Articular syndrom

Articular syndrom– joint pain, shape change,

and impaired joint function
Causes of joint syndrome:
• joint damage
• damage to periarticular tissues
• radiation from other organs
• psychogenic
 Features of Articular syndrom
- morning stiffness in the joints;
- arthralgia at rest;
- arthralgia under load;
- signs of arthritis;
- effect of medications;
Thorough collection of anamnesis !
The presence of other symptoms, syndromes
other than joint (fever! etc.)
Assessment of Articular syndrome
• Joint pain
• Stiffness in the joint/joints
• General stiffness
• Violation of joint function (restriction of
movement volume)
• Changing the shape of the joint
• Changing skin color and temperature
• Crunch in the joint when moving
 The nature of the pain syndrome

• Localization (joint,periarticular tissues)

• Prevalence
• Symmetry
• The nature (inflammatory / mechanical)
• The sharpness of the beginning
• Stiffness (morning 20 min, 2,5? hours)
 The nature of pain:

• Inflammatory: more disturbing at rest, at

night, may decrease with exercise
• Non-inflammatory: increases after physical
activity, in the evening, passes at rest
 Examination of the joints
• Defiguration of the joint due to exudative
phenomena (inflammation-dolor, color, tumor,
functio laesa)
• Joint deformity due to exudative and
proliferative changes, or only proliferative
changes
 Gonarthrosis complicated by reactive
synovitis (inflammation-dolor, color, tumor,
functio laesa)
 rheumatoid
arthritis

narrowing of the joint gap

 Seronegative spondyloarthropathies

Seronegative spondyloarthropathies include

several chronic inflammatory arthritic diseases
The most important diseases in this group
are ankylosing spondylitis, reactive arthritis,
and psoriatic arthritis.

Common features include the absence

of rheumatoid factor (RF) and a strong
genetic association with HLA-B27.
• Spondyloarthropathies disproportionately affect
men, with symptom onset generally occurring
before the age of 45.
• The cardinal sign is slowly progressive pain in the
lower back and sacroiliac joints (especially at night).
• Asymmetrical oligoarthritis and enthesopathy are
also common.
• The diseases differ in the involvement of other
organs, such as the eyes, the genitourinary tract
(particularly in reactive arthritis) or the skin
(particularly in psoriatic arthritis).
 Types of seronegative spondyloarthropathies

The different types of seronegative spondyloarthropathy do

not necessarily represent distinct diseases, but may overlap
significantly in etiology, pathology, clinical features, and
treatment.

• Ankylosing spondylitis (most common)

• Reactive arthritis
• Psoriatic arthritis
• Undifferentiated spondyloarthropathy
• Spondyloarthritis associated with Crohn's disease and
ulcerative colitis
Common features of seronegative spondyloarthropathies

• Negative for rheumatoid factor

• Genetic association with HLA-B27
• Generally more commonly affects men Age
of onset: typically between 20–40 years of
age
• Non-specific symptoms (fever, fatigue,
weight loss)
• Arthritis
– Insidious, often unilateral onset
– Particularly of the sacroiliac joints (especially for ankylosing
spondylitis) Asymmetrical peripheral oligoarthritis
– Stiffness and pain is worse in the morning (typically > 30
minutes) and improves with movement
– Often involves inflammatory enthesopathy (e.g.,
achillodynia)
– Usually responds well to NSAID therapy

• Extra-articular manifestatitons vary according to type,

but involvement of the eye is common (e.g., iritis,
iridocyclitis, uveitis)
 Reactive arthritis (Reiter syndrome)
• Reactive arthritis, (formerly known as Reiter's
syndrome), is an autoimmune condition that occurs after
a bacterial infection of the gastrointestinal or
urinary tract.
• It is categorized as a seronegative spondyloarthritis
because of its association with HLA-B27.
• Reactive arthritis primarily affects young men and
usually presents with musculoskeletal or extra‑articular
symptoms.
• The characteristic triad consists of arthritis,
conjunctivitis, and urethritis.
• The diagnosis is based on clinical features such
as patient history and physical examination;
there are no specific tests for reactive
arthritis.
• Treatment is primarily symptomatic and
consists of the administration of NSAIDs, as
most patients recover spontaneously.
 Etiology

– Post-infectious autoimmune disorder

– Post-urethritis: after infection with Chlamydia

(common), Neisseria gonorrhea, or Ureaplasma
urealyticum
– Post-enteritis: after infection with Shigella,
Yersinia, Salmonella, or Campylobacter
 Clinical features
• Latency period: 1–4 weeks
• Musculoskeletal symptoms
– Polyarthritis
• Acute onset
• Often asymmetrical with a migratory character
Occurs predominantly in the lower extremities
– Sacroiliitis
– Enthesitis
– Dactylitis
 Extra‑articular symptoms

– Conjunctivitis or iritis
– Oral ulcers
– Dermatologic manifestations: skin lesions of the
glans resembling psoriasis (balanitis circinata);
hyperkeratinization of the palms and soles (
keratoderma blenorrhagicum)
• Symptoms from preceding infection
– Diarrhea
– Urogenital tract symptoms (dysuria, pelvic pain,
urethritis, prostatitis)
The classic triad of reactive arthritis
(formerly called Reiter's syndrome)
consists of urethritis, conjunctivitis,
and arthritis, but it is only present in
about a third of cases
Гиперкератинизация ладоней и подошв (keratoderma blenorrhagicum)
у 1/3 пациентов с синдромом Рейтера
 Diagnostics

Reactive arthritis is a clinical diagnosis that may be

supported by diagnostic steps, but there is no
confirmatory test.
• Laboratory tests
– ↑ ESR and CRP
– Test for potentially positive HLA-B27
– Consider performing additional tests to confirm a preceding infection
• Arthrocentesis: may be performed to rule out differentials .
Findings from synovial fluid analysis include:
– ↑ WBC count: 10,000-40,000/μL
– Mostly polymorphonuclear leukocytes predominate
– Gram stain and cultures are negative
 Treatment

There is no curative treatment. The goal of

treatment is to primarily control symptoms as
the disease is usually self-limiting.
• Arthritis
– First line: NSAIDs
– Local treatment: cryotherapy and physiotherapy
– If NSAIDs are not effective: glucocorticoids (intraarticular
or oral)
– In chronic cases : DMARDs, e.g., sulfasalazine or MTX
• Ongoing infection
– Treatment of gastrointestinal infections
 Prognosis

• Resolves spontaneously within a year (80% of

cases)
• High rate of recurrence (15–50% of cases)
 Psoriatic arthritis

• Definition: inflammation of joints (primarily

on hands, feet, spine) that may occur with
psoriasis
• Epidemiology: 5–30% of psoriasis patients
affected
• Clinical features
– Psoriasis and psoriatic arthritis may occur
independently or together
– There are several types of psoriatic arthritis:
• Oligoarthritis (most common, accounting for 70% of
cases): typically with involvement of both the
distal and proximal interphalangeal joints
• Spinal involvement (up to 40% of cases)
– Other rheumatological features
• Enthesitis
• Tenosynovitis
• Dactylitis: inflammation and swelling of fingers or toes
(“sausage digit”)
• Arthritis mutilans: destruction of the IP joints and
resorption of the phalanges; causes the soft tissue of
the fingers to collapse (“telescoping fingers” or “
opera glass hand”)
 Diagnosis

– There is no specific test for diagnosing psoriatic arthritis

– The ClASsification Criteria for Psoriatic ARthritis (CASPAR) is
helpful for diagnosing psoriatic arthritis (≥ 3 out of
the 5 following points required).
• Evidence of psoriasis
• Psoriatic nail dystrophy
• Negative rheumatoid factor (RF)
• Dactylitis
• Radiologic signs
– Imaging studies: joint destruction, ankylosis
• Fingers: pencil-in-cup deformity
• Spine: syndesmophytes, and in
particular asymmetric paravertebral ossification
If first-degree relatives of patients with
psoriasis have joint problems,
psoriatic arthritis should be considered!
Ankylosing spondylitis (Bekhterev's disease…)

- a type of seronegative spondyloarthropathy, is

a chronic inflammatory disease of the axial
skeleton that leads to partial or even complete
fusion and rigidity of the spine.
- Males are disproportionately affected and
upwards of 90% of patients are positive for
the
HLA-B27 genotype, which predisposes to the d
isease.
• The most characteristic early finding is pain and
stiffness in the neck and lower back, caused by
inflammation of the vertebral column and the
sacroiliac joints.
• The pain typically improves with activity and is
especially prominent at night.
• Other articular findings include tenderness to
percussion and displacement of the
sacroiliac joints , as well as limited spine mobility,
which can progress to restrictive pulmonary disease.
• The most common extra-articular manifestation is
acute, unilateral anterior uveitis
Diagnosis is primarily based on symptoms and
x-ray of the sacroiliac joints, with HLA-B27
testing and MRI reserved for inconclusive
cases.
There is no curative treatment, but regular
physiotherapy can slow progression of the
disease. Additionally, NSAIDs and/or tumor
necrosis factor-α inhibitors may improve
symptoms. In severe cases, surgery may be
considered to improve quality of life.
 Treatment
• Physical therapy
– Consistent and rigorous physical therapy
– Independent exercises
• Medical therapy
– First choice: NSAIDs (e.g., indomethacin)
– Additional options
• Tumor necrosis factor-α inhibitors (e.g., etanercept, adalimumab
) In case of peripheral arthritis: DMARDs (especially
[12]

sulfasalazine)
• In severe cases: temporary, intra-articular glucocorticoids
– Surgery: in severe cases to improve quality of life
Indications
 Gout
Gout is a common inflammatory arthropathy characterized
by painful and swollen joints resulting from precipitating
uric acid crystals. Decreased renal excretion and/or
increased production of uric acid leads to hyperuricemia,
which is commonly asymptomatic, but also predisposes
to gout.
Acute gout attacks typically manifest with a severely painful
big toe (podagra) and occur most often in men following
triggers such as alcohol consumption.
Diagnosis is based on clinical presentation and
synovial fluid analysis, which reveals
negatively birefringent monosodium urate crystals.
• Acute attacks are treated with nonsteroidal
anti-inflammatorydrugs
(e.g., naproxen, indomethacin),
while management of chronic gout includes
lifestyle modifications and possibly allopurinol
to control hyperuricemia.