Reiter syndrome

It is a disease framed within reactive arthritis , which, in turn, is classified within spondyloarthropathies. Today, however, the term Reiter’s syndrome has fallen into disuse, and it is more correct to refer to it simply as reactive arthritis.

It is a non-suppurative (sterile) joint inflammation, which affects one or a few joints (mono or oligoarticular) and which appears after an infection (not always demonstrable) gastrointestinal (more frequent in Europe, Africa and Asia), or genitourinary (especially , in the United States and Great Britain), with a latency period of less than one month; It occurs in 1-3% of people who have suffered from such infections. However, it cannot be called infectious arthritis, as it is not possible to isolate germs in the affected joints.

Reiter’s syndrome has been classically defined as the clinical association of arthritis, urethritis, and conjunctivitis .

It has a large hereditary burden, as it is related to the histocompatibility antigen (HLA) B27 gene in 60-80% of cases; There is also a certain family predisposition to suffer from this disease.

It is more frequent in young adults and, when it is of genitourinary origin, it has a slight predominance in males.

Why is it produced?

We have already talked about the genetic association that this disease has.

Regarding the germs that cause the conditions that are later complicated by reactive arthritis, the most frequent are the bacteria Shigella flexneri, Campylobacter jejuni, and various species of Salmonella and Yersinia, in the case of digestive infections. In the genitourinary, the main ones are Chlamydia trachomatis and Ureaplasma urealyticum, also bacteria.

As we have already indicated, the disease generally manifests itself some time after suffering from an infection, which is transmitted either orally or sexually, depending on whether it is digestive or genitourinary, respectively.

The exact mechanism of production of reactive arthritis is not known, although it is quite probable that these are the consequence of autoimmune reactions (that is, of the patient’s immune system against its own antigens) against antigens of the joints that are similar to those of the disease. bacterial. HLA B27 is thought to play a role in the presentation of these antigens to T lymphocytes.

This disease is, especially, frequent in patients with AIDS , especially the form of urogenital origin.

Symptoms of Reiter’s syndrome

General symptoms such as malaise, fever , fatigue, and weight loss are common.

In most cases there is an antecedent infection (generally manifested in the form of diarrhea or urogenital symptoms, depending on its origin), although in a significant minority this is not demonstrable; It should be noted that the intensity of the previous infection does not necessarily agree with the intensity of the arthritic symptoms.

What dominates the picture is usually joint inolvement (arthritis). This normally begins abruptly and intensely, and in one or a few joints, asymmetrically, especially in the lower limbs (knees, ankles and feet).

Severe pain and joint effusions frequently appear (especially in the knee). Sometimes the so-called “sausage finger” (dactylitis), which is diffuse swelling of a toe or hand, can also be observed; this last characteristic is shared by this disease with psoriatic arthritis. Tendinitis, or inflammation of a tendon, can produce talalgia (heel pain), by involvement of the Achilles tendon.

The presence of low back pain can be due to arthritis of the joints of the spine, sacroiliitis (inflammation of the joints of the sacral and iliac bones), inflammation of the areas of insertion of muscles or spasms of these.

There are also extra-articular manifestations, which are mainly ocular, urogenital, and skin and mucous membranes.

Regarding ocular alterations, a mild and transitory conjunctivitis frequently appears, which may even go unnoticed; more rarely, severe anterior uveitis occurs, occasionally causing blindness.

Urogenital lesions can manifest throughout the disease, that is, during the triggering infectious phase or during the reactive phase (the same occurs with diarrhea). These consist mainly of urethritis and, in men, prostatitis , while in women, cystitis , cervicitis, and salpingitis.

Manifestations on the skin and mucous membranes are frequent, highlighting ulcers of the oral cavity, which are usually asymptomatic; Nail alterations may also appear, with hyperkeratosis (similar to what occurs in some form of psoriasis ). The so-called blennorrhagic keratoderma is characteristic, which consists of accumulations of vesicles on the skin with hyperkeratosis, which evolve to crusts and then disappear, and which is especially frequent on the palms of the hands and the soles of the feet. Blennorrhagic keratoderma is more serious in AIDS patients. The balanitis circinada is the appearance on the glans of vesicles that rupture, resulting erosive lesions and painless.

Very infrequently it occurs in this disease affection of the heart, the nervous system or the lungs.

In most patients (60%), the disease becomes chronic or has recurrences, mainly at the cost of episodes of joint symptoms; these symptoms often force the patient to change or abandon their job.

The evolution of the disease is worse in patients who test positive for HLA B27; However, the possibility of a lower tendency to chronicity has been considered in cases triggered by an infection by the Yersinia bacteria.

How is it diagnosed?

The diagnosis of this disease is fundamentally clinical, with the clinical history and physical examination being very important, which will reveal a joint picture compatible with the one described, associated with some other of the typical manifestations already mentioned.

Regarding laboratory data, during the inflammatory phases the erythrocyte sedimentation rate and the acute phase reactants are elevated in the blood analysis. In some cases there may be anemia.

When joint involvement begins, only the findings of the serological tests (existence of certain antibodies) remain as identifying data (and not in all cases) of the triggering infection. If the synovial fluid of the affected joints is analyzed, it shows nonspecific inflammatory changes.

In 60-80% of cases it occurs for HLA B27.

Radiologically, alterations do not usually appear until the advanced stages of the disease, then joint anomalies are found, such as erosions, reduction of joint space …

The main disease to take into account when making the differential diagnosis is psoriatic arthritis, and if there is a urogenital origin, gonorrhea should also be considered. In some cases it is necessary to rule out ankylosing spondylitis.

Treatment of Reiter’s syndrome

There is currently no specific curative treatment for this disease, achieving control of joint manifestations with the use of non-steroidal anti-inflammatory drugs (NSAIDs), mainly indomethacin.

In severe or refractory forms, phenylbutazone (another NSAID) or immunosuppressants, such as methotrexate, azathioprine, or sulfasalazine, can be used.

Corticosteroids are not used systemically, but only intralesionally, thus being effective, for example, for the control of tendinitis or uveitis.

Antibiotics are only useful in cases where the triggering infection is the Chlamydia bacteria (the appropriate antibiotic is then a tetracycline).

Complications are generally treated symptomatically.

The tranquility and rest of the patient are very important, and he must be informed of the most probable course of his disease.

Physical therapy and continuous monitoring are also appropriate.