Reiter’s syndrome is a rheumatic disease characterized by a combined lesion of the urogenital tract (urethritis and prostatitis), joints (mono– or polyarthritis) and the eye mucosa (conjunctivitis), developing sequentially or simultaneously. Reiter’s syndrome is based on an autoimmune process caused by an intestinal or genitourinary infection. Diagnostic criteria are the connection with the transferred infection, laboratory detection of the pathogen and characteristic blood changes, clinical symptom complex. Treatment includes antibiotic therapy for infection and anti-inflammatory therapy for arthritis. Reiter’s syndrome tends to relapse and chronicle the process.
Meaning
In 80% of cases, Reiter’s disease attacks young men from 20 to 40 years old, less often – women and exceptionally rarely – children. The leading etiological agent of Reiter’s syndrome is chlamydia, a microorganism capable of long–term parasitization in host cells in the form of cytoplasmic inclusions. In addition, Reiter’s syndrome can develop after suffering colitis caused by shigella, yersinia, salmonella, and also be provoked by ureaplasma infection. It is assumed that these pathogens, due to their antigenic structure, cause certain immunological reactions in genetically inclined individuals.
During Reiter’s syndrome, there are two stages: infectious, characterized by the presence of the pathogen in the genitourinary or intestinal tract, and immunopathological, accompanied by an immunocomplex reaction with damage to the conjunctiva and synovial membrane of the joints.
Classification
Taking into account the etiofactor, sporadic and epidemic (postenterocolitic) forms of the disease differ. Sporadic form, or Reiter’s disease, develops after a urogenital infection; epidemic – Reiter’s syndrome – after enterocolitis of various etiological nature (dysentery, yersiniosis, salmonella, undifferentiated).
The course of the disease or Reiter’s syndrome can be acute (up to 6 months), prolonged (up to a year) or chronic (longer than 1 year).
Symptoms
For Reiter’s disease (syndrome), lesions of the urogenital tract, eyes, articular tissues, mucous membranes and skin are specific. In Reiter’s disease, urethritis is the first to manifest, accompanied by dysuric disorders, scanty mucous discharge, discomfort and hyperemia in the area of the external urethra. In an asymptomatic clinic, the presence of inflammation is determined based on an increase in the number of leukocytes in the smear. Following urethritis in Reiter’s syndrome, ocular symptoms develop, more often in the form of conjunctivitis, less often – iritis, uveitis, iridocyclitis, retinitis, keratitis, retrobulbar neuritis. The phenomena of conjunctivitis may be of little duration and weakly expressed, unnoticeable to the patient.
The defining sign of Reiter’s syndrome is reactive arthritis, which debuts 1-1.5 months after urogenital infection. For Reiter’s syndrome, asymmetric involvement of the joints of the legs is typical – interphalangeal, metatarsophalangeal, ankle, knee. Arthralgias are more pronounced in the morning and at night, the skin in the joint area is hyperemic, an effusion forms in the joint cavity.
Reiter’s syndrome is characterized by a sequential ladder (from proximal to distal) involvement of the joints for several days. With urogenic arthritis, edema develops, sausage-like defiguration of the fingers; the skin above them acquires a bluish-purple color. With Reiter’s disease, tendinitis, calcaneal bursitis, heel spurs, sacroiliac joint damage – sacroiliitis can develop.
Mucous membranes and skin in Reiter’s syndrome are affected in 30-50% of patients. Ulcerative changes of the oral mucosa (glossitis, stomatitis) and penis (balanitis, balanoposthitis) are characteristic. Red papules, erythematous spots, keratoderma foci appear on the skin – areas of hyperemia of the skin with hyperkeratosis, peeling and cracks mainly on the palms and feet. With Reiter’s syndrome, lymphadenopathy, myocarditis, myocardiodystrophy, focal pneumonia, pleurisy, polyneuritis, nephritis and amyloidosis of the kidneys may develop.
In the complicated form of Reiter’s syndrome, joint dysfunctions, visual disorders, erectile disorders, infertility develop. In the late phase of Reiter’s disease, the kidneys, aorta, and heart can be affected.
Diagnostics
During the diagnosis, a patient with suspected Reiter syndrome may be referred for consultation by a rheumatologist, venereologist, urologist, ophthalmologist, gynecologist. General clinical tests for Reiter’s syndrome reveal hypochromic anemia, ESR growth and leukocytosis of the blood. In urine samples (three-cup, according to Addis-Kakovsky and Nechiporenko), leukocyturia is determined. Microscopy of prostatic secretions shows an increase in white blood cells (>10) in the field of vision and a decrease in the number of lecithin bodies. Changes in blood biochemistry in Reiter’s syndrome are characterized by an increase in α2- and β-globulins, fibrin, sialic acids, seromucoid; the presence of C-reactive protein, a negative test for RF.
Cytological studies of scrapings of the urethra, cervix, conjunctiva, synovial exudate, sperm, prostate secretions with Romanovsky-Giemse staining reveals chlamydia in the form of intracellular cytoplasmic inclusions. In the diagnosis of Reiter’s syndrome, the method of detecting the DNA of the pathogen in biomaterial (PCR) is widely used. In the blood of chlamydia , etc . antibodies are detected by serological reactions – ELISA, RSC, RNGA. A specific sign of Reiter’s syndrome is the carrier of the HLA 27 antigen.
In the analysis of synovial fluid taken by puncture of the joint, inflammatory changes are determined – looseness of the mucin clot, leukocytosis (10-50 × 109 / l), neutrophilosis over 70%, the presence of cytophagocytic macrophages, chlamydial antibodies and antigens, increased complement activity, RF is not detected. Radiographic examination of the joints reveals signs of asymmetric paraarticular osteoporosis, reduction in the size of articular cracks, erosive destruction of the bones of the feet, the presence of heel spurs and spurs of the metacarpal bones, vertebral bodies, in a third of patients – unilateral sacroiliitis.
When diagnosing Reiter’s syndrome, anamnestic information is taken into account (the connection of the disease with urogenital or intestinal infection); the presence of symptoms of conjunctivitis, reactive arthritis, skin manifestations; laboratory confirmation of the pathogen in epithelial scrapings.
Treatment
The tactics of treatment provides for antibiotic therapy (for both sexual partners), immunocorrection, anti-inflammatory course and symptomatic therapy. Antibiotic therapy includes 2-3 consecutive courses (2-3 weeks each) with drugs from various pharmacological groups: tetracyclines (doxycycline), fluoroquinolones (lomefloxacin, ofloxacin, ciprofloxacin) and macrolides (clarithromycin, azithromycin, erythromycin, etc.). With chlamydia infection, preference is given to doxycycline. Simultaneously with antibiotic therapy, antifungal drugs, multivitamins, hepatoprotectors, proteolytic enzymes (pancreatin, trypsin, chymotrypsin) are prescribed.
Immunocorrecting therapy for Reiter’s syndrome includes the use of immunomodulators (thymus preparations), adaptogens, interferon inducers (sodium oxodydroacridinyl acetate, acridonacetic acid in combination with N-methylglucamine), as well as intravenous and intravenous quantum therapy. With severe arthralgic attacks and high activity of inflammation, detoxification and antihistamine therapy is carried out. In order to detoxify Reiter’s disease, extracorporeal hemocorrection is indicated – plasmapheresis, cascade plasma filtration and cryoaferesis.
NSAIDs (rofecoxib, celecoxib, nimesulide, meloxicam), glucocorticosteroids (betamethasone, prednisolone), basic drugs (sulfasalazine, methotrexate) are used to suppress intraarticular inflammation in Reiter’s syndrome. In the presence of intra-articular exudate, a therapeutic puncture of the joint is performed with the introduction of prolonged glucocorticoids (betamethasone, methylprednisolone). Locally applied compresses with a solution of dimethyl sulfoxide, painkillers and anti-inflammatory ointments.
The subsiding of the phenomena of acute arthritis in Reiter’s syndrome allows you to connect physiotherapy sessions of phonophoresis with proteolytic enzymes, glucocorticoids, chondroprotectors; UVI, diathermy, magnetotherapy, laser therapy, massage, mud therapy, hydrogen sulfide and radon baths. In combination with the therapy of Reiter’s syndrome proper, other extragenital foci of inflammation are treated.
Prognosis and prevention
The dynamics of the course is predominantly favorable. In most patients, after six months, the disease goes into persistent remission, which, however, does not exclude an exacerbation of Reiter’s disease many years later. In a quarter of patients, arthritis enters a chronic phase, leading to joint dysfunction, muscle atrophy, and the development of flat feet. The outcome of Reiter’s syndrome can be amyloidosis and other visceropathies.
Prevention includes prevention of intestinal and urogenital infections, timely etiotropic therapy of urethritis and enterocolitis.