An Overview of Psoriasis
Rich Callahan MSPA, PA-C
Fletcher Allen Health Care, Dept. of
Dermatology
Burlington, Vermont
ICM I – Summer 2009
Clinical Overview of Psoriasis: What Is
It?
• True understanding involves knowing the
pathophysiology, which boils down to 3
characteristics:
• The disease you see clinically is a disorder
of cellular differentiation and kinetics
• Psoriasis is mediated by autoimmune
elements which are partially understood.
• Psoriasis is passed on genetically
Epidemiology: Psoriasis in U.S.
• 5 to 7 million Americans have it
• 150,000 to 260,000 new cases/year – mean
age at presentation is 28
• 1.7 million treated – 600,000 of them for
moderate/severe disease
• 400 Psoriasis-related deaths/year. (Toxicity
of medications > Suicide.)
• (Data from Nat’l Psoriasis Foundation – Data on File)
Classification
• Falls under the category of papulosquamous
diseases – skin conditions whose primary features
are scaling papules and plaques.
• There are over a dozen distinct subtypes of
psoriasis: Chronic plaque, guttate, generalized
pustular, scalp sebo-psoriasis, palms and soles
(both plaque and pustular,) inverse psoriasis, nail
psoriasis, psoriatic arthritis, light-sensitive,
erythrodermic, Reiter’s syndrome.
We will focus on 3 most common
Psoriasis subtypes
• Chronic Stable Plaque Psoriasis – Most
common subtype. What most people
visualize when they think of Psoriasis.
• Guttate Psoriais – Acute papulosquamous
eruption. Can evolve into chronic Psoriasis.
• Palmoplantar Pustular Psoriasis (PPP) –
Debilitating, chronic eruption of the palms
and soles.
Clinical Presentation of Psoriasis
• Chronic Stable Plaque: Relatively fixed and
stable pink to erythematous scaling papules and
plaques primarily on trunk, scalp and flexor
extremities. Lesions are sharply marginated and
often slightly raised above surrounding skin.
May/may not be mildly pruritic. Rarely affects
face, genitals, soles of feet. Lesions occassionally
correspond to areas subject to repetetive trauma.
Chronic Stable Plaque Psoriasis
Most common form of the
disease with a wide range
in severity; can be a small,
fixed plaque that doesn’t
move or change. Can also
be large, confluent groups
of papules and plaques
covering 20-70% of a
patients BSA (body
surface area.)
• The problem again is
unpredictability: A
patient with one stable
plaque can suddenly
explode into 20-30% BSA
involvement with no
apparent cause or
explanation, at any stage
in life. Life stress/ETOH
can be precipitants!
Clinical Presentation of Psoriasis
• Guttate: Sudden eruption of brightly
erythematous, round, scaling papules, usually 1cm
or less in diameter, trunk and extremities. Again,
sharply marginated. Spares palms and soles.
Usually preceded by streptococcal or viral URI.
Often a patients first experience with their
psoriasis. Patients often seem sick, with a history
of “not quite getting over that cold a few weeks
ago.”
Guttate Psoriasis
• Comes from the Latin
word for “raindrop” as
patients with this type of
psoriasis literally look like
they have drops of red
paint splattered
haphazardly on their trunk
and extremities.
• Lesions are clearly
defined and often brightly
erythematous, though less
firm and scaly than plaque
psoriasis.
• Often associated with
preceding streptococcal or
viral pharyngitis, URI or
tonsillitis.
• Sometimes it is a young
person’s first experience
with their psoriasis.
Important to instill
realistic expectations in
these patients as many
develop chronic plaque
disease later.
Presentation of Guttate Psoriasis
• Even if patients don’t give a history/show signs of
prior URI/pharyngitis, still a good idea to do
throat culture, lymphatic exam and treat
empirically with antibiotics.
• Many patients will improve after a short course of
antibiotics even if they don’t seem sick.
• Throat cultures sometimes positive for strep.
There are two patterns to this presentation,
and two different prognoses:
• 1.) Middle to older aged patient with long history
of mild chronic stable plaque psoriasis who gets a
nasty URI and has sudden guttate flare. Good
prognosis for return to baseline after treatment
with antibiotics.
• 2.) Young adult without prior history of psoriasis
gets nasty URI and has sudden guttate flare. Often
alarming, often misdiagnosed as infectious.
Guttate lesions often slow to improve with slow
shift into chronic plaque psoriasis.
Clinical Presentation of Psoriasis
• Palmoplantar pustular (PPP): Deeply seated,
non-rupturing pustules on palms/soles which
emerge over time at skin surface to form
scale/crust and then slowly peel. Pustules are
sterile, and only infected secondarily. Tends to
run a chronic course. Resistance to treatment is
common. Patients with severe disease can become
depressed secondary to difficulty performing at
work and ADL’s.
Psychological Impact of
Moderate/Severe Disease
• Patients with extensive
BSA involvement often
afraid to be in public or
wear revealing clothing.
• Some patients shed scale
constantly onto clothing,
furniture, floors, etc.
• Many patients eventually
become depressed if
disease poorly controlled.
• Aggressive treatment of
the patient’s disease is
often warranted in these
cases as the severity of the
disease justifies the
risks/side effects inherent
in the treatments.
• Patients often motivated to
try anything that might be
effective.
It is well documented that drugs can
exacerbate Psoriasis
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•
•
•
ETOH
Beta-blockers
Lithium carbonate
Antimalarials
Interferons
Clinical Pearl – Auspitz’s Sign
• A patient presents with new onset of an erythematous,
crusted, keratotic plaque on the left anterior thigh.
Suspecting fungal disease, the PA scrapes the plaque with
a #15 blade to collect scale for KOH microscopic exam.
The dry, white scale is easily scraped away, yielding
numerous tiny, brisk, pinpoint bleeders in the inflamed
tissue below. This is called Auspitz’s sign, in which
inflamed, dilated capillaries of the hyperactive epidermis
are traumatized. Although it isn’t considered diagnostic of
psoriasis, Auspitz’s is an important hint to look further in
that direction for a diagnosis.
Pathophysiology of Psoriasis – an expert
summary
• As explained by Charles Camisa, MD, in his book
Handbood Of Psoriasis:
• “Psoriasis is the result of a hyperproliferation of
the epidermis, concommitant inflammation and
vascular changes, which occur in response to the
proper combination of genetic and environmental
pressures.”
Camisa, con’t, on pathogenesis of psoraisis
• Psoriatic epidermis has 26.6% of the proliferative cells in
the DNA synthesis (S) phase compared to 7.8% in normal
skin. The growth fraction increases from 60 to 100% and
the size of the population of proliferative cells is doubled,
but the main defect in epidermal kinetics is the overall
eight-fold increase in the germinative cell cycle compared
to that occuring in normal skin. The result is a cell cycle
shortened from 311 to 36 hours and an epidermal turnover
time, that is the time it takes a basal cell reach the stratum
corneum, accelerated from 27 to 4 days.” (From Camisa,
Charles MD, Handbook of Psoriasis, Blackwell Pub., 2004. p. 45)
There is a hyperproliferation of epidermal
cells, but that’s half the story
• Also a disorder of cell differentiation.
• Granular layer is reduced or absent and
there is a massive overproduction of keratin
known histopathologically as hyperkeratosis
and parakeratosis.
• This process creates the thick, white scaly
plaques we see in psoriasis.
The pathophysiology of psoriasis is pretty well
studied, but there is a lot to learn about its
autoimmune basis and underlying etiology.
• Multiple physiologic and immune entities have been
found to play a role in the pathway that mediates the
development of psoriasis: Polymorphonuclear leukocytes,
neuropeptides, T-lymphocytes, inflammatory cytokines,
interleukins, TNF-alpha cells, etc.
• The newest class of psoriasis medications, the “biologics,”
target specific players in this pathway.
• It’s not so much that medical science knows exactly what’s
going on, but rather we do know that when certain immune
elements in the pathway are blocked, patients psoriasis gets
better (sometimes.)
Diagnosis of Psoriasis
• Usually a clinical diagnosis, but skin biopsy
is almost always diagnostic.
• New onset Guttate Psoriasis gets throat
culture to r/o chronic strep infection.
• Occassionally need to biopsy PPP to
differentiate from dyshidrotic eczema.
• Isolated, unilateral lesion should get scraped
to exclude fungus.
Treatment of Plaque Psoriasis
• Moderate to high potency topical steroid creams, gels and
ointment. Classified by potency as I-VII-strong antiinflammatories
• Topical calcipotriene inhibitors (dovonex) – thins
epidermis
• Topical coal tar derivatives (anthralin/LCD) and retinoids
(Tazorac) – anti -inflam
• Phototherapy with narrowband UVB and PUVA
(“psoralen and ultraviolet light”)
• Methotrexate, a potent antimetabolite and immune
suppressant.
• Cyclosporine, a potent immune suppressive drug
Newest on the scene: The Biologics
• Self-injected by patient once or twice weekly, or
bimonthly infusion at IV center.
• Expensive drugs – made of engineered
recombitant proteins.
• We don’t completely understand why they work,
but for some patients they provide dramatic
improvement, without all the side effects inherent
in older immusuppressant medications like
methotrexate or cyclosporine.
Newest on the scene: The Biologics
• Many poorly understood risks/SE’s including
reactivation of prior malignancy/TB. Increased
risk of developing lymphomas/cancers in clinical
trials. Evidence of “unmasking” of prior latent
demyelinating disease – significance not fully
understood.
• Should only be administered by
dermatologists/derm PA’s who are experienced
with them.
How are Biologics Made?
• Derived from whole human cells,
blood, hybridomas, recombitant DNA
technology.
• Produced within living organisms
• Usually large molecules
• Always administered by injection or
IV
The Theory Behind the Biologics
The newly developing psoriasis lesion is precipitated by an
autoimmune reaction wherein there is a genetic defect
inherent in the interaction between keratinocytes,
macrophages (otherwise known as antigen presenting cells,
or APC’s) and T-lymphocytes (T-Cells.)
For reasons that are poorly understood, the macrophages
appear in the epidermis and proceed to identify the
keratinocytes as foreign antigens. These antigens are then
presented to T-lymphocytes which form large populations
which then incite the inflammation of psoriasis. Large
populations of activated T-Cells are found in bases of
Psoriasis plaques.
We don’t have time today for a lecture on the
workings of the immune system in depth.
• Let it suffice to say that numerous experimental
studies and clinical trials have shown that
Psoriasis is a T-Cell mediated disease.
• “Biologic” Psoriasis drugs target and disable
particular steps along the pathway of T-Cell
activation and homing in on target tissues
(keratinocytes in skin) which ultimately results in
clinical disease improvement in most patients.
The Biologics
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Enbrel (etanercept)
Amevive (alefacept)
Humira (adalimumab)
Remicade (infliximab)
Raptiva (efalizumab)
The suffix at the end
of the trade name
denotes class of
protein
• -ximab = chimeric
monoclonal antibody
• -zumab = humanized
monoclonal antibody
• -umab = human
monoclonal antibody
• -cept = receptorantibody fusion
protein
Treatment of Guttate Psoriasis
• Oral antibiotics such as penicillin, erythromycin and
azithromycin.
• Topical steroids
• Narrowband UVB and natural sunlight.
• Tincture of time as majority of cases will resolve
spontaneously in a 4-6 wk period.
• Be ready to explain to younger patients that Guttate
Psoriasis can develop into chronic stable plaque psoriasis
Palmoplantar Pustular Psoriasis (PPP)
Treatment
• This is a stubborn disease – I have several patients on
multiple medications where clinical improvement is
gauged by ability to perform ADL’s/depression.
• First-line is super-potent topical steroid ointments under
occlusion at qhs under plastic wrap. Sometimes it works.
• Can try topical coal tars and UV light treatments
• Most effective for mod/severe disease is acitretin
(Soriatane) an oral retinoid – slows growth of epidermis.
• Combination therapy is usually the rule.