Natasya 1015009

Suciana A.S 1015114

Aghnia H.S 1015130
Adi Widana-1015122
Arni Purnamawati - 0915115
Tutor : dr.Prawindra Irawan, Sp.KK, M.Kes
Fakultas Kedokteran Maranatha
RS Immanuel Bandung
2015

Abstract
Psoriasis: chronic, immune-mediated,
inflammatory disease, affect the skin and joints
Occurs worldwide, prevalence varies between
region
Genetic and environment factor important
role
Gen: PSORS 1- PSORS7
HLA(histocompatibility antigen) HLA-Cw6


Risk factor
Smoking, obesity, alcohol consumption, diet,
infections, medications, stressful life events

Natural history varies depend on clinical subject

Differential diagnosis includes many other
immune-mediated inflammatory disorders

Epidemiology

Prevalence and incidence

Occurs worldwide, has no gender preference
In US affects 2% of population
Incidence 14 per 10.000 persons-years
Extremely rare in certain ethnic groups:
Africans, african-american, japanese, alaskans,
australians, norwegians

Prevalence has not changed with time

Age of onset
75% before age of 40 years
Peak at 20-30 years old
Early onset have positive family history and
associated with HLA-Cw6

Genetic basis
Heritability of psoriasis 60-90%
If both parents have psoriasis, 50% chance of
children have the disease
If only one parent has, the risk decrease 16%
If neither parent is affected, but child develops
psoriasis. Their siblings have and 8% risk

 Major locus for psoriasis located on

chromosome 6p21 (PSORS1)

Chromosomes 1p (PSORS7)
Chromosomes 1q (PSORS4)
Chromosomes 3q (PSORS5)
Chromosomes 4q (PSORS3)
Chromosomes 17q (PSORS2)
Chromosomes 19q (PSORS6)

 Associated with HLA antigen, HLA-Cw6

Expressed in 85-90% of early onset patients

HLA-B13, HLA-B17, HLA-B37, HLA-Bw16

plaque psoriasis
HLA-B27 pustular psoriasis
HLA-B13, HLA-B17 guttate psoriasis in
children

Risk Factor

Smoking and Obesity

Research:
Nurses Health Study II : 30% of psoriasis new
case due to being overweight (BMI >25)
Multivariate relative risk for current smoker was
1.78 and past smoker was 1.37 (p<0.05)
Epidemiologic study from European polpulation:
Second hand smoke is a risk factor

 A recent hospital based cross sectional study: high

intensity of smoking (>20 cigarettes daily) vs a
lower level of consumtion (>10 cigarettes daily)
>2x increased risk for severe psoriasis. The effect
was stronger for women.
Suggest explanation:
Smoking and obesity trigger Th1
immunologic pathway

Alcohol Consumption
Research:
A case control study: the odd ratio was 2.2 for
developing psoriasis at an alcohol intake 100 g/day
Higgins at al: the odds was 8.01 for alcohol as an
independent risk factor
Qureshi et al: multivariate relative risk of psoriasis was
1.72 for an alcohol consumption of 2.3 drinks per
week/more
Metaanalysis of case control studies: the odds was
1.531 (p=0.002)

Suggest Explanation
Heavy drinkers have a tendency to develop
more extensive and inflamed skin lession.
Mechanism: upregulation of pro
inflammatory cytokine, proliferation and
activation of lymphocyte, hyperproliferation of
keratinocyte and increased risk of infection.

Infections
Acute bacterial and viral infection exacerbate
psoriasis. Streptococcal infection triggers og
guttate psoriasis especially in children and young
adult.
HIV infection severe plaque psoriasis which
is often not responsive to standard treatment.

DRUG
MECHANISM
Medication (Drug induced/drug
aggravated)
-Blocker
Lithium

Antimalaria
Antibiotic Tetracyclin
NSAIDs

Epidermal 2-blockade decrease

intra epidermal cAMP &
keratinocyte hyperproliferation
Inhibit inositol monophosphate
depletion intracel Ca and increased
proliferation keratonocyte.
Production TNF- & IFN-
Inhibiting enzyme transglutaminase
& epidermal proliferation
Depeletion of intracel cAMP
Inhibit metabolism of arachidonic
acid accumulation leukotriens
aggravate psoriasis

Psychological Stress
Up to 60% pastient described stress as an
exacerbator.
Suggest mechanism:
-Abnormal neuroendocrine response (HPA axis)
However, the relationship between stress and
psoriasis is likely more complicated.

Natural History
According to the clinical subtype
May present as :
chronic, stable plaques with intermittent
remissions and exacerbations,
acutely with a rapid progression and widespread
involvement.

 Plaque psoriasis
usually chronic with intermittent remissions.
may persist for months to years at the same locations
however, periods of complete remission do occur.
Remissions of 5 years or more have been reported in
approximately 5% of patients.

responds well to topical therapy and phototherapy;

however, systemic therapy may be necessary for severe
disease.
may be associated with internal involvement, including
joints and extra-articular sites such as the eyes.

 Concomitant psoriatic arthritis

occurs in 5%30% of patients with cutaneous
psoriasis.
In a minority of patients, the symptoms of psoriatic
arthritis appear before skin involvement.
The typical presentation : an asymmetric oligoarthritis
with involvement of the distal (DIPs) and proximal
(PIPs) interphalangeal joints of the hands and feet.
Erosive changes may occur years after the presenting
periarticular inflammation.

 The prevalence of ophthalmic involvement in

patients with cutaneous disease is not known;
however, it is thought to occur in approximately
10% of patients.
Psoriasis may affect almost any part of the eye,
leading to blepharitis, peripheral keratopathy,
acute anterior uveitis, posterior synechiae,
conjunctivitis, and cataract formation.

 The prognosis of guttate psoriasis :

excellent in children with spontaneous remissions
occurring over the course of weeks to months.
In adults, the lesions of guttate psoriasis may
become chronic and progress to widespread
involvement with plaque psoriasis..

 Palmoplantar pustulosis
presents with sterile pustules of the palmoplantar
surfaces admixed with yellow-brown macules, is a
chronic disease which tends to remain localized to the
palms and soles.
less responsive to standard treatment and is
commonly associated with sterile inflammatory bone
lesions, such as SAPHO syndrome (synovitis, acne,
pustulosis, hyperostosis, and osteitis).
aggravated by extrinsic factors, such as stress,
smoking, and infections.

 Generalized pustular psoriasis (von Zumbusch)

a severe form of psoriasis which is triggered by pregnancy, rapid
withdrawal of corticosteroids, infections, and hypocalcemia.
It is complicated by systemic symptoms of fever, chills, and
fatigue, as well as electrolyte derangements and liver
abnormalities.
This variant requires systemic immunosuppressive therapy and
often responds by resolution of pustules and extensive scaling
after several days of treatment.
The mortality rate due to sepsis is high without appropriate
treatment.

In addition to the clinical subtype of psoriasis, pregnancy and

HIV infection strongly influence the natural course of disease.

Psoriasis and pregnancy

It is well established that psoriasis fluctuates
during pregnancy, likely due to the hormonal
changes in estrogen and progesterone resulting
in a state of altered immune surveillance.
The majority of women usually experience an
improvement in their cutaneous disease during
pregnancy.

Study by Murase et al, during pregnancy

worsening; 23%

improvement; 56%
no change; 21%

postpartum

improvement; 9%
no change; 26%
worsening; 65%

 In patients with 10% or greater body surface area

involvement who reported improvement, lesions
decreased by 83.8% during pregnancy.

Raychaudhuri et al, pregnancy

no change; 18%

worsened; 26%

improved; 56%

Relapse during the early postpartum period was

common.

 The mechanism by which psoriasis tends to

improve during pregnancy is not well
understood. However, there is now data to
suggest that the upregulation of Th2 cytokines
during pregnancy counteracts the effects of proinflammatory Th1 cytokines which are key
players in the pathogenesis of psoriasis.

Psoriasis and HIV

occurs with a similar to slightly higher prevalence than in the general
population.
may present for the first time in advanced HIV infection, when CD4-cell
count is less than 100 cells per L,and could even be the initial clinical
manifestation of HIV infection.
However, psoriasis also tends to spontaneously improve during endstage AIDS.
The relationship between HIV infection and psoriasis is complicated.
While an expansion of CD8 cells in advanced HIV might explain the
exacerbation of psoriasis
there is now evidence that psoriasis patients are enriched for genetic
variants that protect against HIV-1 disease.Further studies are needed to
shed light on this association.

Psoriasis and its linkage

to another disease
May be at increased risk of developing other
disease due to

shared genetic pathway,

Common immune mechanism,
Treatment related toxicities,
And associated psychological burden

 Linkage to other disease

Inflammatory bowel disease (especially Chrons)
share genetic loci PSORS8 on chromosome 16q
Insulin resistance, atherosclerosis, and
thrombosis chronic Th-1 inflammation
Obesity social isolation, unhealthy dietary
habits, increased depression, alcohol consumption
and decreased physical activity

 Obesity ? psoriasis
Women in the nurses health study II obesity is
a proinflamatory state and adipose tissue is a rich
source of inflammatory mediators (adinopectin,
leptin, resitin, TNF-, IL6, Monocyte
chemmoattractant protein 1. increasing risk to
development of psoriasis

 Psoriasis may also lead to diabetes

Chronic inflammation in the setting of psoriasis,
may predispose to the development of insulin
resistance

Ginsodi et al, 338 patients with chronic plaque

psoriasis and 334 patients with skin disease
other than psoriasis higher prevalence of
metabolic syndrome in the psoriatic group.
However no correlation between severity of
psoriasis and prevalence of metabolic syndrome

 Psoriasis low level of folate and high level of

homocycsteine increased cardiovascular risk
Chen et al showed psoriasis carries an elevated
risk of malignancy, especially younger, male
patients, independent of systemic treatment.

 Psoriasis caused depression and higher

suicidal intention
Rieders et al extent of psoriasis does not
predict severity in psychosocial morbidity.
Continue distressed even after their cutaneous
lesion resolved

Differential Diagnosis

Distinguish the Differential Diagnosis

Clinical subtype various
Skin biopsy
Histopathologic examination

Conclusion
Chronic, multifactorial disorders
Variable

clinical

course

mimic

other

inflammatory and autoimmune skin conditions

Associated

with

physical

and

emotional

comorbidities negative impact on the quality of

life

THANK YOU