Reactive arthritis (ReA) is an autoimmune condition characterized by inflammatory arthritis that develops in response to an infection elsewhere in the body, typically occurring 1–4 weeks after the infection. It is classified as a seronegative spondyloarthropathy and often involves joints, the urogenital tract, and the eyes.

Causes

Reactive arthritis is triggered by specific bacterial infections, most commonly:

• Gastrointestinal infections: Caused by bacteria like Salmonella, Shigella, Campylobacter, or Yersinia.
• Genitourinary infections: Most notably Chlamydia trachomatis, but also Ureaplasma or Mycoplasma.
  The exact mechanism is not fully understood, but it involves an aberrant immune response, likely due to molecular mimicry (where bacterial antigens resemble human tissue proteins) or persistent bacterial antigens in joints. Genetic predisposition, particularly the HLA-B27 gene, increases susceptibility, though not all ReA patients are HLA-B27 positive.

Key Features

Reactive arthritis classically presents with:

• Asymmetric oligoarthritis: Typically affects large joints like knees, ankles, or sacroiliac joints.
• Urogenital symptoms: Urethritis, cervicitis, or dysuria.
• Ocular symptoms: Conjunctivitis or, less commonly, uveitis.
• Mucocutaneous symptoms: Keratoderma blennorrhagicum (scaly skin lesions), circinate balanitis (penile lesions), or oral ulcers.
• Enthesitis: Inflammation at tendon insertions (e.g., Achilles tendon).
  A classic triad of arthritis, urethritis, and conjunctivitis (formerly called Reiter’s syndrome) is seen in some cases but is not universal.

Connection to Secondary Raynaud’s Phenomenon

Reactive arthritis is not a common cause of secondary Raynaud’s phenomenon, and Raynaud’s is rarely reported in ReA. However, a connection could theoretically arise in the following contexts:

• Autoimmune overlap: ReA may coexist with other autoimmune conditions (e.g., systemic lupus erythematosus or scleroderma), which are established causes of secondary Raynaud’s.
• Vascular inflammation: Chronic inflammation in ReA could, in rare cases, affect small blood vessels, potentially leading to vasospasm resembling Raynaud’s.
• Medication side effects: Treatments for ReA, such as NSAIDs or, rarely, immunosuppressive drugs, might influence vascular tone in susceptible individuals, though this is not well-documented.

Given the lack of direct evidence linking ReA to Raynaud’s, if Raynaud’s symptoms are present in a patient with ReA, clinicians should consider:

• Coexisting autoimmune diseases (e.g., lupus or scleroderma).
• Other causes of vasospasm, such as medication effects or environmental triggers.
• Rare vascular complications of ReA, though these are not typical.

Key Points

• Demographics: ReA is more common in young adults (20–40 years), with a slight male predominance, especially in Chlamydia-associated cases.
• Diagnosis: Based on clinical history (recent infection, joint symptoms), physical exam, and lab tests (e.g., elevated ESR/CRP, HLA-B27 testing). Synovial fluid analysis may rule out septic arthritis. Imaging may show enthesitis or sacroiliitis.
• Prognosis: Most cases resolve within 3–12 months, but 15–30% develop chronic arthritis or recurrent episodes, especially HLA-B27-positive patients.
• Treatment:
• Infection management: Antibiotics for active infections (e.g., doxycycline for Chlamydia), though they don’t alter arthritis course.
• Symptom relief: NSAIDs (e.g., ibuprofen) are first-line. Corticosteroids (local or systemic) may be used for severe cases.
• Chronic cases: Disease-modifying antirheumatic drugs (DMARDs) like sulfasalazine or methotrexate, or biologics (e.g., anti-TNF agents) for refractory cases.

If Raynaud’s phenomenon is suspected in a patient with reactive arthritis, a thorough evaluation for other underlying causes is warranted, as ReA alone is unlikely to explain it. Consult a healthcare provider for accurate diagnosis and tailored treatment.

Disclaimer: owerl is not a doctor; please consult one.