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Posted: Sun Jun 5th, 2005 16:14 |
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ARBs and arthritis
Angiotensin receptor blockers suppress antigen-specific T cell responses and ameliorate collagen-induced arthritis in mice.
Arthritis Rheum. 2005 Jun 2;52(6):1920-1928 [Epub ahead of print]
PMID: 15934096 [PubMed - as supplied by publisher]
http://tinyurl.com/dgg29
Dr Marshall:
Here is a study from Japan about joint destruction in mice. So the only thing left to worry about is - are you a man or a mouse? (murine models don't always translate to human disease)
http://tinyurl.com/yalz2c
"Angiotensin receptor blockers suppress antigen-specific T cell responses and ameliorate collagen-induced arthritis in mice
.. olmesartan suppressed the development of severe arthritis and joint destruction in the CIA model."
Carol: Although I developed notable joint damage before I started the MP, I have seen no evidence of progression of this damage since I have been on the MP (taking Benicar every 6 hours). I'm happy I have that in common with these mice .
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Posted: Sat Dec 3rd, 2005 23:03 |
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Osteoarthritis (degenerative arthritis)
(filelink)
This osteoarthritis (degenerative arthritis) website states:
-Osteoarthritis (OA) is a type of arthritis that is caused by the breakdown and eventual loss of the cartilage of one or more joints.
-Osteoarthritis occurs more frequently as we age. Primary osteoarthritis is mostly related to aging.
-Most cases of osteoarthritis have no known cause and are referred to as primary osteoarthritis.
-Osteoarthritis occasionally can be found in multiple members of the same family.
-Unlike many other forms of arthritis that are systemic illnesses, such as rheumatoid arthritis and systemic lupus, osteoarthritis does not affect other organs of the body.
-common x-ray findings of osteoarthritis include loss of joint cartilage, narrowing of the joint space between adjacent bones, and bone spur formation.
I am having more and more difficulty accepting any disease or symptom are merely being part of the 'normal' aging process. How often do patients diagnosed with OA have undiagnosed systemic Th1 inflammation?
Since studies are now showing that tetracycline can slow down the OA process, this suggests that this process is caused by bacteria. I suspect that lost cartilage will not be replaced but that eliminating CWD bacteria can halt the degenerative process.
The Promise of a Tetracycline Antibiotic for Treating Osteoarthritis
An Antibiotic to Slow Osteoarthritis
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Posted: Mon Dec 5th, 2005 06:34 |
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(filelink)
Personal Experience:
marion villa this is a piece of cake my friends... and I am heading for a completely healthy life.
Michele MBK: RA: boost in confidence in resuming life-activities while on MP
John McDonald: RA: Road Back and MP story. other unexpected gains.
Interview with Ival Meyer - arthritis, dyslexia
davbrkr Dave: Lyme 40+ yrs: RA: 1 month-17 days on Phase I
Christina JRA MP summary
Ival RA: MP is the right treatment for RA
Christina: RA - First Anniversary update
Carol: new RA update Phase three
Ival: RA: update: gone back to work. MP 21 months.
Christina: RA - re should I wait to MP?
Carol: RA - MP personal experience
Ival can you work on MP?
Christina RA: food sensitivities lessening. very active. recovering more quickly.
Christina re JRA: personal experience.
Ival: RA: my most active month ever since starting the MP.
Help from RA members
John McDonald: RA: My RA "remission" is more secure now
Ival: RA: Here is my little speech I gave at the Los Angeles conference. see DVDs.
Ival: RA: I've got my life back
Ival: RA improvements..8 months ... 1 year....
Has anyone had evidence of joint improvement?
Carol RA: summary
Carol RA: off thyroid meds
Christina RA personal experience
AmyEliz: RA: my 'positives'.... RA: summary
See also
PAIN CONTROL
see Standard Treatments information link and scroll down
Last edited on Mon Aug 11th, 2008 05:15 by
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Posted: Thu Aug 10th, 2006 03:30 |
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Anti-TNF Antibody Therapy in Rheumatoid Arthritis and the Risk of Serious Infections and Malignancies
(seriousriskfilelink)
JAMA Vol. 295 No. 19, May 17, 2006
Anti-TNF Antibody Therapy in Rheumatoid Arthritis and the Risk of Serious Infections and Malignancies - Systematic Review and Meta-analysis of Rare Harmful Effects in Randomized Controlled Trials
Tim Bongartz, MD; Alex J. Sutton, PhD; Michael J. Sweeting, MSc; Iain Buchan, MD, MFPH; Eric L. Matteson, MD, MPH; Victor Montori, MD, MSc
JAMA. 2006;295:2275-2285.
Context: Tumor necrosis factor (TNF) plays an important role in host defense and tumor growth control. Therefore, anti-TNF antibody therapies may increase the risk of serious infections and malignancies.
Objective: To assess the extent to which anti-TNF antibody therapies may increase the risk of serious infections and malignancies in patients with rheumatoid arthritis by performing a meta-analysis to derive estimates of sparse harmful events occurring in randomized trials of anti-TNF therapy.
Data Sources: A systematic literature search of EMBASE, MEDLINE, Cochrane Library, and electronic abstract databases of the annual scientific meetings of both the European League Against Rheumatism and the American College of Rheumatology was conducted through December 2005. This search was complemented with interviews of the manufacturers of the 2 licensed anti-TNF antibodies.
Study Selection: We included randomized, placebo-controlled trials of the 2 licensed anti-TNF antibodies (infliximab and adalimumab) used for 12 weeks or more in patients with rheumatoid arthritis. Nine trials met our inclusion criteria, including 3493 patients who received anti-TNF antibody treatment and 1512 patients who received placebo.
Data Extraction: Data on study characteristics to assess study quality and intention-to-treat data for serious infections and malignancies were abstracted. Published information from the trials was supplemented by direct contact between principal investigators and industry sponsors.
Data Synthesis: We calculated a pooled odds ratio (Mantel-Haenszel methods with a continuity correction designed for sparse data) for malignancies and serious infections (infection that requires antimicrobial therapy and/or hospitalization) in anti-TNFtreated patients vs placebo patients. We estimated effects for high and low doses separately. The pooled odds ratio for malignancy was 3.3 (95% confidence interval [CI], 1.2-9.1) and for serious infection was 2.0 (95% CI, 1.3-3.1). Malignancies were significantly more common in patients treated with higher doses compared with patients who received lower doses of anti-TNF antibodies. For patients treated with anti-TNF antibodies in the included trials, the number needed to harm was 154 (95% CI, 91-500) for 1 additional malignancy within a treatment period of 6 to 12 months. For serious infections, the number needed to harm was 59 (95% CI, 39-125) within a treatment period of 3 to 12 months.
Conclusions: There is evidence of an increased risk of serious infections and a dose-dependent increased risk of malignancies in patients with rheumatoid arthritis treated with anti-TNF antibody therapy. The formal meta-analysis with pooled sparse adverse events data from randomized controlled trials serves as a tool to assess harmful drug effects.
Author Affiliations: Division of Rheumatology and Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minn (Drs Bongartz and Matteson); Department of Health Sciences, University of Leicester, Leicester, England (Dr Sutton); MRC Biostatistics Unit, Institute of Public Health, Cambridge, England (Mr Sweeting); Northwest Institute for Bio-Health Informatics, University of Manchester, Manchester, England (Dr Buchan); Knowledge and Encounter Research Unit and Department of Medicine, Mayo Clinic College of Medicine, Rochester, Minn (Dr Montori).
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Posted: Thu Aug 10th, 2006 03:36 |
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Cancer Risks Detailed for Arthritis Drugs
(drugrisklink)
By LINDSEY TANNER, AP Medical Writer Tue May 16, 8:18 PM ET
CHICAGO - Rheumatoid arthritis patients taking Humira or Remicade face triple the risk of developing several kinds of cancer and double the risk of getting serious infections, a study led by the Mayo Clinic found.
The analysis builds on previous reports about the risks associated with Abbott Laboratories' Humira and Centocor's Remicade. But the earlier research focused mostly on one kind of cancer — lymphoma — and infections such as tuberculosis and pneumonia.
The new study found an apparent link to other cancers, too, including skin, gastrointestinal, breast and lung tumors. It also quantifies the risks and says high doses appear to be the riskiest.
While the drugs' packaging information mentions some of the risks, the manufacturers said the new study does not prove that the medication is at fault, and they said the research was flawed.
Study co-author Dr. Eric Matteson, a Mayo Clinic rheumatologist, stressed the overall chances of developing cancer while using these drugs is still small. The researchers also noted that the medications' benefits include improving flexibility and range of movement, easing pain and increasing life expectancy, which arthritis can shorten.
In addition, the researchers noted that the risks for individual patients probably vary widely. Older, sicker people who have taken the drugs for several years probably face the highest risks, they said.
Still, the researchers said patients should be made aware of the dangers and told to seek medical help if they develop fevers, coughs or other symptoms of infection. They should also be sure to undergo the cancer screenings recommended for the general public, the researchers said.
Their study appears in Wednesday's Journal of the American Medical Association.
Matteson is working with Centocor in developing a new drug that works similarly, and he and co-author Dr. Tim Bongartz have been paid consultants to Abbott for unrelated work, but neither company funded the study. The Mayo Foundation sponsored the research.
Rheumatoid arthritis affects more than 2 million Americans, and involves a malfunctioning immune system that attacks joints throughout the body, causing pain, deformities and disability.
Dr. John Klippel, president of the Arthritis Foundation, said the study will probably not change doctors' minds, because scores of patients have benefited from the drugs. Remicade was approved in 1998, Humira in 2002.
More than a half-million patients have been treated with the two injectable drugs and a third similar medication, Enbrel, all of which block production of a protein linked with inflammation.
Enbrel was not included in the study because it differs at the molecular level, Matteson said. He said he is getting paid by Enbrel marketers Wyeth and Amgen to do a similar analysis on Enbrel alone.
Matteson's ties to Centocor and his work on Enbrel were among several omissions and errors included in disclosure statements that accompanied the study in JAMA.
He said the omissions were "errors of oversight on my part" and that he was not attempting to conceal anything. Matteson said he brought the issues to JAMA's attention on Friday.
But in an unusual move, journal editors posted a correction Tuesday on JAMA's Web site revealing that they have asked the Mayo Clinic College of Medicine to investigate.
The editors cited "the nature and extensiveness of this incorrect and incomplete reporting."
In a telphone interview Tuesday, Dr. Phil Fontanarosa, JAMA's executive deputy editor, said that "journals are not in a position to conduct full-scale, intense investigations when there are concerns. ... We ask the institutions to help us in getting to the bottom of these sorts of issues."
The researchers analyzed data from nine studies comparing Humira or Remicade with placebos and pooled the results. There were 29 cancers in 3,493 patients who received at least one dose of either drug, compared with three cancers in 1,512 patients on placebos.
Serious infections occurred in 126 patients on drugs and 26 on placebos. They included pneumonia and cellulitis.
An Abbott spokesperson said the analysis "doesn't reflect all the data" on Humira and said the studies were too short to sufficiently monitor cancer incidence.
Tom Schaible, Centocor vice president of medical affairs, said most of the analyzed studies used higher-than-recommended Remicade doses. "There's clearly a favorable benefits-risks ratio" with recommended doses, Schaible said.
On the Net:
JAMA: http://jama.ama-assn.org
Arthritis Foundation: http://www.arthritis.org
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Posted: Mon Sep 18th, 2006 04:56 |
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Reiter's syndrome and HLA axis
(filelink)
I don't believe that the HLA axis genetic changes are necessarily handed down in an individual's DNA, I believe that the HLA axis (HLA-DRA, HLA-DRB and HLA-DQ) are all mutations caused by the pathogens responsible for Th1 infection.
Only that hypothesis explains why so many different diagnoses end up with common HLA haplotypes, yet there is not determinate diagnostic value to be obtained by measuring them. Yes, I know, some of the HLA haplotypes are 50% greater in this, that, or the other diagnosis, but genetics should result in 100% and 0% and anything else is just statistical noise, and should be discarded, IMO.
Ankylosing spondylitis has responded quickly to Benicar blockade, usually with significant reduction of the pain.
..Trevor..
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Aussie Barb
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Posted: Sun Oct 8th, 2006 00:53 |
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Death risk linked to steroid use for arthritis
(filelink)
"Patients with rheumatoid arthritis who are treated with low-dose steroids for more than 10 years are more likely to die than patients who are less exposed to these drugs "
____________________
Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| Depression| 24+ years not Dx| MP Aug04| ABC of MP| MP Search|
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Posted: Mon Oct 16th, 2006 01:50 |
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Angiotensin receptor blockers suppress antigen-specific T cell responses and ameliorate collagen-induced arthritis in mice
(filelink)
Arthritis Rheum. 2005 Jun;52(6):1920-8.
Comment in: Arthritis Rheum. 2005 Dec;52(12):4047-8. Arthritis Rheum. 2005 Nov;52(11):3678-9.
Angiotensin receptor blockers suppress antigen-specific T cell responses and ameliorate collagen-induced arthritis in mice.
Sagawa K, Nagatani K, Komagata Y, Yamamoto K. University of Tokyo, Tokyo, Japan.
OBJECTIVE: The renin-angiotensin system plays an important role in the regulation of cardiovascular, renal, and endocrine functions. Recent studies have demonstrated that angiotensin II has proinflammatory effects that may contribute to the pathogenesis of immune-mediated diseases. We used the collagen-induced arthritis (CIA) model to investigate the influence of angiotensin II receptor blockers (ARBs) on antigen-specific immune responses and determine whether ARBs have preventive or therapeutic effects on the development of arthritis.
METHODS: We administered ARBs (olmesartan, candesartan, and telmisartan) to mice and evaluated antigen-specific T cell proliferation and cytokine production following immunization with ovalbumin (OVA) or type II collagen in Freund's complete adjuvant (CFA) or aluminum hydroxide (alum). Next, we induced CIA in DBA/1 mice and administered olmesartan. The severity and incidence of arthritis were scored according to clinical manifestations, and joint tissue sections were examined histopathologically. RESULTS: ARBs severely suppressed lymphocyte proliferation and interferon-gamma production in mice immunized with OVA or type II collagen in CFA. Olmesartan also suppressed lymphocyte proliferation in mice immunized with ovalbumin in alum. In the CIA model, olmesartan reduced the mean arthritis score and the incidence of severe arthritis, even when it was administered only after disease onset. Histopathologic findings for joint destruction were improved in olmesartan-treated mice.
CONCLUSION: ARBs suppressed antigen-specific immune responses for Th1 and Th2 in vivo. Furthermore, olmesartan suppressed the development of severe arthritis and joint destruction in the CIA model. These findings suggest that ARBs may have therapeutic potential in rheumatoid arthritis.
PMID: 15934096 [PubMed - indexed for MEDLINE]
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