Ch 10. Lichen plans and other lichenoid dermatoses Flashcards
What is typical age of onset for Lichen Planus?
5th-6th decade
2/3 onset between 30-60
rare in kids
How common is LP? Oral LP?
LP up to 1%
Oral LP 1-4%
What % patients with cutaneous LP will get oral involvement
75%
What % of patients presenting with only oral LP will go on to get cutaneous LP
10-20%
Name 4 categories of triggers for LP
- VIRUSES
-Hep C big one, most associated with oral
-HHV6/7, HSV, VZV, HPV - Vaccines
- Contact allergens
-amalgam (mercury), copper, and gold - Drugs-see later cards
Name the top 5 drugs to cause lichenoid drug
Gold
ACEi
Thiazide diuretics
Anti-malarial
Quinidine
What are the classic sites of prediction for classic LP
Wrists-flexor
Forearm-flexor
Dorsal hands
Shins
Pre-sacral
Glans penis
Name 6 classic characteristics of lichen planus
Polygonal
Violaceous
Flat toppes
Papules
Whickams striae-lacy reticulate network fine lines
Pruritic
PIH common
Koebner
Sometimes widely disperse, sometimes coalesced
What 4 subtypes of LP tend to ne more persistent throughout life
Hypetrophic
Oral
Annular
Ulcerative oral
Name 10 variants of lichen
Annular
Atrophic
Actinic
Acute/exanthematous
Hypertrophic
Eosive/ulcerative
Bullous LP
LP pemphigoides
Linear
Lichen planopilaris
Lichen Plans pigmentosus
Oral
Nail
Inverse
Vulvovaginal
DLE/LP overlap
What is the natural course of eruptive/acute LP
Acute onset generalized eruption mostly on classic sites though, trunk, inner wrists, dorsal feet
Self resolves 3-9 months with hyperpigmentation
What are the clinical features of actinic LP
red–brown plaques with an annular configuration, but melasma-like hyperpigmented patches have been observed
Sun exposed areas-face, dorsal arms, neck
Spring/summer
Where are the top 4 sites of annular LP
Axilla>penis >extremity> groin
Where does atrophic LP occur? What is likely happening? What do they look like?
intertriginous and lower extremities
likely resolving LP, maybe be exacerbated by TCS
papules coalesce to form larger plaques that over time become atrophic centrally, with residual hyperpigmentation.
What is the difference between bullous LP and LP pemphigoides
Bullous LP–> vesicles and bullae develop within pre-existing lesions of LP as a result of intense lichenoid inflammation and significant epidermal damage
LP pemphigoides have circulating IgG autoantibodies directed against the 180 kDa BP antigen (BP180; BPAG2), as in idiopathic BP.
Compared to BP though, bullae can arise either within LP lesions or previously uninvolved skin, but the diagnosis of LP usually precedes the LP pemphigoides
Where does hypertrophic LP occur? What does it look like?
Extremely pruritic, thick, hyperkeratotic plaques are seen primarily on the shins or dorsal aspect of the feet and may be covered by a fine adherent scale.
Name a feature on path that may help differentiate hypertrophic LP
increased eosinophils
What is the concern about hypertrophic LP
developing bcc
What is the morphology of inverse psoriasis
Pink to violaceous papules and plaques appear in intertriginous zones OR just hyperpigemtation
What is the presentation of lichen plans pigmentosus
brown to gray-brown macules develops into into diffuse or reticulate pigmentation
sun exposed areas face/neck , can have other locations
Name two variants of lichen plants pigmentosus
-LP inversus–> Also intertriginous variant-can be hard to tell from inverse variant of LP
-Linear variant along lines of blaschko
What is the difference between EDP and Lichen plants pigmentosus
EDP
- is often truncal involvement,
- a younger mean age of onset
-lack of either diffuse pigmentation or lack of coexisting LP lesions.
LPP
-other LP lesions on body
-more photo exposed
-LP lesions is seen in ~20% of patients with LP pigmentosus.
-Occasionally, small nests of keratinocytes are seen within the basal layer and these may be confused with nests of melanocytes.
What is the triad of Graham-Little–Piccardi–Lassueur syndrome
- non-cicatricial loss of pubic and axillary hairs and disseminated spinous or acuminated follicular papules
2.typical cutaneous or mucosal LP
(3) scarring alopecia of the scalp with or without atrophy
What does linear LP refer to
LP lesions that spontaneously pop up in lines of blaschko–> NOT koebner
What % of patients have nail involvement in LP
10%
Name 4 nail findings in LP
Lateral thinning
Longitudinal ridging and fissuring
Dorsal pterygyium
Pitting
Name 4 nail findings in LP
Lateral thinning
Longitudinal ridging and fissuring
Dorsal pterygyium
Pitting
What are the 7 forms of oral LP? Which is most common?
Atrophic
bullous
Erosive
Papular
Pigmented
Plaque like
Reticular-most common
If oral LP, what do you need to ask about
Esophaagesal
Vulvovaginal
What infection is associated with oral LP
Hep C
With Hep C associated LP, where does it often occur? Non Hep C oral LP?
tongue, labial mucosa, and gingivae
Non hep C–> buccal mucosa
What 4 forms of LP are associated with SCC development
- Oral
- Vulvar
- Hypertrophic
- Erosive
Where does ulcerative LP tend to occur
in palmar-plantar lesions
Most common form vulvovaginal LP
Erosive
Often oral involvement too–>vulvovaginal-gingival syndrome
Name 5 clinical differences between LP and lichenoid drug
- Clinically for lichenoid drug:
o Lesions are larger, often more psoriasiform
o Wickham’s striae are usually not apparent
o Mucosal involvement is less common
o Trunk and extremities are favoured over forearms, genitals
o May be photo-distributed (photolichenoid drug)
What are seven histopathologic differences seen in a lichenoid drug eruption as compared to idiopathic lichen planus?
- Focal parakeratosis
- Spongiosis
- Interface change may be patchy
- Epidermis may be thinned
- Less pronounced hypergranulosis (wickham’s striae) or even hypogranulosis
- Cytoid bodies found in the upper granular cell layer (vs. spinous layer in LP)
- Eosinophils
- Plasma cells
- Exocytosis of lymphoid cells
- Perivascular infiltrate in the deeper dermis (especially photolichenoid reactions)
What are seven histopathologic differences seen in a lichenoid drug eruption as compared to idiopathic lichen planus?
- Focal parakeratosis
- Spongiosis
- Interface change may be patchy
- Epidermis may be thinned
- Less pronounced hypergranulosis (wickham’s striae) or even hypogranulosis
- Cytoid bodies found in the upper granular cell layer (vs. spinous layer in LP)
- Eosinophils
- Plasma cells
- Exocytosis of lymphoid cells
- Perivascular infiltrate in the deeper dermis (especially photolichenoid reactions)
Average latent period for drug induced LP
7 or 12 months
What do you see on pathology for giant cell lichenoid dermatitis?
multinucleated giant cells and histiocytes
Name 4 drugs associated with giant cell lichenoid dermatitis
ACE inhibitors,
β-blockers,
lipid-lowering agents,
phenolphthalein,
nonsteroidal anti-inflammatory drugs (NSAIDs).
List 10 features of classic lichen planus seen on histopathology
Hyperkeratosis
Orthokeratosis
Hypergranulosis-wdge shaped
Basal cell degeneration
Lichenoid infiltrate
sub epidermal cleft-max Joseph spaces
Necrotic keratonocytes
Irregular acanthosis
Sawtooth rete ridges
Pigment incontinence
Hypereosinophilia of keratinocytes in malphigian layer
Civatte bodies in the basal layer
Colloid bodies in the papillary dermis
What are two findings seen on direct immunofluorescence of classic lichen planus?
1) Linear fibrillary band of fibrin at the DEJ.
2) Cytoid bodies stain with IgM > IgG, IgA and C3.
What histopathologic finding relates to the Wickham’s striae?
- Wedge-shaped hypergranulosis related to sweat ducts and hair follicles.
Avg remission time for most ppl for cutaneous LP
1 yr
*not erosive lp, often doesn’t remit
