PSORIASIS

Nada El-Saad Debahy

Associate Professor of Clinical Dermatology
American University Hospital
Balamand University
Psoriasis
 Genetic, Autoimmune disorder
(50 proven gene associations)
 Multisystemic disease
 Incidence : 2% of the population
 Variable in duration and extend
Many clinical Variants
 Outline
 Different clinical presentations
 Severity evaluation
 Trigering factors
 Histopathology
 Pathogenesis of the disease
 Comorbidities
 Treatment: Topical,systemic,Biologics
Plaque type

 Well demarcated area

 Thickened
 Erythematous
 Covered with silvery white scales
Guttate Psoriasis
Psoriasis Inversus
Scalp Psoriasis
Plaque without hair loss
Tenia amiantacea
Nail Psoriasis
Palmo-plantar Psoriasis
Pustular Psoriasis
Erythrodermic psoriasis
Clinical Variants
 Plaque type
 Guttate
 Palmo-plantar
 Scalp and Nail
 Flexural
 Pustular
 Erythrodermic
Auspitz sign
Severity Evaluation

 PASI Score:
 Psoriasis surface Area
 Severity Index (Erythema, Induration, Scales)
 Percentage of body surface involved does not
reflect the severity of individual lesions
Triggering factors

 External:
 Koebner elicitated PSO by injury to skin,(K phenomenon)
Lag time between injury and induced lesions is about 2 to 6
weeks. It is seen in 25% of patients.
 Other external triggering factors: Sunburn
Triggering Factors

 Systemic:
 Infections: Bacterial, mainly streptococcal pharyngitis
 Guttate Pso
 Pustular Pso precipitation
 Increase the severity of Plaque Psoriasis
 HIV & other viral infections
 Endocrine Factors: hypocalcemia, pregnancy
 Stress
 Beer intake (more than 5 bottles per week)
 Drugs : Lithium, B bloquers, etc…
 Pathophysiology
 Increased epidermal turnover rate
(proliferation of the basal cells & keratin
accumulation)

 Severe inflammation in the upper dermis

(lymphocytes & blood vessels)
 Autoimmunity in Psoriasis
 Pso is a Tlymphocytes mediated auto immune
disease
 CD4 & CD8 predominant in the infiltrate in
epidermis & dermis
 When activated, they secrete Cytokines
(IL2, IL4, IL5, IFN, TNFal)
 Responsible antigen for the psoriatic process
still unknown

 Its identity remains to be discovered

 Its source is probably stratum corneum

Pathogenesis: Role of cytokines

 IL2 and IFN lead to epidermal proliferation and

lymphocytes & neutrophil accumulation
 IL4 lead to lymphocytes & neutrophil infiltration

Both factors lead to:

 Increased epidermal turn over

 Dermal inflammation with perivascular infiltrate

 Increased blood vessels

 Is Psoriasis a simple skin
disease or a systemic disease?
 Comorbidities in Psoriasis
 Psoriatic Arthritis
 Cardiovascular diseases
 Metabolic syndrome: Diabetes, Hyperlipidemia
 Overweight/Obesity
 Inflammatory bowel diseases
 Depression
 Comorbidities in Psoriasis
 Renal Diseases
 Cancer/Lymphoma
 NASH (non alcoholic steato hepatitis)
 COPD
 Increased mortality

All statistically validated

Psoriasis & Arthropathy
 Psoriatic arthritis
 Many faces:
 Dactylitis (sausage digit) inflammation of entire digit
 Enthesitis: inflammation at sites of insertion of
tendon or ligaments into bone
 Arthritis mutilans: severe inflammation of joints
leading to deformation
 Skin and joints
 Conclusion:
Patients with Pso have increased coronary
artery calcium similar to that of patients with type
2 diabetes,suggesting that patients with Pso
harbour high rates of subclinical atherosclerosis
Course of the disease

 Unpredictable
 Guttate type has a better prognosis
 Early onset and positive Family History, worsen the
prognosis
Treatment:
Treatment depends upon:
 Age
 Sex
 Occupation
 Personality
 general health
 Resources
 Type of the disease
 Extent of the disease
 Duration of the disease
Treatment:
1. TOPICALS:
 Top steroids, IL Steroids

 Tar

 Calcipotriol

 Phototherapy: UVA, UVB, 311B

 Photochemotherapy: PUVA
Treatment:
2. SYSTEMIC
Cyclosporin
Methotrexate
Retinoids

Emerging Therapies : Immunomodulators

Immunomodulators: Biologics
Biologic agents:
• They target selectively CD2 & their cytokines

IL, TNFα, IFN

• thus inhibiting T cell activation & reducing the
inflammatory cytokine response.
• Leading to temporary disease suppression
 First agents
TNFα Inhibitors:

Etanercept (Enbrel)
Adalimumab( Humira )
Infliximab (Remicade )
 New Agents
 TNFα Inh: Cimza: recently approved
 IL17:
 Cosentyx (secukinumab)
 Talz (Ixekisumab)
 Silik
 IL23:
 Tremfya (guselkumab)
 Ilumya
 Both Il23 & IL17 inhibitors are highly promising
targets in the current treatment of moderate to
severe plaque Pso
 Conclusion

 Better comprehension of pathophysiology

 Better and newer therapies
 Research going on