Rheumination

H1N1 and the Color of Phlegm

from  www.newsteamtexas.com/. ../2009/09/flu.jpg

A while ago I wrote a post about my experience with phlegm and how it helped me eliminate respirology as a potential career.  A follow-up post linked to a site that included a color choice labeled 'phlegm' and how I disagreed with the color choice.  It was, as you can imagine, just a joke, but these posts have been some of my most looked up posts of all time.  All last winter I would get regular visits from anxious people the world around trying to figure out if I could help them diagnose what they were harking out. I couldn't.  The visits dwindled out throughout the summer and I thought that was the end of it.  I didn't mind.  It was a bit rude that one of my most successful posts had nothing to do with rheumatology.   

But then came the fall and the visitors returned. I realized that it coincided with the onset of H1N1 in the USA and sure enough, the numbers of visitors continues to rise.  It seems that my post is an H1N1 meter.

Fair enough.  I guess even rheumatologists and others interested in rheumatology get a cough now and again and their phlegm conundrum might lead them to this site.  All the better.  As for me, well I got my vaccine this week so I'm hoping my own sputum will remain pristine.  Mind you, a week in bed might have increased my posting productivity.

Groopman's Wrist

Jerome Groopman is discussed again over at DB's Medical Rants.  I'm sure just about all of you know of Groopman and his book, How Doctors Think.  This book, which discusses how MDs go about their business of making, or missing diagnoses, was the talk of the blogosphere when it first came out in 2007 and seems to pop up regularly since.  I must admit, while the book was an interesting read, his chapter on his own wrist problem lead me wonder exactly how Groopman thinks.

His wrist problem is discussed in mechanical terms, with multiple small traumas, but the problem evolved to the point where it would regularly become "hot, beet red, and swollen".  Now this is the classic triad of inflammatory joint pain, generally seen in arthritic, not orthopaedic conditions.  I would have to think of crystal arthropathy like pseudogout or gout, maybe even palindromic rheumatism.  Instead, it seems like Groopman visits half the orthopedic surgeons on the East coast and discovers, to the surprise of exactly nobody, that surgeons, when they aren't sure what to do, like to operate.  Although the man is an internist, there is no mention of visiting one of his rheumatology buddies who might have done the appropriate diagnostic  procedure, which is a simple joint tap during an attack.

 Sure, maybe it was mechanical, as he suggests by chapters end, but with those symptoms he might have avoided a lot of grief  by staying in the internal medicine wing of the hospital.  For all I know, he's still suffering from pseudogout with an underlying metabolic disease like hemochromatosis.  Just hope he takes the walk  down the corridor to his local rheumatologist.

 

HLA B-27 to the Rescue?

The discovery, in 1973, of the association between ankylosing spondylitis and the Human Leukocyte Antigen HLA B27  raised two still unanswered questions.  The first,  the holy grail of spondyloarthropathy research, is simply; how does the B27 gene confer risk of developing the disease, and the second, somewhat  less funded question; why the hell does this nasty piece of DNA still exist.  Why haven't the Mendelian garbage collectors tossed this unwelcome gene onto the trash heap of failed genetic experiments.

Recent events have rekindled my interest in the latter question.  The H1N1 influenza virus is upon us again and for unknown reasons appears to attack native populations with disproportionate ferocity.  In Canada, many native communities have suffered greatly once the virus touches down.  There is a higher number of affected and a much higher rate of severe infection.  In some respects, it reminds me of the arrival of  Europeans to the continent and their tallships laden with viruses which proved lethal to untold numbers of the original inhabitants.  While the numbers vary wildly, it is suggested that up to 80% of the aboriginal population succumbed to one of the many waves of infectious diseases from abroad.  Given this massive assault, it's possible that a small genetic survival advantage may have had a huge impact.  Could that advantage have been the HLA B27?  I'm starting to wonder.  The clues that lead me to this suggestion start with the inordinately high rate of B27 amongst North American native populations.  While most of the Northern native populations have higher rates of B27, the rate can run as high as 50% in some populations, such as the Haida of the west coast of Canada.  And it isn't because they are immune to the arthritogenic potential of the gene.  20% of the men carrying the gene showed evidence of sacroiliitis on x-ray.  Spondyloarthropathy would likely have  been  a brutal disease among these not-so-long-ago hunter-gatherer peoples, so why is it so prevalent?  Could it be that the B27 gene somehow protected these vulnerable populations from the many plagues that followed the arrival of Europeans? The survivors, though cursed with this unfortunate gene may then have passed it on to future generations.  

Sure, but it's just one of many possibilities.  After all, B27 may simply be linked to any other gene with survival qualities,  like hunting skills or negotiating with ethically challenged governments.  On the other hand, there is some evidence that resisting infections is part of the B27 advantage.  Recent studies have shown that HLA B27 has a protective effect in both HIV and Hepatitis C infections.  While nobody suspects that either of these viruses had anything to do with the massive casualties post Columbus, it makes me wonder whether any of the other diseases such as smallpox or influenza were also less fatal among B27 carriers.  It is known that HLA B27 is involved in the immune response to Influenza A, but I don't know whether this confers any survival advantage.  In fact, it would be a very good study question.  It might even be a good study question for the scary virus flying around the planet today.  

Who knows.  Maybe we'll all be begging for a B27 allele before the end of this modern day pandemic.  

Fibromyalgia Breakthrough

Well, about as big  a breakthrough as has occurred  in the recorded history of fibromyalgia research, which pretty well sets the low end of the scale for scientific breakthroughs.  In fact, the published abstract doesn't even mention fibromyalgia, but hey, you get your good fibromyalgia news where you can.

I could only get the abstract from the Science on-line article but it's pretty intriguing.  In a study of chronic fatigue syndrome, researchers found the presence of retroviral DNA from xenotropic murine leukemia virus-related virus (XMRV), in 68 of 101 (67%) patients as compared to only 8 of 218 (3.7%) controls. Derek Lowe at In The Pipeline notes that the same group has now studied three hundred patients and has found the virus in 98%.  Pretty impressive numbers. Almost too impressive?

So what's this got to do with fibromyalgia.  First of all, CFS and fibromyalgia are very similar diseases. If you look at the criteria for CFS, you could be talking about any one of my fibromyalgia patients.  

The fatigue of CFS is accompanied by characteristic symptoms lasting at least six months. These symptoms include:

• difficulties with memory and concentration
• problems with sleep
• persistent muscle pain
• joint pain (without redness or swelling)
• headaches
• tender lymph nodes
• increased malaise (fatigue and sickness) following exertion
• sore throat

About the only difference is that the focus for CFS is fatigue and for fibromyalgia, it's pain.  Amongst 300 patients, I'd be surprised if there wasn't a lot of patients that would fulfill the criteria for fibromyalgia.  So, if 98% are positive for the virus, well maybe fibro patients will test positive as well.  In fact, the research institute which funded the study says as much, although without any numbers.

So we have here a study that's not about fibromyalgia, in abstract form alone, with no detail about study technique, concerning a virus that nobody has really heard about, from a private research institute with little track record, and nearly unbelievable numbers.

Well, in fibromyalgia terms, we call that progress.