Do you know what a TOCA is? As Yearbook of Rheumatology editor and a department of medicine chair, I have been spoiled—I don’t mean generally, but in the context of reading the literature. The Yearbook staff collected and reviewed all the journals and topics we identified for them and sent original articles. If there was anything I thought I might miss, my institutional library staff routinely circulated to me each month those journals I requested. It made the process of reading the literature incredibly easy for me. Whether or not I learned from this and became a better scientist, educator, or clinician, I certainly had everything imaginable from the literature on my desk.
(I haven’t forgotten about the TOCA; bear with me a moment longer.)
To do this yourself, I suggest the following. Develop a list of journals whose contents would be of interest to you, and follow my instructions in the previous paragraph. Setting up the alerts was not burdensome, although it did take a couple of hours. It will connect you intimately with the worlds of clinical medicine and science—and it helps keep medicine fun.
And now, here are this month’s literature highlights.
COOL RUNNINGS
The Science Times section in The New York Times on April 26 of this year featured, “To beat the heat, drink a slushie first.” Subjects who had ingested ice slushies before running to exhaustion on a treadmill, indoors at 93° F and 54–56% humidity, exercised almost 10 minutes more than participants drinking ice water (50 versus 41 minutes). This may reflect dissipation of body heat to cause the phase change of ice to water necessary to consume the drink. This was a neat study and may be useful for anyone exercising in heat, including patients, whether they are serious or recreational athletes.
In the past five decades, I’ve run about 50 marathons and even one ultramarathon. I bring this up not only because I’m proud, but also because I have a special interest in material relating to exercise. Even though I usually run in the early morning, it’s sometimes virtually impossible to avoid the heat. However, I usually run longer than 40–50 minutes and am not particularly competitive anymore. Also, my running partners (see photo above) stop pretty frequently to smell the flowers and rest, which I’ve come to savor, so this may not have much practical value for me. Although the dogs are approaching 100 in dog years, I can’t tire them out except in extreme heat; when I go for 20–25-mile runs (probably hundreds of dog miles) preparing for a marathon, they just lope along easily, with heart rates never exceeding 110–115 bpm. I might try the slushies for them on hot days (dogs can’t sweat; they must dissipate heat through their paws or from panting; another reason we run when it’s cool and stop often).
Not only might I need to rethink my hydration, but also I may need to change running (and everyday) shoes. Joel Block, Najia Shakoor, and colleagues reported that at least one prototype running shoe may transmit about 8%–12% more peak knee load than flatter, more flexible shoes, specially designed shoes, sandals, or walking barefoot (Arthritis Care Res. 2010;62:917-923). This was walking (not running) patients with osteoarthritis (OA), a controlled environment, only a single measure, only a single time, and only a few shoes. There are probably much better (softer, flatter, more flexible) running and regular shoes, and what does an 8–12% load increase translate into in terms of symptoms or propensity to OA in folks with good biomechanics?
For us runners, there are issues much broader than just the knees; I now have flat feet and have learned more than I ever wanted to know about posterior tibial tendonitis; I depend on orthotics and appropriate shoes for both walking and running. I just had an enjoyable conversation with the authors of this article. They assured me that this change in load is important, that running may be different than walking, and that OA may be different than non-OA. They noted that this work is still early in its evolution.
I commend the authors for their approach and experiments. As a running enthusiast and one-time scientific/medical advisor to the bible of running, Runners World, it’s great to see genuine, serious science brought to a pastime that is suffused with myth, hyperbole, exaggeration, anecdote, hope, marketing, and belief. There are important implications in both these reports for patients (I will rethink my shoe recommendations to those with medial knee disease), as well as for the rest of us.
LESS IS MORE
I recently met with one of my incoming interns for the 2010–2011 academic year. She returned from a medical mission to Malawi earlier this year. She told me this incredibly impoverished country of 14.5 million people is served by approximately 350 physicians. The major medical center where she worked could perform no imaging studies. The only way they could perform blood chemistries was with the kits she brought with her; after her departure, there were no longer any resources to measure sodium, calcium, phosphorus, etc. Imagine, we both said almost together, how useful a country and population like this would find the things that our institution expends unnecessarily in a couple of days.
This made me think of a section in the Archives of Internal Medicine called “Less Is More” (2010;170:584), intending to document where “less health care results in better health and offer commentary on the specific implications” of such instances. The first example in the journal was the “First Physical” (Arch Intern Med. 2010;170:583), about which you may have read in the “Green Journal” or in the media. This critiqued President Obama’s inappropriate electron beam CT for coronary calcium, the attendant unnecessary radiation exposure, his failure to stop smoking, and the inappropriate colon cancer screening prior to age 50 years and by the not-recommended virtual colonoscopy. It was argued that this makes the wrong statement about healthcare and sets a poor example at a time when healthcare policy and leadership is sorely challenged. I heartily agree. Indeed, during this past year, our Department of Medicine morbidity and mortality conferences have addressed this theme and included a regular segment called “Sign(s) of the Apocalypse,” with cases illustrating similar problems in medicine.
For example, we discussed a 21-year-old whose extraordinary inpatient evaluation for a cold and a lipoma cost $9,606; an 83-year-old whose hospitalization and evaluation for possible fracture or infection, costing $9,493, should have been easily recognized as pyrophosphate arthropathy; a man with previously documented acute gout spending 11 unnecessary days in the hospital, at $14,756; a man with longstanding gout, resultant weakness, and normal reflexes treated with plasmapheresis and intravenous immunoglobulin for presumptive Guillain–Barré syndrome, costing $51,275; and a woman with familial Mediterranean fever admitted and evaluated, again and unnecessarily, for $3,655. These instances reflected inappropriate admissions and unneeded, expensive, and excessive care.
In our conference, we also presented patients (e.g., patients with parvovirus infection, pseudo-myxedema) evaluated appropriately and economically as outpatients. These documented the value of thoughtful, reflective, clinical evaluations by knowledgeable physicians—encountered, we think, too infrequently today. We should practice and teach medicine that is safe, effective, patient centered, timely, efficient, equitable, high quality, and cost effective. I wrote some years ago that the best diagnostic test remains a thoughtful and thorough evaluation by a knowledgeable end experienced clinician; science does not substitute for art, nor does sophisticated (or expensive) technology substitute for clinical acumen. Rheumatologists know this.
THE JOINT IS JUMPING. HOW DOES RA SPREAD?
This elegant series of experiments attempted to address the question of how rheumatoid arthritis (RA) spreads from a few to many joints (Nat Med. 2009;15:1414-1420). I must confess that I’ve usually encountered and perceived RA as a polyarthritis and presumed it was multicentric. I have certainly seen mono- or oligo-articular disease evolve to polyarthritis. I accept that the problem is relevant, and certainly of interest, while not necessarily the sole explanation for the propogation of RA. I congratulate the authors on their thinking, approach, experimental design, and controls. They implanted human tissues into immunodeficient (severe combined immunodeficiency disease) mice to show that RA synovial fibroblasts migrated to naive cartilage. These observations suggested that transmigration of these cells, at least in part, participates actively in the disease process. This is another obvious target for intervention. Expect to hear more about this.
ONCE MORE, WITH FEELING
Have you ever complained that recently minted physicians aren’t as well trained as in “the old days”? Don’t have the same skills? Have it easier? And haven’t you heard it said, or read, that empathy has declined? Well, it isn’t true. This fascinating exercise meticulously re-analyzed original data from all those studies allegedly finding loss of empathy by physicians at various stages of training (Acad Med. 2010;85:588-593). The authors noted a negative change in empathy of 0.2, on average, from 5.0–9.0-point rating scales from data with poor returns that was largely self reported. Their conclusion was that a decline in empathy has been greatly exaggerated.
While this study is of general interest to the field of medicine, I was particularly intrigued because our medicine department and program has uniquely embarked on an “educational innovation,” under the aegis of the residency review committee of the Accreditation Council for Graduate Medical Education, which introduces humanities at the bedside. We have found this has a salutary effect on resident performance and perhaps on patient care outcomes. It has significantly changed my faculty, our program, and our identity—and me. It’s been great fun and extraordinarily educational. Among other things, we measure empathy (yes, there are several instruments for this) and find that our residents really do care, deeply, and that our curriculum enhances this, consistent with the message of this article. I heartily and seriously recommend some thoughtful, enlightened reflection (humanities driven or other) to help sustain the passion and excitement for medicine.
FOR CHOCOHOLICS
(AND WHY NOT RHEUMATIC DISEASE PATIENTS?)
Bloomberg News reported on March 31 that “a daily nibble of dark chocolate may slash the risk of heart attacks and strokes by more than one-third.” Intake of 6 gm of chocolate daily was associated with statistically significantly slightly lowered blood pressure (about 1 mmHg) and 39% less risk of stroke or myocardial infarction (Eur Heart J. 2010;31:1616-623). How might this be? Flavonols in cocoa are biologically active. Rheumatologists, with a rich tradition of using therapeutic agents like colchicine, fish oils, plant oils, cyclosporine, and others, shouldn’t be surprised at these potential properties of plants and foodstuffs. Flavonols lower blood pressure, decrease LDL oxidation, diminish C-reactive protein, increase endothelial-dependent dilation, reduce platelet reactivity, and modulate elaboration of cytokines and eicosanoids. Some years ago, I wondered why we hadn’t put statins in the drinking water already, because of their array of salutary effects on general health, and perhaps rheumatic diseases, too. Maybe we should be washing down our statins with some red wine (probably white also) and a healthy bite of chocolate and advising our patients to do the same. Just as we’ve seen studies of statins for various rheumatic diseases, I expect to read about the experimental effects of chocolate or our disorders. But a note of warning—the Archives of Internal Medicine (2010; 170:699-703) reported an association of chocolate consumption with depression.
ARE WE WHAT WE EAT?
A recent JAMA article (2010;303:1848-1856) critically reviewing perceptions of the prevalence of food allergies was highlighted in The New York Times. The review emphasized the paucity of high-quality studies pertaining to food allergies. The authors noted that the prevalence of food allergies was somewhere between 1–2% and 10% of the population; no single diagnostic test merited recommendation; evidence supporting efficacy of therapeutic elimination diets was lacking; value of immunotherapy was unclear; and approaches for managing high-risk infants were still unclear. Otherwise we know everything there is to know about food allergies.
Why should rheumatologists care? Because one of the most common questions patients ask us (after What is it? Why? Why me? What will happen to me? How will you treat it? and What can I do?) is what should I eat? What diet should I follow to make it go away or get better? Who among us has not had a patient who thought their symptoms were related to something ingested and, if so, reasoned that avoiding that food would ameliorate disease? Rheumatology was long intrigued by the seductive notion that the right diet or eliminating offending foodstuffs could moderate rheumatic symptoms. There was the notion of “delayed-onset” food allergies, or non–immunoglobulin-E–mediated food allergic syndromes (like migraine, gastrointestinal, or rheumatologic symptoms).
I came to study this fairly early in my career. As a young academician, food and diet and/or food and arthritis was the furthest topic from my mind; it was not something someone trying to do serious scholarship would even remotely consider. One afternoon in the late 1970s I received a call from my dean. He said there was a wealthy individual in his office willing to donate to the university if we would study diet therapy for arthritis. Would I do it? I responded that I was too busy in my laboratory finding the cause and cure for rheumatoid arthritis (RA) to waste time studying diet; besides, no respectable rheumatologist would want to be identified with such a study. A few years later my dean called again offering that same invitation. He explained that the person requesting the study was again in his office but now with a blank check and that it would be very important for my career to do this. By now the project had piqued my intellectual curiosity, and so I came to examine diet (and learn about complementary and alternative medicine).
We did this rather rigorously, using our clinical research unit and carrying out placebo-controlled diet therapy and food challenges. We found elimination diet therapy ineffective for RA (and osteoarthritis) and could not document food-sensitive or food-related rheumatic symptoms in most patients who thought they had them (just as was reported in the JAMA review). However, we did describe several individuals with such symptoms, notably a lady with clinical and immunological sensitivity to milk. We concluded that food/diet therapy had no general important role in managing rheumatic disease. The occasional patient with clear food-related disease merited formal study. Nothing in the many subsequent reports on this topic has changed these impressions.
Dr. Panush is chair of the department of medicine at Saint Barnabas Medical Center and professor of medicine at the University of Medicine and Dentistry–New Jersey Medical School in Livingston. He is moving soon to be professor of medicine, division of rheumatology, department of medicine, Keck School of Medicine, University of Southern California in Los Angeles.
