Arthrosis-arthritis of the hip joint: ICD-10 code, treatment methods, therapeutic exercises

What is arthrosis-arthritis?

Osteoarthritis affects the cartilage tissue of the joints

Arthrosis-arthritis is a disease that affects both the joint and cartilage tissue. The disease is characterized by the symptoms, causes of development and clinical course of two diseases at once - arthritis and arthrosis.

Arthritis is inflammation of the joint capsule. The pathology may be associated with early injuries, infectious diseases, and autoimmune disorders. Arthritis is often a consequence of gout or psoriasis. The pathology manifests itself at any age and is associated with the functioning of the immune system, since inflammation in the joint begins due to the release of specific antibodies that cause a reaction.

Arthrosis is a degenerative disease that affects the cartilaginous layer located at the junction of bones. This layer plays a vital role - it ensures normal mobility of the joint, cushions the joint when walking, and protects the bones from friction. The main reasons for the development of arthrosis are heavy loads, a sedentary lifestyle, excess weight, and malnutrition of the cartilage due to injuries.

If arthritis is diagnosed in people of all age categories, arthrosis is more typical for older patients, since one of the factors in its development is the natural wear and tear of cartilage tissue.

Both diseases are characterized by pain and impaired mobility of the affected joint.

Osteoarthritis of the hip joint is a fairly common disease. The average age of patients is 50 years and older. Women are more likely to experience pathology than men due to their metabolism, which slows down after menopause.

Damage to the hip joint is associated with increased load on this joint. In the human body, the most vulnerable joints that take part in movement are the hip, knee and ankle joints.

Causes and provoking factors for the development of the disease

The presence of chronic diseases can cause arthrosis-arthritis of the hip joint

The main causes of arthrosis-arthritis of the hip joint:

• natural wear and tear of cartilage tissue;
• excess body weight;
• poor posture, flat feet;
• congenital anomalies of the structure of the musculoskeletal system;
• severe viral and infectious diseases;
• injuries and hypothermia of the joint;
• decreased immunity;
• metabolic disease;
• poor circulation in the lower body;
• chronic diseases.

The cartilage tissue of the hip joint wears out quickly, so about a third of people over the age of 60 experience some form of dysfunction. One of the most common factors leading to the development of the disease is excess weight. If you are overweight, the spine experiences severe stress during movement. This leads to increased load on the hip joint and increases the rate of wear of cartilage tissue. Because of this, blood circulation in the pelvic area and lower extremities is also impaired. The consequence is a malnutrition of the cartilage, its gradual thinning and destruction.

The inflammatory process characteristic of arthritis develops against the background of decreased immunity. If a person has recently had an infectious disease, the risk of developing arthritis increases. Also, in the presence of a chronic source of infection in the body, there is a risk of spread of pathogenic agents through the bloodstream and infection of the joint. Severe hypothermia can lead to the development of inflammation.

Joint injuries, bruises, fractures and other injuries are one of the factors in the development of arthritis. An accidental fall and bruise of the hip joint can cause the onset of an inflammatory process. Due to the structural features of this joint, arthritis and arthrosis often develop simultaneously, since injuries to the hip joint also lead to disruption of local blood circulation, as a result of which the cartilage does not receive additional nutrients.

The risk group for developing the disease includes people over 50 years of age and professional athletes.

Chronic diseases, such as diabetes, gout, psoriasis, systemic lupus erythematosus, scleroderma, are accompanied by circulatory disorders and changes in the functioning of the immune system. All this can lead to the development of problems of the musculoskeletal system, including arthrosis-arthritis of the hip joint.

As you can see, there are many factors that provoke the development of the disease. These also include intoxication of the body, chronic infectious diseases and even bad habits that impair metabolism and blood circulation.

Rheumatoid arthritis: reversibility of changes

Rheumatoid arthritis is a systemic immunoinflammatory disease of connective tissue, manifested by chronic erosive-destructive polyarthritis with predominantly symmetrical damage to the joints of the hands and feet and accompanied in most patients by the formation of a special type of autoantibodies (rheumatoid factor). Women get sick 3–4 times more often than men, and their disease usually begins at the age of 35–45 years.

Painful, stiff joints not only interfere with the most basic everyday movements, but also significantly disrupt the rhythm of normal life.

Rheumatoid polyarthritis is a severe systemic disease that manifests itself as progressive inflammatory synovitis, symmetrically affecting the peripheral joints of the extremities.

In accordance with the recommendations of the American Rheumatological Association (1987), when diagnosing rheumatoid arthritis, it is advisable to adhere to the following criteria:

• morning stiffness of joints or near joints lasting at least 1 hour until it completely disappears;
• soft tissue swelling (arthritis) of three or more joints observed by a physician (i.e., during the examination or in history under the supervision of a physician);
• swelling (arthritis) of the proximal interphalangeal, metacarpophalangeal, or wrist joints;
• symmetrical swelling (arthritis) in at least one pair of joints;
• rheumatoid nodules;
• presence of rheumatoid factor;
• detection by X-ray examination of erosions and (or) periarticular osteoporosis in the joints of the hands and feet.

With a long-term disease, the affected joints become deformed. In addition to the joints, with rheumatoid polyarthritis, periarticular structures (ligaments, tendons, etc.) are damaged, rheumatoid vasculitis (damage to small vessels), osteoporosis, and internal organs are damaged.

The immunopathological/autoimmune nature of the inflammatory process in rheumatoid arthritis is supported by the detection of autoantibodies, rheumatoid factor, in the blood serum and synovial effusion from the affected joints in most patients.

Genetic predisposition is of great importance in the development of rheumatoid arthritis. This is confirmed by the pronounced familial aggregation of the disease, the presence in some patients with rheumatoid arthritis of class II antigens of the major histocompatibility complex HLA DR4 and Dw4 (carriage of which is associated with severe arthritis and rapid progression of erosive changes in the joints). The role of hereditary or acquired disorders of T-suppressor regulation of immune reactions and insufficient function of the monocyte-macrophage system is considered. The triggering role in the development of rheumatoid arthritis can be played by: chronic foci of infection, hormonal changes in the body, food allergies, previous joint injuries, prolonged exposure to damp cold and physical overexertion.

With chronic inflammation at the edge of the articular cartilage at the site of attachment to the epiphyses of the articular capsule, sections of subchondral bone tissue are destroyed and replaced by pannus with the formation of erosions. Sometimes the expanding granulations penetrate through the subchondral endplate into the bone tissue. The products of osteochondral destruction, in turn, have an irritating effect on the synovial membrane, which helps maintain the inflammatory process in it. At the same time, inflammatory changes occur in the joint capsule, ligaments, synovial lining of tendons and synovial bursae, followed by sclerosis, leading to persistent limitation of mobility of the affected joints, subluxations and contractures. Sometimes necrosis and rupture of tendons and synovial bursae are observed. The development of secondary osteoarthritis is often noted.

The inflammatory process in rheumatoid arthritis is characterized by steady progression, the rate of which depends on the activity of the inflammatory process. Even during periods of clinical remission, signs of inflammation remain in the synovium. Gradually, the pannus destroys cartilage on a significant surface of the epiphysis, and the granulation tissue that replaces it connects the opposite articular surfaces and is subsequently transformed first into fibrous and then into bone tissue, which leads to the formation of fibrous and bone ankylosis, respectively, causing complete immobility of the affected joints.

X-ray examination of the joints reveals an asymmetry of erosive changes with frequent and early ankylosis of the wrist joints.

The course of seronegative rheumatoid arthritis is less severe and, in prognosis, more favorable than with the seropositive form of the disease: destructive (erosive) changes and functional disorders of the joints are less pronounced, ulnar deviation of the fingers, contractures and ankylosis are less common (with the exception of ankylosis of the wrist joints). At the same time, seronegative rheumatoid arthritis is less amenable to treatment with basic and immunosuppressive drugs than seropositive rheumatoid arthritis. Secondary amyloidosis develops more often.

In the treatment of rheumatoid arthritis, NSAIDs are used; in severe cases, glucocorticosteroids and immunosuppressants are used; in order to prevent osteoporosis, a combination of calcium and vitamin D preparations is usually prescribed.

Despite all the advances in pharmacology, rheumatoid arthritis still remains a serious disease with a poor prognosis.

Let us give an example from personal experience in managing a patient with rheumatoid arthritis, which, in the author’s opinion, is of scientific interest.

Patient V., age 71 years, consulted a neurologist in August 2006 with complaints of pain in the joints of the hands, knee joints, and lower back. The pain in the joints bothered me day and night, was usually severe, often migrating, and caused the limitation of all active and passive movements in the affected joints. Arthralgia was often combined with severe myalgia, ossalgia, and tendon pain. From the anamnesis: manifestations of polyosteoarthrosis for 15 years, debut of inflammatory articular syndrome in June 2002 (swelling and inflammation in the joints, febrile fever, laboratory-confirmed activity of the inflammatory process). On an outpatient basis (at first periodically, in the last 3 years constantly) she received NSAIDs (ibuprofen, indomethacin, diclofenac, aceclofenac). Since 2004, she regularly took calcium D3 (1 g calcium per day).

She received inpatient treatment at the city rheumatology center of St. Petersburg (April 2003, June–July 2006) with a diagnosis of rheumatoid arthritis, seropositive, with systemic manifestations (low-grade fever, amyotrophy, myalgia), grade 2 activity, functional insufficiency of joints of the 1st–2nd degree. Concomitant pathology: coronary heart disease, angina pectoris FC II. Hypertension of the 3rd degree, stroke (December 2002). Chronic bronchitis without exacerbation. Diffuse goiter of the second stage. Euthyroidism. Polyosteoarthrosis. Cholelithiasis.

Since 2003, he has been constantly receiving methotrexate at a dosage of 2.5 mg 2 times a week. Despite the treatment, joint pain increased, exacerbations became more frequent, and bone condition worsened (osteoporosis, erosion). X-rays of the hands are indicative (Fig. 1–2).

Since August 2006, during treatment with methotrexate, the neurologist additionally prescribed Structum at a dosage of 500 mg 2 times a day. The patient is oriented by the doctor to long-term, up to six months, taking the drug. A slight decrease in the intensity of the pain syndrome (which has been ongoing for the last 2 months) occurred after 3 weeks. There were episodes of exacerbations of rheumatoid arthritis for 4 months. By the end of the 5th month of combination therapy (methotrexate + Structum), the pain syndrome decreased significantly, morning stiffness decreased, and swelling of the wrist and knee joints subsided.

In February 2007, an X-ray of the hands was taken (Fig. 3). The result of comparison with previous x-rays was more than positive (bone erosions decreased). Reception of structum was extended for 3 months. As of May 2007, no exacerbations of the articular syndrome were observed for 4 months; slight swelling remained on the wrist (more on the left) and knee joints. In order to correct antirheumatic therapy (reduce the dose of methotrexate), the patient is recommended to consult at the city rheumatic center.

I. N. Baburin SPbNIPNI im. V. M. Bekhtereva, St. Petersburg

Symptoms of the disease

There is no diagnosis of “arthritis of the hip joint” in the international classification of diseases ICD-10. However, this diagnosis is widespread in domestic medicine. The International Classification of Diseases for Arthrosis Arthritis is classified according to ICD-10 as unspecified arthritis (M13.9) and coxarthrosis (M16).

Symptoms of the disease:

• aching pain in the joints;
• stiffness of movement in the morning;
• local numbness of the joint after prolonged inactivity;
• general malaise (fatigue, fever);
• hyperemia;
• swelling of the skin around the affected joint;
• crunching in the joint when moving the leg to the side.

Unlike arthritis, in which the pain goes away during the day, with arthrosis-arthritis of the hip joint the pain is constant. Discomfort intensifies with exertion, which is typical for arthrosis; pronounced swelling is present during the day, which is one of the main symptoms of arthritis.

In severe cases, the disease leads to severe deformation of the joint.

Arthrosis-arthritis of the hip joint is accompanied by severe swelling of the thigh. The skin around the affected joint may become swollen, red, and hot to the touch.

Symptoms and forms of ankle arthritis

Since the ankle joint is a single, well-coordinated mechanism, any malfunction in its operation is immediately felt in limited movements and pain. Therefore, it is pain that indicates developing degenerative processes. Depending on the form of the disease, it is often accompanied by a number of symptoms.

There are two main forms:

Spicy

Pain increases with increasing load on the joint. The result is limitation and stiffness in movements at the site of inflammation. Swelling and redness are also characteristic. The joint becomes hot, especially after exercise. The main difference between this form is that acute arthritis has a sudden onset and is accompanied by a burning sensation of pain in the cartilage area.

Causes: bacteria - specific, for example, gonococcus and nonspecific - when the disease appears as a result of furunculosis or tonsillitis. Sexually transmitted diseases can also cause infectious arthritis.

Chronic

An increase in temperature, swelling and redness may not be present, however, a combination of stiffness and pain, especially after a prolonged state of inactivity (for example, after sleeping or sitting for a long time) is a characteristic sign.

Causes: gradual accumulation of purines (salts) at the location of the cartilage. This process occurs mainly due to injury.

The listed symptoms, especially the presence of pain, indicate the need to immediately consult a doctor to diagnose the disease. Depending on the factors causing the disease, arthritis can be primary or secondary. The first includes the chronic course of the disease. Secondary indicates that the disease manifested itself as a result of an existing pathology, for example:

• Rheumatoid arthritis.
• Psoriatic arthritis.
• Reactive arthritis.
• Ankylosing spondylitis.
• Systemic lupus erythematosus.

These diseases are caused by autoimmune processes, that is, when a person’s immune system begins to fight against its own joint tissues, considering them foreign.

There are other factors that provoke the occurrence of a focus of the disease:

• Flat feet.
• Excess weight.
• Poor nutrition (especially foods that contribute to the accumulation of salts in the body).
• Genetic predisposition.

Purulent arthritis of the ankle

In this case, the disease progresses rapidly. Although this variant is uncommon, its etiology requires urgent action as the risk remains

blood poisoning and septic reaction of the body.

A purulent process in the joint is more common in children and newborns and less common in adults. However, in the latter, the focus of the disease often affects more than one joint.

Inflammation causes the penetration of bacteria into the synovial fluid, for example, from neighboring tissues, and further spread in its environment. Sometimes the cause can be staphylococcus, E. coli, gonococci and the like: Psev domonas aeruginosa, Enterococcus faecalis. Purulent arthritis manifests itself as follows:

• Sudden malaise.
• Temperature.
• Tachycardia.
• Nausea (in some cases vomiting).
• Smoothing the contour of the joint.

Some symptoms are similar to other types. Therefore, only a thorough examination will allow you to correctly prescribe treatment. Diagnosis is made by blood test, puncture, and x-ray of the affected joint. The purulent type of arthritis is clinically confirmed by the presence of an increased ESR, leukocytosis and determination of the biological composition of the fluid. A detailed list of necessary tests and indicators is compared according to ICD 10 for a detailed assessment.

Gouty arthritis of the ankle

Gouty arthritis of the ankle is always secondary. That is, it occurs against the background of metabolic disorders. As a rule, in such cases, the examination results confirm existing diseases of the endocrine system and kidneys. It is not uncommon for sufferers to be overweight.

Gout is the result of an accumulation of excess uric acid in the blood. This redundancy leads to its transformation into solid crystals. Those who abuse alcohol, meat and fish products also belong to the risk group. The accumulation of uric acid in the blood can also be caused by drugs with a diuretic function.

Acute manifestations of the disease are usually the result of accumulation of uric acid over time. (A more detailed description can be found in the ICD 10 classifier under codes M10.0, 1, 2, 3, 11.) In the initial period, a blood test may not show any obvious deviations from the reference values. Pain attacks can be episodic - lasting one day or more than a week. The further course of the disease has more pronounced symptoms:

• Chills.
• Weakness and malaise.
• Temperature increase.
• The attacks are longer and more severe.

And finally, in the chronic form, the following destructive symptoms are obvious:

• The appearance of tophi (deposits of uric acid in the subcutaneous tissue in the form of granulomas).
• Crunching during physical activity.
• Stiffness (after a long period of inactivity).

Diagnostics

Ultrasound, X-ray and MRI of the hip joint are mandatory when diagnosing arthrosis-arthritis

To make a diagnosis, you must consult a rheumatologist. Necessary examinations:

• blood analysis;
• X-ray of the hip joint;
• Ultrasound of the joint;
• MRI or CT.

A blood test is given to determine the very fact of the presence of an inflammatory process. A study of the level of rheumatoid factor is also carried out. If this antigen is present in the blood, a diagnosis of rheumatoid arthritis is made.

X-ray of the hip joint allows us to identify the degree of damage to bone and cartilage tissue, as well as the exact localization and spread of the pathological process.

Ultrasound is necessary to exclude salt deposits and osteophytes in the joint capsule or around the bone articulation. MRI and CT allows you to visualize the extent of damage to cartilage tissue.

Treatment principle

Treatment of arthrosis-arthritis of the hip joint is prescribed only by a doctor based on examinations

Therapy for joint damage and treatment of arthrosis-arthritis of the hip joint is aimed at:

• restoration of nutrition of cartilage tissue;
• normalization of metabolic processes in the joint;
• reduction of swelling;
• relief of the inflammatory reaction;
• reduction of pain syndrome.

For this purpose, both medicinal and non-medicinal methods are used. Additionally, physiotherapy and massage are prescribed. To restore the motor function of the diseased joint, it is necessary to perform special exercises.

Traditional Treatments

Conservative therapy consists of prescribing the following drugs:

• non-steroidal anti-inflammatory drugs;
• glucocorticosteroids;
• vasodilators;
• chondroprotectors;
• Dietary supplements and vitamins.

Nonsteroidal anti-inflammatory drugs are the first-line drugs of choice for inflammatory joint pathologies accompanied by pain. Medicines in this group relieve inflammation, reduce discomfort, and eliminate symptoms of general malaise, including fever. Usually the drugs Diclofenac, Ibuprofen, Nimesulide are used in any dosage form - ointments, tablets or injections.

Glucocorticosteroids are prescribed for severe inflammation, accompanied by severe swelling. These medications are unsafe and can only be used in a hospital setting. Glucocorticosteroids are administered intra-articularly.

Vasodilator medications are necessary to improve local blood supply. They can be used as a stand-alone remedy or in addition to physical therapy.

Chondroprotectors are a group of drugs that have a positive effect on the condition of cartilage. These medications increase the elasticity of cartilage, improve local metabolic processes and strengthen cartilage tissue.

Dietary supplements are necessary to accelerate the regeneration of the joint and cartilage, vitamins and mineral complexes are used as a prophylactic agent to avoid the progression of the disease.

Physiotherapy

Treatment must be supplemented with physiotherapy. For arthrosis-arthritis the following is prescribed:

• electrophoresis with vasodilators;
• magnetic therapy;
• ultrasound treatment;
• mud therapy;
• phonophoresis.

The choice of the optimal treatment method is made by a doctor. Physiotherapy is prescribed in a course of 10-20 procedures. This treatment is used only after the acute inflammatory process has stopped.

Exercise therapy for arthrosis-arthritis

Performing exercises or therapeutic exercises is an important part of the treatment of arthrosis-arthritis of the hip joint. This allows you to restore normal nutrition to the cartilage and improve the motor function of the diseased joint. A set of exercises will help avoid disability.

Exercise therapy must be performed in a special clinic room, under the supervision of a doctor. The specialist will create an optimal training system.

Simple exercises can be performed at home. They do not require special physical training, so everyone can do them.

1. It is comfortable to lie on your stomach with your arms extended along your body. Slowly raise your right leg, hold it in the upper position for a few seconds, and then lower and raise your left leg.
2. Lying on your stomach, raise both legs as high as possible and hold in the upper position for 15 seconds.
3. Sit on the floor with your legs extended straight in front of you. Smoothly tilt your torso towards your legs without lifting them off the floor, and then slowly straighten up.

All exercises should be performed smoothly, without effort. You should start your workout with five repetitions of each exercise. After a week of daily exercise, the number of repetitions can be increased to 10.

Folk remedies

Traditional medicine methods will help speed up recovery. At home, it is allowed to use warming, salt compresses, and lotions with alcohol tincture of propolis. Additionally, you can take drugs to strengthen the immune system and anti-inflammatory decoctions.

Folk remedies can only be used in addition to conservative treatment methods.

Modern principles of management of patients with early arthritis

In recent years, it has been indisputably proven that it is really possible to change the long-term outcomes of RA only at the very first stages of the disease [3]. The problem of early stage disease is not limited to RA. For all inflammatory rheumatic diseases, it is very typical to have a more or less long initial period, when adequate therapy has the most pronounced effect on their further course (“window of opportunity”). At the same time, RA is the most common chronic inflammatory rheumatic disease. Therefore, the early stage of RA, which represents a major general medical and social problem [4], attracts the greatest attention of researchers around the world.

In recent years, based on domestic and foreign clinical observations [2–5], it has definitely been shown that during the first 1–2 years of the disease in RA, irreversible structural damage to the joints can occur. In this case, the following are distinguished:

• 

“Very early RA” is a disease with a duration of symptoms of up to 3 months, since during this period it is possible to conclude that the arthritis is persistent (this period can be considered a potentially reversible condition), and “early” RA with a disease duration of up to 2 years, when it is possible to determine the presence or absence of a typical erosive process in the joints.

• Early RA

(or “early established RA”) – the first 1–2 years of the disease (when the first signs of disease progression can be identified).

• 

Undifferentiated arthritis (UA) is an inflammatory lesion of the joints that does not (yet?) meet the classification criteria for RA.

According to the scheme proposed by Firestein GS [6], immunopathological processes during the development of RA occur in 3 stages:

• 

The stage of “innate immunity”, when genetically determined immune mechanisms are activated by stimulating dendritic cells, macrophages, fibroblasts, and mast cells.

• 

The stage of “adaptive immunity”, during which the generalization of the process occurs with the inclusion of pro- and anti-inflammatory mechanisms.

• 

The stage of destruction, when pro-inflammatory stimuli prevail, activation of osteoclasts occurs with resorption of bone tissue and the introduction of proliferating synovial cells into cartilage.

This scheme corresponds to the idea that there are several stages in the formation of the clinical picture of the disease, at each of which genetic factors must be combined with the influence of hypothetical environmental factors [7]. This scheme explains the possibility of both typical and atypical (in the form of AN) onset of the disease, as well as the formation of clinical heterogeneity.

Observations of a large cohort of patients [8] within the framework of the Program “Early Arthritis: Diagnosis, Outcome, Criteria, Active Treatment (RADICAL)” showed that of 366 patients with inflammatory joint damage and a disease duration of up to 1 year, only 57.9% had immediate a diagnosis of RA could be established, 36.3% were classified as having AN, 5.7% had other diagnoses made during the initial examination. After 12 months, the diagnosis of RA was established in 33.1% of patients with AN (Fig. 1), which corresponds to the data of foreign researchers [9].

Thus, clinical observations indicate the following features of early RA:

• 

the disease only in 50–60% of cases debuts with a typical clinical picture;

• 

in 1/3 of patients with a picture of inflammatory joint damage, the so-called ON THE;

• 

In patients with AN, RA develops in approximately 30% of cases during 1 year of observation.

Difficulties in objective diagnosis are due to the fact that in RA there are no pathognomonic symptoms. This even applies to such a classic symptom as arthritis of the hands. When diagnosing RA early, the following features must be taken into account [10]:

1) arthritis of the metacarpophalangeal and metatarsophalangeal joints can be asymmetrical;

2) lesions of the periarticular tissues are detected early: tenosynovitis of the flexors and extensors, amyotrophy of the interosseous muscles;

3) there are characteristic symptoms:

• 

positive symptom of hand compression,

• 

flexion contracture of fingers,

• 

inability to clench the hand into a fist.

The most important problem of early diagnosis of RA from the point of view of healthcare organization is the late application of first-time patients for specialized medical care. Since time in this case is a critical factor that largely determines the outcome of treatment, to improve the interaction of primary care physicians with specialist rheumatologists of the European League Against Rheumatism (EULAR), the criteria for clinical suspicion of RA, already tested in our country, are recommended, which are indications for consultation with a rheumatologist [5]:

• 

The presence of 3 or more swollen joints;

• ‑

Involvement of the metacarpophalangeal and metatarsophalangeal joints (positive symptoms of “compression”);

• 

Morning stiffness ≥ 30 minutes.

We recommend, based on our own experience, to suspect RA even in patients with 1-2 swollen joints, since the onset of the disease with mono- and oligoarthritis is not uncommon.

According to the algorithm for staged early diagnosis of RA developed at the Institute of Rheumatology of the Russian Academy of Medical Sciences [8], if there are criteria for clinical suspicion, the patient should be sent to the next stage of diagnosis - examination by a rheumatologist at the clinic, and, if necessary, to the stage of the rheumatology department.

The modern rheumatologist’s “arsenal” for early diagnosis of inflammatory joint diseases is quite wide:

• 

Classification criteria, for the determination of which a thorough clinical examination is of primary importance;

• 

Immunological tests: rheumatoid factor (RF), study of anti-citrullinated antibodies, in particular, antibodies to cyclic citrullinated peptide (ACCP), etc.;

• 

Instrumental methods: in addition to traditional radiography, magnetic resonance imaging (MRI), ultrasound examination (US) of hand joints are increasingly being used;

• 

Immunogenetic studies (typing of certain human leukocyte antigens - HLA) may be relevant;

• 

In some variants of differential diagnosis, especially in the case of the onset of the disease with oligoarthritis of large joints, arthroscopy and biopsy of the synovial membrane may be of utmost importance.

Among the new immunological methods, the determination of ACCP is of greatest importance. This method has now practically become the second standard immunological test (the first is the determination of RF) for diagnosing RA.

This test is quite specific (75–90%) for RA, and its sensitivity at the early stage of the disease also reaches 75% [11]. It is especially important to determine ACCP in patients who are seronegative for RF. As numerous literature data show [12], ACCP, especially the 2nd generation (ACCP-2), is more specific for RA than RF, and can also be successfully used to predict the development of RA in patients with AN. In addition, a high titer of ACCP is associated with a more severe course of the disease (in particular, with a more rapid progression of erosive changes in the joints) [12], as well as with persistently high activity of RA [13], so this test has an undoubted prognostic value.

Methods for the immunological diagnosis of RA are now at a stage of rapid development; many new tests have been proposed, each of which has its own advantages:

• 

Anti-citrullinated antibodies:

– ATsCP-2, ATsP-3,

– ‑A/t to mutated citrullinated vimentin (anti-MCV),

– A/t to citrullinated fibrinogen,

– A/t to citrullinated α-enolase,

– A/T to citrullinated type II collagen,

• 

A/t to RA33 – heterogeneous nuclear nucleoprotein A2 (hnRNP-A2).

An algorithm for the immunological diagnosis of RA has been proposed [14], based on repeated determination of RF, ACCP, anti-MCV, RA33 over time, which, with correct interpretation, should help not only make a nosological diagnosis, but also clarify the prognosis of the disease (Fig. 2).

Identification of early structural changes is one of the main directions of diagnostic search for early RA. MRI of the hand joints currently has the greatest potential in this regard. This modern technique allows:

• 

To objectify the presence of synovitis in doubtful cases;

• 

Carry out differential diagnosis with periarticular lesions;

• 

Identify early erosive and pre-erosive changes (bone marrow edema, cartilage damage), tendon pathology.

MRI is much more sensitive than standard radiography in detecting early signs of osteochondral destruction. Special studies [15] devoted to the comparison of the detection of bone erosions by different methods have shown that X-ray negative erosions detected using MRI and ultrasound can be considered true erosions.

Immunological and instrumental indicators turn out to be interrelated. Thus, we have shown that in the presence of high levels of ACCP and C-reactive protein, high RA activity, high RF and a large number of erosions according to MRI are observed in patients with early RA. Thus, data from immunological and instrumental studies can help in determining the severity of the patient’s condition and, accordingly, in choosing therapy.

It can be especially difficult to clarify the diagnosis in patients with AN, which, according to our observations [16], most often occurs in the following clinical variants:

• 

Oligoarthritis of large joints (knees, ankles, shoulders, hips);

• 

Asymmetrical arthritis of the hand joints;

• 

RF seronegative oligoarthritis of the joints of the hands;

• 

Unstable polyarthritis.

Often, verification of the nosological form requires months of observation and repeated examinations. Special criteria (decision rule) have been proposed to predict the transformation of AN into “real” RA (Table 1) by calculating the sum of points [17]. These criteria were recently tested in 3 independent cohorts of patients with AN [18]. At the same time, the accuracy of prediction turned out to be very high: the accuracy of predicting low risk of transition to RA (≤6 points) was 83–86%, high risk (≥8 points) – 93–100%.

In 2007, EULAR guidelines for the management of early arthritis were published [19]. Just like recommendations for other nosologies (gout, ankylosing spondylitis), these recommendations were developed by a large group of experts according to a specific procedure, assessing the strength of evidence for each point. These recommendations are summarized below.

1. Arthritis is characterized by swelling of the joint accompanied by pain and stiffness. A patient with arthritis in more than one joint should be seen by a rheumatologist, ideally within 6 weeks of symptom onset.

2. Clinical examination is the main method for identifying synovitis. In difficult cases, it is useful to use ultrasound, laser Doppler examination, and MRI.

3. Exclusion of other diseases (non-RA) requires a thorough interview and clinical examination of the patient, as well as at least the following tests: complete blood count, urinalysis, transaminases, antinuclear antibodies.

4. For each patient with early arthritis referred to a rheumatologist, the following factors for the development of persistent erosive arthritis should be determined:

• 

number of swollen and painful joints,

• 

ESR or CRP,

• 

RF and ACCP,

• 

erosion on radiographs.

5. Patients at risk of developing persistent erosive arthritis, even if the patient does not meet the classification criteria for RA, should be prescribed basic therapy as early as possible.

6. It is important to inform the patient about the disease, treatment and outcome. As an additional means, a special educational program can be carried out.

7. Prescription of non-steroidal anti-inflammatory drugs (NSAIDs) should be considered in the presence of symptoms of arthritis after assessing the condition of the gastrointestinal tract, cardiovascular system and kidneys.

8. Systemic glucocorticoid (GC) treatment reduces pain and swelling and should be considered as adjunctive (primarily temporary) therapy as part of a basic treatment strategy. Intra-articular administration of GC should be considered as a means of relieving local symptoms of inflammation.

9. Among disease-modifying anti-inflammatory drugs (DMARDs), methotrexate is considered the main (“anchor”) drug and should be prescribed first in patients at risk of developing persistent disease.

10. The main goal of therapy is to achieve remission. Regular monitoring of disease activity and side effects should lead to decisions regarding the choice and change of therapy (DMARDs and genetically engineered biological drugs).

11. Non-pharmacological methods, such as exercise therapy, physiotherapy, can be used as an addition to drug therapy.

12. Monitoring of disease activity should include the number of swollen and painful joints, assessment of general condition by the patient and physician, ESR and CRP. Disease activity should be assessed at 1–3 month intervals until remission occurs. Structural damage should be assessed with radiographs of the hands and feet every 6 to 12 months during the first few years of the disease. Assessment of function (eg, HAQ) can be added to monitoring activity and structural damage.

The EULAR recommendations represent a major step forward in improving practical care for people with early arthritis. As a comment, I would like to draw your attention to the following main points:

• 

It is emphasized that the main thing in diagnosis is a clinical examination by a rheumatologist;

• 

It was confirmed that the suspicion of RA in oligoarthritis is reasonable; the localization of arthritis is not specifically identified;

• 

ACDCs are recommended for widespread use along with RF;

• 

It is recommended to prescribe DMARD therapy to patients who do not fully meet the 1987 RA criteria in the presence of risk factors for persistent erosive arthritis;

• 

It is emphasized that the main basic drug is methotrexate;

• 

Caution when prescribing NSAIDs;

• 

The important role of HA has been confirmed;

• 

It is emphasized that the key to success is early prescription and regular monitoring of basic therapy.

It is now well known that the first few months from the onset of the disease are the time of the most rapid progression of structural damage, when the basis for the further development of the disease is formed. In this regard, the main concept of therapy for early RA is currently recognized as the concept of a “window of opportunity” [20], when active treatment can affect the further course of the disease.

Practical observations made it possible to formulate new treatment goals – remission or, at a minimum, persistently low disease activity [21].

DMARDs remain the basis of treatment for RA: methotrexate, leflunomide, sulfasalazine. At the same time, DMARD monotherapy (+ NSAIDs as a symptomatic agent) is increasingly being replaced by combination therapy regimens (Fig. 3).

Most often, DMARDs are combined with GCs. Extensive treatment experience has made it possible to identify 2 main areas of use of GCs in early RA:

• 

Rapid suppression of inflammatory activity in the period before the development of the effect of DMARDs (
bridge
therapy);

• 

Achieving higher efficiency, inducing clinical remission, and in some cases slowing down the destruction of joints - with long-term use of low doses (<10 mg/day of prednisolone).

Despite the generally good results of combination therapy with DMARDs and GCs, there remains a significant number of patients with early RA (about 40%), in whom a sufficient clinical response to therapy is not achieved or joint destruction continues. For these patients, the optimal combination of DMARDs and genetically engineered biological drugs (primarily TNF inhibitors). In Russia, chimeric monoclonal antibodies to TNF-α (infliximab) and human monoclonal antibodies to TNF-α (adalimumab) are actively used. The latter have lower immunogenicity, which is manifested in a significantly lower incidence of antibodies to adalimumab and, accordingly, in a decrease in the frequency of hypersensitivity reactions.

Biological drugs have all the features characteristic of DMARDs (suppression of inflammatory activity, inhibition of joint destruction, possible induction of remission), but the effect, as a rule, develops much faster (sometimes immediately after infusion) and is much more pronounced, including in relation to inhibition of destruction joints.

A characteristic feature of therapy with genetically engineered biological drugs is the achievement of clinical remission. The results of randomized studies BeSt [22–24], PREMIER [25], TEMPO [26] show that the rate of stable remission when treated with a combination of methotrexate with each of the TNF-α inhibitors (infliximab, adalimumab and etanercept) when observed for 2–3 years was comparable and amounted to about 50%. A good clinical effect in this case, as a rule, was accompanied by a pronounced slowdown in the progression of joint destruction (in contrast to conventional DMARDs).

Data accumulated over recent years have allowed Suresh E. and Lambert CM [27] to postulate the following:

• 

Combination therapy improves clinical response to treatment, slows radiographic progression, improves joint function outcome, and reduces disability compared with monotherapy;

• 

The “
step-down
” strategy has advantages over the “
step-up
” strategy, since it gives a chance to quickly and effectively suppress inflammation;

• 

GCs and TNF inhibitors are a promising component of combination therapy for early RA, as they allow rapid suppression of inflammatory activity;

• 

Even short-term use of aggressive combination therapy in the early stage of RA provides significant improvement in long-term results compared with monotherapy;

• 

Currently, the effectiveness of combination therapy with the inclusion of GC and TNF inhibitors is most well proven.
Methotrexate plays the role of an “anchor” drug
for all successful combinations;

• 

Despite the previous belief that combination therapy regimens were more toxic, recent large controlled studies have shown that this is not the case.

Unfortunately, the introduction of TNF inhibitors into widespread practice does not completely solve the issue of treating early RA. As a rule, to maintain lasting improvement, ongoing (many months and many years) maintenance treatment is required, so it is difficult to talk about a cure. The same applies to patients with AN. The recently published first placebo-controlled study of a biologic in these patients [28] in a small group (17) of patients showed that a short course (4 infusions) of infliximab did not prevent the development of RA in patients with AN.

Due to the high demand for new genetically engineered biological drugs, more and more new molecules are being introduced into practice, aimed at various mechanisms of pathological activation of the immune system (anti-B-cell drug rituximab, costimulation blocker abatacept, interleukin-6 receptor inhibitor tocilizumab, etc.) .

In general, modern principles of management of patients with early RA can be summarized as follows:

• 

Early diagnosis;

• 

Assessing prognosis is a key point in choosing treatment;

– ‑Determination of immunological markers (anti-citrullinated antibodies),

– ‑Detection of early structural changes (MRI, ultrasound);

• 

All patients should receive methotrexate (or another DMARD), often in combination with GC;

• 

The goal of treatment is remission or at least low disease activity;

• 

With high disease activity, early administration of genetically engineered biological drugs (TNF inhibitors) is required;
•
Long-term use of maintenance doses of DMARDs and genetically engineered biological drugs can stop the destruction of joints.

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Does early rheumatoid arthritis exist? //Best Pract. Res. Clin. Rheumatol., 2005, v.19, No. 1, p. 37–53 8. Karateev D.E., Luchikhina E.L., Tyurina L.N. et al. Early diagnosis of rheumatoid arthritis in clinical practice at the present stage (results of observations of a Moscow cohort of patients with early arthritis within the framework of the RADIKAL program). Ter. Archive, 2008, No. 5, p. 8–13 9. Van Aken J., van Dongen H., le Cessie S. et al. Comparison of long term outcome of patients with rheumatoid arthritis presenting with undifferentiated arthritis or with rheumatoid arthritis: an observational cohort study. Ann Rheum Dis 2006;65;20–25 10. Karateev D.E. Rheumatoid hand. //Consilium medicum, 2005, No. 2, pp. 83–87 11. Aleksandrova E.N., Chemeris N.A., Karateev D.E. et al. Antibodies to cyclic citrullinated peptide in rheumatoid arthritis. Ter. Archive, 2004, No. 12, p. 64–68 12. Avouac J., Gossec L., Dougados M. 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