Spondeloarthropathy Psoriatic Arthritis - PowerPoint Presentation

Slide1

Spondeloarthropathy

Slide2

Psoriatic Arthritis

Slide3

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 inflammatory-type back pain, and who is negative for rheumatoid factor. In such patients, a careful search for psoriasis is warranted.

Slide4

dactylitis

Slide5

dactylitis

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CLINICAL 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,

Slide7

but 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.

Slide8

Clinical 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%).

Slide9

Psoriatic arthritis of the hands with phalangeal joint and nail involvement.

Slide10

Features 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.

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Patients 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.

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Iritis

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.

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LABORATORY 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

.

Slide15

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.

Slide16

TREATMENT

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 .

Slide17

sulfasalazine

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

Slide18

Enteropthic

Arthritis

Slide19

Pathogenesis

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.

Slide20

Jejunal

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

.

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CLINICAL 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.

Slide22

As 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%.

Slide23

Peripheral joint disease in IBD

Slide24

Extraintestinal

manifestationof

IBD

Slide25

Pyoderma gangernosum

Slide26

DIAGNOSIS

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.

Slide27

TREATMENT

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.

Slide28

TNF 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.

Slide29

Reactive 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.

Slide30

A 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 .

Slide31

CAUSE

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

.

Slide32

causes of gastroenteritis lead to reactive arthritis

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PATHOGENESIS

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.

Slide34

The 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.

Slide35

Bacterial

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.

Slide36

CLINICAL 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.

Slide37

Ankle arthritis in a man with

Yersinia

arthritis.

Slide38

The 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.

Slide39

DIAGNOSIS

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.

Slide40

TREATMENT

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.