Joint pain and swelling, rheumatoid arthritis

Rheumatoid arthritis is a chronic systemic inflammatory disease that affects symmetrical joints, usually the hands and feet. They swell, become deformed and lose their mobility.

This pathology belongs to the group of arthritis of an autoimmune nature (in contrast to metabolic arthropathy, such as gouty arthritis, where the pathological process is associated with metabolic disorders), which is characterized primarily by damage to the synovial membrane lining the joint. In the early stages, the disease is similar to a common cold, accompanied by aching joints.

According to statistics, approximately 2 million Russians and about 1% of all people living on our planet suffer from rheumatoid arthritis. Before the advent of modern treatment methods, from 50 to 70% of patients lost their ability to work within 5 years from the onset of the disease. Most often, this type of arthritis affects middle-aged and older women.

Children, although very rarely (6-19 children per 100 thousand people), can also be susceptible to this disease. The childhood form of the disease is called juvenile arthritis (JRA).

1

Consultation with a rheumatologist

2 Diagnosis of arthritis

3 Consultation with a rheumatologist

There are 3 main factors as the cause of the disease (rheumatological triad)

1. Genetic predisposition
   Hereditary tendency to autoimmune reactions
2. More common in carriers of a certain MHC II class antigen: HLA - DR1, DR4
3. Infectious factor
   paramyxoviruses - mumps, measles, respiratory syncytial infection viruses
4. hepatoviruses - hepatitis B virus
5. herpes viruses - herpes simplex viruses, herpes zoster, Cytomegalovirus, Epstein-Barr virus
6. retroviruses - T-lymphotropic virus
7. Triggering factor (hypothermia, hyperinsolation, intoxication, mutagenic medications, endocrinopathies, stress, etc.). For women, breastfeeding for a longer period of time reduces the likelihood of developing RA. Breastfeeding for 24 months or longer reduces the risk of developing RA by half.

Diagnosis of arthritis

Rheumatoid arthritis is diagnosed by a rheumatologist/arthrologist.

Before confirming or denying the diagnosis, the arthrologist/rheumatologist will listen to the patient’s complaints, examine the joints and prescribe the necessary examination.

Diagnosis usually includes the following tests (see also rheumatology examination):

• blood test for rheumatoid factor (the presence of RF indicates so-called seropositive rheumatoid arthritis (prognostically more severe form), the absence of RF indicates a seronegative variant of the disease);
• blood test for ACCP;
• blood test for the level of C-reactive protein (indicates the presence of an inflammatory process);
• blood test for erythrocyte sedimentation rate (determines the phase of the disease - exacerbation or remission);
• radiography of the joints (visualizes the condition of the joints at any stage of arthritis;
• MRI of joints (specifies the condition of the joint and its components).

1 MRI of joints

2 Diagnosis of arthritis

3 X-ray of joints

Diagnosis of the disease

Based on a biochemical blood test , changes in the joints visible on x-rays , and the use of basic clinical markers . A blood test examines ESR, rheumatoid factor, platelet count, etc. The most progressive analysis is the titer of antibodies to cyclic citrulline-containing peptide - ACCP, anti-CCP, anti-CCP. The specificity of this indicator is about 90%, while it is present in 79% of sera from RA patients.

Diagnostically important clinical features are the absence of changes in skin color over the inflamed joints, the development of tenosynovitis of the flexors or extensors of the fingers and the formation of amyotrophies, typical deformities of the hands, the so-called “rheumatoid hand”.

The criteria for an unfavorable prognosis are:

• early damage to large joints and the appearance of rheumatoid nodules;
• swollen lymph nodes;
• involvement of new joints during subsequent exacerbation;
• systemic nature of the disease;
• persistent increase in ESR;
• early appearance (during the first year) and high titers of rheumatoid factor;
• early (up to four months) radiological changes in the affected joints - rapid progression of destructive changes;
• detection of antinuclear antibodies and LE cells;
• carriage of HLA-DR4 antigens; poor tolerability of basic drugs.

In the treatment of rheumatoid arthritis, systemic drug therapy with various groups of drugs is used.

Rheumatoid arthritis - symptoms and treatment

During rheumatoid arthritis, there is a prodromal period , which forms several weeks and/or months before the development of the typical symptom complex inherent in rheumatoid arthritis. It is manifested by general weakness, malaise, pain in muscles and joints, loss of appetite, low-grade fever (from 37.1 to 38 °C) [1][2][8].

The onset of rheumatoid arthritis can clinically manifest itself in various ways:

• nonspecific signs with slightly pronounced articular manifestations (moderate joint pain);
• acute polyarthritis (pain, swelling of two or three joints, limited range of motion in them) with predominant damage to the joints of the hands and feet, severe morning stiffness;
• acute polyarthritis with systemic manifestations: febrile fever (temperature from 38 to 39 °C); lymphadenopathy (enlarged lymph nodes; can increase to the size of a walnut); hepatosplenomegaly (enlarged liver and spleen) [1].

The early stage of RA is characterized by damage to the second and third proximal interphalangeal and metacarpophalangeal joints, as well as a positive symptom of compression of the hand or foot (sharp pain occurs when the hand or foot is compressed) at the level of the metacarpophalangeal and metatarsophalangeal joints. A typical symptom of RA is fusiform defiguration (change in joint shape, such as a swan neck or button loop) of the proximal interflank joints of the hands.

One of the earliest and most characteristic symptoms is morning stiffness (the patient cannot bend and straighten the joints, as if his hands were wearing tight gloves). The severity of stiffness is clearly related to inflammatory activity. With high activity of the inflammatory process, it lasts for many hours, but is especially pronounced in the morning and always decreases after physical activity.

In the advanced and final stages of the disease, destruction, deformation and ankylosis typical of RA appear (fusion of the joint, lack of movement in it).

Brushes:

• ulnar deviation of the metacarpophalangeal joints (fingers deviate to the ulnar side in the form of walrus fins), usually 1-5 years from the onset of the disease;
• lesions of the fingers of the hands in the “boutonniere” type (flexion in the proximal interphalangeal joint) or “swan neck” (hyperextension in the proximal interphalangeal joint);
• deformation of the hand according to the “lornette” type [1][5].

Knee joints: flexion and valgus (knees roll inward) deformity, Baker's cyst (popliteal or knee cyst).

Feet: subluxation of the heads of the metatarsophalangeal joints, lateral deviation (deviation of the big toe towards the other toes), deformation of the big toe.

Cervical spine: subluxations in the area of ​​the atlantoaxial joint, sometimes complicated by compression of the spinal cord or vertebral artery.

Cricoid-arytenoid joint: deepening of the voice, shortness of breath, dysphagia (the patient cannot swallow), recurrent bronchitis.

Ligamentous apparatus and synovial bursae: tenosynovitis (inflammation of the tendon sheaths) in the area of ​​the hand and wrist joint; bursitis (inflammation in the synovial bursa), most often in the elbow joint; synovial cyst on the back of the knee joint (Baker's cyst).

RA is characterized by a variety of extra-articular and systemic manifestations.

Constitutional symptoms : generalized weakness, malaise, weight loss to the point of exhaustion (weight less than 40 kg), low-grade fever.

In the polymorphic picture of rheumatoid arthritis, cardiac involvement is uncommon. Cardiac symptoms can be caused either by the direct inflammatory process in the heart or by a complication of RA—atherosclerosis. With this disease, the myocardium (the thickest muscle of the heart), the pericardium (the outer lining of the heart), the endocardium (the inner lining of the heart), the aorta and the coronary arteries of the heart may be involved in the pathological process. There are diseases such as pericarditis (inflammation of the outer lining of the heart), granulomatous damage to the heart valves (very rare), early development of atherosclerosis, inflammation of the coronary arteries [1][6].

Lung damage is common in RA . It manifests itself:

• pleurisy (inflammation of the pleural layers);
• interstitial lesions of the lungs (inflammation and disruption of the structure of the alveolar walls, pulmonary capillaries);
• obliterating (obstructive) bronchiolitis (persistent, progressive blockage of small bronchi);
• rheumatoid nodules in the lungs (Kaplan syndrome).

The most serious manifestation of lung damage is fibrosing alveolitis , which is caused both by the disease itself and by the use of some basic anti-inflammatory drugs, namely methotrexate, gold drugs and D-penicillamine [1][6][7]. Fibrosing alveolitis is manifested by a nonproductive cough (dry, without sputum), expiratory shortness of breath (difficulty exhaling), gray cyanosis. It leads to increased pressure in the pulmonary artery and the development of cor pulmonale (enlargement of the right side of the heart). The radiograph reveals an increase in the pulmonary pattern, the “honeycomb” phenomenon (a destructive change in the lungs, characterized by the content of numerous cystic air spaces with thick walls).

Skin syndrome has many manifestations. A typical extra-articular symptom is rheumatoid nodules (bone formations on joints the size of a pea or walnut), which are located under the skin most often on the extensor surface of the elbow joints; in an atypical location they can appear on the Achilles tendon, cornea, and tendons.

The development of various pathologies is also considered skin manifestations of rheumatoid arthritis:

• cutaneous vasculitis (inflammation of skin vessels) from ulcerative-necrotic changes to thickening and hypotrophy of the skin;
• digital (digital) arteritis (inflammation and destruction of subcutaneous vessels), rarely with gangrene of the fingers;
• microinfarctions in the nail bed area (circulatory disorders, blockage of a vessel with a microthrombus and the appearance of black dots on the fingers),
• livedo reticularis (reticular asphyxia, or Livedo reticularis) - a delicate blue pattern in the form of lace [8].

Lesions of the peripheral nervous system are explained by compression of the nerve trunks or their vascular damage. Rheumatoid arthritis is characterized by compression neuropathies: carpal tunnel syndrome (prolonged pain, numbness of the fingers), tarsal tunnel (pain in the ankle joint, a feeling of crawling on the arm), etc. Compression of the nerve trunks is manifested by pain, a feeling of crawling, numbness , regional muscle atrophy. Damage to peripheral nerves is also possible, which manifests itself as sensory or sensory-motor disorders.

is of great importance in rheumatoid arthritis : atrophy of the interosseous muscles of the hand, tenor (eminence of the thumb), hypotenor (eminence of the little finger). Characteristic is atrophy of the muscles that are located close to the affected joints, for example, atrophy of the interosseous muscles of the hands, the muscles of the lower third of the thigh in the case of severe arthritis of the knee joints. Amyotrophy (lack of muscle) can be a manifestation of rheumatoid vasculitis, neuropathy, for example, with carpal or cubital tunnel syndrome, long-term use of glucocorticoids, and limitation of muscle activity [1][2][8].

Eye pathology is one of the characteristic manifestations of rheumatoid arthritis . Episcleritis (inflammation of eye tissue) often occurs, which is very rarely accompanied by a severe course or outcome in perforating scleromalacia (softening of tissue) with the formation of holes in the cornea and enucleation (removal of the nucleus).

With scleritis (inflammation of the sclera of the eye) and sclerokeratitis (inflammation of the sclera and cornea of ​​the eye), severe pain and redness of the sclera appears. This disease is also characterized by dry eye syndrome, which is a consequence of the accumulation of lymphocytes in the lacrimal glands and is usually considered within the framework of Sjogren's syndrome.

Kidney pathology is manifested by diffuse glomerulonephritis (damage to the glomerular apparatus of the kidneys), widespread amyloidosis (accumulation of amyloid protein) with predominant damage to the kidneys or drug-induced nephropathy (damage to the tissue and glomerular apparatus of the kidneys). The latter is caused by taking nonsteroidal anti-inflammatory drugs (NSAIDs), such as diclofenac, or combined analgesics with phenacetin, which leads to the development of interstitial nephritis (inflammation in the interstitial tissue of the kidneys).

The blood system reacts to the autoimmune inflammatory process by developing anemia, thrombocytosis (increased platelet content in the blood), neutropenia (decreased number of neutrophils). Secondary, drug-related complications are also possible:

• in response to taking cytostatics in the form of pancytopenia (decrease in the level of all types of blood cells);
• against the background of high doses of glucocorticosteroids in the form of a leukemoid reaction (increase in the total number of leukocytes).

The macrophage system often responds to an active inflammatory process by developing lymphadenopathy (enlarged lymph nodes), splenomegaly (enlarged spleen), and the formation of a special form of rheumatoid arthritis in the form of Felty's syndrome [2][7].

Damage to the gastrointestinal tract (GIT) can be represented by secondary amyloidosis, autoimmune hepatitis, but most often erosive lesions are detected due to the use of NSAIDs or glucocorticosteroids.

Patients with highly active rheumatoid arthritis may develop vasculitis:

• digital arteritis;
• palpable purpura (hemorrhagic rash),
• reticular asphyxia (purple reticular vascular pattern on the skin);
• peripheral polyneuropathy;
• visceral arteritis: coronaryitis (inflammatory damage to the walls of blood vessels supplying the myocardium), mesenteric thrombosis (blockage of blood vessels in the tissue with which the intestine is attached to the abdominal wall), intestinal infarction, acute pneumonitis, alveolitis);
• Raynaud's syndrome (numbness and pain in the fingers).

Endocrine manifestations - due to the autoimmune nature of the disease, autoimmune thyroiditis (a chronic disease of the thyroid gland in which gradual destruction of cells) and Sjögren's syndrome can develop simultaneously.

There are also rare special clinical forms of rheumatoid arthritis:

Felty's syndrome is characterized by the following symptom complex: neutropenia, splenomegaly, hepatomegaly, severe joint damage, extra-articular manifestations (vasculitis, neuropathy, pulmonary fibrosis, Sjogren's syndrome), hyperpigmentation of the skin of the lower extremities, high risk of infectious complications. This syndrome develops in patients with long-term RA.

Still's disease in adults - recurrent febrile fever, arthritis, maculopapular rash, high laboratory activity. It is equally common in men and women. This syndrome is characterized by a debilitating fever that often reaches temperatures above 41 °C. The fever is persistent and reacts paradoxically to therapy. Joint damage is characterized by a benign course. With Still's syndrome, leukocytosis with a shift of the formula to the left, increased activity of liver enzymes, anemia, dysproteinemia (shift in the protein composition of the blood plasma), accelerated erythrocyte sedimentation rate (ESR), increased C-reactive protein, which reflects acute inflammatory processes in the body, hyperferritinemia ( increased ferritin in the blood) [1][8].

Forecast

Rheumatoid arthritis is a disease with a poor prognosis. This means that, despite the treatment, it is impossible to achieve a complete recovery. In addition, treatment drugs are extremely toxic.

The life expectancy of patients with rheumatoid arthritis is on average 5-10 years less than in the general population. In such patients, due to constant chronic inflammation, the risk of sudden cardiovascular death, internal bleeding, and infectious complications is increased.

Reasons for development

The exact factors contributing to the onset of rheumatoid arthritis have not been established. Presumable causes of the development of rheumatoid arthritis:

• weakened immunity and allergies;
• obesity;
• liver and kidney diseases;
• various injuries, surgeries in the anamnesis;
• viruses and bacteria (latent infection);
• stress and long-term depression;
• overdose of hormonal drugs;
• bad habits;
• heredity.

Whatever factor causes this disease, it will certainly lead to disruption of the immune system.

Pathogenesis

Rheumatoid arthritis is classified by specialists as an autoimmune disease. This group of diseases is characterized by the behavior of protective cells - lymphocytes. They, instead of actively diagnosing foreign bacteria, fungi, viruses, and destroying them, begin to attack their own healthy cells.

This pathological process of disruption of the interaction of cells of the immune system in the immune response consists of the following stages:

• Synoviocytes acquire the features of macrophages, secrete proinflammatory cytokines, primarily tumor necrosis factor alpha, interleukin 1, become antigen-presenting cells and cause activation of T-helper type 1 cells.
• In the cells of the synovial fluid and in the synovium of the joint, a large number of T-helper type 1 cells appear, secreting interferon gamma and activating macrophages.
• Activated macrophages and monocytes produce pro-inflammatory cytokines: tumor necrosis factor alpha, IL-1, IL-6.
• An increase in the concentration of IL-8 in the synovial fluid causes a high concentration of neutrophils in it.
• IL-1 causes fever, activation of osteoclasts, which contributes to osteoporosis of the subchondral plate of bone. Tumor necrosis factor causes the appearance of adhesion molecules on the surface of endothelial cells, promoting exudation, causing weight loss, anemia of chronic inflammation. I16, ​​activating hepatocytes, causes an increase in their production of C-reactive protein; activates B lymphocytes (transforming them into plasma cells).
• In the blood, the concentration of plasma cells producing immunoglobulins increases significantly.
• In the blood and synovial fluid of 80% of patients, the concentration of IgM and IgG to the altered Fc region of IgG sharply increases (rheumatoid factors).
• The release of endothelial growth factor promotes the proliferation of capillaries in synovial tissue. Angioneogenesis and proliferation of active fibroblasts and synoviocytes lead to the formation of pannus - aggressive tissue that has signs of tumor-like growth, capable of penetrating into cartilage, the articular surface of the bone, forming erosions, and into the ligamentous apparatus. It is important to note that the clone of uncontrollably multiplying, aggressive synoviocytes that makes up the pannus is formed relatively late - several months after the onset of the disease.
• The formation of immune complexes in the blood as a result of the interaction of IgG with rheumatoid factors leads to complement activation and damage to the microvasculature, which explains the visceral manifestations of rheumatoid arthritis. In the later stages of rheumatoid arthritis, proliferative processes (growth of pannus) may not depend on autoimmune mechanisms and are maintained autonomously.

Treatment of arthritis of the finger joints

Treatment can be carried out therapeutically or surgically. In the initial stages of the development of the disease, complex conservative treatment of the disease can achieve high effectiveness. All medications and additional treatments must be prescribed after a thorough examination to completely eliminate the possibility of an incorrect diagnosis. Under no circumstances should you self-medicate, since the symptoms of arthritis in the joints of the fingers can be confused with the clinical picture of other diseases. Medications are also prescribed based on the individual characteristics of the patient, the stage of development of the disease, and the degree of joint damage.

Arthritis is an inflammatory disease of the joints, so antibiotics and anti-inflammatory drugs are necessarily prescribed for its treatment. During an exacerbation, it is imperative to relieve the inflammatory process and pain. To restore cartilage tissue, chondroprotectors are prescribed. These medications are very effective, but their use must be long-term and consistent.

Massage, physiotherapeutic procedures, mud therapy, traditional medicine can be used as additional methods that increase the effectiveness of the main course of treatment. They are always assigned individually.