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Rheumatology, Volume 39, Issue 2, February 2000, Pages 117–119, https://doi.org/10.1093/rheumatology/39.2.117
01 February 2000
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A. Toivanen, Managing reactive arthritis, Rheumatology, Volume 39, Issue 2, February 2000, Pages 117–119, https://doi.org/10.1093/rheumatology/39.2.117
Reactive arthritis (ReA) is an infectious disease. A healthy but genetically predisposed individual develops it after a suitable triggering infection. Most commonly the initial infection has affected the digestive or the urogenital tract and the terms enteroarthritis or uroarthritis are used, respectively. However, the list of microbes able to trigger ReA is long, and the primary infection may also affect other organs . In spite of intensive research, the pathogenetical process is not yet understood. However, during the period from contracting the initial infection, an incubation time, the primary illness and the following interval period before onset of ReA critical immune reactions are thought to take place. The fact that several quite different microbes lead to a similar clinical entity demonstrates that the classical Koch's postulates do not apply in this instance. As always, when the pathogenesis of a disease is not understood, there exists no definite curative treatment. Luckily enough, the natural prognosis of ReA is rather good. Most patients recover within a few weeks or months, even if the clinical picture is initially severe, and usually no destructive changes take place in the joints. However, there is a tendency of recurrences, and arthralgias, joint swellings, enthesopathies or other manifestations may occur later. In some cases, sacroiliitis or even ankylosing spondylitis may develop, mostly in a mild form.
In the management of ReA some specific aspects have to be kept in mind. First, the disease most commonly affects previously healthy, young adults. Second, the severity of the disease varies from slight arthralgias to invalidating conditions, and the management has to be tailored accordingly. In most instances, the patient is afraid of having a chronic progressively destructive disease. Proper information is the cornerstone of the treatment, to relieve unnecessary anxiety and to have the patient to comply with suggested therapies. The physician should inform the patient about the good prognosis, but also about possible later manifestations. It should further be stressed that new urogenital or enteric infections may trigger relapses, and the patient should avoid them, if possible. A third aspect of importance regarding the management is that the patient seeks medical aid because of the joint inflammation. At that time the triggering infection has already passed and is demonstrable only by serology. Isolation of the causative microbe is only rarely possible. Actually, the signs of the primary, triggering infection may have been quite mild or even passed unnoticed.
The general management depends on the clinical situation. Quite often the general condition is good, but sometimes the patient is severely ill. Rest is advisable and as pointed out below, proper analgesia must be taken care of. Splinting of the affected joints is very rarely indicated, except in severe forms to assure sleep. The patient should also be advised not to use the joints too vigorously even within a few weeks of recovery, as non‐specific factors and minor traumas may lead to a recurrence. When many joints are affected, muscle wasting may occur unless physiotherapy is given.
Non‐steroidal anti‐inflammatory drugs (NSAIDs) form the basis of pharmacological therapy. They should be used in proper dosage and not be stopped too early. Young persons are often reluctant to take ‘pain killers’. It should be explained that not only the analgesia but the anti‐inflammatory effect is wanted, and especially the latter requires sufficient dosage for sufficient time. During recovery, insufficient analgesia may lead to limited use of the joints and actually prolong the rehabilitation. Later on, the patient should not unnecessarily use these drugs. No individual NSAID is definitely superior, but the one with good clinical effect and devoid of side‐effects should be chosen. Patients respond to these drugs very individually. In the case of enthesopathies, locally applied NSAID ointments may be useful.
Corticosteroids are a potent group of drugs to be used in ReA. Intra‐articular application results most often in prompt relief of the joint inflammation. This is of great value for a young, active and employed person. The injection can be repeated a few times, if necessary. In Finland, intra‐articular steroids are widely used with good results. However, this treatment is not applicable if many joints are involved. The risk of infectious complications and true septic arthritis as a differential diagnostic possibility must be kept in mind. In severe cases and when several joints are involved, peroral corticosteroids are useful. They should be started in high dosage, e.g. prednisolone 30–40 mg/day, and tapered rapidly down according to relief of symptoms. The drug should then be continued for a brief period in low dose, and stopped gradually. Corticosteroids are, in a similar manner, also useful in the treatment of acute relapses. If the patient later suffers from chronic arthralgias, corticosteroids should be avoided. In these instances they have poor therapeutic effect and cause more harm than benefit. Corticosteroid ointments may be used for lesions of mucous membranes and skin, and in the case of conjunctivitis local corticosteroids are an obvious choice. In this context it is worthwhile stressing the necessity of proper ophthalmologic investigation if the patient has any degree of eye discomfort, as untreated anterior uveitis may lead to irreversible damage of the eyesight. In aggressive cases of uveitis, systemic corticosteroid treatment is indicated.
The value of disease‐modifying anti‐rheumatic agents or immunosuppressive drugs has not been established. No proper studies are available. However, if the joint inflammations tend to go on, or if there is development towards ankylosing spondylitis, they should be considered. There are some solitary reports of using methotrexate. If there is any evidence that an inflammatory bowel disease such as ulcerative colitis is involved, sulphasalazine is an obvious agent to try. The observations reported by the group of Mielants and Veys  indicate that ileocolonoscopy should be performed for patients with ReA more often than is customary now.
There has been a burning question whether to use antibiotics in ReA. Several facts speak in favour of them. The disease is certainly triggered by an infection, and even late in its course components of the triggering microbes can be detected in the inflamed joints. Persistence and maturation of the antibody responses indicate that the microbe or its components are hiding somewhere in the organism, maintaining an immune stimulation . Regarding Chlamydia, bacterial DNA and RNA have been found by several groups in the inflamed joint [4, 5]. It seems that most general practitioners routinely give a course of antibiotics to patients with ReA. However, there is no solid evidence to support this. Antibiotic treatment in ReA has recently been discussed by Sieper and Braun .
Antibiotics have been proven to be useful in two instances. In rheumatic fever, also a form of ReA, they are used for primary or secondary prevention. However, they do not have an actual role in the treatment of the rheumatic fever itself. Also, in borreliosis the value of antibiotic treatment is definitely established. Early eradication of Borreliae in the initial stages of infection certainly prevents later development of Lyme disease. Yet, in about 10% of patients with borreliosis, antibiotics fail to eradicate the symptoms .
The evidence regarding the effect of antibiotics in enteroarthritis and uroarthritis is somewhat different. There are several reports in which ReA triggered by an enteric infection has been treated with short‐term antibiotics, and the authors definitely agree that this has no effect on the development of ReA or its outcome . Long‐term treatment has been applied, and although some differences exist, the overall conclusion is again that there is no benefit. Recently two systematic, double‐blind, randomized, placebo‐controlled studies on the effect of a 3‐month course of ciprofloxacin on ReA have been carried out. In both instances, no beneficial effect due to the antibiotic could be demonstrated [8, 9].
These observations are also supported by data from an experimental model of ReA induced by intravenous application of Yersinia enterocolitica O:8 into rats. If ciprofloxacin was given instantly after intravenous inoculation of the microbe or when the arthritis was developing, a definite effect was seen, but later it had no effect whatsoever. Actually, some rats turned out to become late carriers of Yersinia, secreting bacteria into the stool [10, 11].
For uroarthritis, the picture is not quite as clear. An interesting study by Bardin and his coworkers in an Inuit Eskimo society demonstrated that proper and prompt treatment of new genitourinary tract infections dramatically reduced relapses of ReA . Also, here it must be stressed that the treatment must rather be considered secondary prophylaxis. In an earlier study Lauhio et al. noticed that lymecycline had a slight beneficial effect in patients with uroarthritis. This possibility is intriguing, as Chlamydiae might persist in the urogenital tract and their eradication by a long treatment could stop the harmful immune response. Also, the observations on long‐term ciprofloxacin indicate that perhaps in Chlamydia‐triggered ReA some beneficial effect could be obtained. However, so far the numbers of such patients have always been too small to permit any firm conclusion . At present, there is a large multinational study on the effect of azithromycin in ReA being undertaken under the auspices of EULAR, and we hope that within a couple of years evidence‐based recommendations can be given.
Regarding Chlamydiae, there is an additional point. The bacteria have a tendency to hide in the epithelium of the genitourinary tract, causing no symptoms. In order to prevent further spread of the infection or an asymptomatic inflammation, eradication of the Chlamydiae with a course of antibiotics is probably advisable. However, this should not be confused with a treatment effort for the ReA.
Altogether, clinical and experimental studies have clearly demonstrated that early and vigorous treatment of a triggering infection before the development of ReA is effective. In real life this goal can almost never be reached. The patient seeks help for joint inflammation, the initial infection has already passed, and antibiotics are no longer effective. At this stage no definitely curative treatment is available, but with individually tailored good management the patient can be helped. Even if the disease takes on a relapsing or chronic course, no serious deformations are to be feared. With this knowledge the patient may tolerate the discomfort and learn to live with his or her disease rather well.
Toivanen A, Toivanen P. Aetiopathogenesis of reactive arthritis.
Mielants H, Veys EM. The gut and reactive arthritis.
Toivanen A, Granfors K, Lahesmaa‐Rantala R et al. Pathogenesis of Yersinia‐triggered reactive arthritis: immunological, microbiological and clinical aspects.
Gérard HC, Branigan PJ, Schumacher HR Jr, Hudson AP. Synovial Chlamydia trachomatis in patients with reactive arthritis/Reiter's syndrome are viable but show aberrant gene expression.
Hughes RA, Keat AC. Reiter's syndrome and reactive arthritis: A current view.
Semin Arthritis Rheum
Sieper J, Braun J. Treatment of reactive arthritis with antibiotics.
Br J Rheumatol
Gross DM, Forsthuber T, Tary‐Lehmann M et al. Identification of LFA‐1 as a candidate autoantigen in treatment‐resistant Lyme arthritis.
Sieper J, Fendler C, Laitko S et al. No benefit of long‐term ciprofloxacin treatment in patients with reactive arthritis and undifferentiated oligoarthritis.
Yli‐Kerttula T, Luukkainen R, Yli‐Kerttula U et al. Effect of a three‐month course of ciprofloxacin on reactive arthritis.
Scand J Immunol
Zhang Y, Gripenberg‐Lerche C, Söderström K‐O et al. Antibiotic prophylaxis and treatment of reactive arthritis. Lessons from an animal model.
Zhang Y, Toivanen A, Toivanen P. Experimental Yersinia‐triggered reactive arthritis; effect of a 3‐week course with ciprofloxacin.
Br J Rheumatol
Bardin T, Enel C, Cornelis F et al. Antibiotic treatment of venereal disease and Reiter's syndrome in a Greenland population.
Lauhio A, Leirisalo‐Repo M, Lähdevirta J et al. Double‐blind, placebo‐controlled study of three‐month treatment with lymecycline in reactive arthritis, with special reference to Chlamydia arthritis.
© British Society for Rheumatology
© British Society for Rheumatology
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Treatment for reactive arthritis
using painkillers such as ibuprofen to relieve joint pain and stiffness. managing any severe or ongoing arthritis, usually using medications such as steroids or disease-modifying anti-rheumatic drugs (DMARDs)
Reactive arthritis is usually temporary, but treatment can help to relieve your symptoms and clear any underlying infection. Most people will make a full recovery within a year, but a small number of people experience long-term joint problems.
Reactive arthritis isn't common. For most people, signs and symptoms come and go, eventually disappearing within 12 months.
Chlamydia is the most common cause of reactive arthritis in the United States and is usually acquired through sexual contact. Salmonella, Shigella, Yersinia, and Campylobacter may cause a gastrointestinal infection that can trigger reactive arthritis.
The longer you're exposed to stress, the more destructive the inflammation can become. In a PLoS One study, people with RA identified stress as a trigger for disease flare-ups. Arthritis symptoms contribute to stress, especially when they're unrelenting.
Treat the disease that's causing your inflammation. Relieve pain with medication and by changing your activities. Maintain joint movement, muscle strength, and overall function with physical therapy and exercise. Lessen stress on your joints by using braces, splints, or canes as needed.
HLA-B27. This blood test looks for the presence of HLA-B27, a genetic risk factor for reactive arthritis. Having this marker is consistent with having reactive arthritis, but it is not definitive—people who test negative can still have reactive arthritis, and not everyone who tests positive has the condition.
Radiographs are a reliable means of diagnosing reactive arthritis, particularly if the typical clinical features are present. In the early stage, radiographs are normal. The synovial joint, symphyses, and entheses are affected. An asymmetrical distribution with predominant involvement of lower extremities is seen.
pain, tenderness and swelling in your joints. pain and tenderness in some tendons, especially at the heels. pain in your lower back and buttocks. sausage-like swelling of your fingers and toes.
It's a possible symptom of reactive arthritis. According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases , about half of all people with reactive arthritis develop pink eye. While treatable, conjunctivitis can return.
X-rays can reveal the status of the joints, including signs of reactive arthritis such as inflammation of the sacroiliac joints in the lower back. They can also help rule out other causes of joint pain. X-rays often do not pick up abnormalities until later in the course of reactive arthritis.
It may be caused by Chlamydia trachomatis, salmonella, or another infection. The condition may cause arthritis symptoms, such as joint pain and inflammation. It may also cause symptoms in the urinary tract and eyes.
The purpose of this study is to determine the effectiveness of long-term combination antibiotic therapy in treating people with chronic reactive arthritis. The study will use two different combinations of common antibiotics: doxycycline paired with rifampin and azithromycin paired with rifampin.
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