Robin is always happy to report potential new journal titles, and a new one has just sprung up courtesy of Gumà et al. 's paper
(Ann Rheum Dis 2002;61:10246).
In the same issue on p. 1030 is one of those wonderful pictures of the OA with Guinea-worm standard a lupus lesion over a butterfly tattoo. Bravo, Drs Canvin and Silver; with colour printing and quality content like that I quite understand why you don't send them to Rheumatology for inclusion in my column. Time to re-investigate the cost of colour. I will get straight on to the Editor.
I am sure everyone has come across overweight patients who are reluctant to undress, as it will reveal the extent of their obesity. Robin last week came across a note in a case file that read unable to weight-bare. He thinks this was not the same thing, in the context. It is certainly most distressing to see how low standards have slipped; even government documents are illiterate these days. But the howler par excellence has to be the sad nursing note recording the death of a patient at Robin's hospital, which read Patient pass away at 11.30 p.m. Relatives sitting on patients bedside. Patient to be satisfied by on call doctor. Something very Belgravian about that, but one does despair.
Azzoni and Cabitza ask whether knee meniscal tears can be diagnosed successfully using ultrasound (J Clinical Ultrasound 2002;30:4726).[CrossRef][ISI][Medline] To save you looking, or trying the same thing, the answer is no, being incorrect in 56%.
Now what does one make, given the slowly growing evidence that glucosamine does something helpful in osteoarthritis, of the paper by Mattei et al. (Osteoarthritis & Cartilage 2002;10:81625)?[CrossRef][ISI][Medline] High doses of the stuff appear to impair the metabolism of bovine chondrocytes in vitro. Robin doesn't like this. He will continue, at present, with his advice on claret.
Of course once the cytokine revolution got really under way it was only a matter of time before the interferons came under scrutiny. Van Holten and colleagues have reviewed the role of ß-interferon in rheumatoid arthritis and conclude that, as with multiple sclerosis, it might be useful Arthritis Res 2002;4:34652). [CrossRef][ISI][Medline] Robin has some experience of the effects in MS; it makes patients feel awful (there is some evidence that its release in large quantities is responsible for the symptoms of influenza). This becomes, therefore, a case for the Journal of Impressions that Need Confirming Before Making Patients Worse...
Another theory takes a knock. Robin has previously reported his enthusiasm for the concept of fetal microchimerism being responsible for the genesis of scleroderma, but Gannage et al. have cunningly done a controlled investigation (Eur J Immunol 2002;12;340513[CrossRef] this is one biiiiiiiig journal!) and found no difference in fetal microchimersim between connective tissue disease patients and controls. Damn. It looked so attractive. Or could it be that the controls with fetal microchimerism are all going to develop CTD, but haven't quite got there yet? It's a bit like the argument of whether a positive IgM rheumatoid factor means you are going to get RA. Perhaps.
Robin does not often venture into molecular stuff but was puzzled by an article
(Graves et al., Molec Pharmacol 2002;6:136472)
Why keep things simple when one can make them complex and interesting? The journal Medical Hypotheses (2003;60:658) [CrossRef][ISI][Medline] contains a fascinating suggestion by Nijs et al. of why chronic fatigue syndrome (CFS) was associated with osteopenia. The abstract is worth quoting, and Robin loves the channelopathy neologism. Firstly, the deregulation of the 2,5A synthetase RNase L antiviral pathway and its associated channelopathy, implicates increased demands for calcium and consequent increased calcium-re-absorption from the skeletal system. Secondly, Mycoplasma fermentans which has been frequently associated with CFS, produces a lipopeptide, named 2-kDa macrophage-activating lipopeptide (MALP-2), which stimulates macrophages. MALP-2 has been shown to enhance bone resorption in a dose-dependent manner, at least in part by stimulating the formation of prostaglandins. Thirdly, decreased levels of insulin-like growth factor I (IGF-I) have been reported in CFS-patients. IGF-I is critical to the proliferation of osteoblasts. Cor. And there was I thinking the bones got thin because CFS sufferers sat around not doing very much.
That swollen knee after surgery may not be infected; a large area of bone is left uncovered in unicondylar knee arthroplasty
(Kobayashi et al., Arch Orthop Trauma Surg 2002;122:46971) [ISI][Medline]
and pyrophosphate may be rubbed off creating pseudo-gout. Try, however, persuading your orthopaedic colleagues to call you in to aspirate the knee before they start the antibiotics. Another reason to insinuate oneself into the swollen joint scenario is reported by Nolan et al.
(Br Med J 2003;326:1512);