Rheumatoid arthritis inflammatory autoimmune disease

It is a cyclic polypeptide with 11 amino acids. It selectively inhibits T-lymphocytes proliferation, IL-2 and other cytokine production. It is the most effective drug for prevention and treatment of graft rejection reaction. It is used in cardiac, hepatic, renal, bone marrow transplantation and as second line drug in rheumatoid arthritis, inflammatory bowel disease, dermato-myositis, bronchial asthma and certain other autoimmune diseases. 

Cyclosporine is used to a somewhat lesser extent in treating autoimmune diseases, but it may be helpful in conditions such as psoriasis, rheumatoid arthritis, inflammatory bowel disease, and glomerulonephri-tiS.i5,32,63 as discussed in Chapter 32, cyclosporine has also been used in the early stages of type 1 diabetes mellitus to help control immune-mediated destruction of pancreatic beta cells, thus decreasing the severity of this disease in some patients.9... 

Maria s medical notes show that she has mild rheumatoid arthritis (an autoimmune disease), the condition is not severe and her joint pain is well controlled by a non-steroidal anti-inflammatory drug (NSAID), taken twice a day. She is not trying to diet and apparently has a well-balanced food intake, but reports that she has recently had several minor stomach upsets and colds. A blood sample is taken for analysis, including a differential white blood cell count. 

Deficiency of thiopurine S-methyl transferase (TPMT) is another phenotype that exhibits inter-ethnic differences in frequency. TPMT is an enzyme that catalyzes methylation of therapeutic agents used in the treatment of acute lymphoblastic leukemia, rheumatoid arthritis, and autoimmune/inflammatory diseases, as well as in organ transplantation. Patients who have TPMT deficiency experience less efficient methylation and are at greater risk of fatal toxicity when treated with standard doses of fhiopurines. TPMT phenotype is defined by erythrocyte 6-mercapto-purine methylation. African American populations exhibit a 20% lower erythrocyte TPMT than Caucasian Americans, and persons of Chinese descent tend to exhibit greater activity than either of these other American subpopulations. 

A glucocorticoid-resistance model has been proposed to provide an explanation for how stress might influence diseases in which excessive inflammation is observed (e.g., allergies, autoimmune diseases, rheumatoid arthritis, and cardiovascular disease). In these cases, chronic stress diminishes the immune system s sensitivity to glucocorticoids that normally terminate the inflammatory response. For example, in a study of a group of 50 parents caring for a child undergoing treatment for pediatric cancer, whole blood of parents of cancer patients exhibited a lesser dexamethasone-dependent suppression of IL-6 production in vitro compared to parents of medically healthy children.94... 

Rheumatoid arthritis is a chronic, inflammatory, autoimmune disease of unknown etiology that if left untreated results in progressive joint destruction, deformity, disability, and premature death. Theories of possible etiologies include genetic, hormonal, viral, autoimmune, and environmental factors. The disease peaks between the fourth through sixth decades of life and is two to three times more common in women than in men. Differences in prevalence rates between ethnic groups are small. 

Sjogren syndrome. Chronic inflammatory autoimmune disease of the exocrine glands of unknown etiology. Its primary symptoms are keratoconjunctivitis sicca and xerostomia. Two types of Sjogren syndrome are distinguished a primary (isolated) type and a secondary type associated with another underlying autoimmune disease (e.g. rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, primary biliary cirrhosis, autoimmune hepatitis, multiple sclerosis, thyroiditis, autoimmune, etc.). Ro/SS-A and La/SS-B autoantibodies are used as classification criteria. 

Pro-inflammatory TNF-a, TNF-aR, Tace, IKK, IL-1, IL-IR, IRAK, IL-6, IL-6R, Toll-like receptors, BlyS, CD40L, LT-j8, GM-CSF Rheumatoid arthritis, Inflammatory diseases, Autoimmune disorders. Cancer... 

Therapeutic Agents Targeting TNF-oc. The Streptococcus pneumoniae host resistance model is also valuable for evaluating the importance of macrophage cytokines on bacterial host resistance. Human biological therapeutics targeting inhibition of TNF-a have been used to treat inflammatory autoimmune diseases such as rheumatoid arthritis. Decreased TNFa as a result of treatment with monoclonal antibodies (mAb) to TNF-a has an effect on several biomarkers of infection (Takashima et al, 1997 van der Poll et al, 1997 Benton et al., 1998 O Brien et al, 1999). These studies have reported that treatment of mice with a mAb to TNF-a results in altered levels of TNF-a in the lungs... 

Inflammatory and immune diseases Autoimmune disease (A,I), asthma (A), osteoarthritis (I), rheumatoid arthritis (I), septic shock (A,I), infections (A,I), familial cold auto-inflammatory syndrome (I), Muckle Wells syndrome (I), chronic infantile neurological cutaneous and articular syndrome/neonatal onset multisystemic inflammatory disease (CINCA/NOMID) (I), Crohn s disease (I), gout (I), acute renal failure (A,l)... 

Immune defense mechanisms can become deleterious for an individual when they are not controlled properly. Then they can cause disease. In such situations therapy is aimed to dampen immune reactions. Important examples are sqttic shock, allergy, autoimmune diseases, and chronic inflammatory diseases such as rheumatoid arthritis. Also, the success of organ transplantation... 

In the pathogenesis of many chronic inflammatory diseases (e.g., rheumatoid arthritis, glomerulonephritis, colitis ulcerosa, Morbus Crohn, atopic dermatitis, psoriasis) autoimmune processes play an important role, too. Although first of all nonsteroidal antiinflammatory agents or glucocorticoids should be applied, immunosuppressive agents may also be indicated. 

IFN- 3 reduces the induction by inflammatory cytokines of adhesion molecules and of MHC class I and II complex on endothelial cells, a process preceding attachment and transendothelial migration of T-cells. These anti-inflammatory effects of IFN- 3 exemplify antagonistic actions of type I and type IIIFN. There is, indeed, much clinical evidence for the involvement of IFN-y in inflammatory processes - through activation of iNOS and subsequent secretion of NO - leading to the establishment of autoimmune diseases as for instance in rheumatoid arthritis. 

Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown aetiology with some autoimmune features. Current thinking favours the hypothesis that interplay between genetic factors, sex hormones, and possibly an infectious agent or another immune activating agent initiates an autoimmune pathogenic mechanism that culminates in a disease with inflammatory and destructive features. 

TNF is a pleiotropic cytokine exerting a wide range of cellular responses, that affect biological processes such as lipid metabolism, coagulation, and insulin resistance and the function of endothelial cells. As a major proinflammatory cytokine TNF is also involved in progression of diseases like cancer, Alzheimer, Diabetes type II, cardiovascular, pulmonary or neurological disorders, and many autoimmune diseases. Blocking the action of TNF clearly reduces its inflammatory potential on various autoimmune disorders like Crohn s disease, rheumatoid arthritis (RA), and psoriasis. 

Besides anemia associated with cancer and CKD, anemia of chronic disease can result from inflammatory processes and occurs commonly in autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus. In treating these types of anemia of chronic disease, the most important principle is treating the underlying disease. These patients also may have iron deficiency and should be treated in the manner already discussed. Erythropoietin therapy such as epoetin-alfa therapy at a dose of 150 units/kg three times a week also may be used in these patients. 

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