Rheumatoid arthritis etiology

In the past number of years a number of studies have shown that in a variety of diseases there is a significant oxidation of Met residues to Met(O) in specific proteins that results in a loss of biological activity. These diseases include cataracts, rheumatoid arthritis, adult respiratory distress syndrome and emphysema. The most convincing evidence that Met(O) in proteins may be involved in the etiology of a pathological condition comes from studies with a-l-PI. It is well accepted that a-l-PI is inactivated upon oxidation of its Met residues. A decreased activity of a-l-PI in lung tissue that would result in an increased elastase activity has been associated with pulmonary emphysema. In patients who have a... 

The musculoskeletal system consists of the muscles, bones, joints, tendons, and ligaments. Disorders related to the musculoskeletal system often are classified by etiology. Acute soft-tissue injuries include strains and sprains of muscles and ligaments. Repeated movements in sports, exercise, work, or activities of daily living may lead to repetitive strain injury, where cumulative damage occurs to the muscles, ligaments, or tendons.1-3 While tendonitis and bursitis can arise from acute injury, more commonly these conditions occur as a result of chronic stress.3,4 Other forms of chronic musculoskeletal pain, such as pain from rheumatoid arthritis (see Chap. 54) or osteoarthritis (see Chap. 55), are discussed elsewhere in this text. 

Brahn E. Animal models of rheumatoid arthritis. Clues to etiology and treatment. Clin Orthop 1991(265) 42-53. 

Rheumatoid arthritis (RA) is a chronic and usually progressive inflammatory disorder of unknown etiology characterized by polyarticular symmetric joint involvement and systemic manifestations. 

The idea of reduced adrenal capacity as a possible model for PTSD has also been recently raised by Heim et ah, who concluded that low cortisol may not be a unique feature of PTSD, but may represent a more universal phenomenon related to bodily disorders, having an etiology related to chronic stress (Heim et al. 2000). There are numerous stress-related disorders such as chronic fatigue syndrome, fibromyalgia, rheumatoid arthritis, chronic pain syndromes, and other disorders that are characterized by hypocortisolism. In one study, Heim et al. showed decreased cortisol responses to low-dose DEX, but failed to observe blunted ACTH responses to CRF in women with chronic pelvic pain, some of whom had PTSD, compared to women with infertility (Heim et al. 1998). Since the data were not analyzed on the basis of the subgroup with and without trauma and/or PTSD, it is not possible to directly compare results of that study to other reports examining PTSD directly. 

Since the recognition of the biological role of lycopene in the prevention of chronic diseases, the emphasis of the scientific community has been in the area of cancer, with special focus on prostate cancer. However, based on the hypothesis that oxidative stress may be an important etiological factor in the causation of most of the degenerative diseases and that lycopene is a potent antioxidant, the scientific community has started to study its role in diseases other than the ones reviewed in this chapter. These health disorders include skin and ocular diseases, rheumatoid arthritis, periodontal diseases, and inflammatory disorders. The scientific information pertaining to the role of lycopene in these diseases is still in its infancy. However, the rationale for undertaking these studies is scientifically valid and it is hoped that in the next 3-5 years several studies will be reported in the literature. 

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. 

There is also a significantly increased incidence of IgA deficiency in patients with autoimmune or potentially autoimmune disorders, and usually it is not clear which came first. It can be argued that autoimmunity is a complication of immune imbalance subsequent to inborn IgA deficiency (H24). With inborn absence of IgA, exposure to normal human colostrum, plasma, and saliva can result in the production of antibodies to IgA. By the time such patients are discovered the etiological mechanisms are often obscured and IgA treatment is out of the question. The incidence of IgA deficiency is known to be 1-4% in the following conditions Still s disease, systemic lupus erythematosus, rheumatoid arthritis, Sjogren s disease, warm hemolytic anemia, megaloblastic anemia, idiopathic pulmonary hemosiderosis, thyrotoxicosis, and cirrhosis. 

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. 

In 1941, Fenz used this antitubercular drug to treat rheumatoid arthritis (RA), since it was thought that arthritis also had an infectious etiology. He found that intravenous doses of 0.01-0.1 g (2-20 mg of Cu) gave modest results, but exceptional results were claimed with some patients given 0.2 g (40 mg of Cu) per injection three times per week with a Umit of 2.5-6 g (475-1140 mg of Cu) per treatment course [229, 230]. Fenz also reported an additional antianaemia effect on anaemias associated with RA which was consistent with observations reported by others, who had found that anaemic... 

The role of both T and B lymphocytes in a variety of disease states beyond transplantation has become increasingly important in the past decade. This is especially true of those diseases frequently referred to as autoimmune in their etiology, such as rheumatoid arthritis, nephrotic syndrome, systemic lupus erythematosus, inflammatory bowel disease, and so on. In addition, several other major diseases are also known to have a component of T- or B-cell-mediated pathogenesis, for example, atopic dermatitis, psoriasis, and asthma. Until very recently, the mainstay of therapy for these diseases was the corticosteroids, which were often less than satisfactory in efficacy and often associated with undesirable side effects, especially in growing children and the elderly. Thus, the search for new agents with different mechanisms of action and which did not have the same adverse event profile as conventional corticosteroids led to the subsequent evaluation of drugs such as tacrolimus and sirolimus to treat several of these diseases. 

Clinical herbalists have reported differing information on the use of Echinacea species in autoimmune conditions. Exacerbation of symptoms has been reported in systemic lupus, ulcerative colitis (autoimmune etiology uncertain), glomerular nephritis, and multiple sclerosis. In "some" cases, effects reoccurred on rechallenge. In rheumatoid arthritis, treatment with Echinacea species for 10 days did not exacerbate the condition (Upton and Graff 2007). A survey of 25 medical herbalists indicated that 12 had used Echinacea species in persons with autoimmune conditions. Of these 12, 11 indicated a beneficial effect and 1 indicated a worsening of symptoms (Upton and Graff 2007). 

Etiology and Pathogenesis - In spite of new arguments for mycoplasma as the cause of rheumatoid arthritis (RA), the etiology of the disease remains uncertain.A brief review article on the pathogenesis of joint inflammation in RA has appeared. ... 

There is very little objective evidence to incriminate food hypersensitivity in the symptoms of patients presenting with joint pains or other physical syndromes unaccompanied by conditions known to have an allergic etiology. Spontaneous variations in the activity of rheumatoid arthritis are notoriously misleading. There are occasional case reports of individual cases of arthritis responding to diet (Parke and Hughes, 1981). However, controlled studies have not yielded any evidence that specific foods provoke rheumatoid disease (Denman et al, 1983). 

---