One of the things I would love to believe about modern medicine is that, once we find a cause for a disease, we’d all know about it. This is second only to my fantasy that if I’m ever involved in a major accident my surgeon will be experienced, sober, and well rested. Well, one out of three anyway.
But what we find is that solutions to disease that don’t fall cleanly into a certain area of medicine get ignored. Rheumatoid Arthritis is a perfect example. I’ve known for almost a decade (see website) what the likely cause of RA is and have helped patients solve the issues. But when I look in my new Harrison’s they continue to say the causative issues are unknown. Balderdash, I say. We’ve got a perfectly good bacterial agent that causes autoimmune cross-reactions in a genetically susceptible population. In English that means bad bug make your body mad. Mad body go after joints and other body parts trying to kill bug. M.D.s use steroids or chemo to kill off immune response but it doesn’t solve the problem because the bug is still in your gut.
How do I know this? Because medline told me. I’ll put the most recent analysis of the bacteria involved below, which is pretty conclusive. But this isn’t a new discovery. I’ll also put the data from 1989 below. We’ve known the likely agent for RA for twenty-two years at least.
So what happens? Do we see our bacteria, Proteus Mirabilis, headlining all the Rheumatology journals? Or do we see absolutely nothing? Keep in mind that a gut bacteria falls squarely in the area of Gastroenterology, far away from Rheumatology. I’m not sure what percentage of a Rheumatologist’s patients are RA sufferers, but I would assume that a switch en masse to Gastroenterology would decimate their patient base. And keep in mind that we’re talking about a causative agent that might lead to a permanent, dare I say it, cure down the line. That means no more quarterly patient visits managing medications for the rest of your life. It means getting better and not having that problem anymore. Sure, you’ll still go to six other doctors for other things, but your Rheumatologist won’t be on that list.
Now, I wouldn’t say that it was unethical for Rheumatologists to ignore the bacteria theory. No more than the MS specialists ignoring the Swank diet, or ALS specialists ignoring the plethora of alternative treatments. Any doctor can say that any treatment needs more research. But when the research mounts to a point where the average layperson can see probable benefit, it becomes a situation where a doctor’s beliefs about a disease can get in the way of his ability to assimilate the newest information about that disease. I can only think that the stomach ulcer surgeons must have had trouble dealing with the reality of Heliobactor pylori as a causative agent for their “stress disease of unknown origin.”
But once we’ve had our moment of empathy with the doctors, we need to think about the patients involved. Twenty-two years is a very long time to have terrible pain, partially controlled by substances that are defined by their side effects. Are any of them being told about the possibility of a bacterial cause? Not that it’s definitive, but that it is a possibility? No, if the medications don’t work, the patient is told: that’s all we can do. The issue is not informed consent by the patient, it is that the physician is not informed. But how is a physician supposed to stay informed when every month s/he is inundated by literature from within his/her field? We all feel the barrage of information, and doctors have the least time for relaxed reading.
So the issue becomes how do we get our physicians to keep learning at the pace we need them to give us all our options? It isn’t possible.
So the informed patients of today need to educate themselves about their illnesses. Again and again I see the patients with the best outcomes are those that ask me and everyone on their treating team all the tough questions. They know the material, or they have a family member who knows the material. I see the very necessary field of medical advocate springing up, individuals who will do the office visits along with you and ask the tough, informed questions. If you haven’t got one, get one.
Autoimmun Rev. 2010 Feb;9(4):216-23. Epub 2009 Nov 4.
Ebringer A, Rashid T, Wilson C.
SourceKing’s College, Analytical Sciences Group, London SE1 9NN, UK. firstname.lastname@example.org
Rheumatoid arthritis (RA) is a crippling joint disease affecting over 20 million people worldwide. The cause of RA is most probably linked to the triad of microbial trigger, genetic association and autoimmunity and can be explained using the philosophical method of Karl Popper or Popperian sequences. Ten “Popper sequences” have been identified which point to the urinary microbe Proteus mirabilis as the cause of RA: Popper sequence 1 establishes that HLA-DR4 lymphocytes injected into a rabbit evoke specific antibodies against Proteus bacteria. Popper sequence 2 establishes that antibodies to Proteus bacteria are present in RA patients from 14 different countries. Popper sequence 3 establishes that antibodies to Proteus bacteria in RA patients are disease specific since no such antibodies are found in other conditions. Popper sequence 4 establishes that when RA patients have high titres of antibodies to Proteus such bacteria are found in urinary cultures. Popper sequence 5 establishes that only Proteus bacteria and no other microbes evoke significantly elevated antibodies in RA patients. Popper sequence 6 establishes that the “shared epitope” EQR(K)RAA shows “molecular mimicry” with the sequence ESRRAL found in Proteus haemolysin. Popper sequence 7 establishes that Proteus urease contains a sequence IRRET which has “molecular mimicry” with LRREI found in collagen XI of hyaline cartilage. Popper sequence 8 establishes that sera obtained from RA patients have cytopathic properties against sheep red cells coated with the cross-reacting EQR(K)RAA and LRREI self-antigen peptides. Popper sequence 9 establishes that Proteus sequences in haemolysin and urease as well as the self antigens, HLA-DR1/4 and collagen XI, each contain an arginine doublet, thereby providing a substrate for peptidyl arginine deiminase (PAD) to give rise to citrulline, which is the main antigenic component of CCP, antibodies to which are found in early cases of RA. Popper sequence 10 establishes that antibodies to Proteus come not only from sequences crossreacting to self antigens but also from non-crossreacting sequences, thereby indicating that active RA patients have been exposed to infection by Proteus. The ten Popper sequences establish that RA is most probably caused by Proteus upper urinary tract infections, which can possibly be treated with anti-Proteus therapy.
Copyright 2009 Elsevier B.V. All rights reserved.
Rheumatol Int. 1989;9(3-5):223-8.
Rheumatoid arthritis and Proteus: a possible aetiological association.
Ebringer A, Khalafpour S, Wilson C.
SourceDepartment of Biochemistry, King’s College, London, UK.
The presence of specific anti-Proteus antibodies in active, rheumatoid arthritis (RA) patients, has been demonstrated by four different techniques: indirect bacterial agglutination, ELISA, Western blotting and immunofluorescence. Furthermore, anti-HLA-DR4 tissue typing sera have been shown to bind to Proteus microorganisms, thereby suggesting some molecular similarity or cross-reactivity between bacteria and HLA antigens. The concept is proposed that Proteus-reactive arthritis occurs during active phases of RA and tissue damage is mediated through immunological activity involving HLA antigens.\
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