About Rheumatoid Arthritis
Rheumatoid arthritis is primarily a disease of the joints. A joint is the point where two or more bones come together. With a few exceptions (in the skull and pelvis, for example), joints are designed to allow movement between the bones and to absorb shock from movements like walking or repetitive motions. The ends of the bones are covered by a tough, elastic tissue called cartilage. The joint is surrounded by a capsule that protects and supports it (see illustration). The joint capsule is lined with a type of tissue called synovium, which produces synovial fluid, a clear substance that lubricates and nourishes the cartilage and bones inside the joint capsule.
Like many other rheumatic diseases, rheumatoid arthritis is an autoimmune disease (auto means self), so-called because a person’s immune system, which normally helps protect the body from infection and disease, attacks joint tissues for unknown reasons. White blood cells, the agents of the immune system, travel to the synovium and cause inflammation (synovitis), characterized by warmth, redness, swelling, and pain—typical symptoms of rheumatoid arthritis. During the inflammation process, the normally thin synovium becomes thick and makes the joint swollen puffy, and sometimes warm to the touch.
As rheumatoid arthritis progresses, the inflamed synovium invades and destroys the cartilage and bone within the joint. The surrounding muscles, ligaments, and tendons that support and stabilize the joint become weak and unable to work normally. These effects lead to the pain and joint damage often seen in rheumatoid arthritis. Researchers studying rheumatoid arthritis now believe that it begins to damage bones during the first year or two that a person has the disease, one reason why early diagnosis and treatment are so important.
Some people with rheumatoid arthritis also have symptoms in places other than their joints. Many people with rheumatoid arthritis develop anemia, or a decrease in the production of red blood cells. Other effects that occur less often include neck pain and dry eyes and mouth. Very rarely, people may have inflammation of the blood vessels (vasculitis), the lining of the lungs (pleurisy), or the sac enclosing the heart (pericarditis).
Symptoms of Rheumatoid Arthritis
- Tender, warm, swollen joints
- Symmetrical pattern of affected joints
- Joint inflammation often affecting the wrist and finger joints closest to the hand
- Joint inflammation sometimes affecting other joints, including the neck, shoulders, elbows, hips, knees, ankles, and feet
- Fatigue, occasional fevers, a loss of energy
- Pain and stiffness lasting for more than 30 minutes in the morning or after a long rest
- Symptoms that last for many years
- Variability of symptoms among people with the disease
An abnormal response of the immune system plays a leading role in the inflammation and joint damage that occurs,but there is scientific evidence that genes, hormones and environmental factors are also involved.
People with a specific genetic marker called the HLA shared epitope have a fivefold greater chance of developing rheumatoid arthritis than do people without the marker. The HLA genetic site controls immune responses. Other genes connected to RA include: STAT4, a gene that plays important roles in the regulation and activation of the immune system; TRAF1 and C5, two genes relevant to chronic inflammation; and PTPN22, a gene associated with both the development and progression of rheumatoid arthritis. Yet not all people with these genes develop RA and not all people with the condition have these genes.
Other factors that may play a role. These factors include infectious agents such as bacteria or viruses, which may trigger development of the disease in a person whose genes make them more likely to get it; female hormones (70 percent of people with RA are women); obesity; and the body’s response to stressful events such as physical or emotional trauma. Research also has indicated that environmental factors may play a role in one’s risk for rheumatoid arthritis. Some include exposure to cigarette smoke, air pollution, insecticides and occupational exposures to mineral oil and silica.
- Sex: Women are more likely to develop rheumatoid arthritis.
- Age: Rheumatoid arthritis can occur at any age, but it most commonly begins between the ages of 40 and 60.
- Family history: If a member of your family has rheumatoid arthritis, you may have an increased risk of the disease.
- Carpal tunnel syndrome.
- Heart problems.
- Lung disease.
ONGOING CLINICAL RESEARCH -Association Between Dyslipidemia and Rheumatoid Arthritis Patients.
About the Study
CVD is the leading cause of death in RA, being responsible for around a half of all RA deaths . CVD in RA presents in many guises including myocardial infarction, congestive cardiac failure, and pericarditis. Of these, it is the ischaemic pathologies attributable to atherosclerotic disease that are the most common and confer the greatest increase in morbidity and mortality Atherosclerotic disease in RA is often silent or presents atypically, therefore creating difficulties in the diagnosis and management of the condition .RA patients also have a poorer prognosis following a myocardial infarction (MI), with significantly higher death rates reported with the initial event.
RA is associated with an increased risk of cardiovascular morbidity and mortality. Dyslipidaemia is a major CVD risk factor in the general population, however, despite the increased CVD risk in RA only limited data exists assessing the impact of chronic inflammation and drug therapies on lipid levels, ratios, structure or function. Furthermore, RA is a condition with strong genetic etiological links, thus it is possible that RA susceptibility genes also contribute to the regulation of lipid metabolism in RA, or that genetic polymorphisms known to regulate lipid metabolism in the general population are more common in RA or have an altered function.
Purpose of the study, Background of the Subject, Factors Prompting to undertake the research project.
The potential harm posed by CVD in RA has sparked an explosion of research in an attempt to identify contributing factors (traditional and novel disease specific) and methods of addressing these. To date the role of several traditional risk factors for CVD has been studied in RA, including hypertension ,insulin resistance ,and obesity .However, in-depth data on the impact of lipid levels, structure and function on the development of atherosclerosis in RA is sparse.
This project attempts to explore the hypothesis that chronic inflammation in RA leads to a disturbed lipid profile and increased CVD risk in this group of patients. In RA, inflammation alters HDL constituents and the concentration of LDL and HDL, thus facilitating atherosclerosis and CVD events. On the other hand, also the increase of oxidative processes, frequently observed in RA, induces atherosclerosis.
Interestingly, some genetic polymorphisms associated with RA occurrence (HLADR4,HLADRB1) enhance atherosclerosis, however, other polymorphisms associated with RA susceptibility do not increase CVD risk. Several other mechanisms may influence atherosclerotic processes in RA. Finally, the effects of RA therapies on cardiovascular system in general and on atherosclerosis in particular are really wide and different. However, the starting point of every RA treatment is that disease control, or better remission, is the best way we have for the reduction of CVD occurrence.
Drugs used in treatment of RA patients also effect on lipid profile. Drugs used in RA , which could alter Lipid profile and cause dyslipidemia, a precursor for CVD incidence are traditional DMARDS MTX, Tofacitinib, Tocilizumab, Glucocoticoids/Prednisone, Azathioprine And Chloroquine Leflunomide (LFN) Cyclosporine (Csa).
Subjects diagnosed with RA as per the ACR criteria will be included in the study.
4) Gonococcal arthritis
5) Systemic Lupus Erythematosus (SLE)
6) Lymes Disease
8) Psoriatic Arthritis
9) Reactive arthritis
Gap 1: Clinicians do not routinely detect and treat traditional CVD risk factors in RA patients . However, the presence of RA as a diagnosis often does not trigger risk factor screening or treatment. LDL‐C and diabetes yearly screening rates in the analyzed patient population with RA are, indicating a need for additional risk detection in this population.
Responsibility for CVD risk screening and treatment is lacking due to vague evidences of the association between Dyslipidaemia & RA.Thus, the care for RA patients, particularly around their heightened CVD risk, is not coordinated between the Rheumatologist and the PCP.
Gap 3: The link between RA and CVD risk has to be affirmed.
Gap 4: Primary care physicians frequently do not correctly calculate CVD risk in RA patients. Primary care physicians are only moderately confident of their abilities to manage patients with arthritis, and only moderately satisfied with their management of these patients due to lack of evident researches on this issue. CVD risk calculator is missing in RA patients.
Gap 5: RA patients have not experienced improvements in survival over the past 4 decades, despite dramatic improvements in the overall rates of mortality in the general population. Further research into the causes of the widening gap in mortality between RA patients and the general population, and the influence of current therapeutic strategies on mortality, is needed in order to develop strategies to reduce the excess mortality observed in RA patients.
Gap 6: To improve the quality of care for RA patients, we need more research on assessing, designing and implementing comprehensive care models. It is important to get RA issues on the primary care agenda by bringing other health professionals to the table to develop inter-professional care models and improve the continuum of care. Tremendous opportunity to look at issues of comorbidity have been jeopardized due to inadequate researches on comorbidities in RA.These inadequancies are the base line cause for lack of Models of comprehensive care in RA patients.
Gap 7 DMARDs are vital to treating inflammatory types of arthritis and should be used in the earliest stages of the disease; they can suppress inflammation, control pain and prevent long-term joint damage. While RA care now emphasizes an early, aggressive treatment plan to counter joint pain and joint damage.This aggressive treatment plan should cover comorbid conditions as part of comprehensive care.Research evidences on the assosciated comorbid conditions with RA & Risk factors behind the screen, are essential to design a screening and treatment protocol.