Related Terms: Rheumatoid disease (RD), lymphedema, osteoarthritis, rhuematoid arthritis, immune system, autoimmune, systemic lupus erythematosus, Ankylosing Spondylitis (AS), joint swelling, joint edema, joint pain, Adaptive immunity, B cells, T cells, Autoantibodies, Anti-citrullinated protein antibodies, Rheumatoid factor, Tolerance, Cartilage oligomeric matrix protein (COMP), Serum COMP-C3b, anti-TNF-alpha treatment, Ankylosing Spondylitis(AS), Sjogren's syndrome.
This is a large group of disorders/diseases (100 diseases) that affects the joints of the patient. The condition can be incredibly painful, causes inflammation and edema. Literally millions of people are affected by it and many become quite disabled from it. The conditions are considered to be autoimmune diseases. In autoimmune disorders, it is believed the body's “defense (immune system)” system attacks the body itself.
The most common rheumatoid diseases in the United States are osteoarthritis (OA), Rheumatoid Arthritis, Ankylosing Spondylitis(AS) and Lupus. Osteoarthritis which causes damage to the cartilage, generally hits the knees, hips, lower back, neck and fingers. The symptoms for this condition include Joint pain, stiffness, and swelling, Involvement of multiple joints (symmetrical pattern), Other organ involvement, Joint stiffness, especially in the morning, Fatigue, Fevers, Lumps called rheumatoid nodules.
Other types of Rheumatic Diseases include: Juvenile idiopathic arthritis, Reiter's Syndrome, Fibromyalgia, Scleroderma, Infectious arthritis, Gout, Polymyalgia rheumatica, Polymyositis, Psoriatic arthritis, Bursitis, Tendinitis (tendonitis)ND, raynaud's Phenomenon. For a brief description of each, please refer to: Arthritis and Rheumatic Diseases
Diagnoses of osteoarthritis is made through physical examination, medical history and blood tests. The blood tests will help rule out any other type of medical problem. A fluid sample from the affected joint may also be taken.
Rhuematoid arthritis affects approximately 1.3 million Americans with 75% of them being female. In RA, the body's immune system attacks its own tissues, causing joint pain, swelling, and stiffness that can be severe.
RA is sometimes called a crippling disease. That's because it can result in permanent joint damage and deformity. RA signs and symptoms include: Joint pain, stiffness, and swelling, Involvement of multiple joints (symmetrical pattern), Other organ involvement, Joint stiffness, especially in the morning, Fatigue, Fevers, Lumps called rheumatoid nodules . (1)
Diagnoses is made through physical examination, history, x-rays, blood tests. The blood test looks for the “rheumatoid factor” which is positive on 70-80% of RA patients.
To diagnose upus, your doctor will ask about your medical history, do a physical exam, and order lab tests of blood and urine samples. One blood test is the antinuclear antibody test (ANA). Most people with lupus have a positive ANA blood test. (1)
To diagnose AS, your doctor (rheumatologist]] will ask about your medical history and perform a physical exam. X-rays of the back looking at the sacroiliac joints may help in making an AS diagnosis. A positive blood test for HLA-B27 protein may help confirm a diagnosis. (1)
To diagnose Sjogren's syndrome, your doctor will do a physical exam and ask about your medical history. Blood tests and other tests may also be performed. A simple biopsy of the inner lip or other area may help confirm the diagnosis.
Osteoarthritis is the result of the wear and tear to the joints. The cause of other conditions such as lupus, and ankylosing spondylitis are unknown but believed to be genetically inherited.
Rheumatic diseases are generally believed to be caused by a combination of genetic and environmental factors. In other words, you may be born with a susceptibility to a disease, but it may take something in your environment to get the disease started.
Treatment of RD of course, would be specific to the particular condition the patient has and any comorbidities.
For the edema, sometimes the joint is drained and otherwise it will resolve itself. If the swelling becomes permanent, then it is lymphedema. For lymphedema a referral is required to a certified lymphedema therapist for a complete evaluation and treatment workup. The protocol treatment consists of complete decongestive therapy with the subsequent wearing of com[ression garments to help control the swelling.
Osteoarthritis treatment consists of a combination of exercise, lifestyle modification and analgesics.
For severe pain, the treating physician may prescribe pain medication.
(1) An Overview of Rheumatic Diseases WebMD
Using the antinuclear antibody test to diagnose rheumatic diseases: when does a positive test warrant further investigation?
Volkmann ER, Taylor M, Ben-Artzi A.
From the Division of Rheumatology, David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, CA.
ABSTRACT: The anti-nuclear antibody (ANA) test is ordered commonly as a screening test for rheumatic diseases. Although ANA positivity is highly sensitive for certain rheumatic diseases, the presence of ANA is nonspecific and can be associated with numerous nonrheumatic factors, including environmental exposures, malignancies, drugs, and infections. This article describes a practical approach for physicians when evaluating patients using a positive ANA test. In the absence of connective tissue disease symptoms, the ANA test has minimal clinical significance in diagnosingrheumatic diseases. Understanding how to use ANA test results appropriately may reduce unnecessary referrals and costly workups.
Adaptive immunity in rheumatic diseases - Bystander or pathogenic player?
Scherer HU, Burmester GR.
Department of Rheumatology, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands.
Keywords: Rheumatoid arthritis Adaptive immunity, B cells, T cells, Autoantibodies, Anti-citrullinated protein antibodies, Rheumatoid factor, Tolerance
Rheumatic diseases comprise a wide spectrum of different conditions. Some are caused by disturbances of the adaptive immune system, while defects in innate immune responses have been identified for others. In between are a variety of multifactorial diseases for which the evidence for a causative involvement of the adaptive immune system is still controversial. In these cases, availability of novel drugs that target key players of the adaptive immune system have improved our understanding of the relevance of adaptive immunity to the disease process, but it has also generated unprecedented findings. Rheumatoid arthritis (RA) is a prototypic example of a disease in which the relative contribution of adaptive immunity to disease pathogenesis is incompletely understood. Although numerous markers have been identified that reflect an activated adaptive immune system, several caveats render interpretation of these findings difficult. For one, the very early immune responses initiating disease are likely to take place before an individual is identified as a patient, and are thus difficult to study in the human. Furthermore, increasing evidence points to pathogenetically distinct subgroups within the clinical diagnosis RA, offering the possibility that adaptive immune responses might be relevant to one subgroup but not the other. In addition, many indications for an adaptive immune system involvement are based on associations for which the underlying mechanism is often unknown. Finally, therapeutic interventions targeting the adaptive immune system have generated heterogeneous results. The present review addresses these issues by placing adaptive immune responses in the context of rheumatic diseases, and by reviewing the evidence for a contribution of adaptive immunity to RA.
Serum COMP-C3b complexes in rheumatic diseases and relation to anti-TNF-alpha treatment.
Happonen KE, Saxne T, Geborek P, Andersson M, Bengtsson A, Hesselstrand R, Heinegard D, Blom AM.
INTRODUCTION: Cartilage oligomeric matrix protein (COMP) is found at elevated concentrations in sera of patients with joint diseases such as rheumatoid arthritis (RA) and osteoarthritis (OA). We recently showed that COMP activates complement via the alternative pathway and that COMP-C3b complexes are present in sera of RA patients, but not healthy controls. We now set out to elaborate on the information provided by this marker in a variety of diseases and larger patient cohorts.
METHODS: COMP-C3b levels in sera were measured using an ELISA capturing COMP and detecting C3b. Serum COMP was measured using ELISA.
RESULTS: COMP-C3b levels were significantly elevated in patients with RA as well as in systemic lupus erythematosus (SLE), compared to healthy controls. SLE patients with arthritis had significantly higher COMP-C3b levels than those without. COMP-C3b was furthermore elevated in patients with ankylosing spondylitis (AS), psoriatic arthritis (PsA), reactive arthritis, systemic sclerosis and OA. COMP-C3b did not correlate with COMP in any of the patient groups. COMP-C3b correlated with disease activity in RA, but not in other diseases. COMP-C3b levels in RA patients decreased upon treatment with TNF-alpha inhibitors whereas the levels increased in patients with AS or PsA. The changes of COMP-C3b did not parallel the changes of C-reactive protein (CRP).
CONCLUSION: COMP-C3b levels are elevated in several rheumatologic diseases and correlate with inflammatory measures in RA. COMP-C3b levels in RA decrease during TNF-alpha inhibition differently from CRP, suggesting that formation of COMP-C3b relates to disease features not reflected by general inflammation measures.
Disease DB 9313
Medline Plus 000423
Systemic lupus erythematosus
ICD-10 [http://apps.who.int/classifications/icd10/browse/2010/en#/L93 |L93]], M32