, hemosiderin, and increased plasma cells (most easily seen in perivascular distribution
near tumor); HHV-81 (Fig. 7.22)
Interstitial histiocytes w/ foci of altered collagen, ↑ mucin, perivascular lymphocytes with eosinophils (Fig 7.23)
Bland dermal spindled fibroblastic proliferation w/ fine collagen fibers; ↑ mucin (Fig 7.24)
Loosely arranged spindle cells with wavy/ “buckled” nuclei , myxoid stroma, and ↑ mast cells (see Fig. 7.25)
cells) arranged in single-cell filing pattern; frequent mitoses ; myeloid/monocytic leukemias typically positive for CD68 and
lysozyme (two most sensitive markers) . MPO . CD34 and CD117 (see Fig. 7.26)
and CD34 (Figs. 7.18)
A B
Fig. 7.17 (A) and (B) Blue nevus. Spindled melanocytes with dendritic processes and cytoplasmic melanin are present between the dermal collagen bundles, which
are often brotic.
A B
Fig. 7.18 (A) Dermatobroma. Scanning section shows the characteristic architecture. The lateral borders of the lesion interdigitate with the adjacent dermis (so-called
“collagen trapping”). The overlying epidermis often shows induction (either epidermal hyperplasia, epidermal hyperpigmentation, hyperkeratosis, or potentially basaloid
or sebaceous differentiation). (B) Dermatobroma, ankle-type. Hemosiderin-laden Touton giant cells (ringed siderophages) are prominent.
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7.3 High-Yield Dermatopathology Differential Diagnoses
A B
Fig. 7.19 (A) Metastatic breast adenocarcinoma, interstitial type. Atypical cells are seen coursing through the dermis single-le, and duct formation is noted. Breast
adenocarcinoma is typically immunoreactive for CK7 stain, with variable expression of ER, PR, and Her2neu. CK20 is usually negative. (B) Metastatic breast adenocarcinoma, inammatory type. Tumor aggregates are noted within dermal lymphatics.
Fig. 7.20 Metastatic colon adenocarcinoma. Dirty necrosis is seen within gland lumina. Colon cancer may stain for CK20 and CDX2; CK7 is usually negative.
A B
Fig. 7.21 (A) and (B) Metastatic renal cell carcinoma (RCC). Atypical clear cells forming ducts with a highly vascular stroma are noted. RCC may stain with keratin
markers such as AE1/AE3, RCC stain, CD10, and PAX8.
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CHAPTER 7 • Dermatopathology
A
B
Fig. 7.22 Kaposi sarcoma (KS; patch stage; (A) H&E; (B) HHV-8 immunohistochemistry
stain). Increased vascularity, spindled cells with adjacent vascular spaces, hemosiderin
deposition, and intermixed plasma cells. The promontory sign, in which new blood
vessel formation is observed within larger vessels, may be present. KS is uniformly immunoreactive for HHV-8 by immunohistochemistry.
A
B
Fig. 7.23 Interstitial granuloma annulare. Increased interstitial histiocytes with
abundant interstitial mucin are seen within the dermis (part of the “busy dermis”
differential).
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C
Fig. 7.24 Scleromyxedema (lichen myxedematosus A): Dermal brosis with increased broblasts (marked with CD34; B) is noted, along with separation of
collagen bers by increased dermal mucin (marked with colloidal iron stain, C).
7.3 High-Yield Dermatopathology Differential Diagnoses
A
Fig. 7.25 Neurobroma (NF), shown at low (A) and high (B) power. This neoplasm is composed of spindled cells with “s-shaped” nuclei. The associated collagen has
a “shredded carrot” appearance (B). Mast cells are usually scattered within the neoplasm. NF is S100 positive and also may stain with CD34.
Fig. 7.26 Acute myeloid leukemia involving the skin. There is a dense inltrate of blasts (dispersed chromatin, nuclear molding), some of which contain conspicuous
eosinophilic granules. The blasts usually are immunoreactive for myeloperoxidase, TdT, CD33, CD34, and CD117 (cKit) immunostains.
B
Table 7.14 Vacuolar Interface Dermatitis DDx
Lupus erythematosus
(SCLE)
Lupus erythematosus
(discoid)
Dermatomyositis
Erythema multiforme Basket-weave (acute) stratum corneum, prominent apoptotic keratinocytes scattered throughout all levels of epidermis, superficial
Fixed drug eruption Basket-weave (acute) stratum corneum, EM-like vacuolar interface, chronic dermal changes (deeper pigment incontinence,
Acute GVHD Orthohyperkeratosis, EM-like vacuolar interface, keratinocyte dysmaturation (from chemo effect), “satellite cell necrosis”;
PLEVA
Orthohyperkeratosis; brisk vacuolar interface diffusely affecting epidermis, superficial (. deep) PV/PA lymphocytic infiltrate ,
BMZ thickening, ↑ mucin; lacks eosinophils (Fig. 7.27)
Orthohyperkeratosis; moderate vacuolar interface centered around follicular epithelium (. interfollicular epidermis),
hyperplastic follicular infundibulae (esp. hypertrophic DLE), dilated follicles w/ follicular plugging, interfollicular epidermal atrophy,
dermal fibrosis/scar, superficial and deep PV/PA lymphocytic infiltrate, BMZ thickening, and ↑ mucin; lacks eosinophils (Fig. 7.28)
Orthohyperkeratosis, epidermal atrophy, sparse lymphocytic infiltrate (,LE), minimal vacuolar interface (,LE, EM, FDE, and PLEVA),
hhh
dermal mucin (>>LE) and vascular ectasia (telangiectasias); lacks deep PV/PA inflammation (vs. LE), lacks eosinophils (Fig. 7.29)
lymphocytic infiltrate w/ lymphocyte exocytosis; lacks eosinophils (vs. frequent eosinophils in SJS/TEN and FDE) (Fig. 7.30)
papillary dermal fibrosis), and mixed dermal inflammation w/ numerous eosinophils
frequently involves follicular and other adnexal epithelium (Fig. 7.31)
Parakeratosis, Lichenoid-to-vacuolar interface, Erythrocyte extravasation, V-shaped (wedge) lymphocytic infiltrate, Acute surface
changes (scale crust 1/– ulceration); never has eosinophils (if more than a few eosinophils present n not PLEVA!) (Fig. 7.32A,B)
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CHAPTER 7 • Dermatopathology
Fig. 7.27 Subacute cutaneous lupus erythematosus. Vacuolar interface inammation
with perivascular mononuclear inammation. Increased dermal mucin and perifollicular
lymphocytic inammation are often noted. Follicular plugging is a feature seen more
frequently in chronic cutaneous lupus erythematosus (discoid lupus; not shown).
Fig. 7.28 Discoid lupus exhibits follicular plugging, supercial and deep perivascular and perifollicular lymphocytes. There is interfollicular atrophy and interface
dermatitis affecting both the epidermis and follicular epithelium. (From Fung MA.
Inammatory diseases of the dermis and epidermis. In: Busam KJ, ed. Dermatopathology: A Volume in the Series: Foundations in Diagnostic Pathology, 2nd ed.
Philadelphia: Elsevier; 2016, pp 11-78.)
Fig. 7.30 Erythema multiforme. This process is characterized by a basket-weave
stratum corneum and brisk interface inltrate with abundant dyskeratotic keratiFig. 7.29 Dermatomyositis: there is hyperkeratosis, epidermal atrophy, mild
basal vacuolar change and marked increase in dermal mucin. (From Luzar B,
Calonje E. Idiopathic connective tissue disorders. In: Calonje E, Brenn T, Lazar AJ,
Billings SD, eds. McKee’s Pathology of the Skin, 5th ed. Philadelphia: Elsevier;
2020, pp 771-825.)
Fig. 7.31 Acute graft-versus-host disease (GVHD), with vacuolar interface changes often extending along the hair follicles and adnexal structures. Though not entirely
specic for GVHD, satellite cell necrosis (juxtaposition of a lymphocyte next to a necrotic keratinocyte) may be observed.
nocytes scattered throughout the epidermis.
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7.3 High-Yield Dermatopathology Differential Diagnoses
A B
Fig. 7.32 (A) and (B) Pityriasis lichenoides. At scanning magnication, there is a lichenoid lymphocytic inltrate with scale crust and occasional necrotic keratinocytes.
In the acute form (pityriasis lichenoides et varioliformis acuta), the inltrate is typically more dense and wedge-shaped, includes erythrocyte extravasation, and has
parakeratosis.
Table 7.15 Lichenoid Interface Dermatitis DDx
Lichen planus Orthohyperkeratosis, irregular acanthosis, V-shaped hypergranulosis , “saw-toothed” rete ridges, and apoptotic
Lichen planus-like keratosis (BLK) Like LP, but may have parakeratosis, eosinophils; frequently see solar lentigo/SK at periphery; often do not have as
Lichenoid drug eruption Looks like LP, but often has parakeratosis and deeper PV inflammatory infiltrate w/ eosinophils
Lichenoid GVHD Infiltrate less dense than LP, satellite cell necrosis , and epidermis often has chemotherapy effect/dysmaturation
Melanoma w/ lichenoid regression Search periphery for atypical melanocytic lesion; prominent pigment incontinence and plasma cells at regressed area
Lichen nitidus Small circumscribed papule, “ball and claw,” and epidermal collarette; dermal infiltrate is more mixed, consisting of
Lichen striatus
Lichenoid pigmented purpura Lichenoid and PV lymphocytic inflammation w/ RBC extravasation and hemosiderin deposition
Lichenoid secondary syphilis “Dirty” infiltrate (lymphocytes, neutrophils, histiocytes, nuclear debris, and plasma cells), slender elongated rete,
Hypertrophic lupus erythematosus Mistaken for SCC because of the hyperplastic follicular epithelium (unlike SCC, the interfollicular epidermis
keratatinocytes limited to lower levels of epidermis; lacks eosinophils (exceptions 5 hypertrophic LP, drug-
induced LP), lacks deep PV/PA inflammation
prominent saw-toothing or hypergranulosis
lymphocytes, histiocytes, and giant cells
Similar to LP, but w/ ↑ spongiosis and deep peri-eccrine inflammation ; usually young patients (solar elastosis rare)
swollen endothelial cells, superficial and deep inflammation
is typically normal-atrophic); lichenoid infiltrate resembles LP but has other features of lupus: deep PV/PA
inflammation, ↑ mucin, and BMZ thickening. Clusters of CD1231 plasmacytoid dendritic cells on IHC
Table 7.16 Weird Endophytic Neoplasms DDx
Poroma Uniform small cuboidal (“poroid”) cells; multifocal epidermal connections; eosinophilic cuticle in ducts (Fig. 7.33)
Trichilemmoma
Clear cell acanthoma Psoriasiform hyperplasia w/ neutrophils in corneum, sharply demarcated from surrounding normal epidermis (“looks
Panfolliculoma (cystic panfolliculoma) Benign, cystic (usually) follicular neoplasm with differentiation toward multiple components of hair follicle apparatus (Fig.7.36)
Pilar sheath acanthoma Acanthotic lobules attached to dilated pore (“dilated pore of Winer on steroids”) ( Fig. 7.37)
Tumor of follicular infundibulum Multiple slender connections to epidermis; fenestrated “ plate-like” architecture, fibrous stroma (Fig. 7.38)
Trichoepithelioma Basaloid tumor cells within highly cellular pink (fibroblast-rich) dermis; minimal to no epidermal attachment (vs. vast
Eccrine syringofibroadenoma Multiple epidermal connections; anastomosing thin strands of epithelial cells, ducts, and fibrovascular stroma (Fig. 7.40)
Lobular architecture, clear (glycogenated) cells w/ peripheral palisade and thick eosinophilic BMZ, 1/– squamous
eddies, 1/– verrucous surface (see Fig. 7.34)
exactly like psoriasis but with clear cells”) (Fig. 7.35)
majority of BCCs); papillary mesenchymal bodies and numerous horn cysts (many calcified) (see Fig. 7.39)
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CHAPTER 7 • Dermatopathology
Fig. 7.33 Poroma. This scanning view shows anastomosing tumor islands with
eccrine differentiation that demonstrate multiple foci of attachment to the epidermis. Cells are monotonous, with more rounded nuclei than typical keratinocytes.
A
Fig. 7.34 Trichilemmoma. An exophytic verrucous growth pattern is associated
with a lobular perifollicular clear cell proliferation at the base of the lesion. (From
Prieto VG, Shea CR, Tok Celebi J, Busam KJ. Adnexal tumors. In: Busam KJ,
ed. Dermatopathology: A Volume in the Series: Foundations in Diagnostic Pa-
thology, 2nd ed. Philadelphia: Elsevier; 2016, pp 388-446.)
Fig. 7.35 Clear cell acanthoma. Although the basal epithelial cells retain their
normal tinctorial properties, most of the epithelium shows marked pallor. Intracorneal neutrophils and loss of the granular layer are frequent ndings.
B
Fig. 7.36 Panfolliculoma. Benign neoplasm with differentiation representing
various regions of the hair follicle. (A) Low power. (B) High power.
Fig. 7.37 Pilar sheath acanthoma. Tumor lobules, composed of outer root
sheath epithelium, radiate from a central depression. (From Patterson JW. Tumors of cutaneous appendages. In: Weedon’s Skin Pathology, 4th ed. Philadelphia: Elsevier; 2016, pp 903-965.)
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Slightly pale keratinocytes
7.3 High-Yield Dermatopathology Differential Diagnoses
Horizontal bridge between
follicles
Fig. 7.38 Tumor of follicular infundibulum (From Rapini RP: Follicular neoplasms. In: Rapini RP, ed. Practical Dermatopathology, 3rd ed. Philadelphia: Elsevier; 2021,
pp 321-329.)
Fig. 7.39 Trichoepithelioma. There are multiple nests of basaloid cells, some
showing abortive hair follicle differentiation. (From Patterson JW. Tumors of cutaneous appendages. In: Weedon’s Skin Pathology. 5th ed. Philadelphia: Elsevier;
2021:951–1016).
Table 7.17 Paisley Tie (“Tadpole”) DDx
DTC Central dell, bland basaloid epithelial strands, numerous horn cysts (many w/ calcification), and fibroblast-rich pink
collagenous stroma; lacks: retraction, myxoid stroma, and perineural involvement (see Fig. 7.41)
MAC Deeply infiltrative tumor (into subcutis/skeletal muscle almost always) with bi-lineage differentiation: horn cysts (follicular)
and small syringoma-like ducts (sweat) in superficial dermis 1 infiltrative epithelial strands in deep dermis/SQ/skeletal muscle;
perineural invasion; scattered lymphoid nodules (see Fig. 7.42)
Syringoma Basaloid epithelial strands and ducts in fibrotic stroma; ducts contain amorphous eosinophilic debris; lacks follicular
differentiation (vs. MAC, DTE and BCC) (see Fig. 7.43)
Morpheaform BCC Sharply angulated strands of atypical basaloid cells in morphea-like stroma, numerous mitoses and apoptotic cells ; fewer
horn cysts and calcifications than DTE; lacks ductal differentiation (vs. MAC and syringoma) and lymphoid nodules (vs. MAC)
(Fig. 7.44)
Fig. 7.40 Eccrine syringobroadenoma: this lesion presented as a solitary tumor.
Arising from the epidermis are numerous anastomosing strands of epithelium
surrounded by a cellular brous stroma. (From Calonje E, Brenn T, Lazar AJ,
Billings SD. Tumors of the sweat glands. In: Calonje E, Brenn T, Lazar AJ, Billings
SD, eds. McKee’s Pathology of the Skin, 5th ed. Philadelphia: Elsevier; 2020,
pp 1611-1679.)
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CHAPTER 7 • Dermatopathology
Fig. 7.41 Desmoplastic trichoepithelioma. Central dell, with paisley-tie epithelial
cords and epithelial cells demonstrating oval nuclei. Dermal calcium deposits
and cysts containing keratin. Usually on the head and neck.
Fig. 7.44 Morpheaform basal cell carcinoma. There is dermal brosis and keloidal collagen formation adjacent to the inltrative islands of tumor. The tumor
demonstrates peripheral palisading and single-cell necrosis. Mucinous stroma
can be scant. The tumor demonstrates epidermal connection.
Fig. 7.42 Microcystic adnexal carcinoma. Combination of cysts and ducts, with
deep extension into subcutis and underlying structures, as well as perineural
invasion, are features.
Table 7.18 Complex Cystic Proliferations (“Rolls and Scrolls”)
Proliferating pilar
cyst
Pilomatricoma Multilobulated dermal tumor; basaloid and
Table 7.19 Epidermoid Cyst Mimickers
Vellus hair cyst Small vellus hairs within cyst cavity
Dermoid cyst Complete array of adnexal structures (follicles,
Steatocystoma Sebaceous glands in cyst wall, eosinosphilic
Dense pink trichilemmal keratin within cyst cavities;
lacks granular layer; multilobular proliferations
of pink squamous cells; lacks anucleate ghost
cells or basaloid germinative cells
pink ghost cells within the tumor lobules;
calcification typically present 1/– ossification
sebaceous glands, and apocrine glands) inserting
in cyst wall
cuticle (“sharktooth” lining), and cyst cavity
appears empty and collapsed
Fig. 7.43 Syringoma. Ducts lined by eosinophilic cuticle and containing proteinaceous, amorphous material. “Tadpoles” with cuboidal nuclei limited to the dermis. (From Patterson JW. Tumors of Cutaneous Appendages. In: Weedon’s Skin
Pathology. 5th ed. Philadelphia: Elsevier; 2021, pp 951–1016.)
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