Reactive Arthritis

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Retrieved

2021-01-23

Source

Orphanet

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HLA-B, IFNG, TRBV20OR9-2, IL17A, TNF, TAP2, HSPD1, HLA-DRB1, TRB, TLR4, CCR5, SLC11A1, CRP, RBM45, IL10, TP53, CDR3, TLR2, USO1, MARCO, PDLIM7, RPL23, BCL2, NCR2, NXF1, HPLH1, TRBV16, TRBV7-9, TRBC1, HSPA14, IL23A, KIR2DL5A, TET1, PCBD2, CTHRC1, SEC14L2, CCL21, TAP1, SOD2, COMP, CRYGD, CYP1A1, FHL1, FLNB, FN1, GLI2, CFH, HLA-C, HRAS, HSPA1L, IL2RA, IL4, CXCL8, IL18, ISG20, KIR2DL1, KIR2DL2, KIR2DS1, MARK1, MMP3, PTGS2, CXCL5, KIR2DL5B

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Reactive arthritis (ReA) is an autoimmune disorder belonging to the group of seronegative spondyloarthropathies and is characterized by the classic triad of arthritis, urethritis and conjunctivitis.

Epidemiology

Prevalence is estimated at 1/30,000. The disease is more common in men and is more frequently reported in whites.

Clinical description

Age of onset varies widely, but there is a peak between 15 and 35 years of age. ReA is rarely seen in children. The disease usually occurs within 1-3 weeks after a urogenital or gastrointestinal infection. Urinary symptoms (polyuria and dysuria) are often the first manifestation. Prostatitis in men, and cervicitis, salpingitis and/or vulvovaginitis in women are frequent findings. Arthritis, manifesting with pain, swelling and tenderness of the large joints, generally appears several weeks or months after the initial symptoms. It often affects one (knee) or a few major joints (knees, ankles or toes). The tendons and ligaments next to the joints may also be inflamed, particularly the Achilles tendon and the lower back joints. Ophthalmologic problems include conjunctivitis with erythema, burning, tearing, and photophobia. Iritis and uveitis are less common. Additional symptoms include scaly skin rashes on the hands or feet, nail changes, diarrhea, balanitis, fever, weight loss, and mouth ulcers. In most patients, the symptoms last for 1-6 months.

Etiology

ReA is typically triggered by Gram-negative infections (Chlamydia, Shigella, Salmonella, and Yersinia). Genetic constitution (many patients are HLA-B27-positive) contributes to the pathogenesis of the disease. However, the exact mechanism by which HLA-B27 results in susceptibility to ReA remains to be determined.

Diagnostic methods

Diagnosis is based on recognition of the clinical triad and blood tests revealing HLA-B27 positivity (about 75% of the patients are HLA-B27-positive).

Differential diagnosis

The differential diagnosis should include other forms of spondyloarthropathy (ankylosing spondylitis, psoriatic arthritis, inflammatory bowel disease-associated spondyloarthropathy, juvenile-onset spondyloarthropathy (see these terms)), and undifferentiated spondyloarthropathy.

Management and treatment

Management aims at eradication of the underlying infection (antibiotics) and reduction of joint pain and inflammation (analgesics, steroids and immunosuppressants, as well as rest, joint protection, and special exercises).

Prognosis

Prognosis is variable. Two-thirds of patients develop prolonged joint discomfort, lower back pain or an enthesopathy after acute ReA. Severe chronic sequelae may develop in up to 30% of cases. However, the majority of patients have a normal life span and nearly normal lifestyle.