Special Section—Contributions From the University of Mississippi Medical Center, Part II
Classic Findings, Mimickers, and Distinguishing Features
in Primary Blistering Skin Disease
Suzanne J. Tintle, MD, MPH; Allison R. Cruse, MD; Robert T. Brodell, MD; Buu Duong, MD
 Context.—Blistering diseases comprise a large group of
clinically polymorphic and sometimes devastating diseas-
es. During the past few decades, we have developed an
elegant understanding of the broad variety of blistering
diseases and the specific histopathologic mechanism of
each.
Objective.—To review examples of the classic findings
of specific blistering diseases and emphasize the impor-
tance of considering unrelated conditions that can mimic
the classic finding.
B listering diseases comprise a large group of clinically
polymorphic and sometimes devastating diseases.
Historically, pemphigus and pemphigoid were broad terms
used in the clinical description of blistering. Today, we have
an elegant understanding of the broad variety of blistering
diseases and the specific histopathologic mechanism of
each. Often, clinical diagnosis is dependent on the skin
biopsy and careful histopathologic evaluation to determine
the exact location of the blister in relationship to the
epidermis.
In approaching blistering diseases, there are 3 fundamen-
tal criteria to consider: (1) the site or level of the blister (or
the lowest level of vesiculation): subcorneal, midepidermis,
suprabasal, subepidermal; (2) the findings that implicate the
mechanism of blister formation (spongiosis, acantholysis,
blistering degeneration, or epidermolysis); and (3) the type
of inflammation (neutrophilic, lymphocytic, eosinophilic,
mixed), if present. A ‘‘top-down’’ approach (evaluating the
histopathologic specimen beginning at the stratum corneum
and moving inferiorly through the epidermis to the
basement membrane zone [BMZ] and then the dermis) is
recommended to characterize blistering processes with
respect to these 3 criteria. Of course, any histopathologic
diagnosis must be considered in the context of the clinical
Accepted for publication July 22, 2019.
Published online October 9, 2019.
From the Departments of Dermatology (Drs Cruse and Brodell)
and Pathology (Drs Tintle, Cruse, and Brodell), and Affiliate Faculty,
Dermatopathology Associates (Dr Duong), University of Mississippi
Medical Center, Jackson; and the Department of Dermatology,
University of Rochester Medical Center, Rochester, New York (Dr
Brodell).
The authors have no relevant financial interest in the products or
companies described in this article.
Corresponding author: Suzanne J. Tintle, MD, MPH, Department
of Pathology, University of Mississippi Medical Center, 2500 North
State Street, Jackson, MS 39216 (email: suzanne.tintle@gmail.com).
136 Arch Pathol Lab Med—Vol 144, February 2020
Data Sources.—This article combines data from expert
review, the medical literature, and dermatology and
pathology texts.
Conclusions.—We have chosen several common exam-
ples of classic blistering diseases that are mimicked by
other cutaneous conditions to highlight the basic findings
in blistering conditions and the importance of clinician-to-
pathologist communication.
(Arch Pathol Lab Med. 2020;144:136–147; doi: 10.5858/
arpa.2019-0175-RA)
stage of disease, the stage of the blister, and the location of
biopsy (perilesional, lesional, or nonlesional). For example,
in a patient with bullous pemphigoid, a subepidermal blister
that is 72 hours old may appear intradermal when re-
epithelialization has begun. In contrast, intraepidermal
blisters can appear subepidermal if the blister ‘‘blows out’’
into the subepidermal zone or if there is prominent papillary
dermal edema.
Biopsy technique also plays a role in the histopathologic
evaluation of blistering diseases. Autoimmune blistering
diseases are associated with autoantibodies that target
specific components of the stratified epithelia or BMZ. In
these cases, direct immunofluorescence (DIF) is often critical
in sample analysis. Optimally, the clinical characteristics of
the blister and the histologic differential diagnosis will be
considered in the approach to biopsy. For example, in the
setting of widespread tense blisters, 1 of 3 approaches is
recommended: (1) choose a small (1–2 mm) blister and
remove in entirety with an 8-mm punch with the blister at
the center of the punch. Bisect and submit half for
hematoxylin-eosin (H&E) staining and half for DIF; (2)
biopsy the edge of a large blister using a 6- or 8-mm punch,
after using a marker to delineate the line along which the
specimen is bisected to provide half for H&E and half for
DIF; or, (3) take 2 biopsies. The first biopsy is taken at the
edge of a blister, including approximately 10% blister and
90% perilesional skin, and the specimen is bisected at the
bedside to demonstrate the ‘‘take-off’’ point of the blister for
H&E. The second biopsy is taken from perilesional skin (1
cm from lesional skin) and is submitted for DIF (Figure 1). In
each situation, the H&E specimen is placed in formalin and
the DIF specimen is placed in Zeus or Michel media.
Pathologists and clinicians must work together to ensure
that the appropriate techniques and media are used.
However, clinicians should be aware of the possibility of a
degenerated stratum corneum and/or stratified epithelium,
Mimickers of Blistering Skin Disease—Tintle et al
Figure 1. Biopsy techniques. (Approach 1) A small (1–2 mm) blister can be removed in its entirety with a 6- to 8-mm punch with the blister at the
center of the punch. (Approach 2) The edge of a large blister can be biopsied using a 6- or 8-mm punch, after using a marker to delineate the line
along which the specimen is bisected. In each of these cases, the specimen is bisected and half of it is placed in formalin (F) for hematoxylin-eosin
(H&E), and half is placed in Zeus or Michel medium (Z) for direct immunofluorescence (DIF). (Approach 3) Take 2 biopsies. The first biopsy is taken
at the edge of a blister, including approximately 10% blister and 90% perilesional skin, and the specimen is bisected at the bedside to demonstrate
the ‘‘takeoff’’ point of the blister for H&E. The second biopsy is taken from perilesional skin (1 cm from lesional skin) and is submitted for DIF.

Figure 2. Pemphigus foliaceus with (A) acantholysis eventuating in a blister within the superficial epidermis. B, A closer view demonstrates stratum
granulosum cells adhering to the overlying stratum corneum (‘‘cling-ons’’; arrow) (hematoxylin-eosin, original magnifications 320 [A] and 340 [B]).

which makes both H&E sections and DIF difficult for the
pathologist to interpret.
This article reviews examples of the classic findings of
specific blistering diseases and emphasizes the importance
of considering unrelated conditions that can mimic the
classic finding.
PEMPHIGUS FOLIACEUS MIMICKED BY
STAPHYLOCOCCAL SCALDED SKIN SYNDROME
Two subcorneal blistering diseases produce widespread
superficial desquamation: pemphigus foliaceus (PF) and
Arch Pathol Lab Med—Vol 144, February 2020
staphylococcal scalded skin syndrome (SSSS). When the
latter disease shows acantholysis, it can mimic the former
(Table 1).
Pemphigus foliaceus classically produces subcorneal
blistering with acantholysis. Individual acantholytic cells
can be identified floating in the blister lumen and may cling
to the underside of the stratum corneum (‘‘cling-ons’’;
Figure 2).1 This disease is caused by autoantibodies to
desmoglein 1 (Dg1), a component of the desmosome, the
adhesion molecule necessary for intercellular (keratinocyte-
to-keratinocyte) adhesion.2 Because Dg1 is found primarily
Mimickers of Blistering Skin Disease—Tintle et al 137
 Table 1. Pemphigus Foliaceus and Its Mimicker Staphylococcal Scalded Skin Syndrome (Confusing Feature: Both Can
Show Subcorneal Blistering With Acantholysis)
Common Distinguishing Features
Histopathologic
Blistering Disease Findings Pathophysiology Clinical Histologic
Pemphigus foliaceus Subcorneal blister with Target Ag: desmoglein 1; No systemic symptoms, Follicular
floating acantholytic Ag-Ab complex produces middle-aged patient acantholysis,
cells and ‘‘cling-ons’’ inflammatory cascade that population chicken-wire IgG
dissolves cement substance deposits in the
upper layers of the
epidermis
Staphylococcal scalded Subcorneal blister without Exfoliative toxin produced by Systemic symptoms, young Negative DIF
skin syndrome acantholysis Staphylococcus aureus children with immature
adheres to desmoglein 1, kidneys or adults with
leading to subcorneal split renal failure
Abbreviations: Ab, antibody; Ag, antigen; DIF, direct immunofluorescence; IgG, immunoglobulin G.

in the granular layer (stratum granulosum), epidermal
acantholysis in PF is mostly confined to the upper layers
of the stratified epithelium.3 ‘‘Acantholytic hypergranulo-
sis,’’ a newly described finding of PF, refers to acantholytic
keratinocytes in the superficial portion of the epidermis
associated with large keratohyaline granules and may be
seen in about one-third of cases.4
Essentially all patients with PF have positive DIF results
demonstrating intercellular immunoglobulin (Ig) G
throughout the epidermis, with heavier deposits character-
istically seen in the upper epidermis.5
Pemphigus foliaceus is seen primarily in otherwise
healthy middle-aged to elderly adults and presents with
recurrent crops of fragile, flaccid bullae that are often
ruptured by the time of presentation.1 Thus, exfoliative
characteristics may predominate on exam, with superficial
erosions and a peripheral, adherent scale crust resembling
corn flakes. Patients may complain of burning, pain, or
pruritus. Systemic symptoms are notably absent.6
Like PF, SSSS is characterized by subcorneal blistering
(Figure 3). Staphylococcal scalded skin syndrome is also due
to the disruption of Dg1, although in SSSS Dg1 is cleaved by
exfoliative toxin A, a serine protease released by certain
strains of Staphylococcus aureus.7
Although the clinical appearance of intact blisters and
bullae in SSSS and PF is very similar, the 2 have otherwise
distinct clinical characteristics and patient populations.
Staphylococcal scalded skin syndrome is seen in neonates
(ages 3–7 days) with immature kidneys, adults with renal
disease, and immunosuppressed patients with kidneys that
do not adequately excrete exfoliative toxin A.8,9 These
patients often have acute systemic symptoms of infection
(fever, irritability, and malaise) compared with the chronic
and nonsystemic course of PF.9 Staphylococcal scalded skin
syndrome is a more rapidly evolving and widespread disease
in which the skin desquamates in sheets. Bacteria are
notably absent on cutaneous histopathology because the
source of infection is not skin but a distant site (such as the
umbilicus, nasopharynx, or urine).8
On H&E, the subcorneal and intragranular pattern of
acantholysis is identical in SSSS and PF.10 However,
epidermal inflammation in SSSS is typically sparse because
bullae are sterile. In contrast, PF typically shows a more
prominent inflammatory infiltrate in the upper dermis,
including eosinophils.11 Direct immunofluorescence on
perilesional skin may be required to differentiate between
138 Arch Pathol Lab Med—Vol 144, February 2020
these 2 entities, revealing intercellular IgG with or without
complement 3 (C3) in PF and negative findings in SSSS.10
It should be noted that pemphigus erythematosus, which
combines clinical features of PF with immunologic features
of lupus erythematosus, histologically appears identical to
pemphigus foliaceus (subcorneal blister containing acan-
tholytic cells).12
PEMPHIGUS VULGARIS MIMICKED BY HAILEY-HAILEY
DISEASE
Acantholysis within the epidermis leading to intraepider-
mal blistering is the characteristic finding of pemphigus
vulgaris (PV), the most common subtype of pemphigus.
Pemphigus vulgaris is usually seen in middle-aged adults
and presents with flaccid, fragile vesicles and bullae most
commonly involving the face, neck, axillae, and groin.13
Pemphigus vulgaris is related to formation of antibodies to
desmoglein 3 (Dg3), another component of the desmosome
(linking keratinocytes to one another).14 Dg3 is thought to
be more prominent than Dg1 in mucosal epithelium. For
this reason, mucosal involvement is almost always seen in
PV (in contrast to PF) and precedes cutaneous involvement
in a significant majority of patients.14
Intraepidermal acantholysis in PV is diffuse and supra-
basal,4 classically leaving a ‘‘tombstone row’’ of basal cells
attached to the dermal papillae (resembling gastrointestinal
‘‘villi’’; Figure 4). Occasional dyskeratosis is seen, and
inflammation is relatively minimal. Although follicular
involvement has historically been associated with PF, See
et al4 recently found a much higher percentage (up to 84%)
of PV cases displaying follicular acantholysis.4 Direct
immunofluorescence can confirm the diagnosis and char-
acteristically shows a ‘‘chicken-wire’’ pattern of IgG and
complement staining within the intercellular spaces, partic-
ularly intense in the lower epidermis.15
A histologic mimicker with some clinical similarities is
Hailey-Hailey disease, formerly known as benign familial
pemphigus (Table 2). As its historical name suggests,
Hailey-Hailey disease is a benign, autosomal dominant
condition with a clinical picture that mimics PV: fragile,
flaccid vesicles that progress to flaccid bullae with subse-
quent rupture and crusting.16 Hailey-Hailey disease typically
is composed of smaller vesicles and involves intertriginous
areas, primarily the axillae, as well as flexures and sides of
the neck (like PV).17 Lesions have usually ruptured by the
time of presentation, appearing instead as painful, well-
demarcated, macerated, or crusted plaques with reticulated
Mimickers of Blistering Skin Disease—Tintle et al
Figure 3. Staphylococcal scalded skin syndrome with (A) a subcorneal blister and underlying superficial lymphohistiocytic perivascular
inflammation. B, A closer view of the subcorneal split (hematoxylin-eosin, original magnifications 34 [A] and 310 [B]).

Figure 4. Pemphigus vulgaris with (A) intraepidermal, predominantly suprabasal blister with acantholysis. Hair follicle involvement is present. B,
Closer magnification reveals ‘‘tombstone row’’ of basal cells (hematoxylin-eosin, original magnifications 34 [A] and 320 [B]).

Table 2. Pemphigus Vulgaris and Its Mimicker Hailey-Hailey Disease (Confusing Feature: Both Can Show Suprabasal
Blistering)
Common Distinguishing Features
Histopathologic
Blistering Disease Findings Pathophysiology Clinical Histologic
Pemphigus vulgaris ‘‘Tombstone row’’ of basal Target Ag: desmoglein 3; Middle-aged adults; Focal dyskeratosis; ‘‘chicken-
cells attached to dermal Ag-Ab complex involvement of face wire’’ pattern of IgG and
papillae produces inflammatory complement staining within
cascade that dissolves intercellular spaces,
cement substance particularly intense in the
lower epidermis; follicular
involvement
Hailey-Hailey Full-thickness acantholysis; Altered calcium Familial history (autosomal Extensive, pronounced
disease ‘‘dilapidated brick wall’’ metabolism in dominant with acantholysis that spares
keratinocytes leading to incomplete penetrance); follicles; negative DIF
disruption of the tight young adults; axillary
junction (mutation in involvement
ATP2C1 gene)
Abbreviations: Ab, antibody; Ag, antigen; DIF, direct immunofluorescence; IgG, immunoglobulin G.

Arch Pathol Lab Med—Vol 144, February 2020 Mimickers of Blistering Skin Disease—Tintle et al 139
 Table 3. Allergic Contact Dermatitis Mimicked by Re-epithelialized Pemphigoid (Confusing Feature: Both Can Show
Intraepidermal Blistering)
Common Distinguishing Features
Histopathologic
Blistering Disease Findings Pathophysiology Clinical Histologic
Allergic contact Intraepidermal blister with Re-exposure to a contact Recent contact with an Spongiosis in epidermis causes
dermatitis eosinophilic spongiosis allergen leading to allergen; pruritic reticular degeneration (cell
and reticular delayed hypersensitivity erythematous papules membranes intact forming a
degeneration reaction and vesicles network pattern)
Bullous pemphigoid Subepidermal blister with Autoimmune disruption of Elderly; multiple pruritic, Regenerative epithelium at
eosinophilic spongiosis the hemidesmosome tense fluid-filled bullae base of blister; eosinophils
(may appear (impairing attachment of lined up at BMZ, positive
intraepidermal if re- epidermis to dermis) DIF, positive ELISA
epithelialized)
Abbreviations: BMZ, basement membrane zone; DIF, direct immunofluorescence; ELISA, enzyme-linked immunosorbent assay.

fissuring.18 The mechanism of acantholysis appears to be
related to altered calcium metabolism in keratinocytes that
disrupts the adherens junction (tight junction).19,20
Histologically, early lesions of Hailey-Hailey disease show
suprabasal clefting and the formation of intraepidermal
lacunae lined by single or clumped acantholytic cells.11 As
disease progresses, intercellular edema between keratino-
cytes with partial acantholysis results in a ‘‘dilapidated brick
wall’’ appearance (Figure 5).11 The acantholysis of Hailey-
Hailey disease is characteristically more extensive (full-
thickness) than that of PV.16 In addition, the dyskeratotic
cells of Hailey-Hailey disease usually show a well-defined
nucleus and preserved cytoplasm, versus the degenerating
dyskeratosis of PV. Hailey-Hailey disease typically spares
adnexal epithelium, as opposed to prominent follicular
involvement in PV. Epidermal hyperplasia is common in
Hailey-Hailey disease, along with a mixed inflammatory cell
infiltrate. Although eosinophils may be present, these are
more characteristic of PV.21 A negative DIF argues against
the diagnosis of PV and supports (but does not confirm) the
diagnosis of Hailey-Hailey disease.
ALLERGIC CONTACT DERMATITIS WITH RETICULAR
DEGENERATION CAUSING INTRAEPIDERMAL BLISTER
MIMICKED BY PEMPHIGOID WITH
RE-EPITHELIALIZATION
Eosinophilic spongiosis is a characteristic finding of both
allergic contact dermatitis (ACD) and bullous pemphigoid
(BP). If spongiosis in ACD is extensive, intraepidermal
vesicles may coalesce to form intraepidermal spongiotic
bullae (Figure 6). Bullous pemphigoid blisters are tense and
sturdy.22 They can persist for many days or even weeks, long
enough to completely re-epithelialize the base of the blister.
Although BP is defined by subepidermal blistering, these re-
epithelialized blisters may appear as intraepidermal bullae.
Partial or complete re-epithelialization may be seen in up to
25% of cases of BP.23
Differentiating factors between these 2 conditions include
the presence of spongiosis, the location of eosinophils, and
immunofluorescence results (Table 3). First, ACD displays
spongiosis with reticular degeneration; intracellular edema
causes keratinocytes to break open, but cell membranes
remain connected and create a network of variably sized
intraepidermal vesicles. In contrast, because the hemides-
mosome is disrupted in BP, keratinocyte-to-keratinocyte
cell membrane adhesion is intact, and hydropic degenera-
tion (as opposed to spongiotic degeneration [or vesicula-
tion]) is seen.24 Thus, in re-epithelialized BP, the floor of the
140 Arch Pathol Lab Med—Vol 144, February 2020
blister will be cleanly split, with regenerative epithelium at
the base (Figure 7).
Secondly, eosinophilic spongiosis (eosinophils within the
epidermis with associated spongiosis) is characteristic of
ACD (and other drug reactions).11 The inflammatory
infiltrate in ACD also consists of a mild to moderately
heavy infiltrate of lymphocytes, macrophages, and Langer-
hans cells in the upper dermis. Lymphocyte exocytosis may
be present.
Eosinophilic spongiosis in BP is often less prominent and
has been described as more at the side of the bulla or at a
distance more lateral within the specimen.24 In older BP
lesions, scale crust, psoriasiform epidermal hyperplasia, and
a denser inflammatory cell infiltrate are seen.
Finally, immunofluorescence can confirm the diagnosis of
BP. Direct immunofluorescence shows IgG and complement
deposited at the BMZ. Alternatively, enzyme-linked immu-
nosorbent assay (ELISA) testing for bullous pemphigoid
antigen 180 (BP180) and bullous pemphigoid antigen 230
(BP230), or indirect immunofluorescence (IIF) on human
salt-split skin or monkey esophagus substrate can be
performed. The IIF will demonstrate IgG at the dermal-
epidermal junction (DEJ), specifically within the roof of the
blister. Direct immunofluorescence, ELISA, and IIF are
negative in ACD.
EARLY ALLERGIC CONTACT DERMATITIS MIMICKED BY
NONBULLOUS ECZEMATOUS OR URTICARIAL
PEMPHIGOID
Nonbullous eczematous or urticarial BP can also closely
resemble ACD, both clinically and histologically (Table 4).
About 20%22,25 of BP cases follow a chronic, relapsing course
that clinically resembles eczema or fixed urticaria.23 Like
ACD, nonbullous BP clinically presents with pruritic,
erythematous papules and plaques (which may progress to
a vesicular, weeping, or bullous stage).11 The vast majority of
these patients never develop clinically significant blister-
ing.26
With the exception of eosinophilic spongiosis, which is
present in only about 8% of cases,23 histologic findings of
nonbullous BP are nonspecific and consist of spongiosis,
mild upper dermal edema, and a perivascular infiltrate with
eosinophils (Figure 8).23 Similarly, early lesions of ACD
show acute spongiotic dermatitis with papillary dermal
edema and a mixed inflammatory perivascular infiltrate
(lymphocytes, macrophages, and Langerhans cells). Eosin-
ophils can be present in both the dermal infiltrate and
Mimickers of Blistering Skin Disease—Tintle et al
Figure 5. A biopsy of Hailey-Hailey disease shows (A) acantholysis creating focal suprabasilar clefting. B, More extensive, full-thickness acantholysis
resulting in ‘‘dilapidated brick wall’’ appearance (hematoxylin-eosin, original magnification 310).

Figure 6. Allergic contact dermatitis featuring (A) vesicular spongiotic dermatitis. B, Closer magnification with intraepidermal blister, adjacent
spongiosis (arrowhead), and eosinophils (arrows) (hematoxylin-eosin, original magnifications 310 [A] and 320 [B]).

Figure 7. A biopsy of an older lesion of bullous pemphigoid reveals (A) a subepidermal bulla containing numerous eosinophils and fibrin, with focal
re-epithelialization providing the appearance of an intraepidermal bulla. B, Closer magnification highlights the same features. Immunofluorescence
studies were confirmatory (hematoxylin-eosin, original magnifications 310 [A] and 320 [B]).

Arch Pathol Lab Med—Vol 144, February 2020 Mimickers of Blistering Skin Disease—Tintle et al 141
 Table 4. Allergic Contact Dermatitis Mimicked by Eczematous Pemphigoid (Confusing Feature: Both Can Show
Spongiotic Dermatitis With Eosinophils)
Common Distinguishing Features
Histopathologic
Blistering Disease Findings Pathophysiology Clinical Histologic
Allergic contact dermatitis Acute spongiotic Re-exposure to a contact Recent contact with an Reticular degeneration;
dermatitis, papillary allergen leading to allergen; pruritic eosinophil and
edema, perivascular delayed hypersensitivity erythematous papules lymphocyte exocytosis
inflammation reaction and vesicles more common
Nonbullous eczematous Acute spongiotic Autoimmune disruption of Elderly; multiple pruritic, Eosinophils lined up at
pemphigoid dermatitis, papillary the hemidesmosome tense fluid-filled bullae BMZ; positive DIF,
edema, perivascular (impairing attachment of positive ELISA
inflammation epidermis to dermis)
Abbreviations: BMZ, basement membrane zone; DIF, direct immunofluorescence; ELISA, enzyme-linked immunosorbent assay.

within areas of spongiosis.11 In early ACD, both stratum
corneum and epidermal thickness are normal (Figure 9).
Differentiating between these 2 conditions histologically
is difficult in the absence of a DEJ split, but the
characteristics described above (reticular degeneration in
ACD) may be helpful in determining a diagnosis.
The diagnosis of non-bullous BP usually requires high
clinical suspicion as well as confirmatory DIF and IIF on
salt-split skin when possible.25 Clinically, nonbullous BP is
more common in the elderly, whereas patients with ACD
will be younger on average and often have a history of
atopy. Patients with ACD often have had exposure to an
allergen in the past 12 to 72 hours,11 and lesions may appear
in geometric or linear shapes, indicating areas of skin
contact with the allergen.
DERMATITIS HERPETIFORMIS MIMICKED BY LINEAR IgA
BULLOUS DERMATOSIS AND BULLOUS SYSTEMIC
LUPUS ERYTHEMATOSUS
Dermatitis herpetiformis (DH) is an autoimmune-derived
disease characterized by intensely pruritic, small papules
and clear fluid-filled vesicles symmetrically distributed on
the dorsal surfaces (extremities, scalp, and sacrum). In DH,
ingestion of gluten is believed to initiate formation of IgA
antibodies to tissue transglutaminase in the gastrointestinal
tract, producing a gluten-sensitive enteropathy (celiac
disease). These antibodies may also recognize epidermal
transglutaminase (TG-3) in the skin, which can activate the
complement cascade with subsequent chemotaxis of neu-
trophils into the papillary dermis. It is not clear why some
patients have only celiac disease, whereas others show only
DH, and yet others show both phenotypes. Dermatitis
herpetiformis is also associated with an increased incidence
of other autoimmune diseases, most commonly autoim-
mune thyroid disease,27 type 1 diabetes mellitus,28 and
pernicious anemia.29
On H&E, DH is characterized by a prominent neutrophilic
infiltrate focused within dermal papillae associated with
papillary dermal edema and subepidermal vesiculation
(Figure 10). There is relative sparing of the rete tips between
each dermal papilla. Eosinophils, lymphocytes, and histio-
cytes migrate into the skin as lesions of DH evolve. Direct
immunofluorescence can provide confirmation of the
diagnosis, showing granular deposits of IgA alone or in
combination with C3 at tips of dermal papillae. There is no
staining for IgM and IgG.
The H&E findings of linear IgA bullous dermatosis
(LABD) can be identical to those seen in DH, but the
immunologic pathogenesis, DIF, and clinical history of the 2
diseases are quite different (Table 5). The antigens in the 2
diseases are both integral to the attachment of the epidermis
to the dermis. In LABD antibodies are directed against

Table 5. Dermatitis Herpetiformis Mimicked by Linear Immunoglobulin (Ig) A Bullous Dermatosis and Bullous Systemic
Lupus Erythematosus (Confusing Feature: Subepidermal Blister With Papillary Dermal Edema and Neutrophilic Infiltrate)
Common Distinguishing Features
Histopathologic
Blistering Disease Findings Pathophysiology Clinical Histologic
Dermatitis Subepidermal vesiculation; IgA antibodies to Dorsal surfaces; grouped, Granular deposits of
herpetiformis papillary dermal edema with epidermal excoriated papules and vesicles; IgA in the dermal
‘‘stuffing’’ of the dermal transglutaminase history of gluten-sensitive papillae on DIF
papillae with neutrophils enteropathy; severe pruritus
Linear IgA bullous Papillary dermal edema with IgA antibodies to Annular, ‘‘string of pearls’’ pruritic Homogeneous, linear
dermatosis dermal-epidermal blistering. BP230 (of vesicles and bullae peripherally pattern of IgA
In some cases, collections of hemidesmosome) surrounding a wheal, deposition at the DEJ
neutrophils ‘‘stuffing’’ the particularly involving groin or on DIF
dermal papillae genitals; drug history (especially
vancomycin)
Bullous lupus Subepidermal blister; superficial, Various autoantibodies Tense vesiculobullous lesions on Granular and linear
erythematosus sparse lichenoid and to components of the sun-exposed skin deposits of IgG and
perivascular mononuclear or BMZ or type VII C3 at the DEJ; IgM
neutrophilic infiltrate in some collagen and IgA may also be
cases with neutrophils present
‘‘stuffing’’ the dermal papillae
Abbreviations: BMZ, basement membrane zone; C3, complement 3; DEJ, dermal-epidermal junction; DIF, direct immunofluorescence.
142 Arch Pathol Lab Med—Vol 144, February 2020 Mimickers of Blistering Skin Disease—Tintle et al
Figure 8. A biopsy of the eczematous phase of bullous pemphigoid shows (A) features of spongiotic dermatitis. B, A perivascular and interstitial
inflammatory infiltrate includes numerous eosinophils. Immunofluorescence studies were confirmatory (hematoxylin-eosin, original magnifications
310 [A] and 320 [B]).

Figure 9. A biopsy of allergic contact dermatitis with features of (A) spongiosis with eosinophils within the epidermis (eosinophilic spongiosis) and
the superficial perivascular and interstitial inflammatory infiltrate. B, Eosinophilic spongiosis (hematoxylin-eosin, original magnifications 310 [A] and
320 [B]).

Figure 10. Dermatitis herpetiformis with (A) neutrophils within the dermal papillae (neutrophilic microabscesses). B, A closer view shows a subtle
subepidermal split. Immunofluorescence studies were confirmatory (hematoxylin-eosin, original magnifications 310 [A] and 320 [B]).

Arch Pathol Lab Med—Vol 144, February 2020 Mimickers of Blistering Skin Disease—Tintle et al 143
BP230 (a component of the hemidesmosome), as opposed
to transglutaminase in DH. The DIF findings of a
homogeneous, linear pattern of IgA deposition at the BMZ
are characteristic of LABD and quite different from the
granular deposits of IgA in the dermal papillae seen in DH.
In the absence of these findings, diagnosis is more difficult,
because salt-split skin studies can yield heterogeneous
results (staining above or below the lamina densa). Linear
IgA bullous dermatosis in adults is usually drug induced;
vancomycin is most commonly implicated, followed by
captopril, other b-lactam antibiotics, and nonsteroidal anti-
inflammatory drugs (NSAIDs). Intact vesicles and tense
bullae, often ringing an erythematous patch, are commonly
seen in LABD, whereas the primary vesicles of DH are
usually excoriated by the time the patient presents.
Both DH and LABD respond clinically to brief courses of
systemic steroids and more prolonged suppression with
dapsone. The latter presumably acts by suppressing
neutrophils. Discontinuation of the offending drug in LABD
and avoidance of gluten in DH are also required.
There are 2 histologic patterns seen in bullous systemic
lupus erythematosus (SLE): 1 predominantly characterized
by mononuclear cells, and 1 characterized predominantly by
neutrophils.30 This latter type closely simulates the findings
of DH and LABD, with papillary microabscesses of
neutrophils ‘‘stuffing’’ the papillae and overlying dermal-
epidermal blistering (Table 5). Nuclear dust in the upper
dermis and surrounding blood vessels can also be seen. On
DIF, there is usually a mix of linear and granular IgG
deposition at the BMZ; IgA and IgM deposits may also be
present. These immunoreactants are below the lamina
densa (on the dermal side of salt-split skin). Some of these
patients have autoantibodies to various components of the
BMZ or to collagen VII.
Bullous SLE is considered a variant of SLE and requires a
clinical diagnosis of SLE. Like SLE, it mainly affects young
women in their second to fourth decades and often presents
acutely with tense vesicles and bullae (overlying either
normal skin or preexisting SLE patches). Another clinically
differentiating factor of bullous SLE is its predilection for
photo-distributed regions (trunk, upper extremities, face
and neck).31 Similarly to DH and LABD, dapsone often
produces a dramatic clinical response.32
TOXIC EPIDERMAL NECROLYSIS MIMICKED BY
PEMPHIGOID WITH EPIDERMAL NECROSIS AND
METHOTREXATE TOXICITY
Most clinicians are familiar with toxic epidermal necrolysis
(TEN), a rapidly progressing dermatologic emergency
associated with high mortality (25% to 50%).33 Timely
diagnosis of TEN is critical and often requires histopatho-
logic confirmation.
Toxic epidermal necrolysis is almost always associated
with a causative drug that must be promptly identified and
discontinued (most commonly implicated are sulfonamides,
anticonvulsants, allopurinol, and NSAIDs).34 Clinically, TEN
is defined by painful sloughing of the skin involving more
than 30% of the body surface area. As it evolves, dusky or
purpuric macules coalesce into patches and plaques that
eventuate in flaccid bullae and subsequent epidermal
sloughing. Mucosal erosions/ulceration (buccal, genital,
ocular) are present in most cases, and a flulike prodrome
usually precedes the appearance of cutaneous lesions.
Stevens-Johnson Syndrome is in the same disease spec-
144 Arch Pathol Lab Med—Vol 144, February 2020
trum, but with less than 10% body surface area involvement.
Involvement of 10% to 30% body surface area is considered
Stevens-Johnson Syndrome/TEN overlap.
The distinctive histologic finding of TEN is full-thickness
epidermal necrosis (although the absence of this finding
does not preclude a diagnosis of TEN; Figure 11). In other
cutaneous diseases, if keratinocyte cell death occurs, it is
often confined to the basal layer. In TEN, on the other hand,
keratinocyte apoptosis is characteristically present within all
layers of the epidermis, taking the form of confluent
necrosis.11 Established lesions of TEN are characterized by
a subepidermal blister, full-thickness necrosis of the
epidermal roof, and a notably absent or sparse inflammatory
infiltrate (‘‘cell-poor’’).11 It is postulated that epidermal
necrosis is mediated by cytokines from drug-specific
cytotoxic T lymphocytes, although apoptosis of keratino-
cytes also occurs.35 The action of cytokines may explain the
apparent discrepancy between the extent of epidermal
damage and the paucity of the dermal infiltrate.11
The characteristic histologic findings of TEN—subepider-
mal clefting and full-thickness epidermal necrosis—are also
observed in the more common condition of BP (Table 6). In
BP, tense blistering occurs at the DEJ. Full-thickness
necrosis occurs in blisters that persist for weeks because
the epidermis is separated from the dermal blood supply
(Figure 12). Because this phenomenon occurs in older
lesions of BP, it is generally recommended that only blisters
less than 48 hours old be sampled.23
Histologically, the most apparent factor differentiating BP
from TEN is the more prominent inflammatory infiltrate and
presence of eosinophils in the former condition.11,36
Additional differentiating factors favoring BP include the
following: (1) absence of dyskeratosis and necrosis in
adjacent nonblistered skin, (2) re-epithelialization of the
dermal-epidermal blister correlating with the age of the
blister, and (3) sampling of younger blisters showing
dermal-epidermal separation without dyskeratosis or ne-
crosis.23 Although DIF sometimes shows diffuse deposition
of immunoreactants in the midepidermis in TEN, it is
usually negative.34 Direct immunofluorescence is a highly
sensitive test for BP, with demonstration of linear IgG and
C3 staining at the DEJ.37,38 Indirect immunofluorescence is a
more specific test for BP; antibody binding to the epidermal
side of split (roof) will be present in 60% to 80% of cases of
BP, with a specificity of 95% to 100%.38 Clinical clues to a
diagnosis of BP include a history of tense, markedly pruritic
blisters, and a negative Nikolsky sign, whereas TEN shows
flaccid painful bullae with a positive Nikolsky sign.23
Although many of the same drugs are associated with BP
and TEN, BP is more commonly caused by furosemide,
captopril, and NSAIDs.
Clinical manifestations of methotrexate (MTX)-induced
cutaneous toxicity are very similar to those of TEN, with
histology that also mimics that of TEN (Table 6). Although
clinically variable, in its most severe form, MTX-induced
toxicity is characterized by widespread erythematous or
dusky macules, blistering, and desquamation.39 Frequent
mucosal involvement (mucositis, stomatitis) often leads
clinicians to consider TEN.40
Methotrexate toxicity is usually seen in patients with renal
failure, or those given a concomitant medication that causes
renal dysfunction or impairs folic acid absorption, especially
trimethoprim-sulfamethoxazole. Without appropriate ad-
justment of MTX dosage, this leads to toxic levels of
systemic MTX. The mechanism of pathogenesis may include
Mimickers of Blistering Skin Disease—Tintle et al
Figure 11. A biopsy of toxic epidermal necrolysis demonstrates (A) epidermal dyskeratosis and confluent necrosis with basket-weave stratum
corneum and sparse underlying inflammation. B, Closer magnification reveals focal dermal-epidermal separation and re-epithelialization
(hematoxylin-eosin, original magnifications 34 [A] and 310 [B]).

Figure 12. A biopsy of bullous pemphigoid with (A) necrosis of the blister roof. B, Closer magnification highlights re-epithelialization of the base.
Immunofluorescence studies were confirmatory (hematoxylin-eosin, original magnifications 34 [A] and 310 [B]).

Figure 13. Full-thickness epidermal necrosis leading to dermal-epidermal separation with sparse underlying inflammation. Patient had renal failure
and was incorrectly dosing methotrexate at 3 times the prescribed amount. Improvement was quickly noted after a rescue dose of leucovorin
(hematoxylin-eosin, original magnification 310).

Arch Pathol Lab Med—Vol 144, February 2020 Mimickers of Blistering Skin Disease—Tintle et al 145
 Table 6. Toxic Epidermal Necrolysis Mimicked by Bullous Pemphigoid With Epidermal Necrosis and by Methotrexate
(MTX)–Induced Toxicity (Confusing Feature: Both Can Show Full-Thickness Epidermal Necrosis Overlying a
Dermal-Epidermal Split)
Common Distinguishing Features
Histopathologic
Blistering Disease Findings Pathophysiology Clinical Histologic
Toxic epidermal Subepidermal blister with Release of cytokines Flulike prodrome followed Cell-poor; negative DIF
necrolysis overlying confluent full- from drug-specific T by development of dusky
thickness epidermal lymphocytes, causing macules that coalesce;
necrosis; sparse or epidermal necrosis flaccid bullae with
absent lymphocytic epidermal sloughing
infiltrate involving .30% BSA;
severe mucosal
involvement
Bullous pemphigoid with Subepidermal blister with Autoantibodies to Initially pruritic and tense; Mixed inflammatory
epidermal necrosis a necrotic (often full- components of the biopsy of lesion ,48 h infiltrate with prominent
thickness) epidermal hemidesmosomes old shows no epidermal eosinophils; positive DIF
roof; eosinophils ‘‘lined (BP180 or BP230) necrosis (linear IgG and C3 at the
up’’ at the DEJ; DEJ); positive IIF
lymphocytes and
neutrophils in papillary
dermis
MTX-induced cutaneous Focal subepidermal Dose-dependent drug- Widespread blistering Subepidermal clefting is
toxicity separation with induced toxicity, direct progressing to focal; greater
keratinocyte dystrophy cell toxicity and desquamation; inflammatory infiltrate
and full-thickness potential allergic significant mucositis, with prominent
epidermal necrosis; reaction component renal insufficiency, and eosinophils
mixed inflammatory cytopenias
infiltrate with eosinophils
Abbreviations: BSA, body surface area; C3, complement 3; DEJ, dermal-epidermal junction; DIF, direct immunofluorescence; IgG, immunoglobulin
G; IIF, indirect immunofluorescence.

an allergic as well as a dose-dependent toxicity reaction.41
Although the cutaneous findings are not life-threatening,
they may herald pancytopenia, which can be fatal.42
On H&E, focal dermal-epidermal clefting and variable
degrees of keratinocyte dystrophy (including full-thickness
epidermal necrosis) are seen (Figure 13).40,42,43 A back-
ground of interface dermatitis and a mixed dermal
inflammatory infiltrate with eosinophils may be present,
which in some cases may be abundant.40 Epidermal
dysmaturation, nuclear pleomorphism, and atypical mitotic
figures have also been reported.43
Helpful features favoring MTX toxicity versus TEN include
especially severe mucositis (including involvement of the
gastrointestinal tract with symptoms such as dysphagia and
diarrhea), concomitant cytopenia(s), and acute renal insuf-
ficiency.40 Neutropenic fever may be seen but typically
follows the onset of cutaneous manifestations,40 whereas
the flulike prodrome of TEN precedes the rash. Histolog-
ically, epidermal necrosis may be less prominent than that
seen in TEN, with a heavier inflammatory infiltrate that
includes eosinophils.
Monitoring serum levels of MTX, particularly in patients
with impaired hepatic or renal function, avoiding medica-
tions that interfere with MTX metabolism (eg, trimetho-
prim-sulfamethoxazole, sulfonamides, NSAIDs), and
quickly initiating leucovorin rescue can help prevent and
treat MTX toxicity.41
SUMMARY
It is not possible to include all possible blistering disease
mimics in an article of this type. Rather, our goal was to
highlight common situations that have confused us initially
or led us to a misdiagnosis. A systematic, ‘‘top-down’’
histopathologic approach can help simplify the evaluation of
blistering diseases. Special attention to biopsy technique,
the clinical stage of disease, the age of the biopsied blister,
and immunofluorescence findings are important for both
clinician and pathologist. Effective communication between
clinician and pathologist to ensure that appropriate biopsy
technique and media are used is critical for accurate
diagnosis.
References
1. James KA, Culton DA, Diaz LA. Diagnosis and clinical features of
pemphigus foliaceus. Dermatol Clin. 2011;29(3):405–412; viii.
2. Diaz LA, Prisayanh PS, Dasher DA, et al; Cooperative Group on Fogo
Selvagem R. The IgM anti-desmoglein 1 response distinguishes Brazilian
pemphigus foliaceus (fogo selvagem) from other forms of pemphigus. J Invest
Dermatol. 2008;128(3):667–675.
3. Maeda JY, Moura AK, Maruta CW, Santi CG, Prisayanh PS, Aoki V. Changes
in the autoimmune blistering response: a clinical and immunopathological shift
from pemphigus foliaceus to bullous pemphigoid. Clin Exp Dermatol. 2006;31(5):
653–655.
4. See SHC, Peternel S, Adams D, North JP. Distinguishing histopathologic
features of acantholytic dermatoses and the pattern of acantholytic hyper-
granulosis. J Cutan Pathol. 2019;46(1):6–15.
5. Mahoney MG, Wang Z, Rothenberger K, Koch PJ, Amagai M, Stanley JR.
Explanations for the clinical and microscopic localization of lesions in
pemphigus foliaceus and vulgaris. J Clin Invest. 1999;103(4):461–468.
6. Dasher D, Rubenstein D, Diaz LA. Pemphigus foliaceus. Curr Dir
Autoimmun. 2008;10:182–194.
7. Pimentel de Araujo F, Tinelli M, Battisti A, et al. An outbreak of skin
infections in neonates due to a Staphylococcus aureus strain producing the
exfoliative toxin A. Infection. 2018;46(1):49–54.
8. Mishra AK, Yadav P, Mishra A. A systemic review on staphylococcal scalded
skin syndrome (SSSS): a rare and critical disease of neonates. Open Microbiol J.
2016;10:150–159.
9. Patel GK, Finlay AY. Staphylococcal scalded skin syndrome: diagnosis and
management. Am J Clin Dermatol. 2003;4(3):165–175.
10. Ho J, Bhawan J. Mimickers of classic acantholytic diseases. J Dermatol.
2017;44(3):232–242.
11. Patterson JW. Weedon’s Skin Pathology. 4th ed. London, UK: Churchill
Livingstone; 2016.

146 Arch Pathol Lab Med—Vol 144, February 2020 Mimickers of Blistering Skin Disease—Tintle et al
 12. Oktarina DA, Poot AM, Kramer D, Diercks GF, Jonkman MF, Pas HH. The
IgG ‘‘lupus-band’’ deposition pattern of pemphigus erythematosus: association
with the desmoglein 1 ectodomain as revealed by 3 cases. Arch Dermatol. 2012;
148(10):1173–1178.
13. Mustafa MB, Porter SR, Smoller BR, Sitaru C. Oral mucosal manifestations
of autoimmune skin diseases. Autoimmun Rev. 2015;14(10):930–951.
14. Amagai M, Tsunoda K, Zillikens D, Nagai T, Nishikawa T. The clinical
phenotype of pemphigus is defined by the anti-desmoglein autoantibody profile. J
Am Acad Dermatol. 1999;40(2, pt 1):167–170.
15. Venugopal SS, Murrell DF. Diagnosis and clinical features of pemphigus
vulgaris. Dermatol Clin. 2011;29(3):373–380; vii.
16. Burge SM. Hailey-Hailey disease: the clinical features, response to
treatment and prognosis. Br J Dermatol. 1992;126(3):275–282.
17. Wolf R, Oumeish OY, Parish LC. Intertriginous eruption. Clin Dermatol.
2011;29(2):173–179.
18. Hurd DS, Johnston C, Bevins A. A case report of Hailey-Hailey disease
treated with alefacept (Amevive). Br J Dermatol. 2008;158(2):399–401.
19. Hakuno M, Shimizu H, Akiyama M, et al. Dissociation of intra- and
extracellular domains of desmosomal cadherins and E-cadherin in Hailey-Hailey
disease and Darier’s disease. Br J Dermatol. 2000;142(4):702–711.
20. Raiko L, Siljamaki E, Mahoney MG, et al. Hailey-Hailey disease and tight
junctions: claudins 1 and 4 are regulated by ATP2C1 gene encoding Ca(2þ) /
Mn(2þ) ATPase SPCA1 in cultured keratinocytes. Exp Dermatol. 2012;21(8):586–
591.
21. Engin B, Kutlubay Z, Celik U, Serdaroglu S, Tuzun Y. Hailey-Hailey disease:
a fold (intertriginous) dermatosis. Clin Dermatol. 2015;33(4):452–455.
22. Bernard P, Antonicelli F. Bullous pemphigoid: a review of its diagnosis,
associations and treatment. Am J Clin Dermatol. 2017;18(4):513–528.
23. Hodge BD, Roach J, Reserva JL, et al. The spectrum of histopathologic
findings in pemphigoid: avoiding diagnostic pitfalls. J Cutan Pathol. 2018;45(11):
831–838.
24. Crotty C, Pittelkow M, Muller SA. Eosinophilic spongiosis: a clinicopath-
ologic review of seventy-one cases. J Am Acad Dermatol. 1983;8(3):337–343.
25. Meijer JM, Diercks GFH, de Lang EWG, Pas HH, Jonkman MF. Assessment
of diagnostic strategy for early recognition of bullous and nonbullous variants of
pemphigoid. JAMA Dermatol. 2019;155(2):158–165.
26. Lamberts A, Meijer JM, Jonkman MF. Nonbullous pemphigoid: a systematic
review. J Am Acad Dermatol. 2018;78(5):989–995.e2.
27. Gaspari AA, Huang CM, Davey RJ, Bondy C, Lawley TJ, Katz SI. Prevalence
of thyroid abnormalities in patients with dermatitis herpetiformis and in control
subjects with HLA-B8/-DR3. Am J Med. 1990;88(2):145–150.
28. Bolotin D, Petronic-Rosic V. Dermatitis herpetiformis, part I: epidemiology,
pathogenesis, and clinical presentation. J Am Acad Dermatol. 2011;64(6):1017–
1024; quiz 1025–1016.
29. Alonso-Llamazares J, Gibson LE, Rogers RS 3rd. Clinical, pathologic, and
immunopathologic features of dermatitis herpetiformis: review of the Mayo Clinic
experience. Int J Dermatol. 2007;46(9):910–919.
30. Merklen-Djafri C, Bessis D, Frances C, et al. Blisters and loss of epidermis in
patients with lupus erythematosus: a clinicopathological study of 22 patients.
Medicine (Baltimore). 2015;94(46):e2102.
31. Contestable JJ, Edhegard KD, Meyerle JH. Bullous systemic lupus
erythematosus: a review and update to diagnosis and treatment. Am J Clin
Dermatol. 2014;15(6):517–524.
32. Chanprapaph K, Sawatwarakul S, Vachiramon V. A 12-year retrospective
review of bullous systemic lupus erythematosus in cutaneous and systemic lupus
erythematosus patients. Lupus. 2017;26(12):1278–1284.
33. Sekula P, Dunant A, Mockenhaupt M, et al. Comprehensive survival
analysis of a cohort of patients with Stevens-Johnson syndrome and toxic
epidermal necrolysis. J Invest Dermatol. 2013;133(5):1197–1204.
34. Wolkenstein P, Revuz J. Toxic epidermal necrolysis. Dermatol Clin. 2000;
18(3):485–495; ix.
35. Kinoshita Y, Saeki H. A review of the pathogenesis of toxic epidermal
necrolysis. J Nippon Med Sch. 2016;83(6):216–222.
36. Mofid MZ, Costarangos C, Bernstein B, Wong L, Munster A, Nousari HC.
Drug-induced linear immunoglobulin A bullous disease that clinically mimics
toxic epidermal necrolysis. J Burn Care Rehabil. 2000;21(3):246–247.
37. Schmidt E, Zillikens D. Modern diagnosis of autoimmune blistering skin
diseases. Autoimmun Rev. 2010;10(2):84–89.
38. Sardy M, Kostaki D, Varga R, Peris K, Ruzicka T. Comparative study of direct
and indirect immunofluorescence and of bullous pemphigoid 180 and 230
enzyme-linked immunosorbent assays for diagnosis of bullous pemphigoid. J Am
Acad Dermatol. 2013;69(5):748–753.
39. Martins da Cunha AC, Rappersberger K, Gadner H. Toxic skin reaction
restricted to palms and soles after high-dose methotrexate. Pediatr Hematol
Oncol. 1991;8(3):277–280.
40. Fridlington JL, Tripple JW, Reichenberg JS, Hall CS, Diven DG. Acute
methotrexate toxicity seen as plaque psoriasis ulceration and necrosis: a
diagnostic clue. Dermatol Online J. 2011;17(11):2.
41. Kataria P, Kendre P, Patel A, Tahiliani N, Ikhar S. Methotrexate-induced
toxic epidermal necrolysis: a rare case report and review of literature. Indian J Crit
Care Med. 2018;22(10):740–742.
42. Jariwala P, Kumar V, Kothari K, Thakkar S, Umrigar DD. Acute methotrexate
toxicity: a fatal condition in two cases of psoriasis. Case Rep Dermatol Med.
2014;2014:946716.
43. Lewis HA, Nemer KM, Chibnall RJ, Musiek AC. Methotrexate-induced
cutaneous ulceration in 3 nonpsoriatic patients: report of a rare side effect. JAAD
Case Rep. 2017;3(3):236–239.

Submit Your Research to the

CAP20 Abstract Program
Abstract and case study submissions to the College of American Pathologists (CAP) 2020 Abstract
Program are now being accepted. Pathologists, laboratory professionals, and researchers in related fields
are encouraged to submit original studies for possible poster presentation at the CAP20 meeting.

Submissions will be accepted until 5 p.m. Central time Tuesday, March 10, 2020. Accepted abstracts and
case studies will appear on the Archives of Pathology & Laboratory Medicine Web site as a Web-only
supplement to the September 2020 issue.

Visit the CAP20 Web site (www.thepathologistsmeeting.org) or the Archives Web site (www.
archivesofpathology.org) for additional abstract program information including a link to the submission
site.

Arch Pathol Lab Med—Vol 144, February 2020 Mimickers of Blistering Skin Disease—Tintle et al 147
Copyright of Archives of Pathology & Laboratory Medicine is the property of College of
American Pathologists and its content may not be copied or emailed to multiple sites or
posted to a listserv without the copyright holder's express written permission. However, users
may print, download, or email articles for individual use.