Ankylosing spondylitis eye symptoms: How Does Ankylosing Spondylitis Affect Eyes and How Is It Treated?

How It Can Affect Your Eyes

Ankylosing spondylitis (AS) is a type of arthritis. It causes pain and stiffness, mainly in your spine. But it can also cause eye inflammation called uveitis. Left untreated, uveitis can harm your vision and, in some cases, lead to blindness.

What Is Uveitis?

Uveitis is a large group of inflammatory eye diseases. It gets its name from the fact that these diseases mostly strike the uvea, the middle part of your eye. But uveitis can show up almost anywhere inside the eye.

Doctors usually describe uveitis based on where you have it:

Anterior uveitis (also called iritis) happens in the front part of your eye. That includes the iris, the colored part. It’s the most common type of uveitis for people with AS. If it’s not treated, anterior uveitis can lead to cataracts, glaucoma, or a buildup of fluid called retinal edema.

Intermediate uveitis is in the vitreous. That’s the big, fluid-filled space in your eye attached to your retina, a layer of cells that sense light and send signals to your brain.


Posterior uveitis (also called choroiditis) attacks the back of your eye. It may affect your retina and your optic nerve, which connects your eye to your brain.

Panuveitis affects all parts of your eye. It’s the most severe type. It can cause blindness if it’s not treated.

Why People With AS Get It

About half of people with ankylosing spondylitis have uveitis at least once. It’s one of the most common complications of that form of arthritis.

Your eye doctor could actually be the first to figure out you have AS. That’s because the same inflammation that makes your back hurt can also cause inflammation in your eyes and other parts of your body.

Some experts think the inflammation starts in a place you might not think of: your gut.

It’s home to trillions of tiny organisms called microbes. They perform so many vital functions that you can’t live without them. One of their main jobs is to control your immune system. When the microbes get out of whack, your immune system does, too.

Uveitis may start when gut bacteria tell immune cells called T cells to attack your eyes. But that’s probably not the whole story. Many people with AS and anterior uveitis have a gene called HLA-B27. This gene makes eye inflammation much more likely.


Keep an eye out for:

These symptoms can come on quickly in one or both eyes. Sometimes uveitis is a one-time thing. In other cases, you may go years between flares. In still others, it can also be long-lasting and need ongoing treatment.


The goal of uveitis treatment is to ease inflammation fast. For anterior uveitis, doctors usually prescribe two types of eye drops:

  • Steroid drops to lower inflammation
  • Drops that widen your pupil to ease pain

For other types of uveitis, you may need steroid pills or shots around your eyes. Sometimes doctors implant a steroid capsule inside your eye.

Steroids can cause serious side effects, including eye diseases like glaucoma and cataracts. Usually, you won’t use steroids for more than 3 months. As you taper off them, your doctor may start you on another medicine.

Some experts think a change in gut bacteria can ease uveitis. You might try:

Probiotics. These are live, friendly bacteria. You find them in yogurt and other fermented foods. They’re in supplements, too.


Prebiotics. These plant fibers feed healthy bacteria in your gut and make them stronger. You can find them in from foods like bananas and onions.

Supplements for gut health like butyrate are another option. A diet that’s mostly plant-based could also help.

Talk with your doctor to find out which treatment might work best for you.

What to know about ankylosing spondylitis and eye health

Ankylosing spondylitis (AS) is a rare form of inflammatory systemic arthritis that mainly affects the back. Because AS is a systemic condition, inflammation associated with it can affect other areas, including the eyes.

As with other types of arthritis, there is no cure for AS. Treatment focuses on relieving the symptoms, slowing the progression of the condition, and preserving the quality of life.

A person with AS should be aware of how it can impact their eyes and speak with their doctor if they have any eye issues.

Below, learn about some common conditions that a person with AS may experience and some general tips for supporting eye health.

Anterior uveitis, also known as iritis, is inflammation of a part of the eye called the uvea, which is located toward the middle of the eye.

Anterior uveitis is one of four types of uveitis — and the most common. It occurs toward the front of the uvea and affects the iris, the colored tissue.

According to one 2017 study, as many as 40% of people with AS develop acute anterior uveitis.

The HLA-B27 gene plays a role in the development of AS, and the same gene is associated with uveitis.

Without treatment, anterior uveitis may lead to permanent damage and possibly blindness. But with early treatment, a person’s prognosis is generally good.


Anterior uveitis causes swelling or inflammation in the eye. As the Spondylitis Association of America note, anterior uveitis causes:

  • pain
  • redness
  • light sensitivity
  • issues with vision

The symptoms generally affect one eye at a time, and they can take a few hours to a few days to develop. An episode of uveitis can last for as long as 6 weeks.


Treatments can vary based on the severity of the condition. Anterior uveitis is commonly treated with corticosteroid eye drops and other drops to dilate the eye.

If drops do not work, the doctor may administer corticosteroid injections.

Treating the underlying AS with biologic drugs called tumor necrosis factor inhibitors can help prevent anterior uveitis.

Speak with a doctor about any symptoms of anterior uveitis. They may make a referral to an optometrist or ophthalmologist, who can rule out other possible conditions and administer treatment. If any symptoms do not improve, let the doctor know.

Glaucoma is actually a group of conditions that put pressure on the optic nerve. This can cause damage that leads to vision issues and potentially vision loss.

The Arthritis Foundation note that anyone with an inflammatory type of arthritis, such as AS, has an increased risk of glaucoma. Those who use corticosteroids also have a higher risk of these eye conditions.


A person typically does not have any symptoms in the early stages of glaucoma.

In later stages, the condition causes a slow loss of peripheral vision.

Without treatment, it can eventually cause blindness. Receiving treatment early can help prevent damage and preserve vision.


There are three main types of treatment for glaucoma:

  • Medications: These are often eye drops, and they can help reduce pressure in the eye and prevent damage to the optic nerve.
  • Laser treatment: Doctors typically use this to help drain fluid from the eye and relieve pressure.
  • Surgery: This can help reduce pressure by draining fluid from the eye, if eye drops or laser treatment are not effective.

A person with AS should tell their doctor about any changes in vision. While glaucoma treatment cannot restore lost vision, early treatment can help prevent the issue from getting worse.

Cataracts causes the lens of the eye to become cloudy as a result of inflammation and pressure.

People who have genetic variations linked with inflammatory conditions, such as AS, have a higher risk of developing cataracts. In addition, taking steroids to treat health conditions can increase the risk of developing this eye problem.


Symptoms may not appear in earlier stages of cataracts. As the issue progresses, the symptoms may include:

  • cloudy or blurry vision
  • double vision
  • low night vision
  • colors appearing faded
  • sensitivity to light, from the sun, lamps, or headlights
  • lights seeming to have halos
  • a need for frequent changes in glasses prescriptions

Over time, cataracts can lead to vision loss.


A person with AS should let their doctor know about any vision changes, which may result from cataracts.

An optometrist or ophthalmologist can diagnose the issue, provide treatment, and recommend management techniques. The plan may involve:

  • new glasses or contacts
  • small changes at home, such as having brighter lights or using magnifying devices when reading or working
  • surgery to remove the cloudy lens and replace it with an artificial lens

Anyone with AS should speak with their doctor about the risk of cataracts. An eye doctor can check for this issue during routine eye exams by dilating the eyes.

For people with AS, having regular eye checkups is important. It can help catch related eye conditions early and prevent damage or vision loss.

Let the doctor know about any changes in vision, including sensitivity to light, blurriness, or eye pain. These can be symptoms of an eye condition.

Receiving treatment early can help improve the prognosis for anterior uveitis and glaucoma.

AS is a systemic type of arthritis that primarily affects the back, but it can cause issues in other areas, including the eyes.

The most common eye condition associated with AS is anterior uveitis, but glaucoma and cataracts are also linked with this form of arthritis. Early detection and treatment can help preserve vision.

Ankylosing Spondylitis & Uveitis: An Ophthalmologist’s Perspective

It’s often said the eyes are the window to the soul, and in the case of ankylosing spondylitis and other spondyloarthropathies, one can also say the eyes are the window to systemic disease. Although uveitis occurs in approximately 2–5% of patients with inflammatory bowel disease, 6–9% of patients with psoriatic arthritis and 25% of patients with reactive arthritis, the prevalence may be as high as 33% in patients with ankylosing spondylitis.1

Jennifer E. Thorne, MD, PhD, is the Cross Family Professor of Ophthalmology and chief of the Division of Ocular Immunology at the Wilmer Eye Institute at Johns Hopkins University, and professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health, Baltimore. In her practice, she evaluates and cares for patients with uveitis and other immune-mediated disorders of the eye, and her insights into diagnosing and treating these conditions provide a great deal of guidance to rheumatologists as they care for their patients.

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Dr. Thorne notes that, based on the anatomic site of the primary inflammation, uveitis can be categorized into four subtypes:

  1. Anterior uveitis, in which the primary inflammation is in the anterior chamber;
  2. Intermediate uveitis, in which the primary source of inflammation is found in the vitreous body;
  3. Posterior uveitis, in which the primary source of inflammation is in the retina and/or choroid; and
  4. Panuveitis, in which the intraocular inflammation is equally distributed in the anterior chamber, vitreous and retina/choroid.

The location of inflammation affects the differential diagnosis. For example, anterior uveitis may be seen in association with spondyloarthritis and other rheumatologic conditions, but posterior uveitis may be due to a primarily ophthalmologic syndrome, such as the white dot syndromes, a group of inflammatory chorioretinopathies of unknown etiology. 2

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Importance of Screening
Once a patient presents with uveitis, it is important to screen for signs and symptoms of possible underlying infection, autoimmune or inflammatory disorder and malignancies, to name just a few of the conditions that can result in a secondary uveitis. Testing for human leukocyte antigen B27 (HLA-B27) is an important step in the evaluation of patients with uveitis. Among patients with ankylosing spondylitis, strong evidence suggests that positive HLA-B27 status is a risk factor for the development of uveitis, as may be the case for presence of hip-joint lesions on imaging, number of involved peripheral arthritic joints, increased antistreptolysin O titers, and increased circulating immune complex levels.3

Spondyloarthropathy Underdiagnosed
Several studies have sought to screen patients with uveitis for the possibility of an underlying spondyloarthritis. In the SENTINEL study, conducted by researchers in Spain, 798 consecutive patients with more than one episode of anterior uveitis separated by at least three months were prospectively evaluated with a series of clinic appointments with an ophthalmologist and a rheumatologist.4

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Your Eyes | National Axial Spondyloarthritis Society

This information is for anyone with axial spondyloarthritis (axial SpA) including people with ankylosing spondylitis (AS)

What is uveitis?

About a quarter of people with axial SpA (AS) will have an attack of uveitis (sometimes known as iritis) at some time in their life.

This is an eye condition caused by inflammation in the front part of the eye between the cornea (the clear window at the front of the eye) and the lens.

What are the signs and symptoms of uveitis

  • Pain in the eye
  • Sensitivity to light. The brighter the light the more pain in the eye as the pupil gets smaller causing pain
  • Redness and soreness of the eye
  • Blurred vision

Uveitis usually comes on suddenly and is likely to recur

Each single attack usually lasts a few weeks and should last no more than 3 months. The inflammation can range from mild to severe and each attack may be different, even in the same person.

What should you do?

If you think you have symptoms of uveitis you should see an eye doctor (ophthalmologist) as soon as possible, ideally within 24 hours, to confirm it and start you on treatment. Early treatment reduces the risk of long term damage to the eye which can affect your vision.

You can find an ophthalmologist by asking your GP to make an urgent referral to the local ophthalmology team or you can go to your local hospital A&E department who will contact the ophthalmologist to arrange an urgent review.

Uveitis is usually treated with a combination of eye drops.

  • Steroid eye drops such as dexamethasone and prednisolone reduce the inflammation
  • Dilating drops dilate the pupil which reduces the risk of the iris sticking to the lens and break any attachments that have already formed

90,000 Ankylosing spondylitis – what is it

The official international name of the disease is ankylosing spondylitis. The term “Ankylosing spondylitis” is used only in Russia and until recently was used in Germany.

Ankylosing spondylitis is a systemic inflammatory disease, a type of spondyloarthritis that affects the joints, spine and entheses (the places where ligaments and tendons attach to the bones).The difference between the disease and other spondyloarthritis lies in the fact that ankylosis (fusion) of the vertebrae occurs among themselves, as a result, the spine can turn into a single bone and deform. The quality of life with this disease is significantly reduced. The second serious complication of ankylosing spondylitis is damage to the hip joints, up to complete loss of mobility and disability.

Why does this disease occur?

The exact cause of the development of the disease is unknown.According to one hypothesis, certain intestinal microbes can trigger pathological inflammation in entheses and joints. For the appearance of a disease, it is not enough for a certain infection to enter the body; a certain state of the body’s immune system is necessary, in which self-sustaining inflammation is possible. Scientifically proven risk factors for the development of ankylosing spondylitis are heredity and smoking.


Ankylosing spondylitis usually begins at a young age.The most common symptom of ankylosing spondylitis is back pain. This pain has a number of characteristics (called “inflammatory back pain”). It increases with prolonged immobility, including during a night’s sleep, and decreases with physical activity. Painful sensations of an inflammatory nature are often accompanied by a feeling of stiffness, especially in the morning when the patient wakes up. The presence of this symptom is a reason for an immediate appeal to a specialist to clarify the diagnosis.Young people often experience pain in the area of ​​the calcaneus or the attachment points of the Achilles tendons.

Most often, the disease begins with sacroiliitis, which is manifested by pain in the lower back (lumbar region). But in some cases, the patient may feel pain in the neck or at the level of the thoracic spine. In the later stages, there is a restriction of movements, in especially severe cases, a “supplicant’s pose” is formed.

Often, patients notice pain, limited mobility and swelling in peripheral joints, for example, shoulder, hip, small joints of the hands and feet, temporomandibular.

The disease can also cause extra-articular manifestations – damage to organs: heart, kidneys, eyes. The latter occurs most often and is manifested by uveitis (pain, photophobia, redness of the eye).

Among the associated conditions, the presence of psoriasis, inflammatory bowel diseases, intestinal or genitourinary infections are distinguished.

Depending on the zone where inflammation develops, central and peripheral forms of the disease are distinguished.


The diagnosis is confirmed using instrumental and laboratory diagnostic methods.X-ray and MRI in the diagnosis of ankylosing spondylitis are used as complementary methods. Often, ultrasound or MRI of the hands and feet can effectively detect enthesitis (inflammatory lesions of entheses).

Laboratory diagnostics play a significant role. 90% of patients with ankylosing spondylitis carry the HLA B-27 gene. It is a genetically determined antigen of leukocytes, which is associated with the possibility of developing an autoinflammatory response. However, the presence of HLA B-27 does not mean the development of the disease, this gene only indicates an increased risk of ankylosing spondylitis.

Early diagnosis is the key to successful treatment of ankylosing spondylitis, but it is not easy to recognize the disease. Much depends on the qualifications of a rheumatologist.

Treatment of ankylosing spondylitis

Drug treatment

The basis of treatment is non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, diclofenac, naproxen, nimesulide, etoricoxib, ketoprofen, aceclofenac, meloxicam, etc. They are able to inhibit ankylosis of the spine, reduce the inflammatory response and improve the prognosis can be used simultaneously as pain relievers.The drugs block the self-sustaining autoinflammatory process and block the disease mechanism. Patients with peripheral involvement, in whom arthritis prevails, are recommended to take basic anti-inflammatory drugs (sulfasalazine, leflunomide, methotrexate). In the absence of the effect of taking non-steroidal anti-inflammatory drugs, patients are prescribed genetically engineered drugs from the group of tumor necrosis factor inhibitors

Surgical treatment

Surgical treatment may be required to correct conditions associated with a complication of the course of the disease, for example, with severe deformities of the spine, vertebral fractures, destruction of the hip joints, and heart damage.


To relieve pain, physiotherapeutic methods can be used: massage, acupuncture and other methods. The disadvantage is that they do not provide long-term sustained effects. Physiotherapy is not included in the official recommendations for the treatment of ankylosing spondylitis.


Regular exercise, in addition to basic therapy, helps maintain joint mobility. Exercises to strengthen the back muscles are especially recommended.


The causes of the development of the disease have not been reliably established, therefore, no special prophylaxis has been developed.

General recommendations can be to maintain an active lifestyle, while trying to avoid injuries of the spine and joints, refrain from smoking, the Mediterranean diet is preferred in food.

Diagnostics and treatment in EMC

Thanks to a wide range of diagnostic methods and modern technologies, most patients with this disease can achieve a good effect in treatment.At the European Medical Center (Moscow), comprehensive care is provided according to the protocols adopted by international rheumatological organizations (ASAS, EULAR, ACR). For patients who cannot come to the clinic, it is possible to organize a correspondence consultation.

Ankylosing spondylitis

The defeat of the joints in ankylosing spondylitis

Ankylosing spondylitis is an ankylosing spondylitis. The disease is an inflammation of the intervertebral joints, which leads to their ankylosis (fusion), due to which the spine appears to be in a hard case that restricts movement.Mostly young men are affected, more often 15-30 years old. The ratio of men to women is 9: 1.


In the development of the disease, a hereditary predisposition is of great importance (a certain feature of the immune system is inherited). The presence of chronic infections (mainly of the intestines and urinary tract) is important. The provoking factor is usually intestinal, genital infections, stress and injuries of the musculoskeletal system.


– Stiffness, pain in the sacroiliac region, which can radiate to the buttocks, lower extremities, intensify in the second half of the night.
– Persistent pain in the calcaneus in young people.
– Pain and stiffness in the thoracic spine.
– Increased ESR in the blood test up to 30-40 mm per hour and above.

If these symptoms persist for more than three months, an immediate consultation with a rheumatologist is required!

The first signs of joint damage are found in the sacroiliac joints. First, inflammatory manifestations occur on the inner (synovial) membrane of the joint in the sacroiliac joints, intervertebral joints or costal-vertebral joints, less often in the joints of the extremities.As a result of inflammation, the amount of intra-articular fluid increases. In the joint cavity, a protein formed as a result of inflammation – fibrin is deposited.

Gradually the inflammation spreads to the cartilage of this joint. Inflammatory-altered cartilage is destroyed, fusion is formed in the joint, which first consists of soft tissues, then fusion of the bone ends is formed – ankylosis. The joint loses its mobility. The disease develops slowly. At the beginning, pains appear in the sacrum, spine.They can be aching, dull. Pain often occurs in the second half of the night or in the morning. Pain in other joints occurs less frequently and is usually less severe. In the morning, patients notice difficulty in starting movement, which gradually disappears. This is a symptom of morning stiffness.

Gradually, the inflammatory process develops further. Inflammation of the sacroiliac joints is manifested by pain in the buttocks. The pain is given to the thigh, knee, less often to the lower leg. Movements in the lumbosacral spine are reduced in volume.When the inflammatory process spreads to the spine, the thoracic spine, the patient develops pain in the thoracic spine with irradiation along the intercostal nerves. This is manifested by symptoms of intercostal neuralgia.

The inflammatory process, which has spread to the cervical spine, causes pain in the neck, radiating to the shoulder, arm. Some patients develop vertebro-basilar insufficiency syndrome. It is manifested by dizziness, staggering when walking, headaches.Peripheral joint involvement is less common. It usually takes a long time. But ankylosis can also occur in the knee, hip joints, leading to loss of joint function.

There are four forms of ankylosing spondylitis:

  • Central form. This form is manifested by the defeat of only the spine. It develops slowly, unnoticed by the patient. The pains appear first in the sacrum, then up the spine. The pain increases with movement, exertion.Night pains often occur. Gradually, the patient’s posture changes: the bending of the cervical spine increases, with a bulge forward, and the thoracic spine with a bulge back. The patient’s head tilts forward, the chin approaches the sternum. In the thoracic region, the spine is flexed and breathing movements of the chest are limited. In the later stages of the disease, movements in the spine are significantly limited. The patient develops asthma attacks, muscle cramps, and blood pressure rises.All this is accompanied by pain in all parts of the spine.
  • Rhizomelic form. In this form of the disease, damage to the spine is accompanied by damage to the large joints. Most often, the shoulder and hip joints are affected. The disease also develops gradually. Depending on the affected joint, pain occurs in the buttocks, thigh, hip joint, radiates to the groin and knee, or shoulder, forearm with pain radiating to the arm.
  • Peripheral form. In the peripheral form of ankylosing spondylitis, the first signs of the disease appear in the sacroiliac joints.Then, after a few months or even several years, inflammatory lesions of the knee and ankle joints develop. Deforming arthrosis develops in the joints, muscle contractures near the joints. This form is more common in adolescents.
  • Scandinavian form of ankylosing spondylitis. This form is similar to the peripheral, but in contrast to it, even smaller joints are affected. These are the joints of the hands and feet. Joint pain in this form of disease is mild.

Ankylosing spondylitis is accompanied by damage to internal organs.On the part of the cardiovascular system, these are myocarditis (inflammatory disease of the heart muscle), inflammation of the aortic valves. With kidney damage, a serious condition develops – renal amyloidosis. Eye damage is manifested by iritis, iridocyclitis.


Treatment is complex, long-term, staged (hospital – sanatorium – polyclinic). It is aimed at reducing pain, reducing inflammation. For this, non-steroidal anti-inflammatory drugs (indomethacin, rheopyrin, diclofenac) are used.In severe and rapid course of the disease, adrenal cortex hormones, immunosuppressants are used. Physiotherapeutic procedures, physiotherapy exercises, spa treatment are prescribed. Therapeutic exercises should be carried out twice a day for 30 minutes, the exercises are selected by the doctor individually. In addition, you need to learn muscle relaxation. In order to inhibit the development of chest immobility, deep breathing is recommended. At the initial stage, it is important not to allow the development of vicious postures of the spine (posture of the proud, the posture of the supplicant).Skiing and swimming are shown to strengthen the muscles of the back and buttocks. The bed should be firm and the pillow should be removed.
For severe forms of joint damage, surgical treatment (arthroplasty) and spinal surgery are used.

Peculiarities of clinical manifestations and treatment of uveitis in ankylosing spondylitis

One of the most common extra-articular manifestations of ankylosing spondylitis (AS) is uveitis (20–40%). The article describes a modern approach to the treatment of patients with uveitis associated with AS, taking into account the peculiarities of the clinical picture and course of the disease.The place of tumor necrosis factor inhibitors in the treatment of patients with uveitis in AS is discussed.

Fig. 1. Acute anterior uveitis: conjunctival injection, hypopyon

Fig. 2. Acute anterior uveitis: posterior synechiae (photo by I.Yu. Razumova)


Spondyloarthritis (SpA) is a large group of inflammatory diseases of the joints and spine, united by common pathogenetic, immunogenetic and clinical signs.The prototype of this group of diseases is ankylosing spondylitis (AS).

In addition to damage to the spine and joints, AS is characterized by a wide range of extra-articular manifestations, of which uveitis is the most common. Uveitis is an inflammation of the structures of the uveal tract of the eye, which includes the iris, ciliary body and the choroid itself, or choroid. Depending on the primary localization of the inflammatory process, uveitis is classified as anterior (iritis, iridocyclitis, cyclitis, keratouveitis), peripheral, or intermediate (parsplanitis), posterior (chorioretinitis, endophthalmitis) and panuveitis (panophthalmitis) [1-3].

Clinical manifestations of uveitis

The inflammatory process in uveitis is characterized by cellular infiltration due to an increase in the permeability of the vascular wall, which can be observed during ophthalmoscopy in various parts of the eye: in the anterior chamber, vitreous body, retina. The activity of uveitis is assessed by the number of inflammatory cells in the anterior chamber of the eye and the severity of inflammatory changes in the structures of the eye. The degree of opacity of the vitreous body is also taken into account.Changes in these parameters make it possible to judge both the presence of exacerbation or remission, and the effectiveness of the therapy [2].

According to various authors, the incidence of uveitis in AS is 20 to 40% [4, 5]. Inflammation primarily affects the anterior structures of the eye: the iris and the ciliary body, then the vitreous body is also included in the process. Clinically, uveitis is manifested by eye pain, photophobia, lacrimation, blurred vision. A common symptom of acute anterior uveitis (AKU) is conjunctival injection, often pericorneal (vascular congestion in the area of ​​the corneoscleral junction) (Fig.one). Biomicroscopy also reveals opalescence of moisture in the anterior chamber of the eye due to the presence of inflammatory cells in it. Fibrin-glued cellular elements can settle on the posterior surface of the cornea, forming precipitates.

Due to the presence of inflammatory exudate in the anterior chamber of the eye, posterior synechiae (adhesion of the pupillary edge of the iris with the anterior lens capsule) and anterior (fusion in the area of ​​the iris root, Fig. 2) occur. The high activity of inflammation is accompanied by a clouding of the moisture of the anterior chamber due to the many inflammatory cells and the formation of hypopyon (sediment at the bottom with a horizontal level).

Uveitis with AS is characterized not by simultaneous damage to both eyes, but by alternating inflammation of the right or left eye. In this regard, uveitis in AS is usually unilateral. It begins acutely, usually lasts less than three months, but tends to recur. Our own observations suggest that in some patients with AS, recurrent uveitis is the dominant clinical manifestation of AS, which determines the severity of the condition. These patients are prone to frequent exacerbations of uveitis – up to 5-6 during the year, which can be protracted and difficult to respond to local anti-inflammatory therapy.As a result of frequent prolonged attacks of uveitis, complications such as cataracts, glaucoma, fibrotic changes in the vitreous can develop. Intense inflammation in the anterior segment of the eye is often accompanied by the formation of anterior and posterior synechiae, which impedes the outflow of ocular fluid.

Observation of 140 patients with AS, who had at least one exacerbation of uveitis in history, showed that in most cases (58% of patients) uveitis developed in the first 10 years after the onset of AS.Complications of uveitis, leading to impaired visual functions, were noted in 29% of patients: synechiae – in 26 (18%), destruction of the vitreous – in 20 (14%), cataract – in 32 (23%), glaucoma – in 13 (9 %), maculopathy – in 6 (4%), ribbon-like corneal degeneration – in 6 (4%), partial atrophy of the optic nerve – in 3 (2%) [6].

With a protracted course or inadequate treatment, inflammation can spread to the posterior parts of the eye with the development of vitritis, retinal vasculitis, cystic macular edema and other vision-threatening conditions.

Pathogenesis of uveitis

Uveitis can develop long before the first manifestation of spondylitis or debut against the background of low-symptom spondylitis, therefore, at present, in accordance with the ASAS classification criteria (SpondyloArthritis international Society – International Society for the Study of Spondyloarthritis), it is taken into account in the early diagnosis of AS [7].

Uveitis is reliably more often observed in patients with other systemic manifestations, in particular, changes in the cardiovascular system in the form of damage to the aorta and valves, as well as rhythm and conduction disturbances [8].When examining 344 patients with AS, observed at the Research Institute of Rheumatology, Russian Academy of Medical Sciences, conduction disturbances (atrioventricular and intraventricular blockade) were observed in 24.3% of patients with uveitis and in 10.6% of those without uveitis (p = 0.006). In addition, uveitis was diagnosed reliably more often in patients with various conduction disturbances compared with those without conduction disturbances (14 (31.8%) out of 44 and 50 (16.7%) out of 300 patients, respectively; p = 0.01 ). A similar pattern was also revealed in relation to the structural changes in the heart, characteristic of AS.For example, thickening of the wall of the aorta and heart valves, subaortic crestal thickening were significantly more often recorded during echocardiography in patients with a history of uveitis than in patients without uveitis (in 16 (59.3%) of 27 and 28 (37.8%) of 74 people, respectively; p = 0.04). Conversely, uveitis was significantly more frequent in patients with changes in the aorta and heart valves compared with patients without structural changes in the heart (in 21 (46.7%) out of 45 and 6 (16.7%) out of 56 people, respectively; p = 0 , 0001).Thus, the presence of uveitis may indicate an increased risk of developing other systemic manifestations in patients with AS.

Of great interest is the study of the pathogenetic role of the histocompatibility antigen HLA-B27 in the development of various manifestations of AS, including eye damage. The relationship between HLA-B27 and OPU was first established by D. Brewerton et al. in 1973 [9]. On the one hand, the majority of AS patients who have at least one attack of uveitis during the course of the disease are carriers of the histocompatibility antigen HLA-B27.On the other hand, almost 30-50% of patients with AKI are HLA-B27-positive, and about 50% of patients from this group have signs of AS [10].

Population genetic studies among Europeans have shown that HLA-B27 accounts for only 16% of the genetic risk of the disease, while in general for the genes of the major histocompatibility complex (MHC) this figure is 50%, which indicates the existence of additional genes in the MHC region, predisposing to the development of the disease [11, 12].A number of studies have shown that MICA, the gene of the main histocompatibility complex, located on the short arm of chromosome 6 next to locus B and characterized by high polymorphism, may be involved in the pathological process leading to the development of AKI. This gene is detected with a high frequency in both HLA-B27-positive and HLA-B27-negative patients with AKI, as well as in patients with ulcerative colitis and psoriasis [13, 14].

Not only genes of the major histocompatibility complex may be involved in the development of uveitis in AS.In particular, this disease can be associated with a genetic region located on the 16th chromosome [15]. This is where the NOD-2 gene, found in patients with Crohn’s disease, AS, psoriasis, and other inflammatory diseases involving the eyes, is located. Previously, this gene was identified as responsible for the development of familial juvenile systemic granulomatosis (Blau syndrome, a rare disease with an autosomal dominant mode of inheritance, one of the main manifestations of which is uveitis).Since AS, Crohn’s disease and reactive arthritis have many common symptoms and can occur in members of the same family, it can be assumed that the NOD-2 gene undergoes a mutation in patients with seronegative spondyloarthritis with systemic manifestations and may be involved in the development of uveitis.

There is information about other genetic markers of OPU, in particular, researchers in Japan established an association between OPA and HLA-DRB1 * 08, but in other studies it was not confirmed [5].Recently, data were obtained on the role of tumor necrosis factor (TNF) alpha promoter gene polymorphism in the development of B27-associated uveitis. It has been shown that HLA-B27-positive patients have an increased risk of developing uveitis in the presence of the A-allele of the TNF-alpha promoter gene in position 238 and a lower risk in the presence of this allele in position 308 [16]. A study of the polymorphism of the TNF-alpha receptor gene (tumor necrosis factor receptor superfamily – the superfamily of tumor necrosis factor receptors, TNFRSF) demonstrated that patients with HLA-B27-associated AKI have an increased risk of complications in the presence of TNFRSF1A-201T and TNFRSF1A-1135T alleles [ ].

The role of the KIR-complex (killer cell immunoglobulin-like receptors) in the pathogenesis of uveitis in AS is of interest. These receptors are expressed on killer cells and some T cells, including activated T cells CD8 + , which interact with HLA class I molecules, including HLA-B27. It turned out that this interaction plays a role in the development of many inflammatory processes, including uveitis in HLA-B27-positive AS patients.HLA-B27 realizes the risk of inflammatory disease in part through interactions with certain KIRs. The KIR – HLA-B27 complex initiates an early NK- or CD8 + -cellular response, leveling the antigenic stimulus. In HLA-B27-positive patients with AS and uveitis, a tendency towards a decrease in the number of KIR 3DS1, 2DS1 and 2DS5 was revealed [18]. HLA-B27, in the absence of these receptors, is unable to activate an early NK- or CD8 + T-cell response mediated by the KIR complex and required to reduce antigenic stimulation, which can lead to the rapid onset of ocular inflammation characteristic of AS.

Modern methods of treatment of patients with uveitis with AS

The relationship between these genetic factors and the role of each of them in the development of uveitis deserves attention and may become the subject of further research.

Treatment of uveitis in patients with AS should be carried out in close cooperation between an ophthalmologist and a rheumatologist. The main method of treatment for AKI, typical for AS, is the topical application of glucocorticosteroids (GCS) in the form of drops and injections in combination with cycloplegic agents.In many cases, when these drugs are used at the onset of the disease, the inflammation can be completely stopped. With insufficient effectiveness of drops, para- or retrobulbar injections of GCS are made, which allow creating a relatively high concentration of the drug in the pathological focus and avoiding undesirable systemic phenomena. With a protracted and recurrent course of uveitis, anti-inflammatory drugs of systemic action are added to the treatment regimen: non-steroidal anti-inflammatory drugs (NSAIDs) and basic anti-inflammatory drugs (DMARDs).

NSAIDs are the first-line drugs for the treatment of patients with AS and, in addition, help to reduce inflammatory infiltration, edema and pain in the eye.

Among DMARDs in the complex treatment of uveitis associated with AS, sulfasalazine is most often used. The data of a number of authors and their own observations show that long-term administration of sulfasalazine significantly reduces the number of exacerbations of uveitis in patients with AS [19, 20].

There is little evidence of a beneficial effect of methotrexate in preventing uveitis attacks [21, 22].However, in the study by S. Gangaputra et al. patients not only with AKI, but also with ocular inflammation of a different etiology, including posterior, intermediate uveitis, panuveitis, scleritis, took part. In this regard, it is difficult to assess the effectiveness of methotrexate in patients with AS with clinical manifestation in the form of uveitis according to the data of this study. In a study by S. Muñoz-Fernandez et al. a small group of patients, 10 people with recurrent AKI, who received methotrexate for a year, was prospectively studied.It has been shown that the number of uveitis attacks per year has significantly decreased.

Another immunosuppressive drug successfully used in the treatment of uveitis is cyclosporin A [23–27]. In most cases, it was used in combination with HA or as monotherapy for the treatment of severe forms of posterior uveitis and panuveitis, recurrent peripheral non-infectious uveitis of various etiologies. Within the framework of AS, such forms of uveitis are rare. Comparative studies of the effectiveness of different DMARDs in the treatment of uveitis in AS have not been conducted, therefore, it is difficult to talk about the advantages of cyclosporin A over sulfasalazine or methotrexate in this case.

Currently, various genetically engineered biological agents are successfully used in the treatment of patients with uveitis, primarily drugs that affect TNF-alpha. Monoclonal antibodies to TNF-alpha (infliximab, adalimumab) are highly effective in the treatment of a number of rheumatic diseases associated with uveitis, including AS, juvenile chronic arthritis, and Crohn’s disease. The theoretical substantiation of the use of anti-TNF-drugs in the treatment of uveitis was the evidence of the key role of TNF-alpha in the development of uveitis, obtained in a number of studies using laboratory animals, as well as data on an increase in the level of TNF-alpha in the serum and intraocular fluid of patients with uveitis.The suggestion that blocking TNF-alpha activity may be effective in the treatment of uveitis has been confirmed in clinical practice. In recent years, more and more data have appeared on anti-TNF therapy for uveitis in humans.

There is information about the use of three TNF inhibitors for different forms of uveitis: infliximab, adalimumab, etanercept.

Infliximab (Remicade) is the ancestor of TNF-alpha inhibitors. It is a chimeric compound based on hybrid monoclonal antibodies to TNF-alpha, consisting of 75% human protein and 25% murine protein.The antigen (TNF-alpha) binds to the mouse protein portion of the molecule. Infliximab with high specificity blocks both circulating and fixed on cell membranes TNF-alpha.

For the first time, infliximab was used for the treatment of uveitis in Behcet’s disease, and later it was successfully used for the treatment of patients with AS with uveitis [28, 29].

Active anti-inflammatory therapy is required for patients with AS and frequent protracted exacerbations of uveitis. TNF-alpha inhibitors have been shown to rapidly relieve uveitis and prevent recurrent exacerbations.The administration of infliximab as the only anti-inflammatory agent was sufficient to suppress the attack of the OPU [30]. The drug was administered at a dose of 10 mg per 1 kg of body weight to eight patients with HLA-B27-associated AKI. The criteria for the effectiveness of treatment were the number of inflammatory cells and precipitates in the anterior chamber of the eye, as well as the level of C-reactive protein in the blood before and after treatment. After one infusion, all patients showed a rapid regression of all symptoms of uveitis, including a decrease in the number of cells in the anterior chamber of the eye.Within 17 months, uveitis did not recur.

Infliximab proved to be highly effective in the treatment of not only anterior, but also posterior uveitis refractory to conventional treatment with corticosteroids and at least one immunosuppressive agent [31]. The authors emphasize the particular efficacy of infliximab in posterior uveitis with predominant retinal vasculitis and vitritis.

Another TNF-alpha inhibitor is actively used for the treatment of uveitis – adalimumab, which is a fully human antibody obtained using recombinant DNA technology.Adalimumab specifically binds to TNF-alpha and blocks its interaction with the p55 and p75 surface cell TNF-alpha receptors, thereby neutralizing the activity of this cytokine. Due to these effects, adalimumab reduces the concentration of matrix metalloproteinases (MMP-1 and 3), adhesion molecules responsible for the migration of leukocytes (ELAM-1, VCAM-1, ICAM-1), reduces the concentration of acute phase proteins. At the same time, the activity of adalimumab is highly specific and is not inhibited by lymphotoxin known as TNF-beta, a cytokine produced by lymphocytes and affecting various cells.TNF-beta modulates various biological responses resulting from TNF-alpha stimulation.

Indicative data from an open study conducted by M. Rudwaleit et al. involving 1250 patients with active AS treated with adalimumab at a dose of 40 mg once every 2 weeks for 20 weeks [32]. The number of attacks of uveitis per 100 patient-years before the initiation of adalimumab therapy and during therapy was compared. It turned out that the frequency of exacerbations of uveitis during treatment with adalimumab decreased by 51% in all patients, by 58% in patients with a history of uveitis, by 68% in people who have had uveitis within the last year, and by 50% in patients who had active uveitis at the time of initiation of treatment.The drug has shown high efficacy in both relief and prevention of exacerbations of uveitis in patients with AS.

The effectiveness of adalimumab has been confirmed in other studies, in particular, in the treatment of patients with refractory autoimmune uveitis: 19 people received adalimumab at a dose of 40 mg once every two weeks for 12 months [33]. All patients showed a decrease in signs of ocular inflammation, an improvement in visual functions at the end of treatment, and complete resolution of cystic macular edema of the eyes in 18 out of 33 cases.Adalimumab is well tolerated.

There is evidence of successful substitution of infliximab for adalimumab in the treatment of uveitis in patients with intolerance or insufficient efficacy of infliximab. K. Takase et al. observed patients with Behcet’s disease and uveitis treated with infliximab and cyclosporine, with infusion reactions to infliximab [34]. At the same time, the termination of anti-TNF therapy led to an exacerbation of uveitis. The administration of adalimumab to these patients led to a rapid relief of the exacerbation of uveitis.In patients with AS and uveitis with insufficient effectiveness of infliximab, it is also possible to improve the course of uveitis after changing the anti-TNF drug.

The following clinical case demonstrates the successful substitution of adalimumab for infliximab.

Clinical case

Patient G., born in 1956, has been observed at the Research Institute of Rheumatology of the Russian Academy of Medical Sciences since 1997 with a diagnosis of AS, HLA-B27-positive, late stage, bilateral coxitis, enthesopathies, extraskeletal manifestations (recurrent anterior uveitis), high activity.

From the anamnesis it is known that inflammatory pain in the spine appeared in a man from the age of 30. The diagnosis of AS was made 7 years after the onset of the disease, when bilateral sacroiliitis, limitation of the mobility of all parts of the spine, were revealed. In 2004 and 2006. episodes of arthritis of the right knee joint were noted. Since 2008, repeated protracted attacks of uveitis in the left eye with a short-term effect against the background of GCS injections have been recorded. Since February 2010, the patient was constantly taking sulfasalazine 2 g / day and NSAIDs, but signs of active ocular inflammation persisted: edema of the iris, cells in the vitreous humor and anterior chamber of the eye.

During examination at the Research Institute of Rheumatology of the Russian Academy of Medical Sciences in September 2010, signs of late stage AS were revealed: increased thoracic kyphosis, smoothness of the cervical and lumbar lordosis, lack of movement in the cervical spine, limitation of the chest excursion to 3 cm, limitation of mobility in the lumbar spine ( Schober test – 2 cm, lateral flexion – 8 cm). High inflammatory activity was determined by the BASDAI index (Bath ankylosing spondylitis disease activity index) (4.5 cm) and laboratory tests (erythrocyte sedimentation rate (ESR) – 26 mm / h, C-reactive protein (CRP) ) – 80 units / ml).

On radiographs of the pelvis, bilateral sacroiliitis of stage IV, narrowing of the hip joints, erosion of the symphysis and ischial tubercles were revealed. X-rays of the spine showed osteoporosis, multiple syndesmophytes in the lumbar and thoracic spine.

The oculist revealed periocular edema of the left eye (OS), grayish-white precipitates on the cornea, opalescence of moisture in the anterior chamber, iris subatrophy, old posterior synechiae, unevenly dilated pupil, opacification of the posterior capsule of the lens, opacity and destruction of the vitreous body; fundus ophthalmoscopy was not performed.Right eye (OD) – no signs of inflammation.

Due to frequent persistent attacks of uveitis, insufficient effect of sulfasalazine therapy and NSAIDs, since September 2010, the patient was started on infliximab (Remicade) at a dose of 3 mg per 1 kg of body weight according to the standard scheme. After the first infusion, a significant improvement in OS was noted in the form of a decrease in the amount of precipitates and edema, as well as a decrease in pain and an increase in the mobility of the spine. One month after the third infusion, an exacerbation of OS uveitis developed, requiring inpatient treatment in the ophthalmology department.After the fourth infusion of infliximab within two months, 3 attacks of OS uveitis were noted.

Due to the recurrence of uveitis during therapy with infliximab, it was decided to replace this drug with adalimumab. Since September 2011, he began treatment with adalimumab at a dose of 40 mg subcutaneously 1 time in 2 weeks.

For six months of therapy with adalimumab, there were no exacerbations of uveitis, the pain in the spine decreased significantly, the BASDAI index was 2.9 cm. Laboratory indicators were without deviations from the norm.The patient continues to take sulfasalazine at a dose of 2 g / day and diclofenac if necessary.

Comparison of the effectiveness of TNF inhibitors

Thus, adalimumab can be successfully used for the treatment of recurrent uveitis in patients with AS. The structural features of adalimumab, consisting only of human protein, can reduce the risk of adverse events associated with the production of anti-chimeric antibodies. The advantages of adalimumab include the subcutaneous route of administration, which is more convenient for patients and does not require a visit to a medical institution.

In AS for a long time, etanercept (Enbrel drug) has been successfully used, which is a dimeric combined protein consisting of a human soluble TNF-alpha p75 receptor connected to the Fc-fragment of human immunoglobulin G1. However, a number of authors question its effectiveness in preventing uveitis in patients with AS [35]. Moreover, there is evidence that etanercept can provoke uveitis in patients with AS and other SpA [36, 37]. In this regard, it is interesting to work on a comparative assessment of the effect of anti-TNF therapy on the prevention of recurrence of uveitis in patients with AS.In a study by J. Braun et al. data on the treatment and follow-up of patients with recurrent AKI in AS with infliximab and etanercept were evaluated based on the results of four placebo-controlled and three open-label studies: 297 patients received etanercept, 90 – infliximab, 190 – placebo [38]. It turned out that the frequency of exacerbations of uveitis in the group of patients receiving anticytokine drugs was significantly lower – 6.8 episodes per 100 patient-years compared with the placebo-control group – 15.6 episodes per 100 patient-years at p = 0.01.Uveitis exacerbations occurred less frequently in patients receiving infliximab than in those receiving etanercept (3.4 per 100 patient-years and 7.9 per 100 patient-years, respectively), although this difference did not reach the level of statistical significance. The authors concluded that anticytokine therapy can significantly reduce the frequency of exacerbations of anterior uveitis in AS, and infliximab was superior to etanercept in this respect.

Similar data were obtained by S. Guignard et al., Who conducted a retrospective analysis of the efficacy of anti-TNF therapy in patients with SpA [39].Of the 46 people included in the study, 13 were treated with etanercept, 25 with infliximab, and 8 with adalimumab. The median duration of anti-TNF therapy was 1.2 years. The number of exacerbations of uveitis per 100 patient-years was 51.8 for all types of therapy before treatment and 21.4 during treatment. For etanercept, this figure was 54.6 and 58.5, for infliximab – 47.4 and 9.0, for adalimumab – 60.5 and 0, respectively. The results of this study showed the superiority of antibodies to TNF, especially adalimumab, over the recombinant soluble receptor in reducing the frequency of exacerbations of uveitis.

In the literature, there are quite intriguing reports of cases of paradoxical development of uveitis against the background of anticytokine therapy. We are talking about both exacerbation and development of uveitis de novo in previously intact eyes [36, 40]. Moreover, in most cases, other manifestations of the disease (arthritis, spondylitis) were successfully controlled by anti-TNF therapy. Cases of exacerbation of uveitis have been described against the background of treatment with etanercept and infliximab (more often in patients with AS), juvenile chronic arthritis was recorded in some patients with psoriatic arthritis (PsA) [40, 41, 42].In most of the described cases, there was a clear chronological relationship between the administration of the drug and the development of uveitis. After stopping uveitis, repeated administration of the drug again led to an exacerbation of eye inflammation. It was noted that the clinical manifestations of uveitis, manifested in AS patients against the background of anti-TNF therapy, differed from those typical in AS in greater severity and torpidity, in some cases with bilateral eye damage. How can we explain the unexpected development of uveitis against the background of powerful anti-inflammatory treatment, are there predictors of a negative eye response to treatment with anti-TNF drugs, which anti-TNF drugs are more successful against uveitis, and does the overall benefit of anti-TNF- treatment of uveitis, the potential risk of exacerbation – these questions remain to be answered.

Using independent adverse event registration databases from 1998 to 2006, L. Lim et al. summarized cases of uveitis during treatment with various anti-TNF drugs [43]. All episodes of uveitis developed during this time period with treatment with etanercept, infliximab and adalimumab were counted. It turned out that 43 cases of uveitis were associated with etanercept therapy, 14 cases with infliximab, and 2.

with adalimumab.

T. Cobo-Ibáñez et al.conducted a study with the participation of patients with SpA with a history of ADR and receiving anti-TNF drugs [44]. Of 19 patients (15 with AS, two with undifferentiated SpA, and two with PsA), 10 received etanercept and 9 received infliximab. The incidence of uveitis in the infliximab group was 61.73 per 100 patient-years before the start of treatment and 2.64 after the start of treatment, in the etanercept group – 34.29 and 60, respectively (p = 0.041). Similar data were obtained in other works [45].

These data suggest that in most cases of uveitis exacerbations are associated with etanercept therapy.Infliximab and adalimumab are also more effective in preventing recurrent attacks in patients with recurrent uveitis [38, 39]. What is the reason for such differences in the effect of anti-TNF drugs remains unclear, while only hypotheses are expressed as an explanation for this phenomenon. It is known that etanercept, in contrast to infliximab, has an additional inhibitory effect on TNF-beta (lymphotoxin-alpha). However, it has been shown in animal models that TNF-beta is also associated with the development of uveitis.In this regard, it is logical to expect that etanercept should even more than infliximab inhibit the development of uveitis. Similar differences in the effectiveness of infliximab and etanercept have been found in the treatment of other diseases, for example, in Crohn’s disease. Perhaps the key to understanding the biological effects of these drugs are differences in their structure and mechanisms of action. Etanercept, being a soluble TNF-alpha receptor, stimulates the T-cell cytokine response, while infliximab and adalimumab suppress it.Another hypothesis is based on the different effects of infliximab and etanercept on apoptosis. Etanercept does not activate apoptosis, which is important in diseases, in the pathogenesis of which, presumably, a defect in apoptosis plays a role. Unlike antibodies to TNF-alpha, etanercept does not kill cells that express the cytokine on its surface. In the case of uveitis, the elimination half-life of TNF-alpha from ocular tissues is prolonged and the likelihood of inflammation increases [43].

Thus, although the three anti-TNF drugs (infliximab, adalimumab, and etanercept) are approximately equally effective for treating patients with arthritis and spondylitis, their effect on uveitis is different.Antibodies to TNF-alpha (infliximab, adalimumab) are more effective than soluble receptors in reducing the incidence of uveitis and, apparently, less frequently associated with the development of uveitis de novo . Nevertheless, the frequency of uveitis attacks in AS patients with etanercept treatment was significantly lower than with placebo; therefore, all anti-TNF drugs can be successfully used to treat rheumatic diseases with eye damage [46, 47]. According to L. Lim, with the development of exacerbations of uveitis against the background of anti-TNF therapy, it is advisable to replace the drug [43].

Our observations confirmed the literature data on the effectiveness of anti-TNF therapy and its superiority compared to traditional anti-inflammatory therapy in patients with uveitis in AS. In 48 patients with AS and recurrent uveitis treated with anti-TNF drugs, the average number of exacerbations of uveitis per year decreased from 2.2 during the period of standard anti-inflammatory therapy to 0.6 per year during the period of anti-TNF therapy (p = 0 , 0007), and all 3 drugs were effective. This allowed us to conclude that there was a significant decrease in the frequency of attacks of uveitis in AS against the background of anti-TNF therapy [48].


In general, anti-TNF therapy can be regarded as a highly effective treatment method that opens up new possibilities and prospects in the treatment of not only arthritis, but also refractory forms of uveitis. However, the mechanisms of action of these drugs on the eye are probably unique, different from the effects on the joints, and require further study.

In the development of immune inflammation in uveitis, not only TNF-alpha is involved, but also other cytokines or signaling molecules, the inhibition or activation of which is theoretically also justified, but the clinical approaches to their use are not sufficiently developed.This, in particular, the receptor complex of interleukin-2 (IL-2), various surface antigens of T-lymphocytes, adhesion molecules (ICAM-1), S-antigen of the retina.

AIN457 (secukinumab), a monoclonal antibodies directed against interleukin-17 (IL-17) [49], is currently being actively studied. IL-17 is secreted by T-helpers 17 and is involved as a key mediator of inflammation in the pathogenesis of autoimmune diseases, including AS, psoriasis, and uveitis.

Another object of research is the drug apremilast (CC-10004), a specific inhibitor of phosphodiesterase-4 (PDE4) and a modulator of pro- and anti-inflammatory mediators [49].PDE4 is one of the major phosphodiesterases expressed by leukocytes. Inhibition of PDE4 leads to the accumulation of intracellular cyclic adenosine monophosphate and, as a consequence, to inhibition of the transcription of proinflammatory cytokines and other cellular reactions, such as neutrophil degranulation, chemotaxis, and cell adhesion. The subject of study, among others, will be the effect of these drugs on the course of uveitis in AS. It can be expected that the development of new approaches to the treatment of uveitis will significantly improve the prognosis and quality of life of patients with AS.

Ankylosing spondylitis

Treatment of ankylosing spondylitis in Kolomna.

Ankylosing spondylitis (ankylosing spondylitis) is a chronic systemic disease characterized by damage to the joints of the spine and the sacroiliac joint, leading to ankylosis (immobility of the joints due to fusion.

To date, the exact causes of this disease have not been fully established. It is believed that one of the factors is a hereditary predisposition.Acquired factors also play an important role.

The pathological process affects the spine and peripheral joints, intervertebral discs, sacroiliac joint, therefore the diagnosis of ankylosing spondylitis requires differential diagnosis with other diseases.

In each case, ankylosing spondylitis is unique and therefore requires an individual approach to treatment.

In our centers, experienced specialists, based on examination, anamnesis and additional research, will develop a treatment plan for this disease, on the basis of which you will maintain your health and regain your mobility.

Symptoms of ankylosing spondylitis.

From the side of the spine: back pain, ameliorated by movement. Morning stiffness, limitation of movement of the spine and chest. Spinal deformity.

From the side of the sacroiliac joint: pain in the buttock and thigh, weakening with movement. Stiffness in the lower back in the morning.

From the side of the joints: affection, as a rule, of large joints. Joint inflammation (pain, swelling, restriction of movement).

Also, damage to the eyes, CVS, kidneys, lungs can be observed.

For the diagnosis of ankylosing spondylitis, functional tests, methods of instrumental diagnostics (X-ray examination, CT, MRI), as well as laboratory tests are used.

Ankylosing spondylitis cannot be cured. The main goal is to prolong the period of remission, which is achieved through complex treatment aimed at reducing pain, relieving inflammation, preventing and reducing stiffness of the joints and spine.

Our specialists will select for you a comprehensive treatment, which, in addition to drug therapy, includes physiotherapeutic procedures (ultrasound, Bernard currents, etc.) that have a good analgesic and anti-inflammatory effect. Also, an individual program for classes in the rehabilitation room will be developed for you, where, under close supervision, you will perform a number of exercises that will allow you to move fully.

Ankylosing spondylitis

Ankylosing spondylitis or ankylosing spondylitis is a term describing a form of arthritis that mainly affects the joints of the spine.This disease usually affects small joints between the vertebrae and reduces the mobility of these joints up to the formation of ankylosis (fusion of bones with each other) …

“Ankylosis” – means to become motionless or rigid; “Spondyl” means the spine; “It” means inflammation.

In ankylosing spondylitis, inflammation occurs outside the joint, where the ligaments and tendons attach to the bone, whereas in most forms of arthritis, inflammation affects the inside of the joint.This condition usually affects the small joints between the vertebrae and reduces the mobility of those joints. Thus, the main feature of joint inflammation is the gradual limitation of their mobility with the formation of ankylosis (bone fusion with each other). At the same time, ossification of the ligaments that strengthen the spine occurs. As a result, the spine can completely lose its flexibility.

Ankylosing spondylitis is a chronic (that is, long-term, long-term) condition, but in most cases the symptoms are moderate.With timely diagnosis and proper treatment, pain and stiffness in ankylosing spondylitis can be minimized, and disability and deformities can be significantly reduced or even prevented.

Ankylosing spondylitis is a systemic disease from the group of rheumatic arthritis, that is, inflammation is noted not only in the area of ​​the intervertebral joints, but also in other tissues. This means that other joints (hip, shoulder, knee, or feet) can be inflamed as well as tissues in the eye, kidneys, heart, and lungs.

Ankylosing spondylitis usually affects young people 13 to 35 years old (mean age 24 years), but may appear in the older age group. Men are affected about three times more often than women.


As with other forms of arthritis, the cause is unknown, but the hereditary factor is not denied.


Usually, the disease develops gradually, there are small pains in the lower back, which intensify over time and spread to other parts of the spine.Pains are persistent and only temporarily decrease after taking medication. Usually in the early morning, lower back stiffness and pain are more severe.

Gradually there is a limitation of the mobility of the spine, which sometimes occurs imperceptibly for the patient himself and is detected only with a special examination by a doctor. Sometimes the pain is very weak or even absent, and the only manifestation of the disease is a violation of the mobility of the spine. Changes in the spine usually spread from the bottom up, so difficulties in moving the neck appear rather late.In some cases, limitation of movement and pain in the cervical spine are observed from the first years of the disease.

Pain is not always limited to the back. Some people have chest pain from time to time.

Along with a decrease in the flexibility of the spine, the mobility of the joints connecting the ribs with the thoracic vertebrae is limited. This leads to impaired breathing and weakening of ventilation of the lungs, which can contribute to the onset of chronic lung disease.

In some patients, in addition to changes in the spine, pain and restriction of movement in the shoulder, hip, temporomandibular joints appear, less often pain and swelling of the joints of the arms and legs, pain in the sternum. These phenomena can be moderate and short-lived, but in some cases they are persistent and rather difficult. One side is usually more painful than the other.

Unlike arthritis in other diseases, inflammation of the joints in ankylosing spodilitis is rarely accompanied by their destruction, but it contributes to the limitation of mobility in them


Take into account the symptoms of the disease, be sure to make an X-ray of the bones and joints (primarily the pelvic bones, where the very first manifestations of the disease are visible).In some cases, blood tests are done for the HLA B27 gene.

Diagnosis is often difficult in the early stages or in mild cases because joint changes occur after several years of illness.


There is currently no specific treatment for ankylosing spondylitis, but there are many therapies for each individual to control symptoms and improve the quality of life of patients.

The main objective of the treatment is to reduce pain and maintain the mobility of the spine, to ensure the correct position of the spine as much as possible.

Ability to operate

People with ankylosing spondylitis are capable of most types of work. The ideal activity is one that allows for alternating periods of sitting, standing and walking, while constantly sedentary work is not suitable for such patients.


As people age, the spine gradually becomes naturally less mobile. In people over 50, this loss of mobility is more pronounced in those with ankylosing spondylitis.