Lichenoid reaction pattern

Lichenoid reaction pattern
Nathan C. Walk, M.D.
Lichenoid dermatoses can be divided into 2 categories:
g
– Lichenoid
– Interface
Lichenoid inflammation is seen in entities that are usually
“benign” and self limited and shows:
– Prominent bandband-like inflammatory infiltrate
– Less prominent basal vacuolar change
Invert this scenario and you have those entities with
more morbidity and mortality:
– Prominent basal vacuolar change
– Less prominent inflammatory infiltrate
Predominately
Predominately….
Lichenoid
–
–
–
–
–
Lichen planus, and variants
Lichen nitidus
Lichen striatus
LPLK
Lichenoid drug eruption
Interface
–
–
–
–
–
–
Fixed drug eruption*
Erythema multiforme/TEN
Graft versus host disease
Eruption of lymphocyte recovery
Lupus erythematosus
Dermatomyositis
Other lichenoid entities:
–
**Poikilodermas
Poikilodermas
–
–
–
–
–
–
–
–
–
–
–
–
–
–
–
–
**Lichen sclerosus et atrophicus
**Pityriasis lichenoides
**Persistent viral
Perniosis
Paraneoplastic pemphigus
Lichenoid purpura
**Lichenoid contact
Late syphillis
Porokeratosis
Drug eruptions
**Phototoxic dermatitis
Prurigo pigmentosa
MF
**Vitiligo
Lichen amyloid
Lichenoid tattoo
Cases 10 & 11
Lichen planus
Clinical:
– Cutaneous
C t
0
0.2
0.22-1 % population,
l ti
oral form 11-4%
– 40s
40s--50s, children uncommon,
elderly rare
– Small,
Small polygonalpolygonal-shaped,
shaped
violaceous, flatflat-topped pruritic
papules that favor the extremities.
– Shiny or transparent surface, with
fine white lines called “Wickham’s
striae
striae”
– + Koebbner phenomenon.
– Flexor surfaces of wrists and
forearms, dorsal hands, anterior
lower legs,
g , neck,, presacral,
p
, oral
>1/2 of cases – sometimes only
site.
– Course depends on subtype –
resolution in 33-12 months in acute
form, oral usually lifetime.
Spontaneous resolution
UNCOMMON.
Histology:
– Prominent Civatte bodies
– Band
Band--like inflammatory infiltrate –
presses against epidermis &
usually does not obscure DD-E
interface or extend into mid
epidermis (EM, fixed drug).
– Hyperkeratosis, NO parakeratosis,
wedge--shaped hypergranulosis
wedge
related to acrosyringia and
acrotrichia,
ac
ot c a, variable
a ab e basal
basa
vacuolar change, variable
acanthosis.
– Pointed or “saw tooth” rete.
– Other:
Oh
Colloid bodies (PAS positive) in
papillary dermis.
DIF shows colloid bodies stain for
complement and IgM.
Some pigment incontinence
incontinence.
Max--Joseph spaces = small clefts at DMax
DE jnx from coalescence of BV change.
Clinical Differential:
– LP variants……atrophic, ulcerative, hypertrophic, linear, actinic,
acute, annular, bullous
– Lichenoid drug eruption (LDE) – more
eczematous/psoriasisform, more likely in sun exposed areas
– Lichen nitidus, lichen striatus, lichen sclerosus
– Pityriasis rosea, EDP
– Psoriasis
– Secondary syphilis
– Paraneoplastic pemphigus, if erosive LP
LP--like
– LE – most difficult to differentiate – especially in patients with
only oral or scalp lesions… try looking for lupus band test
Case 12
Hypertrophic LP
Clinical:
–
Usually on shins…persist for many years, may
develop SCC.
Histology:
–
–
–
Looks LSC
LSC--like with compact orthokeratosis,
psoriasiform hyperplasia.
...but,
but has basal cell damage w/ civatte bodies at
rete tips.
Inflammatory band less pronounced.
Case 13
Lichen planopilaris (LPP)
Clinical:
–
–
–
Keratotic follicular
lesions are present in
a/w other manifestations
off LP.
LP
Most important clinical
group is characterized by
scarring alopecia
alopecia.
Keratotic spines
surrounded by
violaceous rim – scalp,
other hairhair-bearing
surfaces…. Alopecia +
scarring late.
Histology:
gy
– Lichenoid reaction
pattern involving
follicular epithelium –
Infundibulum and
isthmus
– ***Unlike lupus:
Not much PVLI
N t as deep
Not
d
Interfollicular epidermis
characteristically NOT
involved but in reality
involved,
can be in up to 1/3 of
cases involving scalp.
Case 14
Lichen striatus
Clinical:
– Continuous or interrupted
band of discrete or
clustered pink, skin
skin--colored
papules
p
p
that are flat
topped, smooth or scaly,
and range from 22-4 mm.
– Predilection for female
children.
children
– Follow Blaschko’s lines.
– Usually along one side of
body, usually length of
extremity.
t
it
– Spontaneous resolution in
1-2 years.
Histology:
– Lichenoid
Li h
id reaction
ti pattern
tt
occupying 3or 4 adjacent
dermal papillae; irregular and
discontinuous.
– +/
+/-- around follicles
follicles, sweat
glands – c/w LE
– Overlying epidermis –
changes secondary acanthotic with exocytosis of
inflammatory cells, may have
dyskeratotic cells.
– +/
+/-- intraepidermal vesicles
– Infiltrate less dense than in
LP, may extend around hair
follicles or eccrine glands
glands.
Clinical differential:
– LP versus LS
Differ in size and color
hyPOpigmentation is frequent sequela of LS, while
hyPERpigmentation appears in the wake of LP.
– LS – MINIMAL pruritus.
Case 15
Lichen nitidus
Clinical:
– Asymptomatic, numerous,
tiny, discrete, skinskin-colored,
uniform,, pinhead
p
sized
papules.
– Papules are flat with a
shiny
y surface.
– Flexor aspects of upper
extremities, genitalia,
chest,, abdomen,, dorsal
hands.
– + Koebbner phenomenon
Histology:
– Well circumscribed, subepidermal infiltrate, limited to
1-2 dermal papillae.
– Claw
Claw--like acanthotic rete “grasp” the infiltrate
– Thinned epidermis +/
+/-- parakeratosis
– Lymphocytes,
L
h
t
hi
histiocytes,
ti
t
melanophages,
l
h
giant
i t cells.
ll
– Sometimes frankly granulomatous.
Clinical DDx: LP, verruca plana, papular sarcoid,
papular eczema
eczema, lichen scrofulosorum
Case 16
Lichen planus like keratosis
Pathogenesis:
g
–
–
–
–
Arise from pre
pre--existing solar lentigo of SK.
OR
Inflamed actinic keratosis.
Unidentified epidermal antigen – stimulated Langerhaans cells
Æ T cells; i.e. similar to LP
Clinical:
Clinical
–
–
–
–
–
Solitary pink to pink
pink--brown, often scaly, papules from 0.30.3-1.5 cm.
Caucasians, 30s
30s--60s.
A
Asymptomatic,
t
ti or pruritic.
iti
Forearm, upper chest, > H/N; middle aged women.
May appear suddenly.
Histology:
gy
– Lichenoid reaction pattern
with numerous civatte
bodies in the basal layer
and
d mild
ild b
basall vacuolar
l
change.
– Infiltrate usually dense,
may obscure DD-E interface.
interface
– Prominent PI
– Contiguous solar lentigo
may be seen.
– May be subepidermal cleft
from confluent apoptosis of
keratinocytes.
Cases 17 & 18
Erythema multiforme
HSV in minor forms.
M
Mycoplasma
l
and
dd
drugs iin
major forms, SJS/TEN.
Clinical:
– Primary lesion = Round, red
papule which remains fixed for 7
days…may evolve into target
lesion.
– Target lesions: central purple,
outer red.
– Iris lesions: dusky center, then
white, then red.
– Symmetric,
Symmetric predilection for the
extremities.
– Abrupt onset, pruritic or burning
sensations.
– + koebbner
Histology:
gy
– Interface obscuring interface
dermatitis; mainly lymphocytes.
– Prominent epidermal cell death,
not confined to basal layer.
– Basal
B
l vacuolar
l change.
h
– Some spongiosis.
– Vesicular lesions are
characterized by clefting at the D
D-E junction.
junction
– Dermal infiltrate is lymphocytes
and macrophages.
– Eosinophils are usually not
prominent.
– DIF – granular C3, IgM at D
D--E
junction, vessels.
Toxic epidermal necrolysis
– >30% epidermal detachment (helpful guide, not strict
rule).
– NECROSIS and apoptosis.
– Subepidermal bullae with overlying confluent necrosis
of epidermis.
epidermis
– SPARSE inflammatory infiltrate
infiltrate.
– Satellite cell necrosis – early – c/w GVHD.
– More inflammation in those cases a/w EM.
Fixed drug
– Looks a LOT like EM, but….
Deeper inflammatory infiltrate
Neutrophils (NOT in EM)
More p
pigment
g
incontinence
Cases 19 & 20
Graft versus host disease
Clinical:
– Acute form, 1
1--3 weeks after
transplantation usually…could be as
l
long
as 3 months
th
– Morbilliform (maculopapular) exanthem
with sudden onset – begins acrally,
may be generalized.
– Folliculotropic
Folliculotropic.
– If severe, diffuse erythroderma with
bulla formation.
– Chronic form, usually after mean of 4
months, as soon as 40 days
– Divided into:
Lichenoid: erythematous or violaceous
lichenoid papules and plaques affecting
dorsal hands, forearms, and trunk.
Sclerodermoid: plaques of morphea,
eventually generalized scleroderma.
Histology:
– Grade 0 – normal skin
– Grade 1 – basal vacuolar change
– Grade 2 – dyskeratotic cells at all levels in the epidermis and/or follicle,
dermal lymphocytic
y p
y infiltrate
– Grade 3 – fusion of basilar vacuoles to form clefts and microvesicles
– Grade 4 – separation of epidermis from dermis
S t llit cellll necrosis
Satellite
i – said
id tto b
be ““characteristic”.
h
t i ti ”
In early chronic lesions, looks like LP or LPP, although
infiltrate is less dense; PI.
Sclerodermoid phase – mild epidermal changes, such as
atrophy, BV change, dermal fibrosis that extends into
subcutis (septal hyalinization) and may involve skin
appendages; few dyskeratotic cells.
cells
A tough differential
differential…
GVHD
Lymphocyte recovery
Drug reaction
Vi l
Viral
Also…
– Erythema multiforme
What can help….
–
–
–
–
Eosinophils?
Inflammatory pattern? Does is obscure interface?
Timing?
Se erit ?
Severity?
Cases 21 & 22
Lupus erythematosus
Clinical:
– There are several variants of cutaneous lupus, defined in part by the
location and depth of the inflammatory infiltrate.
ACLE
– primarily epidermis and upper dermis + systemic disease
SCLE
– primarily epidermis and upper dermis - 15% systemic disease; a/w antianti-Ro
– Midface spared, V neck, extensor forearms, sides of face; confined to sun
exposed areas,
– Hypo/hyperpigmentation
yp yp p g
after,, no scar
DLE
– epidermis, upper and lower dermis, adnexal structures w/ scarring – NO systemic
dz
– Face almost always +/
+/-- trunk, not related to sun, scarring
LE tumidus
– dermis, no prominent adnexal involvement
LE panniculitis
– subcutaneous tissue, w/ depressed scars
Discoid lupus erythematosus
Sharply demarcated,
erythematous, scaly
patches with follicular
plugging
Face almost always
+/-- trunk, not related
+/
to sun, scarring
Wi h scarring
With
i – NO
systemic dz
Subacute cutaneous lupus
erythematosus
15% systemic
y
disease;;
a/w anti
anti--Ro
Erythematous, slightly
scaly
l – eczematous
t
or
psoriasiform appearance.
Midface spared, V neck,
extensor forearms, sides
of face; confined to sun
exposed areas
Hypo/hyperpigmentation
after, no scar
Histology:
gy
– Lichenoid reaction pattern with S+D PVLI
– Tendency to accumulate around pilosebaceous
follicles.
– Mostly vacuolar change w/ scattered Civatte bodies.
– Thick BM in older lesions – PAS stain.
– Epidermal atrophy
– Follicular plugging
which psoriasiform disease characterized by prominent
follicular plugging?
– Increased dermal mucin
…Lupus
Lupus band test – IgG,
IgG IgM > C3 in broad band along BMZ
Cases 23
Dermatomyositis
Clinical:
– Bimodal age distribution
– Proximal inflammatory
myopathy +
photodistributed violaceous
poikiloderma favoring
scalp,
p, p
periocular,, extensor
skin sites, nailfold
telangiectasias.
Histology:
– Looks like LE, but NO deep inflammation
– Basal vacuolar change
change, occasional civattte
bodies, dermal mucin, thickened BMZ
– May also have poikilodermatous changes
Case 24
Lichen sclerosus et atrophicus
Chronic disorder, men
and women
Usually asymptomatic,
may p/w intractable
pruritus/soreness
Hypopigmentation, thin,
wrinkled atrophic skin
skin.
Scarring disease
Increased risk of SCC?
Relation to morphea?
Clues…
Iff predominately….
Lichenoid
–
–
–
–
–
Lichen planus, and variants
Lichen nitidus
Lichen striatus
LPLK
Lichenoid drug eruption
Interface
–
–
–
–
–
–
Fixed drug eruption
Erythema multiforme/TEN
Graft versus host disease
Eruption of lymphocyte recovery
Lupus erythematosus
Dermatomyositis
Clues
Clues…
Folliculotropic?
– GVHD
Deep inflammation?
– DLE
– FDE
– Lichen
Li h striatus
ti t
Interface obscuring inflammation?
– EM
– FDE
– PLEVA – but also has lymph vasculitis
Prominent pigment incontinence?
– Drugs
– Poikilodermas
Eccrine duct involvement?
– EM (drug induced)
– L. striatus