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Rheumatoid arthritis is a bewilderingly complex disease involving the interactions of many, and varied, cell populations and multiple families of low and high molecular mass mediators. We are only slowly beginning to understand the mechanisms that produce the local and systematic pathology clinically recognized as rheumatoid arthritis. Increasingly, use is being made of experimental models of this disease in an effort to test hypotheses about putative pathological mechanisms and to investigate the effect of novel therapeutic agents. A major section of this book covers these experimental models

Rheumatoid arthritis --- Rheumatoid arthritis. --- Animal models.

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Rheumatoid arthritis. --- Adulthood.

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Background: Treatment with tumour necrosis factor alpha (TNF-α, or simply TNF) inhibitors is considered to be an alternative to the use of traditional disease-modifying anti-rheumatic drugs (DMARDs) in patients with different rheumatic diseases, i.e. rheumatoid arthritis (RA). There are three TNF-inhibitor drugs currently available on the market (brand names in brackets): adalimumab (Humira), etanercept (Enbrel) and infliximab (Remicade). The Norwegian Knowledge Centre for the Health Services has previously summarised the evidence on the drugs' efficacy and safety (in randomised clinical trials and observational studies) while the present report considers cost-effectiveness of the drugs for rheumatoid arthritis. After considerable growth over several years, the aggregate sales of the three drugs amounted to 860 million NOK in 2006. RA is a serious disease, not least from an economic perspective. No cost-of-illness studies have been found for Norway, but studies from Sweden suggest that the costs of the disease are substantial with a large proportion related to loss of work capacity. Methods: We undertook a review of economic evaluations of TNF-inhibitors against RA, and considered an analysis of health-related quality of life data for patients on TNF-inhibitors and DMARD users from a Norwegian observational study. Results: A total of twelve studies from six countries were included in the literature review. The studies were based on health economic models, which were diverse in their characteristics, and therefore the estimates of cost-effectiveness varied significantly. Conclusions: In our review of economic evaluations of TNF-inhibitors, we found significant variation in the type and features of the models used, which led to a wide range of estimates. The potential for direct comparisons of results between the studies, and thus transferability of results into Norwegian setting, is limited. With this in mind, our main conclusions are as follows:1. First line therapy: TNF inhibitors seem not to be cost-effective as first line therapy, based on the one study in which this was considered.2. Second line therapy: We cannot draw any conclusions, since no relevant studies were found.3. Third line therapy: TNF-inhibitors may be cost-effective, particularly in the case of patients in early disease. The drugs are also likely to be more cost-effective for patients who experience a good rather than a moderate response.4. Indirect costs: Prevention of productivity loss may account for considerable savings, but has only been accounted for in a few of the economic evaluations.

Tumor necrosis factor --- Rheumatoid arthritis --- Inhibitors. --- Treatment.

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Arthritis. --- Arthritis, Rheumatoid. --- Rheumatoid arthritis. --- Arthritis. --- Polyarthrite rhumatoïde --- Arthrite

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In recent years there has been a substantial increase in the number of diseases with the inflammatory component such as such as allergy, asthma, rheumatoid arthritis, inflammatory bowl disease (IBD, which includes ulcerative colitis and Crohn's disease), chronic sinusitis, and many other conditions. The majority of these diseases are multifactorial, with the contribution of genetic and environmental factors. Among the latter, the role of certain microorganisms and viruses in triggering or sustaining the inflammatory process is most controversial. In rheumatoid arthritis, for example, the following bacteria and viruses have been implicated in triggering the disease: Mycoplasma spp., Proteus mirabilis, Escherichia coli, Staphylococcus spp., Bordetella spp., Acinetobacter spp., the parvoviruses, Epstein-Barr virus, and retroviruses. The list of putative microbial triggers of rheumatoid arthritis is still growing, and it becomes essentially impossible to make a causation link between certain infectious agents and the disease. In the light of these disappointing results there are calls for even larger studies with the use of more advanced and large-scale technologies. The primary function of the immune system is the maintenance of body homeostasis and protection against any threats to it via several lines of elaborate and complex immune defense. Given even higher complexity that involves the microbiota and the corresponding host-microbe interaction, the conditions for this equilibrium become even more challenging. In the absence of a defined pathogen, for example, the spectrum of microorganisms involved in triggering inappropriate immune responses may include polymicrobial communities or the cumulative effect of several microbial/viral factors. Under the normal circumstances there is a fine-tuned balance between commensal microbiota and the host’s immune responses. However, when this balance is compromised, for example in IBD, a massive immune response is launched against commensal microbiota resulting in chronic inflammation. Besides the microbial/viral factors, the balance of the immune system can be compromised by other causes. Given, for example, the close and inclusive interaction of the immune, nervous and endocrine systems, the list of these provoking factors can expand even more. For instance, it has been demonstrated that even mild sleep deprivation may increase the production of interleukin-6 and C-reactive protein. Understanding the complex role of microbial and environmental factors in inflammatory and autoimmune diseases, therefore, is the main subject of this topic.

environment --- Autoimmune ecology --- Silica exposure --- Rheumatoid arthritis --- Viruses --- Bacteria