Rheumatoid Arthritis is a systemic autoimmune disease that “does not know age”, as it affects even young people. Its frequency is about 1%, with a ratio of 3: 1 women / men and with a global geographical distribution.
Left untreated, Rheumatoid Arthritis causes varying degrees of disability. Seropositive, seronegative arthritis and recurrent rheumatism are forms of RA, which is the most common systemic autoimmune inflammatory arthritis.
Pathogenesis
“Almost every cell type of the immune system and every inflammatory mediator is involved in the disease process: lymphocytes, macrophages and dendritic cells, articular cell fibroblasts, etc., play an important role in the pathogenesis of RA. They produce a variety of chemokines – cytokines and degradation enzymes of the interstitial material, which mediate the interaction with neighboring inflammatory and endothelial cells and are responsible for the progressive inflammation of the joints and the destruction of the articular cartilage and cartilage.
Given the heterogeneous response to treatment, it is clear that RA is not a single disease. In contrast, its pathogenesis involves many pathways that can lead to self-reactivity with similar clinical expression. It results from a complex interaction between genes and the environment, which leads to disruption of immune tolerance and joint inflammation “, points out Eleni Komninou, Rheumatologist, Director of the Metropolitan General Autoimmune Rheumatic Diseases Clinic.
In particular, the following factors are involved:
Genetic factors
Genes of the major class II histocompatibility system (HLA-DR), HLA-DRB1 alleles as well as genes encoding proteins that play a central role in the functioning and regulation of the immune system, such as PTPN22, TRAF1, C5, STAT4 and IRF5.
Environmental factors
Smoking (which increases the risk of developing the disease by 20 to 40 times), stress, etc. Infectious agents (viruses, bacteria) are also blamed.
Disease course – Prognosis
The disease progresses with periods of automatic remission and exacerbation. Specifically, 10% of patients present with a long recession of many years, 75% with a rapid or slow developmental disability, while 15% have an intermittent course with short periods of complete remission.
Poor prognosis indicators
• HIV positive disease
• Rheumatic nodules
• HLA-DR4 gene
• Early corrosion
• Extra-articular manifestations
• Severe disability: 6-12% of patients with RA
• 1/3 to 1/2 of patients show reduced ability to work
• People with RA show reduced survival (7 years in men, 3 years in women)
• After 10 years of illness, 50% of patients with RA develop severe disability.
All of the above will happen if the disease is not treated in a timely and correct manner.
Clinical attack at onset
Polyarticular: 75%: Small joints: 60% (limbs – feet). Large joints: 30%. Big-small: 10%.
Monoarticular: 25%: Knee: 50%, shoulder, wrist, hip 50%.
The symptoms of Rheumatoid Arthritis vary from person to person.
“The main symptoms of Rheumatoid Arthritis are joint pain, swelling and stiffness. It is possible, however, to cause general symptoms and inflammation in other parts of the body. “Some patients, in addition to the symptoms in the joints, may experience more general symptoms, such as fatigue and lack of energy, fever, sweating, decreased appetite and weight loss, dry eyes, and chest pain, if the heart or lungs are affected.” explains the doctor.
Diagnosis
Key useful laboratory indicators in RA are:
- Rheumatoid Factor (RF) which is an autoantibody against the Fc portion of IgG with 75-80% specificity. Antibodies against anti-cyclic citrullinated peptides (anti-CCP antibodies or ACPA) with 96% specificity.
- Their presence (HIV-positive RA) predisposes to a more severe clinical course, although on their own they do not diagnose RA.
General principles of treatment:
1. The treatment of the disease is always done by the rheumatologist in collaboration and with the consent of the well-informed patient.
2. Treatment should be started immediately with the diagnosis of the disease for the best effectiveness of the initial treatment and the prevention of permanent damage.
3. The evaluation of the disease activity and the effectiveness of the treatment is done with established indicators of the disease activity.
The goals of treatment are remission or, if this is not possible, low activity of the disease (control of meningitis and prevention of joint damage). In order to achieve the above therapeutic goals, frequent monitoring of patients is required. The golden rule is: “Treat early – treat efficiently”.
Steps of treatment
Initial treatment includes the administration of conventional synthetic anti-rheumatic drug modifiers (csDMARDs) as monotherapy: methotrexate, leflunomide, sulfasalazine, hydroxychloroquine. Also, in the initial treatment or during outbreaks of the disease, corticosteroids (prednisolone or its analogue at a dose of ≤7.5 mg / day) may be added for a period of time, depending on the patient’s response.
Biological agents drastically changed the landscape of RA treatment
Biological DMARDs (bDMARDs), Anti-TNFs (alphabetically), Adalimumab Certolizumab Pegol Etanercept Golimumab Infliximab or non-anti-TNFs Abatacept Inhibitors IL-6 (Sarilumab or Tocilizumab) Anakinra or corresponding Bacarib .
The combination of the above factors or monotherapy depends on a variety of factors, which are subject to the judgment of the treating rheumatologist. The fact that the disease responds in different ways to different pharmaceutical approaches, shows that RA is not a single disease.
in conclusion
“A better understanding of the various predisposing and triggering factors in early Rheumatoid Arthritis should yield biological markers with prognostic and therapeutic utility for this clinically heterogeneous condition. “Personalized treatment now prevents the establishment of disabilities and ensures a good quality of life”, concludes Ms. Komninou.
Written by Mrs. Eleni Komninou,
Rheumatologist Director of the Metropolitan General Autoimmune Rheumatic Diseases Clinic.
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