Untitled Quiz

Spondyloarthritis (SpA)

• SpA is a group of overlapping disorders sharing clinical features
• Types of SpA include ankylosing spondylitis (AS), reactive arthritis (ReA), psoriatic arthritis (PsA), and arthritis associated with inflammatory bowel disease (IBD)
• The cardinal clinical feature is inflammation of the sacroiliac joints (sacroiliitis) and the spine (spondylitis)
• Also includes inflammation of tendon insertion sites (enthesitis), inflammation of entire digits (dactylitis), and inflammation of one to four lower extremity joints (oligoarthritis)
• Disorders are classified as predominantly axial SpA, affecting the spine, pelvis, and thoracic cage, or predominantly peripheral SpA, affecting the extremities
• Axial spondyloarthritis (axSpA) is the most common inflammatory disorder affecting the axial skeleton, with variable involvement of peripheral joints and extraarticular structures
• Estimated adult prevalence of AS is ~0.17% (range 0.02-0.5%)
• AS shows a strong correlation with the histocompatibility antigen HLA-B27
• In North American whites, the prevalence of B27 is 6%, whereas it is 80-90% in patients with AS
• Sacroiliitis is a typical early manifestation of axSpA, and with progression, the eroded joint margins are replaced by fibrocartilage regeneration and then by ossification
• The larger erosions, progressive sclerosis, and focal narrowing of the articular space are notable features at a slightly later stage
• Eventually, complete ankylosis of the synovial and ligamentous portions of the sacroiliac space on both sides is apparent. The sclerosis may diminish.
• In the spine, outer annular fibers are eroded and replaced by bone, forming early syndesmophytes that could lead to a "bamboo spine"
• HLA-B27 plays a direct role in SpA pathogenesis
• ERAP1 and ERAP2 play a role in AS pathogenesis
• Genes related to TNF pathways are involved
• Genes in the IL-23/IL-17 innate immune cells play roles
• Gut microbiota dysbiosis is also a factor
• Initial SpA symptoms are often noticed in late adolescence or early adulthood, typically during the mid-20s. Symptoms begin after age 40 in 5% of patients

Clinical Manifestations

• Initial symptoms are often insidious, sharp or dull, deep pain in the lower lumbar or gluteal region. Low-back morning stiffness may last for a few hours.
• Pain decreases with activity and returns following inactivity. Within few months, pain tends to be constant and bilateral.
• Nocturnal pain can occur frequently causing the patient to tend to wake up and move around.
• Bony tenderness (likely from enthesitis or osteitis) may accompany back pain or stiffness

Common sites of bony tenderness

• Costosternal junctions
• Spinous processes
• Iliac crests
• Greater trochanters
• Ischial tuberosities
• Tibial tubercles
• Heels

Specific Findings

• Loss of spinal mobility, restricted anterior and lateral flexion and extension of the lumbar spine, and chest expansion.
• Pain in sacroiliac joints may be evoked by direct pressure or stress on the joints

Diagnostic Testing

• No single lab test is diagnostic of SpA.
• HLA-B27 is found in 75-90% of patients in most ethnic groups.
• ESR and CRP are not always elevated.
• Mild anemia may be present.
• Rheumatoid factor (RF), anti-cyclic citrullinated peptide (CCP), and antinuclear antibodies (ANAs) are mostly absent unless caused by another condition. ANAs might appear with anti-TNF therapy.

Radiographic Findings

• Radiography often shows sacroiliitis, typically symmetric.
• Initial radiographic findings include blurred cortical margins of the subchondral bone, followed by erosions and sclerosis.
• Later stages can show "pseudowidening" of the joint space with fibrous and then bony ankylosis, which can lead to the joints becoming obliterated
• In the lumbar spine, loss of lordosis, osteitis of the anterior corners of the vertebral bodies with consequent erosion and bone formation can cause "squaring" or even "barreling" of vertebral bodies. Progressive ossification leads to the formation of marginal syndesmophytes, visible on plain films as bony bridges connecting vertebral bodies
• Specific criteria exist for diagnosis. MRI can often help distinguish various subtypes of the condition.

Clinical Features for Chronic (≥3 months) Back Pain

• Onset of symptoms at ≤40 years
• Insidious onset
• Improvement in symptoms with exercise
• Lack of improvement with rest
• Night pain improving when getting up
• Morning stiffness greater than 30 minutes
• Back pain waking usually only in the latter half of the night
• Alternating buttock pain

Diagnosis of AS

• Classification criteria for ax-SpA, proposed by ASAS, are applicable to individuals with at least three months of back pain and age of onset under 45. Specific criteria exist

Treatment of AS

• Management of SpA should include an exercise program to maintain posture and range of motion
• Non-steroidal anti-inflammatory drugs (NSAIDs) are the first-line pharmacological treatment, reducing pain, tenderness, and increasing mobility
• Continuous high-dose NSAID therapy can potentially slow radiographic progression. Biologic therapy with anti-TNF agents can be helpful for patients with persistent symptoms despite NSAIDS.
• Before starting anti-TNF therapy, patients should be tested and treated for latent tuberculosis (TB) and hepatitis B if found.

Contraindications to TNF Inhibitors

• Active infection or high risk of infection
• History of multiple sclerosis
• Prior history of hematologic malignancy
• Systemic lupus erythematosus (SLE) or other related autoimmunity

Treatment of Uveitis

• Uveitis attacks are generally managed with local glucocorticoids and mydriatic agents. Systemic glucocorticoids, immunomodulating drugs, or anti-TNF therapy may be needed, if necessary.