REACTIVE ARTHRITIS
Arup Kumar Kundu *
Associate Professor, Department of Medicine, In-charge, Division of Rheumatology, Nil Ratan Sircar Medical College, Kolkata, West Bengal. *
Reactive arthritis (ReA) is a joint inflammation (sterile synovitis) developing soon after or during an infection elsewhere in the body, where the organism cannot be isolated or cultured from the affected joint. In the year 1916, Hans Reiter, the physician leader of the Nazi party in Germany during World War II, described a triad of urethritis, conjunctivitis and arthritis in a young German officer who had a bout of bloody dysentery. ReA is a host-microbial interaction in a genetically susceptible individual which induce humoral and cellular immune responses to result in aseptic asymmetrical oligoarthritis. Seventy percent patients recover fully within 6 months but may have a relapse. Severe destructive disease, like rheumatoid arthritis, as sequelae of reactive arthritis is extremely rare.

Seronegative spondyloarthropathy (SpA) is applied to a group of inflammatory joint disorders, distinct from rheumatoid arthritis, that are thought to share a similar pathogenesis as well as cardinal clinical features. They show considerable overlap and a striking genetic association with class I major histocompatibility antigen HLA-B27. Seronegative SpA encompasses diseases like ankylosing spondylitis, reactive arthritis including Reiter's syndrome, psoriatic arthropathy, arthritis associated with inflammatory bowel disease and undifferentiated. Approximately 1-2% of patients develops seronegative SpA after an acute attack of dysentery, or a sexually-acquired infection (non-specific urethritis in male and non-specific cervicitis in female). Due to the wide variation in clinical severity, true incidence of ReA is difficult to assess. Reactive arthritis typically follows a self-limited course, with resolution of symptoms usually by 3-12 months, even in patients who are acutely incapacitated. However, the condition has a high tendency to recur, particularly with ocular and urogenital inflammation. Individuals who are HLA-B27 positive have a higher frequency of recurrence. A new infection/other stress factor could cause a reactivation of the disease.

ReA has been divided into four syndromes: (a) peripheral arthritis syndrome (b) enthesopathic syndrome (c) pelvi-axial syndrome and (d) extramuscular skeletal syndrome.

Mucocutaneous lesions are not uncommon. Three classical lesions commonly encountered are: Keratoderma blenorrhagica, circinate balanitis and nail dystrophy. Ocular lesions include conjunctivitis, uveitis, keratitis and episcleritis. - Few of the uncommon features include cardiac abnormalities (aortitis, aortic regurgitation, conduction defects, pleuro-pericarditis), peripheral neuropathy (ulnar neuritis, foot drop), and CNS disease (seizures, meningoencephalitis). Painless oral ulcers or shiny patches in the palate, tongue, and mucosa of the cheeks and lips have been described. Mild to moderate proteinuria, microhaematuria, and aseptic pyuria are seen in few of the patients. Erythema nodosum is not commonly encountered with ReA. In severe chronic cases, amyloid deposits and immunoglobulin A (IgA) nephropathy have been reported.

There is no definite cure for ReA and the management is mainly symptomatic and supportive. The treatment of ReA is modified according to the severity of symptoms. In symptomatic treatment, in the acute phase, NSAIDs form the foundation of therapy, and they should be used on a regular basis judiciously to achieve maximum anti-inflammatory effect. The current concepts on the pathogenesis of reactive arthritis indicate that an infectious agent is the trigger of the disease, but antibiotic treatment does not change the course of the disease, even when a micro-organism is isolated. To diminish the spread of infection, antibiotics like ciprofloxacin, co-trimoxazole and tetracycline have been tried in the early phase of illness. Recently, lymecycline (tetracycline-derivative) showed a reduction in the duration of acute Chlamydia-associated, but not enteric-related, ReA when administered for 3 months. No evidence indicates that antibiotic therapy benefits enteric-related ReA or chronic ReA of any aetiology. It is very difficult to treat chronic or recurrent ReA because with time patients get less benefit from NSAIDs, and corticosteroids are not indicated in those settings because of their less well defined therapeutic effects. Comprehensive management includes counseling of patients to avoid sexually transmitted diseases, and enteropathogens, as well as to treat the sexual partner, to use proper physical therapy, vocational counseling along with continued surveillance for longterm complications.
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