Rheumatoid Arthritis: Bos JD

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A digest of articles written 1999 and later, on the topic "Arthritis, Rheumatoid," originating from Planet Earth —» Bos JD.  Display:  All Citations ·  All Abstracts
1 Guideline Review and expert opinion on prevention and treatment of infliximab-related infusion reactions. 2008

Lecluse LL, Piskin G, Mekkes JR, Bos JD, de Rie MA. · Department of Dermatology, Academic Medical Center, University of Amsterdam, PO Box 22700, 1100 DE Amsterdam, The Netherlands. · Br J Dermatol. · Pubmed #18627374 No free full text.

Abstract: Infliximab (Remicade; Schering-Plough, Kenilworth, NJ, U.S.A.) is a chimeric monoclonal antibody that acts as a tumour necrosis factor-alpha inhibitor. Infliximab is registered for the treatment of rheumatoid arthritis, psoriatic arthritis, Crohn disease, ulcerative colitis, ankylosing spondylitis and plaque-type psoriasis. Like other foreign protein-derived agents, infliximab may lead to infusion reactions during and after infusion. Infusion reactions occur in 3-22% of patients with psoriasis treated with infliximab. Most of these reactions are mild or moderate and only few are severe. Nevertheless, they may lead to discontinuation of treatment. As infliximab for psoriasis is prescribed as a last resort and is in most cases very effective, discontinuation of treatment is undesirable. With proper care and prevention of the infusion reactions the need to discontinue treatment with infliximab can be diminished. The objective of this article is to present a guideline for the management of infliximab-related infusion reactions, based on the best available evidence. This guideline can be used in patients with psoriasis as well as in dermatology patients receiving infliximab for off-label indications such as hidradenitis suppurativa or pyoderma gangrenosum.

2 Review Psoriasis, innate immunity, and gene pools. 2007

Bos JD. · Department of Dermatology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands. · J Am Acad Dermatol. · Pubmed #17317489 No free full text.

Abstract: Recently, emphasis has shifted from T cells to innate (natural) immunity as the possible major culprit in psoriasis. All known elements of innate immune responses are up-regulated in psoriasis lesions, which must have a polygenetic origin. We hypothesize that urbanized populations have been under evolutionary pressure that selects for increased innate immunity responses because those offer relative but immediate protection from epidemic infections. That would have resulted in a changing gene pool, in which alleles of polymorphisms associated with increased innate immunity responses have amplified in these populations. Having too many of these genes together in one individual would result in a relatively low number of infections. On the other hand, it would also result in a higher prevalence of diseases related to increased innate immunity, such as psoriasis, and perhaps also multiple sclerosis and rheumatoid arthritis. Indeed, in indigenous people (Inuit, Aborigines, Ami) who have not been under this selection pressure, morbidity due to infections is high and the prevalence of psoriasis is low or even absent.