Dermatology: Practical and Conceptual


Research  |  Dermatol Pract Concept 2019;9(2):7 119

Dermatology Practical & Conceptual

Mucous Membrane Pemphigoid-Associated 
Malignancies: Case Series and a Brief  

Overview of the Literature
Michelangelo La Placa1, Riccardo Balestri1, Federico Tartari1, Andrea Sechi1, Francesca Ferrara1, 

Camilla Loi1, Annalisa Patrizi1, Federico Bardazzi1

1 Dermatology Division, Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Bologna, Italy

Key words: mucous membrane pemphigoid, malignancy, autoimmune bullous disorders, paraneoplastic pemphigus, laminin-332, blistering 
diseases, laminin-5, anti-epiligrin, cicatricial pemphigoid, adenocarcinoma

Citation: La Placa M, Balestri R, Tartari F, Sechi A, Ferrara F, Loi C, Patrizi A, Bardazzi F. Mucous membrane pemphigoid-associated 
malignancies: Case series and a brief overview of the literature. Dermatol Pract Concept. 2019;9(2):119-125. DOI: https://doi.org/10.5826/
dpc.0902a07

Accepted: February 6, 2019; Published: April 30, 2019

Copyright: ©2019 La Placa et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, 
which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: None.

Competing interests: The authors have no conflicts of interest to disclose.

Authorship: All authors have contributed significantly to this publication.

Corresponding author: Michelangelo La Placa, MD, Dermatology Division, Department of Experimental, Diagnostic and Specialty 
Medicine, University of Bologna, Via Massarenti 1, 40138, Bologna, Italy. Email: michelangelo.laplaca@unibo.it

Background: Mucous membrane pemphigoid (MMP) is a heterogeneous group of blistering disorders 
affecting the mucosae with or without skin involvement, characterized by the presence of autoantibod-
ies to components of the basement membrane zone, including the bullous pemphigoid antigen BP180 
and β4 integrin. Current literature has shown that a minority of patients present circulating antibodies 
to laminin-332 and this population seems to be associated with a relatively high risk of malignancy.

Objective: To present our personal case series of patients with MMP-associated malignancy from a 
dermatology university hospital.

Methods: Twenty-two patients affected by MMP were seen in the period between 2001 and 2016; in 
4 patients (18%) an associated cancer was detected.

Results: These patients were 2 men and 2 women, with a mean age of 69.7 years (range, 48-83). The 
associated malignancies included a breast cancer, a pancreatic adenocarcinoma, a metastatic laryngeal 
carcinoma, and a hepatic carcinoma. All patients had negative results for both BP180 and laminin-332 
autoantibodies.

Conclusion: We confirm that MMP patients have a relatively high possibility of developing a solid 
cancer, but the autoantibody detection is not mandatory and is probably correlated with the severity 
of the disease.

ABSTRACT

Introduction

Mucous membrane pemphigoid (MMP), formerly cicatricial 

pemphigoid, is a rare heterogeneous group of autoimmune 

subepithelial blistering disorders involving the mucous mem-

branes and occasionally the skin with a chronic course and 

tendency toward scarring [1]. Previously, other names have 

been used to describe these conditions, including benign 

MMP, anti-laminin-5 cicatricial pemphigoid, oral pemphi-

goid, and ocular pemphigoid. Because it is difficult to clini-



120 Research  |  Dermatol Pract Concept 2019;9(2):7

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cally distinguish the various MMP subgroups, the collective 

term MMP is now accepted [2].

MMP commonly affects the oral mucosa, but ocular and 

nasal epithelia, the first aerodigestive tract and the genitals 

may be involved. Cutaneous involvement may be absent or 

limited. MMP usually affects patients aged between 60 and 

80 years, with a female prevalence [1-3]. The disease is mainly 

controlled with corticosteroids and other immunosuppressive 

drugs, including cyclosporine, mycophenolate, cyclophospha-

mide, and azathioprine [3].

Most of the MMP autoantibody profile shares the same 

target antigens of other autoimmune blistering diseases 

from the pemphigoid group and paraneoplastic pemphigus, 

namely circulating IgG and/or IgA autoantibodies targeting 

the basement membrane zone (BMZ) components, includ-

ing the bullous pemphigoid antigens BP180 and BP230, and 

the β4 integrin [1-6]. Current evidence demonstrates that a 
minority of MMP patients with autoantibodies to IgG anti-

laminin-332 (formerly anti-laminin-5 or anti-epiligrin) have 

an increased relative risk of cancer [1,7]. Previously, this 

subgroup was named anti-epiligrin cicatricial pemphigoid 

(AECP), to differentiate it from the majority of cicatricial 

pemphigoid patients without these specific autoantibodies. 

Finally, there is no report of MMP-associated malignancies 

with autoantibodies to BP180 [1,2,8-14].

We present a case series of MMP patients with associated 

malignancies and a brief overview of the current literature.

Case Series

During the period between 2001 and 2016, at the Department 

of Dermatology at the University of Bologna, we diagnosed 

and followed up 22 patients affected by MMP. From this 

group, we selected 4 individuals (18%) who developed a 

solid tumor (a breast cancer, a pancreatic adenocarcinoma, 

a metastatic laryngeal carcinoma, and a hepatocarcinoma) 

before the MMP diagnosis or during the MMP follow-up. 

They were 2 men and 2 women, with a mean age of 69.7 

years (range, 48-83). In general, our patients had mainly oral 

and/or genital mucous involvement. Only patient 2 had con-

comitant skin lesions, characterized by blisters and erosions 

on the trunk and limbs, and patient 4 had exclusive conjunc-

tival involvement, undergoing a complete loss of eyelashes 

due to synechiae. Cancer detection was preceding in case 1 

(diagnosed 1 year before MMP) and metachronous in the 

remaining cases: 1 year after MMP in cases 2 and 4, and 3 

years after in case 3. All patients’ data, treatment, and follow-

up are summarized in Table 1. Another patient, a 73-year-old 

woman, received the diagnosis of breast cancer 6 years pre-

ceding MMP occurrence. She is still under follow-up in our 



Research  |  Dermatol Pract Concept 2019;9(2):7 121

lular matrix [1,2,6-9]. These individuals cannot be distin-

guished clinically from those with other variants of MMP 

[10]. Because it has been reported that these patients with 

anti-laminin-332 have an increased relative risk of develop-

ing cancer, in particular adenocarcinoma, prompt diagnosis 

and treatments are crucial [8-12]. Various pathogenetic 

hypotheses have been put forward, including the theory that 

tumor cells secrete laminin-332 with the consequent loss of 

keratinocyte adhesion and blister formation [10].

A literature search revealed several case reports and ret-

rospective cohort studies regarding MMP and malignancy 

[8,12-36]. In particular, Egan et al described a cohort of 35 

patients affected by AECP followed up in a period of 12 years; 

10 patients (28.6%) developed a solitary cancer [8]. Eight 

of these patients had cancer after the onset of AECP, most 

within 12 to 14 months, and all deaths were cancer-related. 

The associated malignancies included 3 lung, 3 stomach, 2 

colon, and 2 endometrial cancers. They estimated a relative 

risk of 6.8% for solid cancer, but 15.4% if diagnosed within 

the first year of blister formation. They also documented 

the short interval occurring between the onset of AECP and 

cancer (average 14 months). This was the first cohort study 

regarding MMP and associated malignancies. Later, Letko 

et al have published a retrospective study of 79 patients 

affected by MMP [11]. Only in 3 patients was a cancer 

associated with MMP; a breast ductal carcinoma in situ, a 

lung squamous cell carcinoma, and a colon adenocarcinoma. 

Three other oncology patients had been excluded from the 

study because the cancer diagnosis preceded the MMP (13, 

clinic, but was excluded from the study because of the long 

interval between cancer occurrence and the MMP diagnosis.

An MMP diagnosis was made by combining the clinical 

and histopathological findings. In particular, clinical findings 

included active mucous membrane involvement characterized 

by blisters and/or erosions. In addition, direct and indirect 

immunofluorescence from perilesional mucosa revealed a lin-

ear deposition of IgG and/or C3 at the BMZ and circulating 

IgG anti-BMZ autoantibodies, respectively (Figure 1). Immu-

noblot analysis was negative for anti-BP180 and anti-BP230 

autoantibodies, as well as anti-purified human laminin-332.

The investigation described was carried out on residual 

biopsy sections following diagnostic analysis during the 

course of institutional diagnostic services, and the study was 

exempted from institutional review board review.

Discussion

MMP is an autoimmune bullous disorder with predominant 

or exclusive mucosal involvement. As reported for para-

neoplastic pemphigus and bullous pemphigoid, MMP is a 

pathogenetic example of cell-mediated immunity involve-

ment, characterized by the presence of different autoantibody 

responses to basement membrane antigens, including the 

BP180 and BP230, or β4 integrin [3]. Moreover, whereas 
most of MMP patients share BP180 autoantigen and oral 

or cutaneous involvement [12], a minority of individuals 

express laminin-332 antigen, which is a glycoprotein that 

interacts with other BMZ molecules to stabilize the extracel-

A

D

B

E

C

F

Figure 1. (A) Ocular MMP with conjunctival involvement, with symblepharon formation. (B) Polymorphic manifestation of MMP with cu-

taneous involvement, characterized by tense, serous, or hemorrhagic bullae. (C) Oral MMP with hemorrhagic crusting and lip erosions. (D) 

Low magnification of subepidermal blister with inflammatory cell infiltrate (hematoxylin and eosin [H&E], ×4). (E,F) MMP inflammatory 

infiltrate of the upper dermis, with numerous eosinophils (H&E, ×10; H&E, ×20). [Copyright: ©2019 La Placa et al.]



122 Research  |  Dermatol Pract Concept 2019;9(2):7

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2
 

su
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im
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3
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.

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, 2

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8
 

[2
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4
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 i
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2
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 M
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, 1

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[2
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]

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]

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 s

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as
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 r

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ic

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 a
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2
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 [

2
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]

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L
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ep

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ll
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 n

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cl
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2

0
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, d

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n
e 

7
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, a

n
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ra

l 
p
re

d
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is

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e 

3
0

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g/

d
. P

at
ie

n
t 

d
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d
.

P
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ll
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ck
, 1

9
6
8
 [

2
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]

C
as

e 
re

p
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rt

N
D

T
h
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o
id

 A
C

P
M

M
P
 n

o
t 

re
sp

o
n

si
ve

 t
o

 p
re

d
n

is
o

lo
n

e 
an

d
 s

u
lf

ap
yr

id
in

e 
u

n
ti

l 
fa

ta
l 

o
u

tc
o

m
e.

Ta
b

le
 2

. 
C

as
e 

R
ep

o
rt

s 
o
f 

M
M

P
-A

ss
o
ci

at
ed

 M
al

ig
n
an

ci
es

 F
ro

m
 t

h
e 

L
it

er
at

u
re



Research  |  Dermatol Pract Concept 2019;9(2):7 123

S
tu

d
y

S
tu

d
y
 D

e
si

g
n

M
M

P
 A

n
ti

b
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d
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D

ia
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o
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M
a
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g
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a
n

cy

T
im

e
 o

f 
M

a
li

g
n

a
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cy
 

D
ia

g
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s
Tr

e
a

tm
e

n
t 

a
n

d
 F

o
ll

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p

H
o
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e-

R
o
ss

 e
t 

al
, 

1
9
9
0
 [

2
9
]

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re

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rt

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D

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p
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ea
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x
cl

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 o

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lv

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en

t 
tr

ea
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d
 w

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o

p
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 d

ex
am

et
h

as
o

n
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cy
st

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w
it

h
 g

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.

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, 1
9
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[3
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]

C
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p
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C
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ad

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er
ap

y,
 M

M
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 w
as

 w
el

l 
co

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tr

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ll

ed
 w

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h

 p
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d
n

is
o

n
e.

K
il
b
y,

 1
9
6
5
 [

3
1
]

C
as

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re

p
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rt

N
D

M
et

as
ta

ti
c 

p
an

cr
ea

s 
C

A
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U
n
su

cc
es

sf
u

l 
tr

ea
tm

en
t 

w
it

h
 2

0
 m

g/
d

 o
f 

p
re

d
n

is
o

lo
n

e.

G
ib

so
n
 e

t 
al

, 1
9
9
7
 

[3
2
]

A
E

C
P
 c

as
e 

re
p
o
rt

L
am

in
in

-5
 b

y 
im

m
u
n
o
p
re

ci
p
it

at
io

n
L

u
n
g 

C
A

P
G

o
o
d
 r

es
p

o
n

se
 o

f 
M

M
P

 w
it

h
 m

u
lt

ip
le

 c
o

u
rs

es
 o

f 
p

re
d

n
is

o
n

e,
 

cy
cl

o
p

h
o

sp
h

am
id

e,
 a

n
d

 d
ap

so
n

e.

F
u
ji
m

o
to

 e
t 

al
, 

1
9
9
8
 [

3
3
]

A
E

C
P
 c

as
e 

re
p
o
rt

N
D

G
as

tr
ic

 C
A

S
A

ft
er

 g
as

tr
ec

to
m

y,
 s

p
le

n
ec

to
m

y,
 a

n
d

 c
h

o
le

cy
st

ec
to

m
y,

 M
M

P
 h

ea
le

d
 a

n
d

 
co

rt
ic

o
st

er
o

id
s 

w
er

e 
d

is
co

n
ti

n
u

ed
. F

ew
 w

ee
k

s 
af

te
r 

b
et

am
et

h
as

o
n

e 
w

as
 

st
o
p
p
ed

, b
li

st
er

s 
re

la
p

se
d

 a
n

d
 t

h
e 

p
at

ie
n

t 
d

ie
d

 o
f 

m
et

as
ta

se
s.

D
in

g 
et

 a
l, 

2
0
1
4
 

[3
4
]

A
E

C
P
 c

as
e 

re
p
o
rt

N
eg

at
iv

e 
C

er
vi

ca
l A

C
P

M
M

P
 h

ea
le

d
 a

ft
er

 h
ys

te
ro

an
n

es
si

ec
to

m
y 

an
d

 l
ym

p
h

ad
en

ec
to

m
y.

F
u
k
u
ch

i 
et

 a
l, 

2
0
1
3
 

[3
5
]

C
as

e 
re

p
o
rt

L
am

in
in

-3
3
2
 a

n
d
 

B
P
2
3
0
 p

o
si

ti
ve

U
n
k
n
o
w

n
 o

ri
gi

n
 A

C
P

M
M

P
 r

em
is

si
o

n
 w

it
h

 p
re

d
n

is
o

n
e 

6
0

 m
g/

d
, b

u
t 

th
e 

p
at

ie
n

t 
d

ie
d

 a
n

d
 d

ia
gn

o
si

s 
o
f 

lo
w

-g
ra

d
e 

A
C

 o
f 

u
n

k
n

o
w

n
 p

ri
m

ar
y 

si
te

 w
as

 m
ad

e 
af

te
r 

au
to

p
sy

.

D
em

it
su

 e
t 

al
, 2

0
0
9
 

[3
6
]

C
as

e 
re

p
o
rt

L
am

in
in

-3
3
2
 a

n
d
 

B
P
1
8
0

P
an

cr
ea

s 
C

A
S

B
et

am
et

h
as

o
n

e 
4

 m
g 

an
d

 p
la

sm
a 

ex
ch

an
ge

 g
av

e 
b

en
efi

t 
to

 M
M

P
 r

es
o

lu
ti

o
n

, 
b
u
t 

p
at

ie
n

t 
d

ie
d

 o
f 

in
tr

ah
ep

at
ic

 c
h

o
la

n
gi

ti
s 

fo
ll

o
w

ed
 b

y 
se

p
si

s.

Sh
an

n
o
n
 e

t 
al

, 
2
0
0
3
 [

1
4
]

C
as

e 
re

p
o
rt

L
am

in
in

-5
 b

y 
im

m
u
n
o
b
lo

t
L

ar
ge

 B
-c

el
l 

n
o
n
-

H
o
d
gk

in
 l

ym
p
h
o
m

a
M

M
M

P
 d

ev
el

o
p

ed
 a

ft
er

 2
 c

yc
le

s 
o

f 
ch

em
o

th
er

ap
y 

w
it

h
 r

em
is

si
o

n
 o

f 
ly

m
p
h
o

m
a.

 H
ig

h
-d

o
se

 s
ys

te
m

ic
 s

te
ro

id
s 

an
d

 a
za

th
io

p
ri

n
e 

co
n

tr
o

ll
ed

 t
h

e 
p
em

p
h
ig

o
id

 u
p

 t
o

 r
es

o
lu

ti
o

n
.

Sa
d
le

r 
et

 a
l, 

2
0

0
7
 

[9
]

A
E

C
P
 c

as
e 

re
p
o
rt

 a
n
d
 

re
p
o
rt

ed
 c

as
es

 
re

vi
ew

L
am

in
in

-5
 b

y 
im

m
u
n
o
b
lo

t
M

yc
o
si

s 
fu

n
go

id
es

M
C

u
ta

n
eo

u
s 

ly
m

p
h

o
m

a 
co

n
tr

o
ll

ed
 w

it
h

 t
o

p
ic

al
 c

lo
b

et
as

o
l 

fo
r 

1
2

 y
ea

rs
 b

ef
o

re
 

o
cc

u
rr

en
ce

 o
f 

o
ra

l 
an

d
 n

as
al

 M
M

P.

A
C

 =
 a

de
no

ca
rc

in
om

a;
 B

P 
= 

bu
llo

us
 p

em
ph

ig
oi

d;
 C

A
 =

 c
ar

ci
no

m
a;

 M
 =

 m
et

ac
hr

on
ou

s;
 N

A
 =

 n
ot

 a
va

ila
bl

e;
 N

D
 =

 n
ot

 d
et

ec
te

d;
 P

 =
 p

re
ce

di
ng

 th
e 

ca
nc

er
 d

ia
gn

os
is

; S
 =

 s
yn

ch
ro

no
us

.

Ta
b

le
 2

. 
(C

o
n
ti

n
u
ed

)



124 Research  |  Dermatol Pract Concept 2019;9(2):7

5, and 4 years, respectively). In another report, Sadler et al 

described a patient with mycosis fungoides treated for 12 

years with topical clobetasol ointment who developed oral 

and nasal erosions; histopathology led to the diagnosis of 

AECP [9]. This is the first association between MMP and 

lymphoma. Moreover, the authors provided a summary 

overview of all MMP (or AECP) cancer-associated cases 

published until 2007, including a letter from Shannon and 

colleagues [14], reporting a case of cicatricial pemphigoid 

and non-Hodgkin lymphoma. More recently, Bernard and 

colleagues analyzed a large cohort of 154 MMP patients, and 

an associated neoplasia was found in 18 (11.7%) of them 

[13]. In this French study, the prevalence and significance of 

anti-laminin-332 was analyzed, showing that the presence of 

these antibodies is directly correlated with the severity of the 

disease, but not exclusively with the presence of a neoplasm. 

In fact, of these 18 patients, they showed that only 2 (6.4%) 

were laminin-332 positive, while 16 (13%) were laminin-332 

negative, concluding that this frequency does not differ from 

that of the general population in the same age range. It is 

noteworthy, finally, that in most of these cases the interval 

between cancer detection and MMP occurrence was very 

long (more than 8 years), and the cancer diagnosis frequently 

preceded the MMP occurrence.

On the other hand, case reports published to date include 

23 MMP or AECP patients with 25 solid tumors, in particular 

lung, gastric, ovarian, cervical, and pancreatic adenocarcino-

mas; and renal, prostatic, thyroid, hepatocellular, and esopha-

geal carcinomas [8,14-36]. In addition, a case of large B-cell 

non-Hodgkin lymphoma and a case of mycosis fungoides are 

cited above [8,14]. Although it is sometimes impossible to 

clarify the time of cancer detection, in 16 cases the diagnosis 

of MMP preceded the tumor diagnosis or was synchronous 

(11 and 5 cases, respectively), whereas in 9 patients the bul-

lous disorder occurred after the cancer detection (metachro-

nous) (Table 2).

Determining a true paraneoplastic syndrome is often 

impossible. In fact, most neoplasms are initially occult and 

asymptomatic. In particular, a true paraneoplastic syndrome 

comprises the contemporaneous presence (or detection) of 

both dermatosis and cancer, with resolution of symptoms 

after cancer healing, and possible recurrence after cancer 

relapse. Therefore, the term “paraneoplastic” is used only for 

a subtype of pemphigus, while the term “associated malignan-

cies” must be preferred in the other autoimmune blistering 

disorders, including MMP [37].

In our case series, 3 patients developed the malignancy 

1 to 3 years after the MMP diagnosis. A woman had breast 

cancer 1 year before MMP occurrence. Although 1 of our 

patients died from metastases 1.5 year after MMP diagnosis 

(case 2), the others cleared their bullous disease after cancer 

removal and are still under follow-up (range, 2-5 years) in 

our clinic without recurrences.

Conclusions

The clinical importance of determining specific antibodies in 

autoimmune blistering disorders is well known. For example, 

the presence of BP180 and/or BP230 in bullous pemphigoid 

may represent an active disease also in the absence of clinical 

symptoms [38]. In this regard, various studies demonstrate 

the correlation between laminin-332 MMP and cancer, under-

scoring the importance of immunological diagnosis of these 

autoantibodies [7,10].

On the other hand, and in accordance with the recent 

study by Bernard and coworkers [13], our data demonstrate 

the relatively frequent association of MMP with a solid 

cancer, but no significant correlation with autoantibody 

detection. However, it is possible that laminin-332 reactivity 

is correlated with the severity of the disease, but needs to be 

determined by further studies.

References

 1. Kartan S, Shi VY, Clark AK, Chan LS. Paraneoplastic pemphigus 

and autoimmune blistering diseases associated with neoplasm: 

characteristics, diagnosis, associated neoplasms, proposed patho-

genesis, treatment. Am J Clin Dermatol. 2017;18(1):105-126.

 2. Chan LS, Ahmed AR, Anhalt GJ, et al. The first international con-

sensus on mucous membrane pemphigoid: definition, diagnostic 

criteria, pathogenic factors, medical treatment, and prognostic 

indicators. Arch Dermatol. 2002;138 (3):370-379.

 3. Broussard KC, Leung TG, Moradi A, Thorne JE, Fine JD. Autoim-

mune bullous diseases with skin and eye involvement: cicatricial 

pemphigoid, pemphigus vulgaris, and pemphigus paraneoplastica. 

Clin Dermatol. 2016;34(2):205-213.

 4. Anhalt GJ, Kim SC, Stanley JR, et al. Paraneoplastic pemphigus: 

an autoimmune mucocutaneous disease associated with neoplasia. 

N Engl J Med. 1990;323(25):1729-1735.

 5. Mutasim DF, Pelc NJ, Anhalt GJ. Paraneoplastic pemphigus, 

pemphigus vulgaris, and pemphigus foliaceous. Clin Dermatol. 

1993;11(3):173-181.

 6. Bhol KC, Colon JE, Ahmed AR. Autoantibody in mucous mem-

brane pemphigoid binds to an intracellular epitope on human 

beta4 integrin and causes basement membrane zone separation 

in oral mucosa in an organ culture model. J Invest Dermatol. 

2003;120(4):701-702.

 7. Lazarova Z, Salato VK, Lanschuetzer CM, Janson M, Fairley 

JA, Yancey KB. IgG anti-laminin-332 autoantibodies are present 

in a subset of patients with mucous membrane, but not bullous, 

pemphigoid. J Am Acad Dermatol. 2008;58(6):951-958.

 8. Egan CA, Lazarova Z, Darling TN, Yee C, Coté T, Yancey KB. 

Anti-epiligrin cicatricial pemphigoid and relative risk of cancer. 

Lancet. 2001;357 (9271):1850-1851.

 9. Sadler E, Lazarova Z, Sarasombath P, Yancey KB. A widening 

perspective regarding the relationship between anti-epiligrin 

cicatricial pemphigoid and cancer. J Dermatol Sci. 2007;47(1):1-7.



Research  |  Dermatol Pract Concept 2019;9(2):7 125

10. Egan CA, Lazarova Z, Darling TN, Yee C, Yancey KB. Anti-

epiligrin cicatricial pemphigoid: clinical findings, immunopatho-

genesis, and significant associations. Medicine (Baltimore). 

2003;82(3):177-186.

11. Letko E, Gürcan HM, Papaliodis GN, Christen W, Foster CS, 

Ahmed AR. Relative risk for cancer in mucous membrane pem-

phigoid associated with antibodies to the beta4 integrin subunit. 

Clin Exp Dermatol. 2007;32(6):637-641.

12. Cozzani E, Di Zenzo G, Calabresi V, et al. Autoantibody pro-

file of a cohort of 78 Italian patients with mucous membrane 

pemphigoid: correlation between reactivity profile and clinical 

involvement. Acta Derm Venereol. 2016;96(6):768-773.

13. Bernard P, Antonicelli F, Bedane C, et al. Prevalence and clinical 

significance of anti-laminin 332 autoantibodies detected by a 

novel enzyme-linked immunosorbent assay in mucous membrane 

pemphigoid. JAMA Dermatol. 2013;149(5):533-540.

14. Shannon JF, Mackenzie-Wood A, Wood G, Goldstein D. Cica-

tricial pemphigoid in non-Hodgkin’s lymphoma. Intern Med J. 

2003;33(8):396-397.

15. Taniuchi K, Takata M, Matsui C, et al. Antiepiligrin (laminin 5) 

cicatricial pemphigoid associated with an underlying gastric carci-

noma producing laminin 5. Br J Dermatol. 1999;140(4):696-700.

16. Chamberlain AJ, Cooper SM, Allen J, et al. Paraneoplastic immu-

nobullous disease with an epidermolysis bullosa acquisita pheno-

type: two cases demonstrating remission with treatment of gynae-

cological malignancy. Australas J Dermatol. 2004;45(2):136-139.

17. Yamada H, Nobeyama Y, Matsuo K, et al. A case of paraneoplas-

tic pemphigus associated with triple malignancies in combination 

with antilaminin-332 mucous membrane pemphigoid. Br J Der-

matol. 2012;166(1):230-231.

18. Fukushima S, Egawa K, Nishi H, et al. Two cases of anti-epiligrin 

cicatricial pemphigoid with and without associated malignancy. 

Acta Derm Venereol. 2008;88(5):484-487.

19. Matsushima S, Horiguchi Y, Honda T, et al. A case of anti-epiligrin 

cicatricial pemphigoid associated with lung carcinoma and severe 

laryngeal stenosis: review of Japanese cases and evaluation of risk 

for internal malignancy. J Dermatol. 2004;31(1):10-15.

20. Setterfield J, Shirlaw PJ, Lazarova Z, et al. Paraneoplastic cicatri-

cial pemphigoid. Br J Dermatol. 1999;141(1):127-131.

21. Shibuya T, Komatsu S, Takahashi I, et al. Mucous membrane 

pemphigoid accompanied by ovarian cancer: a case with autoan-

tibodies solely against γ(2)-subunit of laminin-332. J Dermatol. 
2012;39(10):882-884.

22. Mitsuya J, Hara H, Ito K, Ishii N, Hashimoto T, Terui T. Meta-

static ovarian carcinoma-associated subepidermal blistering dis-

ease with autoantibodies to both the p200 dermal antigen and the 

gamma 2 subunit of laminin 5 showing unusual clinical features. 

Br J Dermatol. 2008;158(6):1354-1357.

23. Saravanan K, Baer ST, Meredith A, Dyson A, von der Werth J. 

Benign mucous membrane pemphigoid of the upper aero-digestive 

tract: rare paraneoplastic syndrome presentation in renal cell 

carcinoma. J Laryngol Otol. 2006;120(3):237-239.

24. Young AL, Bailey EE, Colaço SM, Engler DE, Grossman ME. 

Anti-laminin-332 mucous membrane pemphigoid associated with 

recurrent metastatic prostate carcinoma: hypothesis for a para-

neoplastic phenomenon. Eur J Dermatol. 2011;21(3):401-404.

25. Ostlere LS, Branfoot AC, Staughton RC. Cicatricial pemphi-

goid and carcinoma of the pancreas. Clin Exp Dermatol. 

1992;17(1):67-68.

26. Uchiyama K, Yamamoto Y, Taniuchi K, Matsui C, Fushida Y, 

Shirao Y. Remission of antiepiligrin (laminin-5) cicatricial pemphi-

goid after excision of gastric carcinoma. Cornea. 2000;19(4):564-

566.

27. Dainichi T, Hirakawa Y, Ishii N, et al. Mucous membrane pem-

phigoid with autoantibodies to all the laminin 332 subunits and 

fatal outcome resulting from liver cirrhosis and hepatocellular 

carcinoma. J Am Acad Dermatol. 2011;64(6):1199-1200.

28. Polliack A. Benign mucous membrane pemphigoid with laryn-

geal stenosis in a patient with thyroid carcinoma. Arch Pathol. 

1968;86(1):48-51.

29. Hope-Ross M, Benedict-Smith A, Hillery M, Mullaney P, Condon 

P, Collum LM. Ocular cicatricial pemphigoid and oesophageal 

carcinoma. Acta Ophthalmol (Copenh). 1990;68(3):361-363.

30. Greer KE, Beacham BE, Askew FC Jr. Benign mucous membrane 

pemphigoid in association with internal malignancy. Cutis. 

1980;25(2):183-185.

31. Kilby PE. Carcinoma of the pancreas presenting with “benign 

mucous membrane pemphigoid.” Cancer. 1965;18:847-850.

32. Gibson GE, Daoud MS, Pittelkow MR. Anti-epiligrin (laminin 

5) cicatricial pemphigoid and lung carcinoma: coincidence or 

association? Br J Dermatol. 1997;137(5):780-782.

33. Fujimoto W, Ishida-Yamamoto A, Hsu R, et al. Anti-epiligrin 

cicatricial pemphigoid: a case associated with gastric carcinoma 

and features resembling epidermolysis bullosa acquisita. Br J 

Dermatol. 1998;139(4):682-687.

34. Ding DC, Chu TY, Hsu YH. Remission of anti-epiligrin cicatricial 

pemphigoid after excision of cervical adenocarcinoma. J Cutan 

Pathol. 2014;41(8):692-693.

35. Fukuchi O, Suko A, Matsuzaki H, et al. Anti-laminin-332 mu-

cous membrane pemphigoid with autoantibodies to α3, β3 and 
γ2 subunits of laminin-332 as well as to BP230 and periplakin 
associated with adenocarcinoma from an unknown primary site. 

J Dermatol. 2013;40(1):61-62.

36. Demitsu T, Yoneda K, Iida E, et al. A case of mucous membrane 

pemphigoid with IgG antibodies against all the α3, β3 and γ2 sub-
units of laminin-332 and BP180 C-terminal domain, associated 

with pancreatic cancer. Clin Exp Dermatol. 2009;34(8):e992-

e994.

37. Balestri R, Magnano M, La Placa M, et al. Malignancies in 

bullous pemphigoid: a controversial association. J Dermatol. 

2016;43(2):125-133.

38. Schmidt E, Obe K, Bröcker EB, Zillikens D. Serum levels of au-

toantibodies to BP180 correlate with disease activity in patients 

with bullous pemphigoid. Arch Dermatol. 2000;136(2):174-178.