Psoriatic arthritis should be suspected in a patient with an asymmetric joint distribution pattern who may have additional clinical features such as dactylitis enthesitis or inflammatorytype back pain and who is negative for rheumatoid factor In such patients a careful search for psor ID: 914528
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Slide1
Spondeloarthropathy
Slide2Psoriatic Arthritis
Slide3Psoriatic arthritis should be suspected in a patient with an asymmetric joint distribution pattern who may have additional clinical features, such as
dactylitis
,
enthesitis
, or inflammatory-type back pain, and who is negative for rheumatoid factor. In such patients, a careful search for psoriasis is warranted.
Slide4dactylitis
Slide5dactylitis
Slide6CLINICAL FEATURES
Plaque psoriasis or psoriasis
vulgaris
is the most common skin phenotype in patients with psoriatic arthritis. Other patterns of skin involvement may be seen
Although the arthritis usually develops in a setting of an established diagnosis of psoriasis
,(80%)
some patients may be unaware that they have psoriasis, or psoriasis may develop after the onset of arthritis in approximately 15% of cases
.
If
a patient presents with the classic
articular
manifestations of psoriatic arthritis,
Slide7but does not volunteer psoriasis or the presence of a rash, it is incumbent on the physician to examine the patient’s skin carefully, including the scalp and nails because psoriasis frequently lurks in such areas.
in clinical practice, there seems to be little relationship between severity of skin involvement and severity of arthritis.
Patients with psoriatic arthritis present with symptoms and signs of joint,
entheseal
, or spinal inflammation.
Slide8Clinical patterns of P.A
five clinical patterns of psoriatic arthritis
1. Asymmetric
oligoarthritis
2. Symmetric
polyarthritis
3
. Predominant distal
interphalangeal
(DIP) joint involvement
4. Predominant
spondyloarthritis
5
. Destructive (
mutilans
)
arthritis(5%).
Slide9Psoriatic arthritis of the hands with phalangeal joint and nail involvement.
Slide10Features that are typical of psoriatic arthritis are helpful in diagnosis, including
dactylitis
and
enthesitis
.
Dactylitis
, in which there is a sausage-shaped swelling of the fingers or toes
(may
be found
at
first presentation,
or during follow-up).
Ultrasound
and magnetic resonance imaging (MRI) studies have shown that joint and
tenosynovial
inflammation are prominent in involved digits.
Enthesitis
, inflammation at tendon or ligament insertion into bone, is a feature of all of the
spondyloarthropathies
and may be a presenting feature in psoriatic arthritis.
Slide11Patients with
enthesitis
complain of pain at these sites with tenderness and sometimes swelling found on examination
.
Entheseal
involvement may be asymptomatic, with ultrasound being more sensitive than clinical palpation. Often spurs are detected on x-ray, although spurs are not always associated with symptoms.
Slide12Iritis
or
uveitis
occurs
more
bilateral than in
ankylosing
spondylitis
, but usually found in patients with spinal involvement.
Numerous
studies have suggested that psoriatic arthritis patients have a higher prevalence of inflammatory bowel disease, sometimes asymptomatic and detected only on biopsy specimen.
Whether
this inflammatory bowel disease is coincidental or possibly related to medication effects remains to be clarified. Distal limb edema or
lymphedema
may occur more commonly in psoriatic
arthritis
Finally
,
amyloid
is rare, but is described in psoriatic arthritis.
Slide13Slide14LABORATORY FEATURES
There is no diagnostic laboratory test for psoriatic arthritis. Although the absence of rheumatoid factor is considered an important distinguishing feature from
RA Until
there is a more definitive diagnostic test, it is difficult to be categorical about diagnosis in these patients
.
Cyclic
citrullinated
peptide antibodies were initially thought to be specific to RA, but it is now recognized that cyclic
citrullinated
peptide antibodies are found in approximately 5% of psoriatic arthritis patients as well
.
Acute-phase markers, such as ESR, C-reactive protein, or serum
amyloid
A, all may be elevated in psoriatic arthritis patients, but less commonly and to a lesser degree than in RA patients.
These markers are elevated in particular in patients with
polyarticular
disease and act as a marker of poor prognosis .
Finally, as mentioned previously,
hyperuricemia
may be found in association with metabolic abnormalities in psoriatic arthritis patients and not reflecting the extent of skin involvement.
Slide16TREATMENT
nonsteroidal
anti-inflammatory drugs
are most often the agents first used in psoriatic arthritis although occasional exacerbations of psoriasis have been reported.
The use of systemic corticosteroids
is no evidence-based ,although 24% of patients in one study were taking
prednisolone
.There are concerns that exacerbations of psoriasis may follow corticosteroid withdrawal.
intra-
articular
steroids
in psoriatic arthritis or of local
entheseal
or
dactylitis
injections. intra-
articular
steroids is effective, especially in
oligoarticular
disease or where there is localized
entheseal
involvement, such as in plantar fasciitis .
Slide17sulfasalazine
is used in psoriatic arthritis .
Methotrexate
remains for many rheumatologists the DMARD of first choice for patients with psoriatic arthritis, but evidence for its use is limited . A small, prospective randomized controlled trial concluded that
methotrexate
was as effective as cyclosporine,
gold salts and
antimalarials
, there is no evidence of treatment benefit; exacerbation of psoriasis is reported,
Biological agent
also used in the treatment as TNF-
alfa
Slide18Enteropthic
Arthritis
Slide19Pathogenesis
The interplay between the intestinal
microflora
and genetic host factors is disturbed in IBD. The microbial contribution is still largely unclear, and animal work indicates that parts of the normal gut flora may be involved. In addition, pathogenic organisms, such as Clostridium
difficile
, have been linked to exacerbations of IBD.
genetic factors related to innate immunity are involved in susceptibility to IBD
HLA-B27 is clearly one predisposing factor, but only in the minority of cases with spinal joint involvement.
Slide20Jejunal
fluid from patients with
ankylosing
spondylitis
(AS) and rheumatoid arthritis collected with the closed-segment endoscopic technique contained antibodies against
Klebsiella
pneumoniae
, Escherichia coli, and Proteus mirabilis.
Increased gut permeability has already been alluded to as an important factor in pathogenesis. Bacteria recovered from the gut lumen in IBD are covered by immunoglobulin, part of which is circulatory
IgG
.
Slide21CLINICAL FEATURES
Spinal involvement occurs in 10% to 20% of cases. The back symptoms are often silent, so their prevalence is underestimated; they may precede the onset of IBD or appear later. In contrast to AS, there is an equal sex distribution. In general, the involvement is similar to or identical with that in classic AS, although small differences have been found.
Changes in
enteropathic
disease tended to be milder than AS, squaring was more prevalent, . The majority of radiographic features were similar.
Slide22As noted, spinal involvement is often asymptomatic, but when symptoms are present, they do not correlate with intestinal symptoms as that of peripheral arthritis.
The issue is complicated by the association of AS with silent
Crohn's
disease, as diagnosed by biopsy. Isolated
sacroiliitis
is not strongly associated with HLA-B27. In full-blown IBD-related AS, the prevalence of B27 is between 50% and 70%.
Peripheral joint disease in IBD
Slide24Extraintestinal
manifestationof
IBD
Slide25Pyoderma gangernosum
Slide26DIAGNOSIS
A careful history and clinical examination, supplemented by imaging, are the principal diagnostic tools.
As mentioned, genetic mapping has shown interesting clinical correlates, but genotyping is not part of the routine clinical workup at present, except perhaps for HLA-B27.
Stool cultures should be performed when infection with special pathogens is suspected.
Slide27TREATMENT
Sulfasalazine
and its derivative 5-ASA which have efficacy of compared with placebo in ulcerative colitis but not in
Crohn's
disease.
Glucocorticoids
are effective in both forms of IBD, although the response of
uveitis
to topical therapy with
glucocorticoids
may be less prompt than in
uveitis
of other causes .
Azathioprine
has been widely used to maintain remission in IBD. It has proven long-term efficacy in both ulcerative colitis and
Crohn's
disease, according to a large European study .It should not be combined with 5-ASA owing to a pharmacokinetic interaction.
Slide28TNF inhibition with
infliximab
(but not with
etanercept
) results in remission of gastrointestinal manifestations in close to 60% of patients with
Crohn's
disease, as confirmed in several placebo-controlled studies.
More recently,
infliximab
was found to be superior to placebo in ulcerative colitis patients resistant to conventional drug therapy,
efficacy of
infliximab
in the treatment of
pyoderma
gangrenosum
Pain control with
nonsteroidal
anti-inflammatory
drugs is a potential problem owing to their potential induction of flares. However, they are widely used and often well tolerated.
Slide29Reactive arthritis
The occurrence of enteric reactive arthritis is determined by the prevalence of exposure to triggering agents and the susceptibility of infected individuals. Therefore, incidence and prevalence figures vary among populations and over time.
The risk of developing enteric reactive arthritis in exposed individuals varies from very low to 20% in different outbreaks
; it may be lower in children .The prevalence of
Yersinia
infections has diminished in recent years, probably as a consequence of improved slaughterhouse hygiene. Salmonella and Campylobacter are presently the two dominant causes of enteric reactive arthritis in most countries.
Slide30A history of
urethritis
(
dysuria
or discharge) or
diarrhoea
must be specifically sought for several reasons.
The interval between these symptoms and the development of arthritis means that patients may not connect these apparently unrelated events.
Secondly, preceding infection may be virtually asymptomatic. Chlamydia infection in women is notoriously silent, and in men these symptoms or a sexual history are often not volunteered spontaneously.
Of gastrointestinal infections, salmonella is likely to produce symptoms in those who go on to reactive arthritis , whereas in
yersinia
-related arthritis many patients have sub-clinical or mild gastrointestinal symptoms .
Slide31CAUSE
The triggering agents are usually gram-negative obligate or facultative intracellular organisms In most series, no organism can be identified in one quarter of patients.
clearly only a small number of microorganisms have the potency to trigger reactive arthritis
.
Slide32causes of gastroenteritis lead to reactive arthritis
Slide33PATHOGENESIS
In enteric reactive arthritis, a triggering gut pathogen starts an inflammatory reaction in the gut; immune cells and antigenic material then disseminate into the joint.
By definition, no living organisms are present in the joint after the outbreak of arthritis. Several steps in the pathogenesis remain elusive.
The
humoral
immune response to the trigger involves
secretory
IgA
and
IgM
and also
IgG
, and it is prolonged in comparison to patients who do not develop enteric reactive arthritis.
Slide34The role of HLA-B27 has been studied intensely for decades. Some evidence indicates that it enhances the expression of
proinflammatory
signals, resulting in a
glutamic
acid located in the B pocket. In vitro experiments have shown normal cellular uptake of bacteria but delayed elimination.
Ex vivo studies have identified antigenic material, in part in the form of processed
lipopolysaccharid
, and DNA in the joints.
It is not known how this material gets into the joints.
Slide35Bacterial
lipopolysaccharide
and heat shock protein can be found in joint tissue up to 4 years after the acute episode. Carriage of HLA-B27 does not influence the duration of bacterial presence in feces in
salmonellosis
, and joint involvement does not correlate with carriage.
Slide36CLINICAL FEATURES
Reactive arthritis is characterized by the acute onset of asymmetric
oligoarthritis
, with dominant localization to the lower extremities and often affecting the large joints
Aseptic
urethritis
is a common feature, and the presence of
circinate
balanitis
is almost
pathognomonic
.
Enthesopathy
, manifested by heel pain, is very common.
Erythema
nodosum
is rather unusual.
Unequivocal signs of
synovitis
are often accompanied by less distinct
arthralgias
, which may outlast
synovitis
by several months.
Slide37Ankle arthritis in a man with
Yersinia
arthritis.
Slide38The enteritis is typically mild and may escape recognition, suggesting that a vigorous inflammatory response in the gut may provide protection against arthritis. Fever and acute-phase reactants may be low grade or intense.
Self-limited
glomerulonephritis
,
myocarditis
, and conjunctivitis are other clinical features.
Slide39DIAGNOSIS
Asymmetric, nondestructive
oligoarthritis
starting some weeks after mild gastroenteritis in a previously healthy individual should raise the suspicion of enteric reactive arthritis.
The presence of
balanitis
blennorrhagica
in males is almost
pathognomonic
&
Keratoderma
blennorrhagica
. Rheumatoid factor and
anticyclic
citrullinated
peptide antibody (anti-CCP) should be negative.
A triggering agent may be cultured from the stools or traced serologically in the blood. However, even a systematic search reveals a trigger in only 60% of cases. Conversely, it is not unusual to find triggers in patients without previous symptomatic disease.
Slide40TREATMENT
Importantly, reactive arthritis cannot be prevented with aggressive antibiotic therapy, even when started early.
Symptomatic analgesic treatment is usually sufficient but may be supplemented by short periods of systemic
glucocorticoids
or
antimalarials
.
Short-term antibiotic therapy is usually administered if a triggering agent can be identified. The rationale for the use of antibiotics is to eradicate remaining microorganisms (e.g., Salmonella) in carriers and to prevent recurrence. However, there is no evidence that antibiotics influence the outcome.