The spondyloarthropathies comprise a diverse group of inflammatory arthritis conditions that share certain genetic predisposing factors and clinical features. The pathogenesis of spondyloarthropathies is still not well defined. Recent studies have provided insight into distinct pathogenetic mechanisms underlying ankylosing spondylitis and reactive arthritis that arise from a complex interplay between genetic factors (including HLA-B27) and environmental factors.2
The pathogenesis of Reiter's syndrome may involve molecular mimicry between bacterial fragments in synovial fluid and the HLA-B27 molecule. Most (70-80%) patients with Reiter's syndrome are positive for HLA-B27, as compared with only 6% of the general population. The arthritis may be perpetuated by the induction of cytotoxic T lymphocytes by microbial fragments in the joints, but these cytotoxic T lymphocytes have specificity for HLA-B27-positive cells. The presence of HLA-B27 may allow stronger or persistent microbial invasion.3
Reactive arthritis usually has a self-limited course of 3 to 12 months, but up to 50% of patients experience recurrent bouts of arthritis, and 15% to 30% of them develop chronic symptoms of the disease.4
Extra-articular manifestations such as ocular inflammation, enteritis, mucocutaneous lesions, urethritis, and (rarely) carditis provide essential support for a diagnosis of reactive arthritis. However, neurological complications are rare.5
There have been only a few case reports of polyneuropathy, cranial nerve palsy, or myelopathy in Reiter's syndrome.6,7
Whilst there were gastrointestinal symptoms in this case, stool examinations provided no laboratory evidence of preceding infection. There also was no preceding urethral discharge or notable infections. The patient visited our clinic at 7 months after the onset of the first symptoms. The high dose of steroids administered might have inhibited a systemic inflammatory reaction. According to a previous report, approximately only 60% of such cases have evidence of previous infection detected either by serology or by cultures from urogenital or stool samples.8
Nonsteroid anti-inflammatory drugs (NSAIDs) and sulfasalazine are effective treatments for reactive arthritis, and methotrexate can also be beneficial.9
Our patient did not respond to NSAIDs, but methotrexate and sulfasalazine relieved his neurological symptoms and arthralgia, making them stable during a 5-year follow-up.
The association between reactive arthritis and cervical myelopathy was not clear in this patient, but there were some features suggesting Reiter's syndrome as a cause of the myelitis. First, the gastrointestinal symptoms that appeared before the development of cervical myelopathy might have reflected a preceding infection that initiated an autoimmune reaction, which led to myelitis and systemic inflammation. Initial urinary tract infection and costochondral tenderness at the time of the first attack of myelitis might be indicative of Reiter's syndrome. Second, despite the application of steroid pulse therapy, recurrences of progressive myelopathy associated with systemic symptoms of the skin and joints, and the positivity for HLA-B27 suggest other causes of myelitis. Third, both neurological symptoms and the arthritis that was resistant to the steroid pulse therapy did not recur after sulfasalazine and methotrexate treatment.
In conclusion, Reiter's syndrome should be considered in the differential diagnosis of cases of progressive myelopathy with multiple arthritis, urethritis, and skin lesions.