INTRODUCTION TO RHEUMATOLOGY

The origins of Rheumatology

Rheumatology - a branch of medicine devoted to the study of rheumatic diseases and disorders of the function and / or structure of the musculoskeletal system.

In the I century AD was the first appeared in the literature, the concept of rheuma (revma). The word "rheuma" of Greek origin. Rheuma refers to "a substance that flows", probably formed from phlegm. This is the "primary juice," by definition of the ancients, which was formed in the brain and flowed in different parts of the body, causing illness.

The origins of Rheumatology

In 1642, the term "rheumatism" was introduced in the literature by french physician Dr. G. Baillou, who supposed that arthritis can be a manifestation of systemic disease.

The origins of Rheumatology

In 1928, in the USA Dr. R. Pemberton organized the American Committee for the treatment of rheumatism, which was renamed the American Association for the Study and Treatment of rheumatic diseases (1934), followed by the American Association of rheumaticism (1937) and, finally, the American Rheumatology Association (1988).

The origins of Rheumatology

In 1940, Bernard Comroe suggested the term "rheumatologist.

In 1949, Hollander uses the term "rheumatology" in his textbook on arthritis and painful condition (Arthritis and Allied Conditions).

History of the discovery of some rheumatic diseases

Acute rheumatic fever

Acute rheumatic fever

The doctrine of rheumatism has a long history. For the first time information about rheumatic arthritis appeared in the writings of Hippocrates. There was humoralism (Latin humor - fluid) - current through the joint process. In the early XX century, all were regarded as diseases of the joints and rheumatism. Classic works consecrated to the ARF, have been written by Jean-Bapite Bomllard and Walter B Cheadle and published in 1836, which detailed the "rheumatic arthritis" and carditis. At one time Lasegue said: "Rheumatism licks the joints but bites the heart. S. Botkin has been shown that ARF affects many organs: kidneys, skin, nervous system, liver and lungs.

Acute rheumatic fever

In 1904 morphologist Ludwig Aschoff first discovered and described the morphological substrate of rheumatic fever - a kind of cell granuloma. In 1929 Talalayev showed that rheumatic granuloma Aschoff - only one stage, but it has 3 phases: exudative, proliferative phase, cell proliferation and sclerosis. So now the rheumatic granulomacalled Aschoff Talalayev. In 1933, Rebecca Lancefield was divided into groups hemolytic streptococci, helping researchers clarify the epidemiology of the disease. For the first time the criteria for leadership in the diagnosis of ARF were developed by Dr. T Duckett Jones and published in 1944. Later they were adopted and revised by the American Heart Association.

Rheumatoid arthritis

Rheumatoid arthritis
The earliest signs of rheumatoid arthritis were found in 4500 BC. They were found on the remains of skeletons of Indians in Tennessee, USA. The first paper describing the symptoms are very reminiscent of the symptoms of rheumatoid arthritis dates back to 123 a year.

The first clinical description of this pathology in 1800, is credited with Augustin-Jacob LandreBeauvais. The author called the disease variant of gout - a "simple asthenic gout" (goutte asthenique primitif). Benjamin Brodie described the slow progression of synovitis by involving joint capsule and tendon sheath.

Joint swelling in early rheumatoid arthritis

Deformities of long-standing rheumatoid arthritis

Rheumatoid arthritis

A. Garrod suggested the term "rheumatoid arthritis" in 1858 and differentiate it from gout in 1892, the disease got its present name.

Systemic lupus erythematosus

The name lupus, the Latin version as Lupus erythematosus, comes from the Latin "lupus", which means wolf and "eritematozus" - red, because of its similarity to the bite injuries hungry wolf.

This disease is known to doctors since 1828, after describing the French dermatologist Biett skin symptoms

45 years later Kaposhi (dermatologist) observed that some patients with skin symptoms are also symptoms of internal organs.

In 1845, Ferdinand von Hebra described a rash on the type of "butterflies" on her nose and cheeks.

Systemic lupus erythematosus

In 1948,William Hargraves described the LEcells. This discovery allowed doctors to identify many patients with systemic lupus erythematosus. In 1956, Miescher, described the absorption of LE-cell factor kernels. In 1958, George Friou described a method for identification of antinuclear antibodies.

Spondyloarthropathies (ankylosing spondylitis)

The archaeological study of Egyptian mummies found the disease, which is now called ankylosing spondylitis is known to mankind since ancient times. The first historical description of the disease in the literature refers to 1559, when Realdo Colombo described the two skeletons with typical changes of ankylosing spondylitis in his book "Anatomy. 100 years later, in 1693, an Irish physician Bernard Connor described the skeleton of a man with signs of scoliosis, in which the sacrum, hip bone, lumbar vertebrae and 10 thoracic vertebrae with ribs are fused into one bone.

Spondyloarthropathies (ankylosing spondylitis)

In the late 1890s, Russian doctor, Vladimir Bekhterev and French doctors Adolf Strumpell and Pierre Marie described ankylosing spondylitis. Linking disease to a gene class I HLA-B27 belongs to the Americans Lee Schlosstein, Rodney Bluestone and Paul Terasaki, as well as the British Derrick Brewerton, Caffrey and Nichols.

Classification of rheumatic / musculoskeletal syndromes in different years

Rheumatology as a specialty

Rheumatology as an independent scientific and practical discipline was formed 45 years ago. Rheumatic diseases are one of the most common pathologies of the human body. The term "rheumatic disease" include a variety of origins of the disease predominantly systemic, less local character, proceeding with persistent or transient articular syndrome.

The origins of the classification

Theoretical basis for combining these various diseases in the same group was the fact that their basis is a preferential loss of connective tissue, as dense, which include the dermis, tendons, ligaments, cartilage, bone and others, and its special types (synovial and serous membranes, basal membranes of blood vessels and epithelium, etc.).

Working classification and nomenclature of rheumatic diseases (1999)

I. Rheumatism (rheumatic fever) II. Diffuse diseases of connective tissue

1.0. Lupus Erythematosus 2.0. Systemic Scleroderma 3.0. Diffuse Fasciitis 4.0. Dermatomyositis (polimiozit) 5.0. Disease hoegren 6.0. Mixed connective tissue disease 7.0. Rheumatic polimialgia 8.0. Recurrent polihondritis, including Tietze disease 9.0. Recurrent pannikulitis (Weber-Christian disease)

 Working

classification and nomenclature of rheumatic diseases (1999) III. Systemic Vasculitis

1.0. periarteritis nodosa 2.0. Granulomatous arteritis:

2.1. Wegener's granulomatosis 2.2. Eosinophilic granulomatous vasculitis 2.3. Giant cell arteritis temporal (Horton's disease) 2.4. Nonspecific aortoarteriit (Takayasu's disease)

3.0. Hyperergic angiitis

3.1. Hemorrhagic vasculitis (Henoch disease - purpura) 3.2. Goodpasture's syndrome 3.3. Mixed cryoglobulinemia (cryoglobulinemc purpura)

4.0. Thromboangiitis obliterans (Buerger's disease) 5.0. Behcet's syndrome 6.0. Kawasaki syndrome (muco-cutaneous-glandular syndrome)

Working classification and nomenclature of rheumatic diseases (1999)

IV. Rheumatoid arthritis V. Juvenile arthritis VI. Ankylosing spondylitis (Bechterew) VII. Arthritis, combined with spondylarthritis 1.0. psoriatic arthritis 2.0. Reiter's disease 3.0. Arthritis in chronic nonspecific bowel disease (ulcerative colitis, ileitis regionar-ny Crohn's disease) 4.0. Arthritis, and (or) sacroiliitis unspecified etiology

VIII. Arthritis associated with infection 1.0. infectious arthritis 1.1. Bacterial (staphylococcal, brucellosis, syphilis, spirochetal, mycobacterial, tuberculosis, etc.) 1.1.1. Lyme disease 1.1.2. Whipple's disease 1.2. viral 1.3. fungal 1.4. parasitic

2.0. Reactive arthritis 2.1. Postenterocolitic (shigellosis, yersiniosis, salmonellosis, klebsiellosis, etc.) 2.2. Urogenital (excluding Reiter's disease and gonorrhea) 2.3. After nasopharyngeal infection 2.4. After vaccination

2.0. 2.1. (, , , .) 2.2. ( ) 2.3. 2.4.

IX. microcrystalline arthritis 1.0. primary gout 2.0. Gout secondary (drug, renal insufficiency, lead intoxication, etc.) 3.0. Chondrocalcinosis (pseudogout) 4.0. hydroxyapatite arthropathy

 (1999)

IX.
1.0.

2.0. (, , .) 3.0. () 4.0.

X. osteoarthritis XI. Other joint diseases 1.0. palindromic rheumatism 2.0. intermittent hydrarthrosis 3.0. multiple retikulohystiocytosis 4.0. Sinovioma 5.0. chondromatosis of the joint 6.0. Villonodulary synovitis

X. XI.
1.0.

2.0. 3.0. 4.0. 5.0. 6.0.

XII. Non-rheumatic diseases with arthropathy

1.0. allergic diseases 2.0. Metabolic disorders 2.1. Amyloidosis 2.2. Ochronosis 2.3. Hyperlipidemia

2.4. hemochromatosis 3.0. Congenital defects of the connective tissue metabolism

3.1. Marfan's syndrome 3.2. Desmogenez imperfecta (Ehlers - Danlos syndrome)

3.3. Hypermobility syndrome

3.4. MPS

 (1999)

XII.
1.0. 2.0. 2.1. 2.2. 2.3. 2.4. 3.0. 3.1. 3.2. ( ) 3.3. 3.4.

4.0. endocrine diseases 5.0. nervous 6.0. Diseases of the blood 7.0. Paraneoplastic syndrome (malignant tumors of various sites) 8.0. occupational diseases 9.0. Other diseases 9.1. Sarcoidosis is 9.2. Periodic disease 9.3. Chronic active hepatitis 9.4. hypovitaminosis C

 4.0.

5.0. 6.0. 7.0. ( ) 8.0. 9.0. 9.1. 9.2. 9.3. 9.4.

XIII. Diseases of the extra-articular soft tissues 1.0. Diseases of the muscles of 1.1. Myositis 1.2. Ossifitsiruyuschy myositis 2.0. Diseases of the tissues around 3.0. Diseases of the fascia and aponeuroses 4.0, subcutaneous disease. Fat 5.0. Poliosteoartromialgiya (psychogenic rheumatism)

 (1999)

XIII. 1.0. 1.1. 1.2. 2.0. 3.0. 4.0, . 5.0. ( )

XIV. Bone disease and osteochondropathy 1.0. bone disease 1.1. Osteoporosis (osteopenia), generalized 1.2. osteomalacia 1.3. Osteopathy hypertrophic pulmonary (Marie-Bamberger syndrome) 1.4. Osteitis deformans (Paget's disease) 1.5. Osteolysis (unspecified etiology)

XIV. 1.0.
1.1.

() 1.2. 1.3. ( ) 1.4. ( ) 1.5. ( )

2.0. osteochondropathy 2.1. Aseptic necrosis of the femoral head (Perthes disease) and other sites (Khler's disease I and II, disease Kenbeka, etc.) 2.2. osteochondritis dissecans 2.3. Osteochondropathy vertebral disease (Sheyermana - May, Calve's disease) 2.4. Osteochondropathy tuberosity of the tibia (Osgood disease - Schlatter

2.0.
2.1.

( ) ( I II, .) 2.2. 2.3. ( May, ) 2.4. (

Laboratory studies

The values of laboratory data

Laboratory tests may help in diagnosis and to confirm data obtained by history taking and examination, but are not independently diagnostic criteria. In addition, laboratory tests can help monitoring disease activity, but they are meaningful only when correlated with clinical outcome.

Laboratory studies in rheumatic diseases

Anemia

Normochromic - Correlation with disease activity Iron - NSAID-associated gastrointestinal pathology Hemolytic - SLE, APS Aplastic - Citostatic, phenylbutazone, D-penicillamine, etc.

Leukocytes

Leukocytosis - A high activity of inflammation, with Still, the infection Leukopenia - SCR (lymphopenia), with m-Felty (neutropenia)
Thrombocytosis - The high activity of inflammation Thrombocytopenia - SLE, APS

Platelets

KLF - Increase - Inflammatory myopathies

Laboratory studies in rheumatic diseases

Transaminases, bilirubin - Increase - Pathology of the liver with "rheumatologic" manifestations of the toxicity of drugs (methotrexate, NSAIDs) Uric acid - Hyperuricemia Gout Markers of inflammation

Increased ESR - Active inflammation , a diagnostic criterion for polymyalgia rheumatica and giant cell arteritis, intercurrent infection Increased CRP - PA - activity of inflammation, joint destruction, SLE - intercurrent infection

Uroscopy

Microhematuria nephritidis (SLE, systemic vasculitis), toxic drugs Proteinuria nephritidis (SLE, systemic vasculitis, amyloidosis), the toxicity of drugs

The value of immunological tests in rheumatic diseases

Test
Anti-nuclear Anti-DNA

Disease
SLE SLE

Diagnosis in tipical clinic manifest +++ +++

DifDiagnosis ++ +

Scrining
-

Monitoring
? +++

Anti-body -Sm, RNP

3, 4

SLE, Mixt path

Nephrop aties in SLE SLE RA

+++

+++

++

++

+++

50 Rheumatoid factor

+ +++

+ +

+ +

The value of immunological tests in rheumatic diseases

Test CRP Cryoglobulins SL-0 ANCA ntiphosfolipides HLA B-27 Disease AR AR, SLE ARF Vasculiti dis APhS AS Diagnosis in tipical clinic manifest + + ++ +++ +++ ++ DifDiagnosis + ++ ++ ++ Scrining ? Monitoring +++ + + + + -

Anti-body at Lyme

Lyme d.

+++

++

The disease, in which can increase the RF in the serum

Subacute bacterial endocarditis Leprosy Chronic inflammatory disease of unknown etiology Tuberculosis Syphilis Sarcoidosis Lyme Disease Periodontal disease Interstitial lung disease Viral diseases Liver disease Rubella Cytomegalovirus Mixed cryoglobulinemia

Autoantibodies in rheumatic diseases

Type nti ds DNA Description Antibodies to double strand of DNA, have greater specificity than antibodies to ssDNA Most diagnostic tools are not shared by antibodies to the five main types of histones Typical diagnosticum to 2 extractable nuclear antibodies (Sm and RNP ribonucleoprotein) ribonucleoprotein Clinical interface Highly specific for SLE, rarely detected in other diseases and in healthy people SLE, lupus medication, other autoimmune diseases Highly specific for SLE

Anti Histon

Anti ENA

Anti SSA/Ro

Anti SSB/La

ribonucleoprotein

SLE (especially subacute cutaneous lupus), lupus neonatal syndrome Shogren Shogren's syndrome, lupus erythematosus, SLE newborn

Autoantibodies in rheumatic diseases

Type Anti centromer Description Antibodies to the centromere / kinetochore region of chromosome Antibodies to topoisomerase 1 DNA Antibodies to the transfer-RNA synthetase Clinical interface Limited scleroderma (CREST)

Anti Scl 70
Anti Jo-1

scleroderma

Anti PM-Scl Anti Mi-2

Poly / dermatomyositis, particularly in patients with insterstitsialnym lung disease, Raynaud's phenomenon, cracked skin of hands (mechanical arm), arthritis, and resistance to therapy Antibodies to nuclear Polymyositis / scleroderma Overlap components of granular syndrome Antibodies to nuclear antigens dermatomyositis of unknown function

The main indications for diagnostic arthrocentesis

Monoartritis Trauma with effusion into the joint cavity Suspected purulent arthritis Suspicion of microcrystalline (urate, hydroxyapatite), arthritis unclear diagnosis

The value of radiology in rheumatic diseases

Disease Rheumatoid arthritis Osteoarthritis AS Reactive arthritis SLE Scleroderma Gout Osteoporosis Thorax + +++ +++ Hand and foot +++ ++ ++ ++ ++ ++ Sacroi liac + +++ +++ +++ ++ Knee joints + +++ other The thoracic spine Lumbar spine Heel bone The Esophagus Densitometry, spine

Minimum set of laboratory tests to diagnose the causes of joint pain

The total blood count, platelets ESR Bilirubin Transaminase CK Creatinine uric acid Urinalysis, daily urine for protein Microscopic analysis of synovial fluid, including crystals

CRP rheumatoid factor antinuclear factor Anti-DNA A/b to extractable nuclear antigen (RNP) ANCA ASL-O Determination of chlamydial antigen A/b to B.burgdorferi HLA B-27

Minimum set of radiographic studies to diagnose the causes of joint pain

Chest Hands and distal foot in front projection Pelvis in frontal projection Knee in frontal and lateral projections Cervical spine in a straight line and lateral projections The lumbar spine and lateral projections Heel bone Esophagus Densitometry

Application of the morphological study (biopsy) in diagnosis of rheumatic diseases and their complications

Polymyositis Sjogren's disease Diffuse eosinophilic fasciitis Systemic vasculitis Secondary amyloidosis Differential Diagnosis in subcutaneous sites (rheumatoid nodule / tophi) Differential diagnosis of suspected tumor of the synovial

Drugs used to treat rheumatic diseases

Non-steroidal anti-inflammatory drugs for treatment of rheumatic diseases

Medication Diclofenac potassium Diclofenac sodium Etodolak Ibuprofen Indomethacin Dose 100-200 mg/24 h, divided into 2-4 reception Possible side effects

Ketoprofen Meloxicam Naproxen Nimesulide Piroxicam

100-200 mg/24 h, divided into 2-4, or 100 mg in the form of retard 800-1200 mg/24 h, divided into 2-4 reception. In the form of retard 1 dose 400-1000mg/24 h 1200-3200 mg/24 h, divided into 3-4 reception 50-200 mg/24 h, divided into 2-4, either in the form of retard 75 mg 1 times a day, 75 mg 2 times daily 200-225 mg/24 h divided into 3-4 reception or retard-150-200 mg/24 h 1 times 7.5 -15 mg/24 h 1 times per day 500-1500 mg/24 h divided 2 reception 100-200 mg/24 to 1-2 reception 20 mg/24 h in 1-2 reception

For all NSAIDS: abdominal pain, or stomach, cramps, discomfort, edema (oedema), diarrhea, nausea, vomiting, heartburn, dizziness, headache, allergic reactions

Prevention and treatment of GASTROINTESTINAL pathologies resulting from receiving NSAIDS Antacids have no data about their effectiveness H2-blockers Cure duodenal injury duodenal injury in Warn high doses were effective at the level of the stomach and eliminate symptoms caused by NSAIDS Improve semiology Inhibitors proton pump is effective for the prevention and treatment of gastroduodenal of defeats Improves semiology

Risk factors for the development of renal failure in the application of NSAIDs
High risk Reducing the volume of circulating blood, as significant bleeding or hemodynamic disturbances on the type of shock Severe heart failure Cirrhosis of the liver with / without ascites Clinically significant dehydration

Low - medium risk True kidney disease diabetic nephropathy nephrotic syndrome hypertensive nephropathy beginning of anesthesia
The controversial risk advanced age

Corticosteroids

Corticosteroids are widely used in the treatment of inflammatory forms of arthritis and related systemic autoimmune diseases. In addition to their strong anti-inflammatory effect, they regulate a wide range of metabolic, immunological and central nervous system function. For systemic therapy have been issued numerous synthetic derivatives, but the prednisone, prednisolone, and methylprednisolone are used most widely.

Corticosteroids
Form Hydrocortisone Cortisone Prednisone Methylprednisolone Prednisolone Dexamethasone Relative antiinflammatory potential 1 0,8 4 5 5 20-30 Equivalent dose (mg) 20 25 5 4 4 0,75 Elimination halflife (h) 8-12 8-12 12-36 12-36 12-36 36-54

Side effects of long-term Cortico-Therapy

Frequent
Hypertension Negative calcium balance and secondary hyperparathyroidism Negative nitrogen balance Obesity, moon face, supraclavicular fat accumulation in the area, fat accumulation in the form of a mountain on his back, Slowing of wound healing, erythema face, thin, fragile skin, blue striae, petechiae and ecchymosis Acne

Side effects of long-term Cortico-Therapy

Growth retardation in children Adrenal insufficiency, resulting in suppression of the hypothalamic-pituitary-adrenal system Hyperglycemia, diabetes mellitus, dyslipidemia, atherosclerosis Sodium retention, hypokalemia Increased risk of infection, neutrophilia, lymphopenia Osteoporosis, compression fractures of vertebrae, Osteonecrosis Mood changes such as euphoria, emotional lability, insomnia, depression, increased appetite subcapsular cataract

Side effects of long-term Cortico-Therapy

medium frequency
metabolic alkalosis Diabetic ketoacidosis, hyperosmolar diabetic coma Peptic ulcer (usually the stomach), gastric bleeding "Silent" intestinal perforation Increased intraocular pressure and glaucoma Mild intracranial hypertension or pseudotumor of the brain spontaneous fractures psychosis

Side effects of long-term Cortico-Therapy

Rare
Sudden death in the rapid introduction of high-dose, pulse therapy Valvular damage in SLE In susceptible patients may develop heart failure Cellulitis (after cancellation) Hirsutism or virilism, impotence, secondary amenorrhea Hepatomegaly as a result of fatty liver exophthalmos Allergies to synthetic corticosteroids (urticaria, angioedema)

Pathogenic (Basic) therapy of inflammatory rheumatic diseases

Disease modifying antirheumatic drugs (DMARDs) - the basic drugs from diverse group of funds that reduce the symptoms of rheumatoid arthritis (RA) and other inflammatory autoimmune diseases. In addition, there is increasing evidence that treatment with DMARD, especially if appointed early in the course of the disease, can delay the progression of cartilage and bone. When the RA is not responding to treatment DMARD, can be applied biological therapy. Biologicals alter the action of cytokines

Basic therapy

When to start - an understanding that changes in the joints can occur within the first 12 months of the debut of RA, led to the earlier introduction of DMARD and more aggressive combination DMARD. Monotherapy - Methotrexate is considered standard therapy for DMARD.

Combination therapy - Join one or two DMARD therapy with methotrexate for the background is often used in an attempt to improve clinical response in those patients who did not give an answer to monotherapy with methotrexate. The most commonly used combinations of DMARD - "triple therapy" (methotrexate + hydroxychloroquine sulfosalazin +) or methotrexate plus a biological agent.

Pathogenetic (Basic) drugs

Medication Azathioprine Possible side effects Leukopenia, increased transaminase Flatulence, change the color and smell of urine, 15-9 drops in 3 reception rarely allergic reactions in the form of urticaria Hematuria, hair loss, 50-150 mg per day in leukopenia, amenorrhea, single dose nausea, vomiting Hypertension, increased hair growth, reduced 100-400 mg daily in 2 kidney function, reception hypertrophy of gum, tremor 200-600 mg daily in 2-1 Violation of, diarrhea, rash reception Dosage 50-150 mg/day in 1-3 reception

Wobenzym

Cyclophosphamide

Cyclosporine

Hydroxychloroquine

Pathogenetic (Basic) drugs

Medication
Leflunomid

Dosage
10-20 mg/day in 1. Treatment begins with a dose of 100 mg support screens from 3 consecutive days

Possible side effects

Diarrhea, dizziness, hair loss, hypertension, increased transaminase, leukopenia, rash on the skin Discomfort in the stomach, skin rash, headache, photosensitivity, increased transaminase, leukopenia, ulcers in the mouth, weakness, fatigue Diarrhea, moderate leukopenia Abdominal pain, diarrhea, increased sensitivity, reduced appetite, nausea, vomiting, rash on the skin The feeling of crowding in the stomach, nausea, allergies (skin rashes).

Methotrexate

7.5-20 mg/week

Mycophenolate Mikofenolat Sulfasalazine

1.5-day 500-3000 mg daily in 2-4 reception

Wobenzym

9-15 drops in 3 reception

Treatment strategies with drugs

1. Sequential monotherapy

2. Step-up (ascending) combination therapy

3. Step-down (descending) combination therapy 4. Combination with a biological agent

Biological therapy

One of the most important achievements of the pharmacotherapy of inflammatory rheumatic diseases associated with the development of entirely new group of drugs, which are called "biological" agents. Their mechanism of action is associated with suppression of synthesis of "inflammatory" cytokines, play a fundamental role in the immunopathogenesis of these diseases, especially RA.

Immunomodulating and proinflammatory effects of cytokines in the pathogenesis of inflammatory rheumatic diseases (1)

Vascular endothelial cells - enhance the expression of adhesion molecules (ISAM-1, VSAM-1, E-selectin) through the activation of NF-kV stimulate angiogenesis, leading to disruption of anticoagulant activity (stimulation of the synthesis of tissue factor, suppression of synthesis of thrombomodulin). Lymphocytes - contribute to the development of lymphoid tissue, modification of SV44 and the ability to bind to the ligand. Dendritic cells - cells induce the maturation and migration from nonlymphoid organs to secondary lymphocyte organs. Neutrophils and platelets - contribute to activation.

Immunomodulating and proinflammatory effects of cytokines in the pathogenesis of inflammatory rheumatic diseases (2)

Fibroblasts and synoviocytes - lead to proliferation. Pro-inflammatory cytokines - in addition induce the synthesis of IL-1, IL-6, granulocyte-macrophage colonystimulating factor. Other pro-inflammatory mediators - induce the synthesis of PGE2 through activation of COX-2, leukotrienes, platelet activating factor, nitric oxide and reactive oxygen species. Metalloproteinases - induce the synthesis of collagenase, gelatinase, stromelysin. Other effects - increase pain, induce cachexia, induce fever, mobilize calcium from the bones; modulate apoptosis.

Biological therapy

The particular interest is the use of monoclonal antibodies. These drugs have very high specificity, which provides a selective effect on certain links in the immunopathogenesis of disease, minimally affecting normal functioning mechanisms of the immune system. This can significantly reduce the risk of "generalized" imunosupresed, which is typical of many drugs, especially glucocorticoids and cytotoxic drugs.

Monoclonal antibody to TNF-

Hummanised Kimerik Mouse Humman

100% human protein 5% -10% protein of the mouse

25% protein of the mouse 100% mouse protein

Adalimumab Golimumab (Adalimumab)

Adalimumab

Infliximab

Biological therapy

The main target for anticytokine monoclonal antibody therapy is:

TNF-alpha

(infliximab, adalimumab, etc.) IL-6 (tocilizumab) CD20 B cells (rituximab) IL-1, IL-2, etc.

Contraindications of biological therapy

Congestive heart failure, Severe infection Latent tuberculosis Malignant neoplasms Pregnancy and lactation.

The need for biological specimens

The gravity of the condition of the patient

Biologicals

Corticosteroids

Basic drugs (methotrexate, sulfasalazine, leflunomid)

The number of patients

THANK YOU!

What is Rheumatology?
Rheumatology is the non-surgical subspecialty of internal medicine that focuses on common and complex problems that may affect the entire body, and frequently involves the musculoskeletal system. Such diseases include: rheumatoid arthritis; gout; lupus;

scleroderma; osteoporosis; fibromyalgia and spondylitis. Common problems such as tendonitis, back pain, bursitis and carpel tunnel syndrome can be a result of rheumatologic disorders as well. There are more than 100 types of rheumatological disorders, some of which are very serious and difficult to diagnose and treat.