Robin Goodfellow (43-10)

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A young lady with RA came in to the clinic this morning— designer safari suit, crop top, colour-coordinated all the way down to her flip-flops. She then told me how bad her feet were; as it was clear her metatarsalgia was being made worse by the fact she had to claw her toes to stay in them, I suggested, when the weather was hot, that sandals with a back would be better. ‘But mine don’t match the outfit’, she pouted, and then smiled. ‘I suppose’ she said ‘it's a fine line between looking good and being a cripple!’ I decided not to point out that crippled feet don’t look good.

Robert Marshall writes: ‘As an avid reader of your mischievous monthly missive, I wonder if your fancies would be tickled by a typo that occurred in one of my letters recently. I had dictated that the young lady in question suffered from costochondritis. However, the letter that came back for signature cheerily talked of a "caustic introitus"! The mind boggles ... perhaps the fancies had been tickled once too often!’ Thank you, Robert, and remember that long term oral steroids cause thrush.

Robin has just received Chris Dyos’ full ‘Ode to a Rheumatologist’ (he also sent rather a clever one about bubonic plague to his GP— a very useable talent, this). Robin feels that it should be published in an eminent medical journal but it would occupy the whole of a month's column, so pro tem will have simply to email a copy to anyone who requests it, except George Ehrlich, who will get one anyway for telling me that he is indeed related to the eponymous Paul. Email away to robingoodfellow_rhu{at}hotmail.com. It's worth it, though there may be a small delay while Robin delivers his boy to university and then heads off to Marrakech for a well-deserved break à deux.

Our esteemed Editor took pity on this poor (his back pay under the new contract has not yet come) goblin and, after Robin's rude remark last month about the tight-fistedness of the journal and failure to pay expenses, mailed him a copy of the Aceves-Avila paper on culture driven disorders. I would take it all back, except he forgot to put a stamp on it and Robin's secretary is now £1.21 out of pocket for the excess charge.

Further to Robin's statin tale (are you all calling it statinomyalgia yet?), Thompson et al. ( JAMA 2003;289:1681–90[Abstract/Free Full Text]) suggest that statin myopathy is rare, but Robin thinks otherwise. The mechanism, says Thompson, may be that statins reduce the production of small regulatory proteins that are important for myocyte maintenance. All that matters to Robin, now he has stopped his, is that he can shovel muck and trim hedges like a young 'un. His brain gets tired of too much science, and so he would like to recommend a book. Entitled Hippocratic Oaths and by a geriatrician (or gerontologist, if you must) called Raymond Tallis (London, Atlantic Books, 2004), it describes the demise of medicine in the UK as a profession and describes much of the stupid, politically correct icing that has been thickly applied to the NHS cake. Robin is jealous of the style, although he, as he is sure many readers will find, tastes a lot of déjà in the nutty bits. Put it on your Christmas list tout de suite.

Shanahan and colleagues ( Ann Rheum Dis 2004;63:1035–40[Abstract/Free Full Text]) have done their bit for economy. They tested to see whether suprascapular nerve blocks are as good when using the landmark technique as when done with CT guidance by radiologists. They are. Always a fan, and proponent, of one-stop outpatients, Robin will continue doing them in clinic. Mind you he has had a few problems putting hyaluronic acid preparations into joints other than knees; being so viscous, it's difficult to feel, through needle resistance, where you are, so he has started finding his way into ankles, elbows and occasionally shoulders using local anaesthetic first.

Robin has always fondly believed that hypermobility predisposed to osteoarthritis (on the theoretical basis that hypermobile subjects’ connective tissue was less robust). So it was a surprise to read the article by Kraus et al. ( Arthritis Rheum 2004;50:2178–83[CrossRef][ISI][Medline]) which indicates that in hand OA it may be protective. Which gives Robin the opportunity to use another favourite word—counter-intuitive.

Dr Pearce from Hull has a turn of phrase that is enviable, but makes me jealous; he writes ( Eur Neurol 2004;52:67–72[CrossRef][Medline]) thus: ‘The terms myofascial pain, fibromyalgia and fibrositis are critically examined. They constitute diagnostic labels for non-specific musculoskeletal aches and pains. Analysis of the evidence shows that none of these labels is substantiated by hard physical signs or by laboratory evidence of consistent pathological or biochemical abnormality. What is the objective evidence for disorder(s) of muscle, fascia or fibrous tissues, so clearly indicated by these diagnostic names? Alternative terms such as "regional pain syndrome" or "chronic pain syndrome" merely redefine the clinical problem without providing a mechanism or basis for diagnosis. Despite different diagnostic criteria, these conditions, along with chronic fatigue syndrome, have many demographic and clinical similarities, most notably tender trigger points. Indeed, the terms are often used interchangeably. There are few differences in the symptoms, physical findings, laboratory tests, functional status, psychosocial features and psychiatric disorders. This paper seeks not to deny the existence of aches and pains, but to critically examine the utility of these terms. The only claimed physical sign is the presence of tender trigger points over muscles or muscle attachments. Research suggests that tender points are a measure of general distress related to pain complaints but separately associated with fatigue and depression. They are present in some normal subjects and are variable in occurrence in time in the same individual. They reflect no demonstrable pathology. It is therefore argued that none of these commonly used diagnoses represent distinct disease entities. A possible but unproven alternative hypothesis is that such symptoms relate to neural pain with both peripheral and central components, and in some instances psychological or wilful embellishment.’

So there.

And for those who wish for a dose of real science, Robin can do no better than point them at J Immunol 2004;173:1463–76[Abstract/Free Full Text], where Miranda-Carus and Madrid friends describe how they have characterized the molecules responsible for synovial fibroblast-T lymphocyte (TL) cross-talk in rheumatoid arthritis (RA), and what effect methotrexate has on them. In summary, RASFib production of IL-15 induces the proinflammatory cytokines TNF-{alpha}, IFN-{gamma}, and IL-17 in cocultured TLs through a cell contact-dependent mechanism. In turn, these cytokines stimulate the expression of IL-15, IL-8, and IL-6 in RASFibs, thereby creating a feedback loop that favours persistent synovial inflammation. Methotrexate seems to disrupt this loop by decreasing cell adhesion (that is a quote, by the way; Robin could not remember past the word proinflammatory). He intends to print this out for those awkward patients who insist not only that they know all the side-effects—and Robin has a nice leaflet for those—but also how this toxic drug works. And good luck to them!





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