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Monday, 25 November 2013

Rheumatoid Arthritis (RA) - The Causes

Rheumatoid Arthritis
Rheumatoid Arthritis is defined a chronic disorder as a result of inflammation, affecting mostly the flexible (synovial) joints and tissues and organs in the body. The disease affects more women than in men and generally occurs after the ages of 40 and diminishes the quality of life of many elders.

B.1. Causes
The probable causes of  Rheumatoid Arthritis may include the following
1. Abnormal autoimmune response
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic synovitis that progresses to destruction of cartilage and bone. Scientists in the study of Abnormal networks of immune response-related molecules in bone marrow cells from patients with rheumatoid arthritis as revealed by DNA microarray analysis, indicated that abnormal regulatory networks in the immune response and cell cycle categories were identified in BM mononuclear cells from RA patients, indicating that the BM is pathologically involved in RA(10).
2. Abnormal lipid profile
In the study to observe the association between inflammation status/autoimmune antibodies and plasma lipid in patients with rheumatoid arthritis (RA), found that (1) There were 12.9%, 10.2% and 14.2% patients with elevated TC, LDL-C and TC respectively, patients with reduced HDL-C accounted for 43.6%. (2) C(3) was higher in elevated TC group than normal TC group (P < 0.05). ESR and CRP were significantly higher in decreased HDL-C group than in normal HDL-C group (P < 0.05). CRP, C(3) and C(4) were significantly higher in elevated LDL-C group than in normal LDL-C group (P < 0.05). (3) Multiple stepwise regression analysis showed that C(3) was positively correlated with TC (R(2) = 0.067, P < 0.05). Both ESR and CRP were negative correlated with HDL-C (R(2) = 0.202, P < 0.05). CRP and anti-CCP were positively correlated with LDL-C (R(2) = 0.129, P < 0.05). ESR and C(4) were positively correlated with AIP (R(2) = 0.046, P < 0.05)(11).
3. Genetic susceptibility
In exploring the overlap between T1D, CeD and RA, there is strong evidence that variation within the TAGAP gene is associated with all three autoimmune diseases. Interestingly a number of loci appear to be specific to one of the three diseases currently studied suggesting that they may play a role in determining the particular autoimmune phenotype at presentation(12). Others suggest that this CCR5 promoter polymorphism seems to play an important role in determining different clinical courses in both forms of rheumatoid arthritis(13).
4. Inflammatory and infectious connections
Chronic inflammation of the joint can result of thickens the synovium, of that affect the cartilage and bone within the joint.Some researchers suggested that rheumatoid arthritis (RA) is a associated with the T helper 17 cells (Th17) as major effector cells in several chronic inflammatory states(14). Others indicated that Periodontal infection (P. gingivalis) carries a unique risk for development of autoimmune antibodies associated with RA. Patients with RA have either lost many teeth or usually have severe periodontitis. Additional research, both in regards to basic mechanisms as well as clinical studies, are necessary before it can be said that there are causative links between RA and periodontitis(15).
5. Etc.

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Sources
(10) http://www.ncbi.nlm.nih.gov/pubmed/21679443
(11) http://www.ncbi.nlm.nih.gov/pubmed/22321280
(12) http://www.ncbi.nlm.nih.gov/pubmed/20854658
(13) http://www.ncbi.nlm.nih.gov/pubmed/22665517
(14) http://www.ncbi.nlm.nih.gov/pubmed/21616040
(15) http://www.ncbi.nlm.nih.gov/pubmed/22347541