A 56-year-old woman complains of pain in the small joints of her hands and feet. She has been experiencing these symptoms for the last 12 years. Examination of her hands detects a subluxation of the metacarpophalangeal joints with fingers bent outwards («walrus flippers»). There are high molecular weight immune complexes in the patient's blood. What diagnosis can be made in this case?

Чому це правильна відповідь

Rheumatoid arthritis is a chronic autoimmune inflammatory disease that primarily affects synovial joints, leading to progressive destruction of articular cartilage, subchondral bone, and periarticular structures. The disease is mediated by persistent synovitis driven by immune complexes, activated T lymphocytes, macrophages, and pro-inflammatory cytokines, which stimulate synovial hyperplasia and pannus formation. The pannus, composed of proliferating fibroblast-like synoviocytes, granulation tissue, and inflammatory cells, invades cartilage and bone causing erosion and deformity. Chronicity of the disease state explains the long duration of symptoms described in the case. Macroscopically, rheumatoid arthritis leads to joint deformities due to cartilage loss, ligament laxity, and erosion of bone surfaces. One of the classic deformities is ulnar deviation and subluxation of the metacarpophalangeal joints, producing the characteristic outward bending of fingers. Subluxation of the joints reflects destruction of articular surfaces and capsular structures, accompanied by chronic synovial expansion, which displaces and destabilizes joint alignment. These deformities are irreversible and progress over time with continuing inflammation. Microscopically, the hallmark changes include synovial lining hyperplasia, fibrin deposition, lymphoplasmacytic infiltration, and formation of rheumatoid nodules composed of central fibrinoid necrosis surrounded by palisading histiocytes. Immune complex deposition plays a central role in propagating inflammation, complement activation, and neutrophil recruitment. The presence of high molecular weight immune complexes in circulation, as noted in the case, supports ongoing immune-mediated pathology characteristic of rheumatoid arthritis rather than metabolic or infectious arthropathies. Pathogenesis involves loss of tolerance to self-antigens, especially citrullinated proteins, leading to autoantibody formation (RF, anti-CCP) and systemic immune activation. Cytokines such as TNF-alpha, IL-1, and IL-6 drive synovial proliferation, osteoclast activation, and progressive joint destruction. These mechanisms explain both pain and deformity as late manifestations of chronic immune-driven joint damage continued over many years. Long-term complications of rheumatoid arthritis include severe disability, contractures, secondary degenerative changes, amyloidosis, and systemic manifestations such as pulmonary fibrosis or vasculitis. The chronicity and severity of deformities observed in this case suggest advanced disease stage. Importantly, the combination of long duration of symptoms, small-joint involvement, ulnar deviation deformities, and circulating immune complexes is highly characteristic of rheumatoid arthritis and not consistent with other inflammatory or metabolic joint diseases.