AIDS AND REACTIVE ARTHRITIS.
An aggressive form of Reiter's syndrome may develop in patients with AIDS (seeChapter 417). Early reports suggested that Reiter's syndrome developed in many HIV-infected individuals after profound immunosuppression. Although it has been suggested that AIDS patients are at increased risk of reactive arthritis, a number of prospective analyses of HIV-infected populations failed to reveal an increased incidence or prevalence of Reiter's syndrome when compared with that observed in an HIV-negative population matched for other risk factors. It seems clear that HIV infection alters the clinical expression of Reiter's syndrome. The vast majority of AIDS patients with Reiter's syndrome are HLA-B27+ and have incomplete symptoms and signs of Reiter's syndrome. The arthritis evolves in two main patterns: (1) an additive, asymmetrical polyarthritis or (2) an intermittent oligoarthritis that most commonly affects the lower extremities. Enthesitis, fasciitis, conjunctivitis, and urethritis are early and prominent symptoms. Although sacroiliitis does occur, HIV-associated reactive arthritis is rarely associated with axial disease or uveitis. HIV-associated disease also differs from classic Reiter's syndrome in the severity and chronicity of disease, prominent enthesitis, and a poor response to non-steroidal anti-inflammatory drugs (NSAIDs).
PSORIATIC ARTHRITIS.
Psoriatic arthritis develops in 5 to 7% of patients with cutaneous psoriasis. Although most cases arise in patients with established, active cutaneous disease, other patients (especially children) have articular disease that antedates the development of psoriasis. Although the extent of psoriatic skin disease correlates poorly with the onset of arthritis, the risk of psoriatic arthritis increases with a family history of spondyloarthropathy or extensive nail pitting. The age of onset is usually between 30 and 55 years, and psoriatic arthritis has been shown to affect men and women equally. Psoriatic spondylitis, however, has a male-female ratio of 2.3:1.
The genetic associations with psoriatic arthritis are heterogeneous. Cutaneous psoriasis is associated with HLA-B13, HLA-Bw17, and HLA-Cw6. By contrast, HLA-B39 and HLA-B27 have been associated with sacroiliitis and axial involvement, and HLA-Cw6, HLA-Bw38, HLA-DR4, and HLA-DR7 have been associated with peripheral arthropathy. No etiologic agent or reactive process has been proved, although stress, trauma, the expression of heat shock proteins, and antecedent infection withStreptococcusorStaphylococcushave been suggested to play a role. The histopathology of psoriatic synovitis is similar to that seen in other inflammatory arthritides, with a notable lack of intrasynovial immunoglobulin and rheumatoid factor production and a greater propensity for fibrous ankylosis, osseous resorption, and heterotopic bone formation. Like HIV-associated Reiter's syndrome, disease severity in psoriatic arthritis is enhanced by coexistent HIV infection.
Psoriatic arthritis has an insidious onset and a progressive course. Five major variants of psoriatic arthritis have been described. These variants are not mutually exclusive, and patients
may progress from one form to another. The 1st form is an asymmetrical oligoarthritis that is observed in 30 to 50% of patients and may involve both large and small joints. Dactylitis, or "sausage digits," may be seen in the fingers or toes. In this group, cutaneous features may be minimal and are often missed. The 2nd variant involves the distal interphalangeal joint and is seen in 10 to 15% of patients. It is strongly associated with nail changes of pitting, onycholysis, subungual hyperkeratosis, transverse ridging, and/or leukonychia(Fig. 287-7). Periungual erythema may reflect the extent of nail and joint disease. The 3rd variant is a rheumatoid arthritis-like symmetrical polyarthritis that is seen in 15 to 30% of patients who lack serum rheumatoid factor and rheumatoid nodules. The 4th variant is psoriatic spondylitis, which is seen in approximately 20% of psoriatic arthritis patients, 50% of whom are HLA-B27+. Finally, arthritis mutilans is seen in 5% of patients and is manifested as a destructive, erosive, polyarticular arthritis affecting the hands, feet, and spine. It often leads to progressive deformity and substantial disability.
Extra-articular features and laboratory findings are similar to those seen in Reiter's syndrome, although keratoconjunctivitis sicca, and mitral valve prolapse are less common. Hyperuricemia may be found and often correlates with the severity of cutaneous psoriasis.
Radiographic changes in psoriatic arthritis are similar to those seen in Reiter's syndrome and include soft tissue swelling ("sausage digits"), erosions, periostitis, asymmetrical sacroiliitis, and Reiter's-like spondylitis with asymmetrical non-marginal bulky syndesmophytes (s