Psoriatic Arthritis
Epidemiology
1-3% Caucasian, 0.1-0.3% American/African-American, but 20-30% of those with PsO.
Psoriasis 2-3%. Up to 40% of patients with PsA have a family history of PsO. 30-50yrs.
Unlike other inflammatory arthritis, M=F or M>F.
• Psoriasis precedes arthritis by 8-10yrs in ≈65%
• Simultaneous onset of PsA and psoriasis occurs in ≈25%
• Arthritis precedes psoriasis in ≈5-10% (particularly in childhood)
Risk factors for PsA development in PsO patients
difficult sites of psoriasis (nails, scalp, genitals), severity of PsO, obesity, 1st-degree relative
with PsO/PsA, uveitis.
Causes
Genetics
PsA is a polygenic disorder. Concordance among monozygotic twins ranges from 35-70%,
versus 12-20% for dizygotic twins. Up to 40% of PsA have a family history of PsO.
-HLA: HLA-C6 is associated with severe, early-onset skin psoriasis. HLA-B38 and HLA-
B39 are associated with PsA and HLA-B27 (15-45%) is associated with sacroiliitis and
spondylitis. HLA-DR*04 is associated with worse radiographic progression.
-non-HLA: polymorphisms of IL-23R, IL-36R (DITRA), CARD14 (familial PsO,
autosomal dominant), PTPN22, TNFAIP3 (=A20, an E3 ligase which functions as a negative
regulator of the NF-kB, an adaptor protein in the IL-17R complex, mutation leads to
increased production of IL-22).
Infection
the link with post-streptococcal tonsillitis and subsequent guttate psoriasis. A role of
bacterial colonization of psoriatic skin plaques and associated dysregulation of the skin
barrier has also been hypothesized. Improvement in skin lesions in psoriasis patients who
underwent tonsillectomy. Abnormal mucosal permeability of the large intestine has been
reported in about 20% of PsA cases + dysbiosis.
Trauma
Trauma to a joint (deep Koebner phenomenon) is reported in 25% of patients before the
onset of PsA. Trauma is important in PsA, the target entheses, which are sites of high
mechanical stress, might exhibit signs of microdamage → microscopic inflammatory
changes. Subclinical trauma may explain DIP involvement.
Obesity
increases the risk of PsA in psoriasis patients. Obesity is a low-grade inflammation and
increases burden load at entheses.
CASPAR criteria
for trials mainly but also in “diagnosis”.
≥3 points have 99% specificity and 92% sensitivity.
A patient must have inflammatory articular disease (joint, spine, or entheseal
inflammation) and score ≥3 points from the following categories:
i) Psoriasis: current (2 points) / past or family history (1 point each).
ii) Nail dystrophy: 1 point.
iii) Dactylitis: 1 point.
iv) Juxta-articular new bone formation: 1 point.
v) Negative RF: 1 point.
, Enthesitis is not a criterion!
Wright & Moll criteria
inflammatory arthritis (either peripheral arthritis and/or axial) + psoriasis, RF (-).
Metrology
BSA
is estimated based on the number of palm-size areas affected (1 palm = 1% BSA).
<3% mild disease
3-10% moderate
≥10% severe
PASI
The body is divided into 4 regions, each weighted differently.
Head x0.1
Upper Limbs x0.2
Trunk x0.3
Lower Limbs x0.4
For each region, severity is scored (0–4) based on: erythema, induration, desquamation
(0-72)
Mild: PASI <10
Moderate: PASI: 10–20
Severe: PASI >20
ASDAS score for axial
1) Total back pain (BASDAI question 2)
2) Patient global of disease activity
3) Peripheral pain/swelling (BASDAI question 3)
4) Duration of morning stiffness (BASDAI question 6)
5) CRP in (mg/L) or ESR
<1,3: inactive
1,3 -2,1: low disease activity
2,1 - 3,5: high disease activity
>3,5: very high disease activity
Memo: “I fix up a bad spine”
DAPSA score for peripheral
-Tender joint count (out of 68 joints)
-Swollen joint count (out of 66 joints)
-PtGDA
-Patient pain assessment
-CRP (mg/dL)
≤4: Remission
>4 to ≤14: Low disease activity
>14 to ≤28: Moderate disease activity
>28: High disease activity
Minimal disease activity (MDA) is a PsA T2T state defined by meeting pre-specified criteria
for disease activity across PsA pathophysiologic manifestations (swollen and tender joints,
PASI or BSA, SPARCC) and PROs (joint pain VAS, patient global disease activity VAS, HAQ-DI).
Epidemiology
1-3% Caucasian, 0.1-0.3% American/African-American, but 20-30% of those with PsO.
Psoriasis 2-3%. Up to 40% of patients with PsA have a family history of PsO. 30-50yrs.
Unlike other inflammatory arthritis, M=F or M>F.
• Psoriasis precedes arthritis by 8-10yrs in ≈65%
• Simultaneous onset of PsA and psoriasis occurs in ≈25%
• Arthritis precedes psoriasis in ≈5-10% (particularly in childhood)
Risk factors for PsA development in PsO patients
difficult sites of psoriasis (nails, scalp, genitals), severity of PsO, obesity, 1st-degree relative
with PsO/PsA, uveitis.
Causes
Genetics
PsA is a polygenic disorder. Concordance among monozygotic twins ranges from 35-70%,
versus 12-20% for dizygotic twins. Up to 40% of PsA have a family history of PsO.
-HLA: HLA-C6 is associated with severe, early-onset skin psoriasis. HLA-B38 and HLA-
B39 are associated with PsA and HLA-B27 (15-45%) is associated with sacroiliitis and
spondylitis. HLA-DR*04 is associated with worse radiographic progression.
-non-HLA: polymorphisms of IL-23R, IL-36R (DITRA), CARD14 (familial PsO,
autosomal dominant), PTPN22, TNFAIP3 (=A20, an E3 ligase which functions as a negative
regulator of the NF-kB, an adaptor protein in the IL-17R complex, mutation leads to
increased production of IL-22).
Infection
the link with post-streptococcal tonsillitis and subsequent guttate psoriasis. A role of
bacterial colonization of psoriatic skin plaques and associated dysregulation of the skin
barrier has also been hypothesized. Improvement in skin lesions in psoriasis patients who
underwent tonsillectomy. Abnormal mucosal permeability of the large intestine has been
reported in about 20% of PsA cases + dysbiosis.
Trauma
Trauma to a joint (deep Koebner phenomenon) is reported in 25% of patients before the
onset of PsA. Trauma is important in PsA, the target entheses, which are sites of high
mechanical stress, might exhibit signs of microdamage → microscopic inflammatory
changes. Subclinical trauma may explain DIP involvement.
Obesity
increases the risk of PsA in psoriasis patients. Obesity is a low-grade inflammation and
increases burden load at entheses.
CASPAR criteria
for trials mainly but also in “diagnosis”.
≥3 points have 99% specificity and 92% sensitivity.
A patient must have inflammatory articular disease (joint, spine, or entheseal
inflammation) and score ≥3 points from the following categories:
i) Psoriasis: current (2 points) / past or family history (1 point each).
ii) Nail dystrophy: 1 point.
iii) Dactylitis: 1 point.
iv) Juxta-articular new bone formation: 1 point.
v) Negative RF: 1 point.
, Enthesitis is not a criterion!
Wright & Moll criteria
inflammatory arthritis (either peripheral arthritis and/or axial) + psoriasis, RF (-).
Metrology
BSA
is estimated based on the number of palm-size areas affected (1 palm = 1% BSA).
<3% mild disease
3-10% moderate
≥10% severe
PASI
The body is divided into 4 regions, each weighted differently.
Head x0.1
Upper Limbs x0.2
Trunk x0.3
Lower Limbs x0.4
For each region, severity is scored (0–4) based on: erythema, induration, desquamation
(0-72)
Mild: PASI <10
Moderate: PASI: 10–20
Severe: PASI >20
ASDAS score for axial
1) Total back pain (BASDAI question 2)
2) Patient global of disease activity
3) Peripheral pain/swelling (BASDAI question 3)
4) Duration of morning stiffness (BASDAI question 6)
5) CRP in (mg/L) or ESR
<1,3: inactive
1,3 -2,1: low disease activity
2,1 - 3,5: high disease activity
>3,5: very high disease activity
Memo: “I fix up a bad spine”
DAPSA score for peripheral
-Tender joint count (out of 68 joints)
-Swollen joint count (out of 66 joints)
-PtGDA
-Patient pain assessment
-CRP (mg/dL)
≤4: Remission
>4 to ≤14: Low disease activity
>14 to ≤28: Moderate disease activity
>28: High disease activity
Minimal disease activity (MDA) is a PsA T2T state defined by meeting pre-specified criteria
for disease activity across PsA pathophysiologic manifestations (swollen and tender joints,
PASI or BSA, SPARCC) and PROs (joint pain VAS, patient global disease activity VAS, HAQ-DI).
