Talk:Rheumatoid arthritis/Archive 1

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"The name is based on the term "rheumatic fever", an illness which includes joint pain and is derived from the Greek word rheumatos ("flowing"). The suffix -oid ("resembling") gives the translation as joint inflammation that resembles rheumatic fever. The first recognized description of rheumatoid arthritis was made in 1800 by Dr Augustin Jacob Landré-Beauvais (1772–1840) of Paris.[2]"

Is this true? First, the [Rheumatic fever] or [Rheumatism] articles make no mention of a name origin. Secondly, it seems dubious to me that someone would name a disease based on the fact that it's similar to another disease... using the prefix the disease is named from. Couldn't it just as well be "joint inflammation that has a flowing resemblance"? Clarification would be helpful. 90.227.230.219 (talk) 15:05, 21 May 2010 (UTC)

Apparently, the disease is eased by pregnancy. This is probably because pregnancy induce higher concentration of female hormones in the body. "It is already known that female sex hormones play a large part in easing RA during pregnancy, but it is not known why." [1] Unsigned by User:Wk muriithi

Ah, a news article. Many

chronic fatigue syndrome) are eased by pregnancy. Sadly, they rebound mercilessly after parturition. Oddly, lupus erythematosus

often develops during pregnancy. It is temping that fetal alloimmunisation is to blame, although nulliparous females and males also get lupus.

This phenomenon has various explanations. Just "female hormones" does not explain this at all, because females are much more at risk for autoimmune disease than males (up to 10x in some diseases).

It is actually more likely that the pregnant female auto-immunosuppresses to prevent immune rejection of the placenta and fetus, which are not necessarily HLA-identical.

PMID 9500514 has a good review on this. It would be nice if the articles actually mentioned in which medical journal this research was going to get published. JFW | T@lk

20:14, 6 Feb 2005 (UTC)

If somebody wants to expand the history section here is a link with good information: [2] --WS 10:39, 14 August 2005 (UTC) The Legacy of Thomas McPherson Brown, MD MIRA Therapy for Connective Tissue Disease by Henry Scammell

THERE IS A CURE!

The Road Back and other web sites have very convincing evidence, including double blind clinical trials that demonstrate the efficacy of Antibiotic Therapy (AT) for the treatment of Rheumatoid Arthritis and other suppossed "autoimmune diseases". [3]and [4]

Nothing is likely to ruin a good reputation in medicine faster than being the first to come up with the right answer while the rest of the institution is comfortably bedded down with familiar folly. When the truth finally does come out, even after decades, that doesn't always mean the world immediately stops punishing the prophet. Heretics make great scapegoats, and the process often continues for a time even after they're safely dead.

Thomas McPherson Brown, MD, is a case in point. Working with Albert Sabin (later of polio vaccine fame) at the Rockefeller Institute just before World War II, Brown isolated a bacter ia-like agent from the joint fluid of an arthritic woman and speculated that it might be the infectious trigger for her disease. The bug in question, then generically classified as an L-form, was too small to identify precisely, but with the advent of electron microscopy it was shown to be a class of cell-wall-deficient organisms which scientists named mycoplasma, for watery fungus.

Mycoplasma is ubiquitous and not at all easy to get rid of, but Brown found that it usually could be controlled by long-term, low-level doses of tetracycline. As that class of antibiotic evolved, he got even better results with the second and third generation, doxycycline and minocycline. Up to then, the only treatments for the various forms of inflammatory arthritis were for the symptoms, and this was the first credible therapy aimed at a probable cause.

Of course, because Brown's treatment generally produced positive results, he became immensely popular with his patients, a vocal, partisan constituency eventually some 10,000 strong, which proudly referred to itself as "Doctor Brown's Army." But very possibly for these same reasons, among his peers and many of his colleagues he was variously dismissed as a misguided zealot, a benign eccentric, or a serious, boat-rocking troublemaker, and he found himself progressively cut off from the usual sources for the funding of research. As painful as this must have been, it hardly seemed to slow him down.

After the war Brown headed up arthritis research for the Veterans' Administration, and eventually became Dean of Medicine at George Washington University Medical School and a medical consultant to the White House. By the time I met him 1988, he had retired from GWU but still maintained a thriving clinical practice and directed the Arthritis Institute at the National Hospital just outside Washington. Although he depended on a cane, he still had the handshake of a lifelong tennis player, a warm, gentle laugh, and the smiling, caring attentiveness of a natural healer. It was easy to see why he was so widely loved.

The reason for our meeting was to collaborate on a book that set forth his theory and treatment for the inflammatory forms of arthritis. Our effort gained some poignant urgency from the fact that we both knew he was dying of cancer. Although he was the author of over 100 medical articles in prestigious peer-reviewed journals, the general public was still in the dark about the benefits and promise of antibiotic therapy. A book seemed the only way to continue Tom's lifelong battle against mankind's oldest and most widespread crippling disease, and to make the therapy available to the millions who would still need it when he was gone.

Although in many cases the therapy brought about remission or even reversal of rheumatoid arthritis, Dr. Brown cautioned me at our first meeting against presenting antibiotics as a cure. While they didn't work for everyone, he estimated his success rate at above 90 percent for those who stuck with the therapy (an estimate I have since heard from other physicians who treat large numbers of patients with his protocol.) The timetable and degree of response could vary for individual patients, Brown said, by such factors as how much time had elapsed since o nset of the disease, the severity of symptoms, age at diagnosis, family history, and not least, any damage that already may have been done to the patient's overall health and particularly to their immune systems by the more widely accepted therapies for a rthritis. Ironically, many doctors who dismissed minocycline as either unproven or unsafe for rheumatic disease were perfectly happy to prescribe a frightening pharmacopoeia of other "standard" therapies including the potent cancer drug methotrexate, or g old salts, possibly the most lethal prescription drug ever passed by the FDA. None of these other therapies had ever been proven to produce long-term benefits, and most let the disease worsen while masking symptoms.

Tom Brown lived just a year aft er the book's publication. That was plenty of time to experience the further slings and arrows of his peers ("I just hope he isn't hurting anybody," one of them observed piously for the cameras of 20/20), but not nearly long enough for vindication. The first serious study of his therapy didn't begin until nearly three years later.

The treatment described in our book is now widely referred to as MIRA therapy, from that landmark, NIH-sponsored study of Minocycline In Rheumatoid Arthritis. But the MIRA trials were hardly undertaken as a tardy attempt at salvaging Tom Brown's reputation; quite the contrary. As one of the principals recently told me, at the outset at least half of the six participating centers entered the study with open skepticism. For one thing, Brown's theory and treatment flew in the face of almost everything that was then held to be true of rheumatoid arthritis. For another, because the NIH appeared to be bending to pressure from Congress in the wake of our book, the study rekindled serious resentment against the persistence of his influence even from beyond the grave. Many expected the MIRA trials would simply drive Tom Brown's ghost from the stage, and rheumatology would be able to settle back into its familiar rut of empty hopes and unfilled promises.

That all began to change even before the MIRA trials were finished. Without decoding which patients were receiving placebo and which got minocycline, it was obvious that more of them were improving than would be expected for that size group. When the results were finally published in Annals of Internal Medicine in 1995, it was revealed that well over half of the minocycline patients had improved by at least 50% according to subjective criteria of joint tenderness and swelling. Even more experienced dramatic improvements in objective measurements of their blood work.

Not everyone was surprised. When Tom Brown had made his final television appearance on Good Morning America back in 1988, Joan Lunden said his approach to arthritis was "turning the medical world upside down." His answer was a quiet, "I'm trying to turn it rightside up." Seven years later, with the decoding of the MIRA study, for those who still remembered that exchange the words now rang like prophesy. It was only logical to the members of Dr. Brown's Army that the therapy that had turned around their diseases and given them back their lives would work as well for others. That was the whole point of the book.

An editorial accompanying the MIRA study described the outcome as "highly significant...with minimal adverse events." It said that together with similar results from a smaller study in the Netherlands, the results "could be submitted to the Food and Drug Administration as the two positive 'pivotal' controlled clinical trials required for approval of a new drug application."

What are those 'minimal adverse events' sometimes associated with minocycline? The best known is sun sensitivity, which is easily avoided by a good blocker and the proper clothing. While none of the MIRA patients showed serious toxicity, seven dropped out of the study, most commonly for dizziness. This is a known problem with minocycline, but apparently not with doxycycline, which Tom Brown would often use as an alternative. Another adverse reaction, so infrequent that it was not reported in the MIRA study, can be hyperpigmentation, a darkening of the skin in patches, usually on the hands and forearms, which disappears when the therapy is stopped. It also can discolor teeth of small children. The most serious-sounding objection to minocycline is that it is an antibiotic, a class of pharmaceuticals under considerable - and legitimate - criticism for wide scale overuse, particularly in diseases where it encourages resistant forms of the organisms it attacks. But that argument ignores the benign profile of antibiotics in the tetracycline family, proven least prone to this disadvantage in literally billions of doses for conditions no more serious than teenage acne. And it also overlooks the special nature of mycoplasmas. When most bacteria are attacked by an antibiotic, they immediately put up a defense in the form of mutation, based on a decision formed at the point of impact in the cell wall. But because mycoplasmas are cell-wall-deficient organisms (toroidal in shape, they look like partially nibbled donuts), the antibiotic action takes place primarily in the cell's core, where no such response occurs. I have met several of Tom Brown's patients who have controlled their connective tissue disease with minocycline for decades, and the only other effect they ever noticed was that they almost never were bothered by the common cold.

There now have been at least seven major studies of Tom Brown's theory and treatment, including publication of O'Dell's landmark trials in Nebraska where one-third of the patients who had improved on minocycline in the first year achieved remission by the end of three years. The results were even better for year four. In 1998, The Lancet published a small, open study of usually fatal systemic scleroderma at Harvard Medical School, sponsored by The Road Back Foundation and the National Institutes of Health; two-thirds of the completers were in remission after 48 weeks of this therapy. Today, minocycline and doxycycline are widely prescribed for the various inflammatory forms of arthritis and other connective tissue diseases such as scleroderma, lupus and fibromyalgia. Minocycline is now listed as a standard treatment for both rheumatoid arthritis and Lyme disease by the Arthritis Foundation and the USP.

But at the same time Tom Brown's safe, inexpensive and highly effective therapy is becoming the new standard treatment for many of those diseases, the paradox remains. Even though the specialty of rheumatology proved the treatment works, many practitioners in that field still resent the way the MIRA study happened, and either refuse to give it or they limit its availability to those fortunate few patients who are informed enough to ask for it. Along the way, perhaps because the institution has lost the capacity for change and renewal, rheumatology has become the fastest declining specialty in medicine.

Meanwhile, the rehabilitation of Tom Brown's reputation is progressing nicely, as they like to say in medicine, with full recovery just around the corner. When he and I set out to preserve his theory and treatment for those who would live after him, we had no idea our effort would prove so durable. But the new edition of our book is updated with results of the latest clinical trials and illustrated with new case histories and pictures of recovered patients doing the most improbable things such as rock-climbing and scuba diving. Ten years after we wrote the first version and nine years since his death, Tom Brown's legacy, updated and reissued as The New Arthritis Breakthrough, was ranked by Library Journal as the #1 best-selling health book in America. I can hear Tom's warm, familiar chuckle at how it's turning out.

—Preceding unsigned comment added by Selfhelp (talk • contribs) 19:00, 10 July 2006

Effect, mechanism & cause are quiet distinct features. The fact that a tetracycline antibiotic may help does not prove that the demonstrated benefit is due to antibiotic action and thus a causation by bacteria. You will note from some of the articles in the PubMed Search criteria given that minocycline in particular seems to be more helpful than other tetracyclines:

It seems likely that the tetracyclines have direct immuno-modifying activity, quite separate from any antibacterial action: "The present study thus shows that Minocycline and tetracycline exhibit immunomodulatory properties, which may contribute significantly to their beneficial effects in rheumatoid arthritis." - Reeta K, Mediratta P, Mahajan P, Sharma K (2002). "Effect of minocycline and tetracycline on immunological responses in experimental animals". Indian J Med Sci. 56 (11): 553–9.

PMID 14510338.{{cite journal}}: CS1 maint: multiple names: authors list (link

)

Similarly much of the benefit of tetracycline in rosacea may be anti-inflammatory in nature rather than any killing of bacteria on/in the skin.

The article already mentions that a number of bacterial triggers have been previously considered - so it is not Rheumatologists being blind to a visionary colleague, but a number of suggestions that have been made and , to date, found wanting as a full explanation.

These ideas are not currently accepted by mainstream medicine and are de facto therefore the minority viewpoint. NPOV requires mentioning of the opinion. It is not trivial minority I grant (which need not be mention at all in wikipedia), but nor does NPOV grant comparable coverage.

Merely providing a search list of 'Minocycline in Rheumatoid Arthritis' to PubMed is not citing evidence for a position (all the 102 found papers could be refuting the idea) - so some selectivity as to which of these is to be used to support a claim needs be made. The other 2 links given [5] is a personal website (and fails meet

WP:Reliable source criteria) and [6]

is a campaigning patient group - again this would constitute a tertiary source rather than appropriate peer reviewed primary source studies.

The information may or may not have good evidence behind it, but for now none of the present links acts to

WP:Verify

the claims made, and as such the claim does not deserve to stay in the article (remember wikipedia is not a soap box, however passionate about a topic one is) - but with suitable rewrite and a change in citation/reference approach there is clearly lots of interesting stuff to add (even if just that tetracyclines useful immunomodifiers that are less toxic than other agents)...

For now, I shall have a go a writing/phrasing some of the additional material, applying wikistyling and moving non-mainstream ideas out from the main flow - this is "controversy" in the normal scientific meaning (i.e. a range of differing ideas and debate rather than necessarily accusations of pseudoscience) and research, rather than established/accepted knowledge. David Ruben ^Talk 21:29, 10 July 2006 (UTC)

I have just revert Selfhelp's POV recent edits in which it was stated that "complete remission" was shown by the papers cited - this was unfounded - the www.annals.org link concludes "modest" improvements & "neither ...study addressed possible mechanisms of action". Adding 2 additional links to Roadback seems to be spamming/POV pushing. I agree the studies are interesting and worthy further research, likewise that Minocycline seems a nicer drug than many others used in RhA (not least, given my dislike of phlebotomy, the lack of any requirement for monthly blood testing as with methotrexate). But studies, as indicated in the www.annals.org citation given, have not consistently supported benefits of tetracycline - although latest 2 studies are helping to suggest a research trend. Certainly there is no medical consensus (yet) on their overall role: ?useful just for mild disease, ?usefulness exceeds that of current treatments or ? useful for all degrees of severity and might help reduce dosages of more side-effect prone DMARDs ? But all this amounts to speculation (albeit likely quite positive), that should not be included in wikipedia as an encyclopaedia of established knowledge. David Ruben ^Talk 00:33, 15 July 2006 (UTC)

This section REALLY needs some information backing it up its claims... even if there's no actual scientific backing, some citation of books or websites promoting an "Eastern" approach to RA would be good. Elfbabe 06:20, 20 March 2006 (UTC)

I changed a statement in the diagnostic criteria so that it reflects the actual one. Jfmarchini 17:17, 9 September 2006 (UTC)

The person who wrote some of these dreadful symptoms must have the most depressing life. Dry eyes = leaking of eye contents? Good grief. Could you be a little less dramatic and just talk about major symptoms rather than freak occurrences? Cyborg Ninja 01:48, 29 October 2006 (UTC)

I heard that in the 1940's (US) that RA was treated with gold which was injected into the bloodstream, and apparently was quite popular and effective. But now one knows how or why it works. —The preceding

It also caused thrombocytopenia in 1% of patients, which is probably why it's no longer popular. Nbauman 02:30, 16 August 2007 (UTC)

Might be interesting to note that R. A. is a disease not a product of old age.

The article lacks a discussion of the juvenile version of RA. Might put some info in this week. Novickas 18:57, 12 March 2007 (UTC)

Hi everyone. Is it possible to condense some of the material on this article to make it more concise?

Rowan 15:07, 24 March 2007 (UTC)Rowan

Hi,

Does anyone have sources for the paragraph on prognosis and disability, particularly:

   * Daily living activities are impaired in most patients.
   * After 5 years of disease, approximately 33% of patients will not be working
   * After 10 years, approximately half will have substantial functional disability.

If reliable sources are not found for this paragraph I propose to remove the information as the top 4 google results for "rheumatoid arthritis prognosis" all contradict this information:

• http://www.merck.com/mmhe/sec05/ch067/ch067b.html
• http://arthritis.about.com/od/arthqa/f/rafuture.htm
• http://www.wrongdiagnosis.com/r/rheumatoid_arthritis/prognosis.htm
• http://www.usnews.com/usnews/health/bones/rheumatoid_arthritis/ra.test.prognosis.htm

The reason I feel that this information should be removed if unsourced is that when people are diagnosed (myself included) they often use Wikipedia as a "swot up" about the illness they have just been told they have. If this information is incorrect it should be removed as it may cause alarm to newly diagnosed patients. Martin Hinks 12:55, 23 May 2007 (UTC)

Unfortunately those prognoses are accurate. The Merck Manual, which you cited above, says that 10% will ultimately have severe disability. The most complete statistics I could find were in Harrison's Internal Medicine, a standard textbook that most medical students in the U.S. read, which is unfortunately only available online if you've paid $150 for the textbook. It says:

Harrison's Internal Medicine > Part 13. Disorders of the Immune System, Connective Tissue, and Joints > Section 2. Disorders of Immune-Mediated Injury >

Chapter 301. Rheumatoid Arthritis

Clinical Course and Prognosis

The course of RA is quite variable and difficult to predict in an individual patient. Most patients experience persistent but fluctuating disease activity, accompanied by a variable degree of joint abnormalities and functional impairment. After 10 to 12 years, <20% of patients will have no evidence of disability or joint abnormalities. Within 10 years, 50% of patients will have work disability. A number of features are correlated with a greater likelihood of developing joint abnormalities or disabilities. These include the presence of >20 inflamed joints, a markedly elevated erythrocyte sedimentation rate, radiographic evidence of bone erosions, the presence of rheumatoid nodules, high titers of serum rheumatoid factor, the presence of functional disability, persistent inflammation, advanced age at onset, the presence of comorbid conditions, low socioeconomic status or educational level, or the presence of HLA-DR1*0401 or -DR*0404. The presence of one or more of these implies the presence of more aggressive disease with a greater likelihood of developing progressive joint abnormalities and disability. Persistent elevation of the erythrocyte sedimentation rate, disability, and pain on longitudinal follow-up are good predictors of work disability. Patients who lack these features have more indolent disease with a slower progression to joint abnormalities and disability. The pattern of disease onset does not appear to predict the development of disabilities. Approximately 15% of patients with RA will have a short-lived inflammatory process that remits without major disability. These individuals tend to lack the aforementioned features associated with more aggressive disease....

The median life expectancy of persons with RA is shortened by 3 to 7 years. Of the 2.5-fold increase in mortality rate, RA itself is a contributing feature in 15 to 30%. The increased mortality rate seems to be limited to patients with more severe articular disease and can be attributed largely to infection and gastrointestinal bleeding. Recent evidence has also shown an important role of cardiovascular disease in the increased mortality of RA patients, and this appears to diminish with effective anti-inflammatory therapy. Drug therapy may also play a role in the increased mortality rate seen in individuals with RA. Factors correlated with early death include disability, disease duration or severity, glucocorticoid use, age at onset, and low socioeconomic or educational status.

I sympathize with the feeling that we should not cause needless alarm, but I also believe that we have an obligation to tell readers the truth. If people are coming to the Internet to research their disease, they are presumably looking for the truth.

Patients need to know their prognosis so they can plan for the future. In the U.S., there are financial issues of health insurance and disability. If you're likely to be unable to work in 10 years, you better use that time to prepare for it.

People should also know that there are diagnostic tests, like erythrocyte sedementation, that can give them a more accurate prognosis.

Severe arthritis can be treated with disease-modifying drugs that can themselves have severe and sometimes life-threatening adverse effects (and are very expensive). In order to decide whether to use these drugs, you need the candid facts about your prognosis. If you have bad prognostic factors, the drugs are probably worth the risk.

A lot of patient information is deceptively upbeat. If you read it, you wouldn't realize how serious arthritis is and how important it is to treat it quickly and aggressively. Nbauman 01:12, 16 August 2007 (UTC)

P.S. Here's another source that is free on the web:

Rheumatoid arthritis

Designing and implementing a treatment plan

Richard B. Gremillion, MD Ronald F. van Vollenhoven, MD, PhD

VOL 103 / NO 2 / FEBRUARY 1998 / POSTGRADUATE MEDICINE

Rheumatoid arthritis is not a benign disease. A 25-year prospective study (1) showed that median life expectancy is shortened by 7 years in males and 3 years in females. A significant decline in functional status also occurs over time. About 50% of patients with rheumatoid arthritis cannot function in their jobs within 10 years of disease onset. According to one study, (2) 48% of patients with a recent diagnosis were highly functional compared with 17% who had had the disease for 12 years. An important discovery was that joint destruction occurs early in disease (3). Within 3 years of onset, 70% of patients show radiographic damage, which is more pronounced during the first year of disease than during the second or third year. [end quote]

The significance of this is that it's very important for people with severe disease to know right away what they're facing, because they only have 3 years to prevent the worst damage -- but they must then take drugs that have dangerous side effects. Nbauman 01:43, 16 August 2007 (UTC)

NOTE - The last reference is from 1998. Surely the development of new drugs in the last decade, including the biologics, makes a BIG difference to this? —Preceding unsigned comment added by 24.161.97.249 (talk) 02:18, 12 December 2007 (UTC)

Prognosis

I completely agree with the above comment and think this should be updated as a matter of urgency. I have noted that RA charities in the UK (e.g. the Arthritis Research Campaign) quote much more encouraging statistics than US charities information sites in which I have seen the 50% off work in 10 years figure. In ARC's information page (http://www.arc.org.uk/arthinfo/patpubs/6033/6033.asp), I see 5% on people with RA have severely disabling arthritis, 20% have very mild symptoms or spontaneous remission and the remaining 75% have flare-ups and moderate symptoms but, with treatment and some level of adaptation, lead normal lives.

Like previous disputers of this article, I think this article does not present a fair review of the tetracycline+ anti-inflammatory drug treatment pioneered by Dr. Thomas_McPherson_Brown. I have a million objections to this article, but I will not be drawn into a long polemic like the previous disputers, and then be brow beaten into silence. I will start real simple: I will not go away until the book "The New Arthritis Breakthrough"[7], by H. Scammell is referenced prominently in the antibiotics section.

Real scientists fix their theory so it agrees with the data. Quacks fix the data so it agrees with their theory; they will hide or ignore any data that does not support their pet theory. There is incontrovertible evidence, both from double blind placebo controlled studies[8] and from anecdotal evidence[9], that antibiotic therapy works far better than any other available treatment for RA. And yet the writers of this article say: "The bacteria/antibiotic hypothesis therefore has very little support amongst the majority of rheumatologists and researchers, but is seen by a small number of integrative physicians and caregivers as part of the web of factors that produce the disease." One can only conclude that the writers of this article are quacks. If they aren't, why would they fail to mention, with clarity, the studies I just mentioned, the book by H. Scammell, and the Road Back Foundation website[10]? I cannot in good conscience allow the NPOV tag to be removed from this article until the article is fixed to reflect science instead of quackery. If anybody removes the tag before then, I will put it right back up. If we have to bring this to the attention of the highest levels of Wikipedia, so be it.Superperro 06:55, 8 August 2007 (UTC)

I have removed your entire paragraph. Please discuss your views here first before holding an article hostage in the way that you have done before. Obviously, antibiotics are not accepted treatment for RA and have their own problems (hypernatremia, intracranial hypertension). You are clearly new to the process, and I urge you to read

WP:NOR

before trying to reinsert your content.

If you want the theory to be accepted, you need some scientists to do proper clinical large trails with objective endpoints. In the absence of those, "my drug works better than your drug" becomes an empty argument. JFW | T@lk 13:14, 20 August 2007 (UTC)

The rules for NPOV are that the flag is removed only AFTER the dispute is settled, not before. Removing the entire antibiotics section is not an acceptable respose to a dispute. It is clear vandallism. Superperro 19:50, 20 August 2007 (UTC)

Firstly, do not move recent discussions to the top. See

WP:TALK

for talkpage guidelines.

Secondly, the {{

arbitration committee

case shows what happens when NPOV tags are sprayed around liberally.

Thirdly, just because one guy has done some research and written some books does not make his work notable. What I want from you is a reasonable discussion (without all the forceful language above) that takes into account the following points: (1) Do any professional guidelines regard antibiotic therapy as an advisable therapeutic modality in RA? (2) Is there a survey of rheumatologists that indicates that AP is a commonly-used modality? (3) Are there double-blind placebo-controlled randomised trials with reproducible and objective endpoints that demonstrate a benefit of AP? If none of these questions is answered with "yes", you are fighting an uphill battle to make this content relevant for an encyclopedia. I am simply explaining some very basic principles. If you continue to revert, there is a reasonable chance someone will have to

protect the article to force all contributors around the negotiating table. JFW | T@lk

01:01, 21 August 2007 (UTC)

I will file a complaint with the arbitration committee. The flag clearly states, do not remove until the dispute is settled. Removing it repeatedly is probably cause for being banned from wikipediaSuperperro 02:08, 21 August 2007 (UTC)

The NPOV flag is unnecessary. I wish you would focus on the content, rather than some brighly coloured box.

There is no point complaining to the ArbComm. Perhaps you ought to read

dispute resolution guidelines

first.

Could you now please address my three questions in my previous post? JFW | T@lk 04:36, 21 August 2007 (UTC)

I believe this article is seriously flawed and is giving bad (even dangerous) advice to the public on serious health matters. It definitely deserves an NPOV flag, according to my conscience. Stop making your own rules about NPOV. You have no right to take the NPOV flag down until the dispute is settled. You are not dealing in good faith. The flag states explicitly "Please do not remove this message until the dispute is resolved." There is no room for interpretation. Superperro 05:18, 21 August 2007 (UTC)

Your conscience is not the decisive factor. Do not confuse the flag with a reasonable discussion, which you have still not participated in. In perfect honesty, I couldn't care less whether the article is flagged, but you placed for inadequate reasons. The fact that you disagree with the mainstream management of rheumatoid arthritis perhaps reflects more on your POV than on anything else.

Could you now please tell me the answer to my question above: what evidence do you have that Thomas_McPherson_Brown's treatments were ever accepted in the medical community. JFW | T@lk 08:26, 21 August 2007 (UTC)

In my first statement, I pointed out a whole web page of clinical studies [11]. In particular, the 10th item on that list [12], the famous MIRA study, was an NIH conducted, double blind placebo controlled study. Antibiotic therapy for Rheumatoid Arthritis is approved by the American College of Rheumatology. JFW, stop changing the topic. Stop making up your own NPOV rules. Stop misrepresenting NPOV policy. There is no question that your removing the NPOV flag is illegal. I cannot engage in any civil discussion with someone who thinks the law does not apply to himSuperperro 12:44, 21 August 2007 (UTC)

These studies merely show that tetracyclines - specifically minocycline - show some promise as a treatment for RA. They do not show any bacterial cause; minocycline is known to be anti-inflammatory in its own right, and no studies show any benefit from non-tetracycline antibiotics. Your attempts to insert a long section on a treatment which is in no way considered to be a mainstream treatment are not appreciated, and clearly give it undue weight. This may deserve a brief paragraph as an experimental treatment, but no more than that. PeteThePill 17:31, 21 August 2007 (UTC)

I will commit an act of

request for comments

will be necessary.

PeteThePill has made a point that DavidRuben made a bit earlier on: effect from an antibiotic (which is also an immune modulator) does not immediately demonstrate bacterial etiology. In any case, if the arthritis is a "molecular mimicry"-like "allergic" reaction, eliminating the supposed bacterial cause by no means means that the reaction will resolve too. The whole theory is built on quicksand.

Let me try a compromise. The paragraph I will support is about as long as the paragraph on methotrexate and infliximab (both of which have solid evidence bases). Any longer is in direct violation of

WP:WEIGHT

.

"Some studies demonstrate benefit from tetracycline antibiotics, specifically minocycline (ref, ref). This may be the result of immune modulating effects of this class of antibiotics (ref), but some see this as a proof that rheumatoid arthritis is caused by bacterial infection (mycoplasma) or the body's cross-reaction to bacterial antigens (ref by Thomas McPherson Brown)."

Will you agree to such a paragraph, Superperro? JFW | T@lk 18:45, 21 August 2007 (UTC)

PeteThePill, your comment is so illogical, it's hard to address it.

• "These studies merely show that tetracyclines - specifically minocycline - show some promise as a treatment for RA. They do not show any bacterial cause" Pete, I was asked by JFW in his question (3) for a double blind clinical study. I gave one. Clinical studies are not meant to determine the cause of a disease. They only decide whether a treatment is effective. The MIRA study proved effectiveness of minocin, with flying colors. I was never asked what evidence is there that RA is a continuing infection.
• "no studies show any benefit from non-tetracycline antibiotics". False. Dr. Brown also used Clindamycin. I've heard of other antibotics being used (Zythromax, Levaquin). I can't quote studies but my ignorance is not an excuse for a wikipedia article to be flawed, or for you making dogmatic statements that you can't prove.
• "Your attempts to insert a long section". I never said that. You made that up. I haven't inserted a single comma into the article. My claim is that the article is flawed and biased.

Pete, you are attacking two different issues: antibiotics treatments (which the MIRA study proves very effective) and the infectious disease hypothesis. This is what the article says about the infectious disease hypothesis: "The bacteria/antibiotic hypothesis therefore has very little support amongst the majority of rheumatologists and researchers, but is seen by a small number of integrative physicians and caregivers as part of the web of factors that produce the disease." I assume you find this comment unbiased, ethical and scientific, because you don't seem to be complaining about it. This is what the article never mentions.

• (1)Sabin, inventor of the oral polio vaccine, was able to take liquid from the joint of a mouse with RA, inject it into the joint of a healthy mouse, and induce, almost immediately, RA in the healthy mouse. In recent times, this result has been reproduced with chimpazees. This is easily explained by the infectious disease hypothesis. Please answer me Pete, how does the auto-inmune disease hypothesis explain this? The inmune system of the healthy chimp learns to attack itself by coming into contact with the genetic material of another, genetically distinct chimpanzee?
• (2)There are many, many documented cases of patients who went to doctor Brown, patients who had had RA for 5 to 10 years, and Dr. Brown was able to put their disease into remission. Again this is easily explained by the infectious disease hypothesis. Please answer me Pete, how does the auto-inmune hypothesis explain this? The patient's inmune system, which had been attacking the patient for more than 5 years, was taught not to attack the patient by the mildly anti-inflammatory effects of tetracyclines? Why don't other anti-inflamatories have a similar power to cause remission?
• (3)The archeological record shows that RA did not exist in Europe before the 18th century (except for spondylitis), but it existed among American Indians much earlier than that. Most archeologist agree that this is simply explained if RA is an infectious disease. Please answer me Pete, how does the auto-inmmune disease explain this?

Of course, (1)(2)(3) are not proof that RA is an infectious disease, they just point in that direction. So far, there is no research that proves OR DISPROVES the infectious disease hypothesis. If there is an experiment that DISPROVES the infectious disease hypothesis, I beg you to mention it Pete.Superperro 19:28, 21 August 2007 (UTC)

JFW, thanks for restoring the NPOV flag. Hopefully, it will be removed soon. Your paragraph is a vast improvement in quality and fairness over the abomination that was there before. But I find it a bit too dry and terse. I would propose a small section entitled "Antibiotic Therapy and Infectious Disease Hypothesis". The content of this section would be the following paragraph:

Two separate but related questions have been the source of some controversy:

• Does antibiotic therapy help to alleviate Rheumatoid Arthritis? The MIRA(ref?) study---an NIH sponsored, double blind, placebo controlled clinical study---showed that this is the case for the antibiotic minocycline. In response to the MIRA study, the American College of Rheumatology has approved minocycline as one possible DMARD.
• Is Rheumatoid Arthritis a continuing bacterial infection, or is it purely an auto-immune response? The main proponent of the infectious disease hypothesis was Thomas McPherson Brown M.D. His belief in the infectious nature of the disease led him to treat Rheumatoid Arthritis with a combination of antibiotics like tetracycline and clindamycin, combined with anti-inflammatory drugs. Detractors(ref?) of the infectious disease hypothesis claim that the beneficial effects of antibiotic treatment are due to the anti-inflammatory effect of the antibiotic, rather than to its anti-bacterial effects.Superperro 02:54, 22 August 2007 (UTC)

It is meant to be dry and terse. McPherson Brown was obviously an outsider, and while minocycline may be a useful DMARD, that does not prove his point. In that way would you want to expand the paragraph that I've written? I don't know of anyone who has directly criticised this approach, but by not recommending it the makers of official guidelines are certainly showing they are not greatly impressed. JFW | T@lk 03:42, 22 August 2007 (UTC)

I would add that Wikipedia does not seek to correct current misunderstanding (it does not follow

Notablility) - lack of a rebutal is insufficient argument, journals and testbooks are not required to consider any and all hypothesis, hence why at wikipedia we need reliable 3rd party sources to positively confirm information. David Ruben ^Talk

04:02, 22 August 2007 (UTC)

PS

WP:AfD if this (newly identified) problem with the footnoted sources can not be addressed (see Talk:Thomas McPherson Brown) David Ruben ^Talk

04:07, 22 August 2007 (UTC)

I note Thomas McPherson Brown was "Speedy deleted per (CSD g12), was a blatant copyright infringement. using TW" by another editor.David Ruben ^Talk 20:53, 22 August 2007 (UTC)

David, do you agree with the paragraph in the way I've rephrased it? "Some studies demonstrate benefit from tetracycline antibiotics, specifically minocycline (ref, ref). This may be the result of immune modulating effects of this class of antibiotics (ref), but some see this as a proof that rheumatoid arthritis is caused by bacterial infection (mycoplasma) or the body's cross-reaction to bacterial antigens (ref by Thomas McPherson Brown)." Or do you think any mention of TMcPB is disproportionate? JFW | T@lk 21:57, 22 August 2007 (UTC)

Hi JFW, 1st sentance and a half is quite proper, but unless there can be presented some reliable source to confirm that microbiobial hypothesis is a significant minority viewpoint (vs just a trivial minority), then I would leave out the speculation. As written, it is not stated definitely that minocycline is not working by antibiotic action, but more cautiously (NPOV) that "may be the result of ...". So I would, for now use just "Some studies demonstrate benefit from tetracycline antibiotics, specifically minocycline (ref, ref). This may be the result of immune modulating effects of this class of antibiotics.(ref)" - but if can be shown via third party sources that TMcPB views have notability, then your version would be of proportionate & appropriate weight :-) David Ruben ^Talk 00:04, 23 August 2007 (UTC)

I've said all I can say, so this is my last message. Do with the article whatever your conscience dictates. For the medical doctors among you, I remind you that you have dedicated your life to upholding the best interest of your patients, and to do them no harm.

It is now clear that the controllers of this article want to hide or mis-represent the beneficial effects of antibiotic treatments. It would be nice if wikipedia had a fair article on RA, but it doesn't look like it's going to happen. The original article was fine, except for the antibiotics section which was comically biased and unscientific; it appear that those controllers want to re-instate the bias and pseudo-science of the original antibiotics section. It doesn't bother me that much anymore, because, due to the miraculous capacity of the internet to spread the word, more and more patients are demanding antibiotic treatments from their rheumatologists. Rheumatologists who refuse to offer antibiotics will soon be out of a job.

RA sufferers are not dumb. Why would they prefer lethal medicines that give some relief for a few years, but are eventually rejected by the body. Medicines that preserve the joints, but cause dangerous irreversible damage to the rest of the body. Medicines that almost never bring remission. Dr. Brown put into remission an astounding 80% of his patients. His treatments have only a few, easily controlled side effects.

It would be nice if the conscience of a rheumatologist is what caused him/her to use Dr. Brown type treatments, but if that is not the case, then the iron hand of the market place will take care of him/her in the next few years. —The preceding unsigned comment was added by Superperro (talk • contribs) 19:05, August 23, 2007 (UTC).

JFW said:

"(1) Do any professional guidelines regard antibiotic therapy as an advisable therapeutic modality in RA? (2) Is there a survey of rheumatologists that indicates that AP is a commonly-used modality? (3) Are there double-blind placebo-controlled randomised trials with reproducible and objective endpoints that demonstrate a benefit of AP?"

(1)Yes, The ACR (American College of Rheumatology) lists Minocycline as an approved DMARD (Disease-Modifying Antirheumatic Drug) for Rheumatoid Arthritis (http://www.rheumatology.org/public/factsheets/minocycline.asp). (2) Whether it is commonly used or not depends on the rheumatologist and his/her personal beliefs. However, the fact that the association that represents rheumatologists, and is made up of rheumatologists, lists Minocyline as a DMARD clearly shows that clinical studies have proved Minocycline as effective in the treatment of RA. (3) Here are some studies which should prove helpful in demonstrating there is benefit to antibiotics for RA:

1. http://www.annals.org/cgi/content/full/122/2/81 Tilley MIRA 48 wks minocycline vs placebo, 1995

2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10446869&dopt=Abstract O’Dell 4 year Minocycline vs placebo, early-onset RA, 1999

3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16447240&dopt=Abstract Doxycycline + MTX vs MTX alone, no previous DMARD, <1 year with RA, 2006

4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11273473&dopt=Abstract India study, 6 months, Doxycycline vs MTX 6 months, 2000

5. http://www.medscape.com/medline/abstract/11665963 Minocycline vs Plaquenil O’Dell 2001

6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9592865&dopt=Abstract Chinese, Minocycline + unspecified DMARD, DMARD resistant before study, 1998

7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10047718&dopt=Abstract Japanese study, DMARD resistant, 6 mos, 1 yr, minocycline only, 1998

8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1334514&dopt=Abstract Israeli study, DMARD resistant, 48 weeks, minocycline only. 1992.

9. http://www.jrheum.com/abstracts/abstracts06/224.html London study. Tetracycline plus clindamycin vs no treatment, 1 year, DMARD resistant, 2006

JFW: Thank you for addressing this very important subject of antibiotics to treat rheumatoid arthritis. I have been in remission from my severe, crippling rheumatoid arthritis for 2 years. I am on Minocycline alone. Do not let any doctor (or otherwise) tell you that he or she knows the mode of action behind Minocycline, or any other DMARD. The fact is, there is still no poven cause or cure for RA. They do not know the mode of action behind Minocycline on rheumatoid arthritis. The fact that some rheumatologists state that it only works because of its anti-inflammatory or immune-modulatory effects, is simply pure speculation. Jason —Preceding unsigned comment added by Jason22175 (talk • contribs) 06:55, August 24, 2007 (UTC)

Somewhat of a side issue, minocycline is now thought to help treat rosacea through an antiinflammatory effect (see newly added 1st paragraph of Rosacea#Causes), but presumably there must be some antibiotic effect given that other non-tetracycline antibiotics are also used for that condition (unless they all have the same additoinal activity).

To the above two editors, thank you for the references. What is needed in wikipedia for any "new" treatment approach is two levels of citation (proof). The less rigorous (and usually easiest to verify) is whether a significant number of people believe or use a particular approach. This should on simple citing be easy to prove in a NPOV way - either there is, or is not, a significant number who hold a viewpoint. Much harder of course is to confirm whether that view is right or wrong, and suitable references for random controlled pacebo trials, or biochemical studies to prove underlying mechanism of action are often harder to locate. Hence for this article:

1. Confirmation of approach being used? Other than Road Back Foundation's or Scammell's own claims, are there Rheumatology journals or National Media reports of significant numbers treated. I know Road Back Foundation's website so claims, but the artice will need an independant 3rd party source?
   • If so, then no question, the article must mention that this approach used .
   • The
     weight
     given over in the artcle will depend on current de facto size of those who follow this approach. So if only a (significant) minority of rheumatologists would so use (and for wikipedia, we are talking of the worldwide collection of specialists), then only a small mention would be appropropriate. If in time became the primary treatment by most rheumatologists, then the article would need be ammended to reflect what would then be the majority viewpoint.
   • Please realise that wikipedia reflects current accepted practice, even if research papers are starting to emerge that contradicts this and one suspects that day-to-day clinical practice is about to change (
     good faith
     .
2. Does an approach actually work, or at least work in the way that is claimed ? Refs above suggest yes might work, but as Jason22175 points out may not be for certain understood why, so language needs to reflect this.

Quite honestly would it really matter if it were proved minocycline worked as a DMARD and not by any anti-infective process, if it were also shown that it worked better and more safely than any other existing drug ? It would still be an interesting and useful additional tool. What counts is helping the patient, and if research suggests new possible underlying mechanisms or approaches in treatment, then that is where specialists and patients will follow... and wikipedia, one step behind, will no doubt be reflecting these changes.

I'll let others look up on those references now kindly given above, and discuss how this meets the

WP:NPOV guidelines that apply - I'm shortly off on holiday in the real world :-) David Ruben ^Talk

19:57, 24 August 2007 (UTC)

"Much harder of course is to confirm whether that view is right or wrong, and suitable references for random controlled pacebo trials, or biochemical studies to prove underlying mechanism of action are often harder to locate."

--Jason —Preceding unsigned comment added by Jason22175 (talk • contribs) 06:19, August 25, 2007 (UTC)

After years of "suicidal" chronic pain I was diagnosed with RA and AS. Both my brothers have it too with advanced spinal fusion. Over the counter medications and steroids did not work. Viox for 2 years nearly killed me and was useless too until I quit them just before the recall as I was having constant 24 / 7 heart pain. Somebody introduced me to the book "the infection connection". Only the third Dr. I contacted was prepared to prescribe Tetracycline but with little faith even after I purchased several books and gave them to the Dr's to read. Anyway I got dramatic relief in just days. I took the tetracycline for one year then stopped. The relief lasted months and then flared up again. Another short dose and it cleared up. The flare ups are becoming more infrequent and I have no doubt that the tetracycline saved my life. I was at the end of my rope without health insurance and unable to sleep/work or do anything. Had become a zombie. In my twenties I was a highly successful tri-athlete. This was a death sentence and the pain had become so excruciating that I had no more interest in continuing. Unable to work, no health insurance and just enough income to pay rent and food from my games, see www.dreamgreen.org I had to do something. Please, tetracycline does work. Occasionally I still have flare ups and I accept there will always be some pain now but at least now I can sleep better, I can get up without chronic stiffness and pain and walk and swim again. I am in my mid 40's and considering going to med school if I can find the funds because of tetracycline. Thanks to Katherine Poehlmann, Ph.D. and her book The Infection Connection. —Preceding unsigned comment added by 76.125.252.84 (talk) 18:03, 22 January 2010 (UTC)

Why do people recommend using acetaminophen which is not anit-inflammatory instead of Advil which is anti-inflammatory? Just because its more popular pain killer? BryanTree 03:32, 5 October 2007 (UTC)

Acetaminophen is recommended when an arthritis sufferer is taking methotrexate. Using NSAIDs with methotrexate can cause liver damage. 12.31.17.65 15:53, 16 October 2007 (UTC)edobrzen

With the advent of biologics (enbrel, humira, remicade) I suspect that much of the information in this article will be outdated within the next couple years, if it is not already. Properly treated, most people can lead normal lives with RA. The problem stems from diagnosis taking too long, and unnecessary damage occuring during this sometimes long process. Family doctors who suspect RA should screen for rheumatoid factor and anti-CCP and refer positive patients to a rheumatologist asap. Also, we need to provide for the uninsured to gain access to biologics. The most recent studies indicate a favorable cost-benefit ratio of biologics, even though they are very expensive. Allowing an unnecesary disability and then paying for it for life is even more expensive, on so many levels. For references, go to www.medscape.com and search on rheumatoid arthritis.159.121.9.50 19:00, 15 November 2007 (UTC)SDrake, Portland, OR

How about you provide references yourself, rather than directing people to search Medscape? Also, your vision of the future sounds interesting but not suitable for inclusion at present. JFW | T@lk 01:56, 23 November 2007 (UTC)

Ann Intern Med has put out a systematic review on which DMARD is better, and are combinations better than monotherapy. JFW | T@lk 01:56, 23 November 2007 (UTC)

This is actually a pretty important paper that is actually available free now. JFW | T@lk 08:49, 5 May 2008 (UTC)

33% of RA patients undergoing HRCT have some changes of interstitial lung disease, even if they are asymptomatic: http://archinte.ama-assn.org/cgi/content/abstract/168/2/159 JFW | T@lk 19:16, 29 January 2008 (UTC)

Just making a quick list of what i've noticed needs doing, feel free to add to the list as you notice something. Please remove an item from this list when it's been fixed:

• Image for the infobox
• Use more peer reviewed articles to cite things, there are lots of good but not necessarily
  reliable sources
  .
• Clean up introduction, move the naming information to the top next to the name of the article. (The name is derived from the Greek rheumatos means "flowing"...)
• Rheumatoid arthritis#Other needs tidying up and expanding if possible. Internal red links need to be fixed (by either making their respective articles or simply removing the link and just having normal text).

Regards, CycloneNimrod^Talk? 11:45, 26 April 2008 (UTC)

MEDMOS needs to be applied, and sections populated as usual. I would suggest we identify a good recent free review article as a scaffold for most of the essential information. JFW | T@lk 21:45, 28 April 2008 (UTC)

I've been searching through PubMed and found "Kennedy T, McCabe C, Struthers G; et al. (2005). "BSR guidelines on standards of care for persons with rheumatoid arthritis".

NICE and found this guideline: http://www.nice.org.uk/nicemedia/pdf/coxiifullguidance.pdf Regards, CycloneNimrod^Talk?

13:28, 29 April 2008 (UTC)