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ASAS/EULAR recommendations for management of AS
mig
07/15/11 08:39 PM
Published on www.ard.bmj.com Annuals of Rheumatic Diseases, The EULAR Journal website, is the following article:
Title: 2010 update of the ASAS/EULAR recommendations for the management of ankylosing spondylitis
Author:
J Braun, R van den Berg, X Baraliakos, H Boehm, R Burgos-Vargas, E Collantes-Estevez, H Dagfinrud, B Dijkmans, M Dougados, P Emery, P Geher, M Hammoudeh, RD Inman, M Jongkees, MA Khan, U Kiltz, TK Kvien, M Leirisalo-Repo, WP Maksymowych, I Olivieri, K Pavelka, J Sieper, E Stanislawska-Biernat, D Wendling, S Özgocmen, C van Drogen, BJ van Royen, D van der Heijde
Publication: Annals of the Rheumatic Diseases
Publisher: BMJ Publishing Group Ltd.
Date: Jun 1, 2011
Copyright © 2011, BMJ Publishing Group Ltd and the European League Against Rheumatism
"AS is the prototype,24 a subtype, and an outcome of spondyloarthritis, particularly of the axial form of spondyloarthritis. Recent new classification criteria have widened the spectrum of spondyloarthritis by including earlier forms in addition to AS.25 26 This project has also led to a separation in the classification to predominantly axial and peripheral forms of spondyloarthritis. The term ‘axial spondyloarthritis’ covers patients with chronic back pain who have AS, which is defined by the presence of definite structural changes on radiographs in the sacroiliac joints, and patients with early or abortive forms of spondyloarthritis, which is defined by the presence of sacroiliac inflammation as detected by MRI or the presence of HLA B27 in combination with the presence of features typical of spondyloarthritis.27 28 It can be anticipated that future trials will increasingly target axial spondyloarthritis rather than AS. Some trials with that aim have already been performed and some have started. However, as the evidence from such trials is currently limited it has been decided to restrict the recommendations to AS, although the project group unanimously agreed that these recommendations can equally be applied to patients with axial spondyloarthritis."
You can discuss this topic here.
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New Styles Available
mig
06/29/11 09:22 PM
There are 2 new style 'skins' available on KA.
Scroll to the bottom-left corner of the page to find a drop-down box with a style-chooser list. 2 new skins are now available to select as a preference.
Look for a new one on the list called Blues, and another recent addition, an imported style called light-blue. 
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Clues to Why Humira Fails Some
jessxo
04/13/11 07:22 PM
REPRINT
Copyright © 2011 HealthDay. All rights reserved.Link: http://consumer.healthday.com/Article.asp?AID=651830
Nearly a third develop an immune reaction to the drug that thwarts its effectiveness, study finds
By Jenifer Goodwin
HealthDay Reporter
TUESDAY, April 12 (HealthDay News) -- In a new study, close to a third of patients taking the arthritis drug Humira developed an immune system reaction to it that rendered it ineffective.
Researchers say the finding helps to explain why some people get relief from their rheumatoid arthritis symptoms while on Humira (adalimumab), which is made by Abbott Laboratories, while others gain little or no benefit. Humira belongs to a class of drugs known as biologics.
In those people for whom the drug is ineffective, the immune system realizes the drug is a foreign substance and develops antibodies to it, researchers explained. Those antibodies bind to the drug and prevent it from working.
"What the publication shows is that Humira, like many other biologic agents, may induce an immunological response against the drug," said senior study author Dr. Gerrit Jan Wolbink, a rheumatologist at Jan van Breemen Research Institute in the Netherlands. "The immunological response works against the drug. This is one of the explanations why some patients do not respond the way we hope they will."
Patients who were also taking methotrexate, another arthritis drug and an immunosuppressant, were less likely to develop the antibodies, according to the study in the April 13 issue of the Journal of the American Medical Association.
Researchers followed 272 patients taking Humira for about three years.
About 28 percent developed immune system antibodies against the drug. The reaction tended to happen within the first few months of starting treatment: About 67 percent of those who developed antibodies did so during the first 28 weeks.
Patients without antibodies had more of the drug circulating in their blood. Lower levels of the drug are a sign that the body's immune system is fighting the drug and it's being removed from the body, Jan Wolbink explained.
Whether or not patients developed antibodies was also linked to whether they got relief from their rheumatoid arthritis while on Humira.
Nearly half -- 48 percent -- of those without antibodies experienced a significant reduction of their arthritis symptoms while taking the drug, while only 13 percent of those who developed antidrug antibodies got similar relief.
And while 34 percent of patients without antibodies experienced remission, only 4 percent of those who developed antibodies did.
Patients who developed antibodies were also more likely to drop out of the study because of "treatment failure."
Humira is a tumor necrosis factor (TNF) inhibitor, which works by blocking the action of TNF, a substance known as a cytokine that contributes to the inflammation of rheumatoid arthritis and other conditions.
"If you make antibodies, then Humira doesn't block the action of TNF, and it doesn't work," Jan Wolbink said.
Dr. Olga Belostotsky, a rheumatologist and chief of allergy and immunology at Lennox Hill Hospital in New York City, said the research helps explain why some patients don't respond to Humira, and yet they do respond when switched to another drug in the same class of TNF inhibitors.
"It's because they don't have antibodies to the other drugs, even when it's another drug in the same group of medications," she said.
Belostotsky said the research suggests it's very important that patients start methotrexate to suppress the immune system before starting Humira.
What isn't known is why those 28 percent of patients developed antidrug antibodies while the rest didn't.
"Why antibodies develop in some people more than the others is unclear, and why people react more to some drugs than others is unclear," Belostotsky said.
More information
The Arthritis Foundation has more on rheumatoid arthritis.
SOURCES: Gerrit Jan Wolbink, M.D., Ph.D., rheumatologist, Jan van Breemen Research Institute, Amsterdam, Netherlands; Olga Belostotsky, M.D., Ph.D., rheumatologist and chief, allergy and immunology, Lenox Hill Hospital, New York City; Journal of the American Medical Association, April, 13, 2011
Last Updated: April 12, 2011
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NIH scientists discover secrets of helper T cells
jessxo
11/04/10 08:13 PM
Press Release (reprint) October 20, 2010Recent NIH scientific findings
Scientists at the National Institutes of Health have redefined the roles of several cytokines involved in the generation of immune cells implicated in severe autoimmune diseases. The study in mice showed that development of Th17 immune cells can occur without the presence of transforming growth factor (TGF)-beta, a mediator thought to be required for Th17 cell development. The study demonstrates that the interaction of three inflammatory cytokines (proteins that influence the behavior of cells) – interleukin-6 (IL-6), IL-1-beta and IL-23 – is responsible for the creation of Th17 cells that are more active in promoting autoimmunity than Th17 cells generated with IL-6, IL-1-beta and TGF-beta. These findings reemphasize the separate roles of IL-23 and TGF-beta in immunity and autoimmunity, and open up possibilities for the development of new therapies. The study appears in the current issue of the journal Nature.
The immune systems of mice and humans mainly consist of B cells and T cells. While B cells fight infections and can induce autoimmunity by producing antibodies that directly target foreign antigens or a person’s own tissue, T cells are involved in overall cell-mediated immunity. Importantly, how a T helper (Th) cell differentiates (develops from an immature, unspecialized cell into a mature, specialized cell) determines how it mediates immune responses. Th17 cells produce IL-17, a powerful inflammatory cytokine, and have been implicated in multiple autoimmune diseases, including rheumatoid arthritis, psoriasis and multiple sclerosis. The established belief has been that Th17 cells initially differentiate in response to activation by IL-6 and TGF-beta. However, previous research has shown that TGF-beta is primarily associated with suppressing immune functions and promoting regulatory T cells (Treg), which can produce inhibitory cytokines that dampen inflammatory immune responses.
In the present study, the NIH scientists first looked at the conditions to differentiate Th17 cells from naïve T cells outside of the mouse (in vitro) and tried several different cocktails of cytokines to see which combinations would promote Th17 development. They found two combinations that efficiently induced Th17 differentiation. As previously described, IL-6, IL-1-beta, and TGF-beta-1 together created Th17 cells. Surprisingly, IL-6, IL-1-beta, and IL-23 without TGF-beta also created Th17 cells. Most interestingly, the action of Th17 cells generated with IL-23, designated Th17(23), was different from the action of Th17 cells generated with TGF-beta (Th17(beta)). The researchers compared transcription factors, receptors and mediators of the two Th17 subtypes and looked at the pathogenic activity of both Th17 subtypes in mice during experimental autoimmune encephalomyelitis (EAE), a common model of autoimmunity that mimics some aspects of multiple sclerosis. They found that Th17(23) cells provoked significantly more severe disease than did Th17(beta) cells.
These findings suggest a new model for Th17 generation and the existence of functionally different subtypes of Th17 cells. This study also provides a better understanding of the array of immune components involved in autoimmunity and suggests possibilities for new targeted therapies.
NIH scientists contributing to this study are affiliated with the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), the National Institute of Dental and Craniofacial Research (NIDCR), and the National Institute of Allergy and Infectious Diseases (NIAID). Additional support was provided by Merck Research Laboratories (Schering-Plough Biopharma), Palo Alto, Calif.
Reference
Ghoreschi K, Laurence A, Yang XP, Tato CM, McGeachy MJ, Konkel J, Ramos HL, Wei L, Davidson T, Bouladoux N, Grainger J, Chen Q, Kanno Y, Watford WT, Sun HW, Eberl G, Shevach E, Belkaid Y, Cua DJ, Chen W, O’Shea JJ. Enhanced Pathogenicity of Th17 cells Generated in the Absence of Transforming Growth Factor-ß Signaling. Nature. 2010 October 21;467(7318): 967-971.
Who
John J. O’Shea, M.D. Scientific Director, National Institute of Arthritis and Musculoskeletal and Skin Diseases, is available to comment on this article.
Contact
To schedule interviews, please contact Trish Reynolds, 301-496-8190, reynoldsp2@mail.nih.gov.
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ASR HIP RECALL BY DEPUY
seancadogan1
09/20/10 12:15 PM
Are there any AS members out there who had a Hip replacement and the implants used were the faulty ASR DePuy types?
Love to hear from you
Regards
Sean
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Johninco's (John S) story
Johninco
07/01/10 12:22 AM
Hey, everyone. I'm a newbie here and my story has just been published on the Stories page.
If you read it you'll have a better understanding of the comments I make in the forums.
I look forward to getting to know all of you.
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Houston - AS Support Group Meeting
ankyspon
12/01/09 11:21 PM
Well, I am not sure if its a great idea but I am going to this AS Support Group Meeting in Houston and expect Shauna to be there. I was wondering if there's anybody else who lives in or around Houston who might treat this to be a good opportunity to meet me and others in person.
Its going to be an evening dinner meeting on Tuesday, December 11. If there's anybody who's interested to be there, please pm me and I can share the address with you.
Thanks.
Ankush
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