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7.3 High-Yield Dermatopathology Differential Diagnoses
Table 7.20 Blue Balls in Dermis
Cylindroma Multiple basaloid tumor micronodules fused together in jigsaw pattern, small ducts, and thick hyaline (pink) BMZ material
Spiradenoma Larger basophilic dermal nodules with sweat ducts, hyaline droplets within tumor micronodules, and lymphocytes “peppered
Dermal duct tumor Nodule of monomorphous poroid cells w/ cuticle-lined sweat ducts. No epidermal connection
Glomus tumor Monomorphous glomus cells encircling delicate blood vessels ; lacks sweat ducts (vs. dermal duct tumor)
Hidradenoma
Trichoblastoma Dermal/SQ basaloid nodules (solid or cribriform), fibroblast-rich pink collagenous stroma, papillary mesenchymal bodies , and
Table 7.21 Clonal SK vs. Hidroacanthoma Simplex vs. Bowen’s Disease
Clonal SK
Hidroacanthoma
simplex
Bowen’s disease Full thickness keratinocyte atypia (“windblown” appearance) with atypical mitoses, dyskeratotic keratinocytes (not seen in other
Table 7.22 Pagetoid DDx
Disease Essential Features Immunostaining Profile
Pagetoid Bowen’s disease Clear cytoplasm, intercellular bridges, and involves basal layer
EMPD/Paget’s disease Mucin in cytoplasm; nests of Paget cells compress the healthy basal layer
Melanoma in situ Pigmented, expect to see some nesting at base of rete
Mycosis fungoides Lymphocytes lining up at DEJ; irregular nuclear contours (“cerebriform”),
Peri-ocular sebaceous
carcinoma
surrounding each tumor micronodule
into tumor”
Nodule comprised of a mixture of squamoid and clear cells with sweat ducts; keloidal/hyalinized stroma; 1/– cystic
degeneration (“solid-cystic hidradenoma”)
horn cysts; lacks stromal mucin and retraction (vs. BCC), lacks ducts (vs. sweat gland neoplasms)
Intraepidermal nests of keratinocytes w/ minimal atypia; cell size $ surrounding keratinocytes; lacks ducts
Acanthotic epidermis w/ intraepidermal nests of small poroid cells (smaller than surrounding keratinocytes); small ducts present at
least focally
two entities)
CK5/61, CK7-(usually), BerEP4–
of keratinocytes; 1/– ducts (Fig. 7.45)
perinuclear halo around lymphocytes (“lumps of coal resting on a
pillow”), and “wiry” papillary dermal fibrosis (abnormally thickened
collagen fibers in papillary dermis entrapping lymphocytes) ( Fig. 7.46)
Eyelid skin (pagetoid spread is rare in extra-ocular sebaceous carcinoma),
pale vacuolated cytoplasm with indented/scalloped central nuclei
Cytokeratin 71, CK20–, CEA1, BerEP41 (helps
to distinguish from pagetoid Bowen’s, which is
negative)
1
, Melan-A1, HMB-45
S100
CD31, CD41, CD8 (Exception 5
hypopigmented MF, which is usually CD81 and
CD4–). Often see loss of CD5 and CD7 (most
common aberrant staining pattern)
Adipophilin1, AR1, EMA1, BER-EP4-
1
Fig. 7.45 Extramammary Paget disease. Pagetoid cells with ample cytoplasm,
sometimes containing vacuoles 1/– mucin. Basal keratinocytes are often compressed/crushed by tumor nests (helps to DDx from melanoma, where the tumor
nests do not compress the basal layer of epidermis).
Fig. 7.46 Mycosis fungoides.
425
CHAPTER 7 • Dermatopathology
Table 7.23 Square Biopsy DDx
Disease
Chronic radiation
dermatitis
Necrobiosis
lipoidica
Normal skin of the
back
Scar Yes (fibroblasts) “East-West” collagen
SclerEdema No
SclerOderma/
Morphea
Sclerodermoid
GVHD
Scleromyxedema/
NSF
Increased
Cellularity? Essential Features
No Homogenized (“sick-appearing”)
Yes
(granulomatous)
No Normal thickness of collagen
No (exception:
early/inflammatory
morphea has
perivascular
lymphoplasmacytic
inflammation)
No Thick collagen bundles,
Yes (fibroblasts)
dermis, prominent superficial
telangiectasias, stellate
fibroblasts, and loss of
adnexae (Fig. 7.47)
Diffuse granulomatous
inflammation w/ “cake-
layered” necrobiosis,
dermal sclerosis (late-stage),
multinucleated GCs, and
↑ plasma cells
bundles—they just extend
deeper!.
orientation with ↑
broblast cellularity, vertically
oriented blood vessels
Hypertrophic scars have
“whorled” broblastic nodules
↑ Space and ↑ mucin
between normal-sized
collagen fibers (Fig. 7.48)
Thick hyalinized (pink)
collagen bundles, loss of
perieccrine fat, and deep PV
inflammatory infiltrate with
plasma cells (Fig. 7.49)
mild vacuolar interface,
pigment incontinence,
and loss of adnexae
↑ Fibroblasts in dermis (NSF
extends deeper into SQ), mild
collagen thickening,
and ↑ mucin (see Fig. 7.24)
Fig. 7.48 Scleredema. (From Ferringer T: Metabolic disorders. In: Elston DM,
Ferringer T, eds. Dermatopathology, 3rd ed. Philadelphia: Elsevier; 2019; pp 251-263.)
Fig. 7.47 Chronic radiation dermatitis. Dermal sclerosis, with ectatic supercial
vessels and bizarre broblasts.
426
A
B
Fig. 7.49 Morphea. Sclerosis of collagen bers centered in the deep reticular
dermis, with trapping/ablation of adnexal structures, and lymphoplasmacytic
inammation in a perivascular pattern (often present at dermo-pannicular
junction)
7.3 High-Yield Dermatopathology Differential Diagnoses
Table 7.24 “SLAM” DDx: Malignant Dermal Spindle Cell Tumor “Slammed” Up Against the Epidermis
Disease Essential Features Immunostaining Profile
SCC (spindle cell type)
Leiomyosarcoma Hyperchromatic spindle cells w/ fascicular
AFX Bizarre/atypical mitotic figures; mixture of cell
Melanoma, (desmoplastic/
spindle cell type)
Overlying epidermal keratinocytic atypia 1/
epidermal connection
architecture and cigar-shaped nuclei w/
perinuclear vacuoles (glycogen)
types (multinucleated GCs, histiocyte-like cells,
foam cells, and spindle cells)
Atypical junctional melanocytic proliferation (often subtle),
solar elastosis, blue-gray myxoid stroma, and
nodular lymphocyte aggregates, PNI (Fig. 7.50)
Cytokeratin1 (CK5/6, CK903 and MNF116 are most sensitive),
p631, p401 (most specific marker for SCC vs. AFX)
SMA1, Desmin1
AFX is a diagnosis of exclusion!
Most importantly, must be negative for: Cytokeratin, p63, p40,
S100, SOX-10, and Desmin (caution: SMA may have “tram
track”/myobroblast-like staining in AFX)
Most useful positive stains: CD101 (also positive in many spin-
dle cell SCCs), Procollagen-1 1
Other positive stains: CD681, CD741 (weak in AFX, strong in
UPS), CD991 and CD1171 (latter two stains are non-specic)
S1001, SOX-101 (differentiates from scar), and p75/NGFR1 (useful
desmoplastic melanomas)
for S100
A B
Fig. 7.50 Malignant melanoma with a junctional and desmoplastic component. Dermal lymphoid aggregates may be a clue to the presence of a desmoplastic
component.
Table 7.25 Psoriasiform and Spongiotic Disorders
Plaque psoriasis Regular (“psoriasiform”) acanthosis, neutrophil microabscesses in stratum corneum (Munro) and spinosum (Kugoj),
Guttate psoriasis
Pustular psoriasis Sub- and intracorneal neutrophilic abscesses
Lichen simplex chronicus Irregular acanthosis, hypergranulosis, and vertical collagen in dermal papillae; lacks neutrophilic microabscesses
Mycosis fungoides Hyperchromatic, cerebriform epidermotropic lymphocytes w/ perinuclear halo (“lumps of coal on a pillow”); minimal
PRP Hyperkeratosis out of proportion to degree of acanthosis, “checkerboard” parakeratosis (parakeratosis horizontally and
Secondary syphilis Psoriasiform hyperplasia (long, “sexy & slender” rete); supercial and deep inammation; “dirty” lichenoid inammation
Subacute spongiotic
dermatitis
hypogranulosis, confluent parakeratosis, suprapapillary plate thinning, dilated vessels in dermal papillae, and little or no
serum crust
Minimal acanthosis, 1spongiosis, mounds of neutrophils w/ underlying parakeratosis (thicker and more adherent than
pityriasis rosea) (Fig. 7.51)
spongiosis relative to number of lymphocytes in epidermis, band-like superficial dermal lymphocytic infiltrate with minimal
to no inflammation deep to superficial vessels (“bare underbelly sign”), lymphocytes “tagging” basal layer of epidermis
(“pigs lining up at the trough”), wiry papillary dermal fibrosis, and absence of intraepidermal neutrophils (see Fig. 7.26)
vertically alternating with orthohyperkeratosis), follicular plugging , “shoulder parakeratosis” (around follicular ostia), focal
acantholysis (helpful clue), and thickened suprapapillary plates ; NO NEUTS! (Fig. 7.52)
w/ neutrophils and plasma cells, lymphocyte exocytosis, and swollen endothelial cells
CAUTION: has neutrophils in horn!
Mild to moderate acanthosis 1/– parakeratosis, prominent spongiosis, Langerhans cell “microabscesses” in spinous
layer (esp. allergic contact dermatitis)
CAUTION: neutrophils may be seen but are limited to areas of serum crust; lacks intraspinous neutrophil microabscesses
Continued
427
CHAPTER 7 • Dermatopathology
Table 7.25 Psoriasiform and Spongiotic Disorders—cont'd
Pityriasis rosea Subacute spongiotic dermatitis w/ thin mounds of parakeratosis (lacks neutrophils seen in psoriasis), and extravasated
ILVEN Horizontally alternating orthokeratosis (WITH granular layer) and parakeratosis (WITHOUT granular layer). Low-power view is
Tinea
Nutritional deficiency
dermatitis
RBCs around superficial dermal vessels (Fig. 7.53)
helpful.
Epidermal changes may resemble psoriasis or spongiotic dermatitis → clue: “layered” stratum corneum (compact stratum
corneum immediately above granular layer), “bullet holes” (hyphae) in compact keratin, and sub/intracorneal neutrophil
abscesses
Psoriasiform hyperplasia with confluent parakeratosis AND pallor of upper 1/3 of epidermis (Fig. 7.54)
Fig. 7.51 Guttate psoriasis. Adherent mounds of parakeratosis with overlying
neutrophilic microabscesses. Only focal hypogranulosis 1/– mild spongiosis.
Acanthosis is far more subtle than that in classic psoriasis.
Fig. 7.53 Pityriasis rosea. RBC, red blood cell. (From Elston DM: Psoriasiform
and spongiotic dermatitis. In: Elston DM, Ferringer T, eds. Dermatopathology,
3rd ed. Philadelphia: Elsevier, 2019; pp 153-164.)
Fig. 7.52 Pityriasis rubra pilaris. Hyperkeratosis out of proportion to degree of
acanthosis. Alternating “checkerboard” parakeratosis.
428
Fig. 7.54 Nutritional deciency. (From Ferringer T: Metabolic disorders. In: Elston DM,
Ferringer T, eds. Dermatopathology, 2nd ed. Philadelphia: Elsevier, 2014;
pp 224-233.)
7.3 High-Yield Dermatopathology Differential Diagnoses
Box 7.1 Mnemonic
“Neuts in the horn (stratum corneum) = PTICSS”
Psoriasis, Tinea, Impetigo, Candida, Seborrheic dermatitis, Syphilis
From Elston DM, Ferringer T, eds. Dermatopathology, 3rd ed. Philadelphia:
Elsevier; 2019, p 505.
Table 7.26 Acantholytic Disorders
Disease H&E DIF Notes
Pemphigus
foliaceus
Pemphigus
vulgaris
Pemphigus
vegetans
Pemphigus
erythematosus
Paraneoplastic
pemphigus
Hailey-Hailey Epidermal hyperplasia, full-thickness
Darier’s disease Acantholytic dyskeratosis (prominent) with
Grover’s disease May appear in a pemphigus-like, Darier-like, or
Warty
dyskeratoma
Subcorneal split, acantholysis in granular layer like
“shingles blowing off of a roof”
Suprabasilar split, “tombstoning of basal layer,”
and acantholysis extends down hair follicles
PEH with eosinophilic abscesses in epidermis;
subtle suprabasilar clefting
Similar to pemphigus foliaceus
Combination of suprabasilar acantholysis and
interface dermatitis
intraepidermal acantholysis (“dilapidated brick
wall”), mild dyskeratosis, and keratinocytes have
distinct pink-red cytoplasm (Fig. 7.55)
suprabasilar clefting (Fig. 7.56)
Hailey-Hailey-like pattern
Endophytic with either cup shape
hair follicle; prominent acantholytic dyskeratosis
with cells expelled into the center of the crater
leaving dermal papillae looking like “villi”
or resembling
Intercellular IgG and C3 Due to anti-Dsg1 antibodies
Same as pemphigus foliaceus,
Pemphigus pattern (intercellular
BMZ (linear to granular) 1
DIF:classically shows combo
IIF: positive on rat bladder
Negative Less dyskeratosis compared with Darier’s
Negative Dyskeratosis manifests as corps ronds/grains
Negative May have mix of all three patterns. If a mix of patterns
Negative Solitary nature and cup-shaped architecture are
Box 7.2 Mnemonic
“Subcorneal pustules = CAT PISS”
Candida, Acropustulosis of infancy, Transient neonatal pustular melanosis,
Pustular psoriasis, Impetigo, Sneddon-Wilkinson (and IgA pemphigus),
Staph scalded skin
Modied from Elston DM, Ferringer T, eds. Dermatopathology, 3rd ed.
Philadelphia: Elsevier; 2019, p 505.
Most important Ddx is staph scalded skin → DIF
distinguishes
but w/ ↑ staining in lower half
of epidermis
IgG and C3)
intercellular pemphigus
pattern
of intercellular pemphigus
pattern 1 lichenoid changes;
appears similar to
pemphigus erythematosus
epithelium (because rat
bladder contains plakins)
Due to anti-Dsg1 and anti-Dsg3 antibodies
Clinical variant of PV
Overlap of pemphigus foliaceus and cutaneous
lupus erythematosus
Anti-desmoglein 1 and ANA 1
Antiplakin family antibodies (including BP-230)
detected with immunoblotting or ELISA
May be associated with B-cell lymphoproliferative
disorders (most common), thymoma,
Castleman’s disease, some carcinomas,
sarcomas, and even melanoma
Associated with life-threatening bronchiolitis
obliterans (#2 cause of death; #1 is underlying
malignancy progression)
seen on path, favor Grover’s, but CPC required
the most helpful clues to distinguish from Darier’s.
Acantholytic acanthoma is not cup-shaped
Fig. 7.55 Hailey-Hailey disease. In contrast to Darier disease, dyskeratosis is
usually minimal or even absent.
Fig. 7.56 Darier disease. Acantholytic dyskeratosis is seen.
429
CHAPTER 7 • Dermatopathology
Table 7.27 High-Yield Granulomatous Disorders (Fig. 7.57)
GA (interstitial)
GA (palisaded) Palisaded histiocytes in superficial-mid dermis (except deep GA) encircling and degrading collagen fibers;
Gout Palisaded granuloma around light pink/gray feathery needle-shaped crystals (best seen if fixed in ethanol) (Fig. 7.59)
Lupus miliaris disseminatus faciei Large foci of caseation necrosis (amorphic pink debris) surrounded by histiocytes on facial skin
Necrobiosis lipoidica
NXG X-shaped red zones of necrosis w/ nuclear debris within granulomas; cholesterol clefts and bizarre, HUGE
Rheumatoid nodule Deep dermal-SQ palisaded granuloma surrounding pink fibrin; no mucin (Fig. 7.62)
Sarcoid Well-formed epithelioid granulomas w/ minimal surrounding lymphocytic inflammation (“ naked”); often difficult to
Patchy interstitial histiocytes, ↑ mucin, lymphocytes, and ↑ eosinophils
↑ mucin; PV infiltrate with ↑ eosinophils (Fig 7.58a and 7.58b)
Layered pan-dermal granulomatous inflammation and necrobiosis ( “layered lasagna”), pan-dermal process n
entire dermis appears altered, with “square biopsy” sign, and plasma cells; lacks eosinophils (vs. GA) (Fig. 7.60)
multinucleate giant cells (often with 50–100 nuclei in horseshoe or osteoclast-like pattern)( Fig. 7.61)
distinguish from Crohn’s disease, Melkersson-Rosenthal syndrome, zirconium/beryllium deposition, Blau syndrome,
perioral dermatitis, and tuberculoid leprosy. Foreign material may be present (“scar-coid”) and does not exclude
diagnosis (Fig. 7.63)
NONINFECTIOUS GRANULOMAS: ALGORITHM FOR HISTOLOGIC DIAGNOSIS
Non-infectious granulomas
With plasma
“Naked”
Sarcoidosis
Epithelioid
tubercle
Caseation
Crohn’s
disease
Appreciable
lymphocytes
Consider
infection
Syphilis
cells
With
lymphocytes
Granulomatous
slack skin
Diffuse infiltrate,
no palisade
With
neutrophils
Ruptured cyst
or follicle
Palisaded
granuloma
Horizontal
“tiers”
Prominent
Necrobiosis
lipoidica
Necrobiotic
xanthogranuloma
Granuloma
annulare*
Elastophagocytosis
Superficial
dermal
Nodular
infiltrate
Diffuse infiltrate,
marked collagen
alteration
Subcutis
cholesterol
clefts
Annular elastolytic
giant cell granuloma
Fig. 7.57 Non-infectious granulomas: algorithm for histopathologic diagnosis. Interstitial granulomatous dermatitis and palisaded neutrophilic and granulomatous
dermatitis may represent an additional diagnostic consideration. May also have a patchy dermal interstitial pattern without palisades, or subcutaneous palisades, with
more mucin than rheumatoid nodules. (From Rosenbach MA, Wanat KA, Reisenauer A, White KP, Korcheva V, White CR Jr. Non-infectious granulomas. In: Bolognia JL,
Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Philadelphia: Elsevier; 2018:1644–1663.)
Rheumatoid
nodule
430
7.3 High-Yield Dermatopathology Differential Diagnoses
A B
Fig. 7.58 Granuloma annulare (palisaded variant) with palisading granulomatous inammation, central necrobiosis of collage, and increased mucin. Palisaded appearance is best observed at low power.
Fig. 7.59 Gout. Granulomatous inammation surrounding light pink, needleshaped crystals.
A
B
Fig. 7.60 Necrobiosis lipoidica. (A) Low magnication reveals layered pan-dermal
granulomatous inammation with necrobiosis; “wall-to-wall” process with no
remaining normal dermis. (B) High magnication.
431
CHAPTER 7 • Dermatopathology
A
Fig. 7.62 Rheumatoid nodule. Deep and large palisaded granuloma with central
pink brin; lacks mucin (vs GA)
B
Fig. 7.61 Necrobiotic xanthogranuloma. Low power (A) showing pan-dermal
granulomatous inammation. High power (B) demonstrates cholesterol clefts
and bizarre, large multinucleated histiocytic giant cells. (From Johnston RB.
Granulomatous reaction pattern. In: Weedon’s Skin Pathology Essentials, 2nd
ed. Philadelphia: Elsevier, 2017, pp 134-162.)
Fig. 7.63 Sacroidosis. “Naked, well-formed granulomas” comprised of discrete
balls of granulomatous inammatory cells (histiocytes and giant cells) with
minimal-to-no surrounding lymphocytes.
432
7.3 High-Yield Dermatopathology Differential Diagnoses
Table 7.28 Histopathologic Features of the Major Granulomatous Dermatitides (See also Fig. 7.57)
Palisading
Neutrophilic and
Granulomatous
Dermatitis
Entire dermis
Palisading;
prominent
neutrophils and
leukocytoclasia
Variable
Sarcoidosis
Typical location Superficial and
deep dermis
Granuloma pattern Tubercle with
few peripheral
lymphocytes
(“naked”)
Granuloma
Annulare
Superficial and
a
mid dermis
Palisading or
interstitial
Necrobiosis
Lipoidica AEGCG
Entire dermis,
a
subcutis
Diffuse
palisading
and interstitial;
horizontal
Superficial
and mid
dermis
Palisading,
irregular
Cutaneous
Crohn’s
Disease
Superficial and
deep dermis
Tubercle with
surrounding
lymphocytes
Rheumatoid
Nodule
Deep
dermis,
subcutis
Palisading Palisading in
Interstitial
Granulomatous
Dermatitis
Mid and deep
dermis
small “rosettes”
“tiers”
Necrobiosis (altered
No Yes (“blue”) Yes (“red”) No No Yes (“red”) Yes (“blue”) Yes (“blue”)
collagen)
Giant cells Yes Variable Yes Yes Yes Yes Variable Variable
Elastolysis No Variable Variable Yes No No Variable Variable
Elastophagocytosis No No No Yes No No No No
Asteroid bodies Yes Variable Variable Yes No No Variable Variable
Mucin No Yes Minimal No No Variable Yes (but less than
palisaded GA)l
Extracellular lipid No Variable Yes No No Variable No No
Vascular changes No Variable Yes
a
Subcutaneous variant can also occur.
No No Yes No Yes
AEGCG, Annular elastolytic giant cell granuloma.
Modied from Rosenbach MA, Wanat KA, Reisenauer A, White KP, Korcheva V, White CR Jr. Non-infectious granulomas. In: Bolognia JL, Schaffer JV, Cerroni L,
eds. Dermatology. 4th ed. Philadelphia: Elsevier; 2018: 1644–1663.
Table 7.29 High-Yield Inammatory and Occlusive Vascular Disorders
Vasculitides (Vessel Inammation and Destruction, Fibrin in Vessel Wall, RBC Extravasation, and Leukocytoclasis)
Henoch-Schönlein purpura LCV, IgA in vessel walls (DIF)
Mixed cryoglobulinemia LCV
Granulomatosis with polyangiitis
(Wegener’s)
Eosinophilic granulomatosis with
polyangiitis (Churg-Strauss)
LCV involving vessels high up (postcapillary venules) and down low (medium-sized vessels) → may evolve into palisading
granuloma with giant cells surrounding neutrophil-rich abscess, 1/– granulomatous vasculitis
LCV involving vessels up high (postcapillary venules) and down low (medium-sized vessels) → may evolve into palisading
granuloma with central degranulating eosinophils and flame figures, 1/– granulomatous vasculitis (Fig. 7.64)
Erythema elevatum diutinum LCV with numerous eosinophils, “ onion-skin” fibrosis, and nonfacial location (Fig. 7.65)
Granuloma faciale
LCV w/ numerous eosinophils, plasma cells and histiocytes, Grenz zone, mild fibrosis (,EED), and most commonly on face (Fig. 7.66)
Occlusive vasculopathies (“Plugged” Vessels w/ Minimal Primary Vascular Inammation)
Thrombotic Intravascular thrombus
Causes: cryoglobulinemia type I (intravascular deposits are PAS positive; uorescence with multiple conjugates on DIF),
warfarin necrosis, DIC, lupus anticoagulant, Factor V Leiden mutation, and protein C or S deciency → all are essentially
indistinguishable histopathologically
Livedoid vasculopathy Bright pink-red hyalinized vessel walls (“red crayon-like”), intravascular thrombosis of superficial dermal vessels, and
background stasis changes
Calciphylaxis
Levamisole-associated
vasculopathy
Calcified vessel walls w/ thrombosis deep in the fat, 1/– extravascular calcium debris (esp. peri-eccrine)
Mixed features of LCV 1 small vessel thrombosis high in dermis
Patients also have neutropenia and P- and/or C-ANCA antibodies
Fig. 7.64 Flame gure, seen in eosinophilic cellulitis (Wells syndrome), Churg-Strauss, and other brisk
allergic or dermal hypersensitivity reactions (bug bite, drug, etc). Due to eosinophil degranulation onto
collagen bers.
433
CHAPTER 7 • Dermatopathology
A
Fig. 7.65 Erythema elevatum diutinum, (A) Low power, (B) High power: Characterized by multiple dermal nodules comprised of nodules of storiform (“onion skin”) brosis
around destroyed vessels, and subtle features of LCV with conspicuous eosinophils. Differentiated from g. faciale by high degree of onion skin brosis and non-facial
location. (B, from Elston DM: Inammatory vascular diseases. In: Elston DM, Ferringer T, eds. Dermatopathology, 3rd ed. Philadelphia: Elsevier, 2019; pp 193-219.)
B
A B
Fig. 7.66 Granuloma faciale. (A) Low power, (B) High power: Characterized by Grenz zone, dense dermal perivascular LCV with numerous eosinophils, plasma cells
and histiocytes. Much less onion-skin brosis compared to EED.
Table 7.30 High-Yield Panniculitides
Cold panniculitis (deep perniosis)
Erythema induratum/nodular
vasculitis
Erythema nodosum
Lupus panniculitis
Sclerema neonatorum Lobular panniculitis w/ radiating needle-shaped crystals within adipocytes; lacks surrounding granulomatous inflammation
SQ fat necrosis of newborn
(and poststeroid panniculitis)
PAN Vasculitis of solitary medium-sized vessel (artery) in deep dermis/SQ tissue with fibrin in vessel wall and obliteration of
Pancreatic panniculitis Lobular panniculitis w/ amorphous purple aggregates in fat lobules representing enzymatic fat necrosis (“ghost cells”) (Fig. 7.68)
Lipodermatosclerosis (stasis
panniculitis)
Lobular fat necrosis with lymphocytes, histiocytes, and neuts at dermal-pannicular junction; 1/– overlying dermal perniosis
Caseous necrosis of fat lobules (neutrophil-rich) 1 vasculitis of small and medium (PAN-sized) lobular and septal
vessels 1 septal thickening
Major clue: involves lobules and septae diffusely, whereas PAN involves one lobule and only damages a small amount of fat
immediately surrounding the affected vessel
Septal panniculitis with neutrophils in septum (early) → progresses to septal thickening w/ small granulomas with
central clefting (Miescher’s granulomas)
Note: there is only slight spill-over of inammation into the lobules
Lobular fat necrosis w/ pink hyalinization around fat, nodular PV/PA lymphoplasmacytic aggregates, 1/ clusters
CD1231 plasmacytoid dendritic cells in vast majority of cases (very helpful to DDx from SPTCL, which lacks CD123+
cells) 1/– ↑ mucin and interface dermatitis
Lobular panniculitis w/ radiating needle-shaped crystals within adipocytes w/ associated brisk granulomatous
inflammation
lumen, 1/ very mild lobular panniculitis in area immediately adjacent to affected vessel ( Fig. 7.67)
Lobular panniculitis w/ cystic fat necrosis and with lipomembranous change (“frost on a window pane”), septal
fibrosis, lipophages, and overlying stasis changes
434