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240 BRITISH JOURNAL OF RHEUMATOLOGY VOL. XXV NO. 3 11. Anonymous. Examinations. Lancet 1956;ii: 385-7. 12. Ziman J. Exams. Listener 1968;80:419-501. 13. Stone E. The evaluation of learning. BrJMed Educ 1969;3:135-42. 14. King LS. Medical thinking: a historical preface. Princeton, NJ: Princeton University Press, 1982;6-7. 15. Thomas L. Late night thoughts on listening to Mahler's Ninth Symphony. New York: Viking Press, 1983;143-55. 16. Hamilton JD. The McMaster curriculum: a critique. BrMedJ 1976;l:1191-6. 17. Fraenkel GT. McMaster revisited. Br Med J 1978;ii: 1072-6. 18. Wood PHN, Badley EM. Rheumatology and medical education. London: The Arthritis Council, 1979. 19. William WO. A study of general practitioners' 20. 21. 22. 23. workload in South Wales, 1956-1966: a survey of 68 doctors. Reports from General Practice No.12, London: Royal College of General Practitioners, 1970. Bjelle A, Magi M. Rheumatic disorders in primary care. Scand J. Rheumatol 1981 ;10: 331-41. Potter S, Bellamy N, and Buchanan WW. The McMaster experiment in medical education with special reference to the teaching of rheumatology. Hung Rheumatol 1983; 24(Suppl):39-51. Gordon DA, Urowitz MB, Smythe MD. The founding editor—Metro A. Ogryzlo. J Rheumatol 1977;4:l-3. Osier W. Teacher and student. In: Aequanimatas and other addresses. P. Blakiston, Son & Co., Philadelphia: 2nd edn. 1914. RHEUMATOID ARTHRITIS AND OSTEOPOROSIS IN this edition there are two papers reporting accelerated bone loss and increased skeletal metabolism, together with two letters reporting fractures, occurring in rheumatoid arthritis (RA). In serial studies Reid etal. [1] have found increased rates of bone loss at around 3-4% per year, while Gevers et al. [2] have found elevated serum osteocalcin levels, a noncollagenous matrix protein which is produced by osteoblasts, reflecting increased bone formation and hence skeletal metabolism. While these studies appear to be in good agreement, previous reports have indicated that in RA skeletal metabolism may be normal [3], increased [4] or suppressed [5]; that serum calcium may be elevated [6] or low [7] and that osteocalcin may be normal [3] or low [8]. A histomorphometric study of rib biopsies showed that bone formation was reduced, but resorption rates were increased [9]. These results provide conflicting data. There is no adequate explanation for this although the time after onset of disease that is chosen for study may be relevant. For example, following immobilization rapid bone loss occurs but the skeleton eventually becomes quiescent [10]. Thus, while there is little doubt that patients with RA lose bone at an accelerated rate fl, 11], have lower bone mass [12-rl4] and are at increased risk of fracture [14-16], why the bone loss should occur at all is not well established. Periarticular osteoporosis, which may be due to a local increase in vascularity, paracrine factors, direct erosion by pannus and immobility of affected joints, is a characteristic feature of RA but the concept of a generalized alteration in skeletal metabolism specifically related to the disease is controversial. The problem is that there are so many potential factors which may contribute to bone loss—the patient's age, sex, menopausal status [17], duration of arthritis [18], coexistent disease, immobility, calcium malabsorption [19], drugs, nutrition, vitamin D status [14], etc. Osteoporosis is essentially a disease of elderly women, and women with RA who are postmenopausal will be at greatest risk. Steroid therapy can cause accelerated bone loss, although patients may have a variable skeletal response to this drug [18]. Of the other factors, immobility is likely to be the most important. Rheumatoid arthritis is a multisystem disease and it is clearly possible that there is skeletal involvement. However, this issue cannot be resolved on the basis of the data that are currently available. With the newer techniques of dual photon absorptiometry and computerized tomography, it is possible to measure bone mineral at sites of clinical relevance such as the spine and femur [20]. It is now recognized that different rates of bone loss may occur at various sites throughout the skeleton, e.g. in postmenopausal osteoporosis there is predominantly spinal bone loss [21] while in anorexia nervosa there is greater bone loss in the femoral neck than in the spine, which has greater loss than the distal radius [22]. Sodium fluoride and low-dose parathyroid hormone, which have 241 EDITORIAL been evaluated in the treatment of osteoporosis, increase trabecular bone volume but apparently at the expense of cortical bone [23]. To obtain further information in RA, up-to-date methodology should be used to study patients with early disease at a time when they are fully mobile. Nevertheless, in a study of early disease (mean duration 14 months), reduced total body potassium—an index of skeletal muscle mass— was found [3] and it may not be possible to eliminate the influence of mobility completely. Ideally, patients should be premenopausal to avoid the accelerated bone loss which occurs following withdrawal of the protective effect of oestrogen on the skeleton. Why accelerated bone loss should occur is of academic interest. It does occur and patients sustain fractures, which is of practical relevance. In a population who may already be elderly and infirm, housebound and taking an inadequate diet, a fracture may be a catastrophic event. Currently, it is not possible to increase bone mass predictably in patients with established osteoporosis and it would therefore appear likely that advances in therapy will need to be related to prophylaxis. This may partially come about by educating the population at large. Such an approach seems possible since alteration in diet appears to have been effective in reducing coronary artery disease in the United States [24]. In preventing osteoporosis it is clearly desirable that peak adult bone mass should be attained, and it is probable that regular exercise and an adequate calcium intake are important to the growing skeleton [25]. Adults should also ensure an adequate calcium intake, although the benefit here is much more controversial [26]. In patients with RA the importance of mobility should be emphasized and an adequate diet ensured. However, in considering the prevention of bone loss, most therapies will only have a trivial effect when compared with oestrogen [27, 28]. The possibility of routine oestrogen therapy in women with RA at the time of the menopause should be considered. Low-dose oestrogen therapy is safe and, even if there is a small incidence of side-effects, this is surely an acceptable price to pay when one considers that fracture of the femur is now the leading cause of accidental death amongst the elderly [29]. IGNAC FOGELMAN Department of Nuclear Medicine, Guy's Hospital, London SE1 9RT, UK REFERENCES 1. Reid DM, Kennedy NSJ, Smith MA, et al. Bone loss in rheumatoid arthritis and primary generalized osteoarthrosis: effects of corticosteroids, suppressive antirheumatic drugs and calcium supplements. Br J Rheumatol 1986;25:253-9. 2. Gevers G, Devos P, De Roo M, Dequeker J. Increased levels of osteocalcin (serum bone GLA-protein) in rheumatoid arthritis. Br J Rheumatol 1986;25:260-2. 3. Sambrook PN, Ansell BM, Foster S, et al. Bone turnover in early rheumatoid arthritis: 1. Biochemical and kinetic indexes. Ann Rheum Dis 1985;44:575-9. 4. Steven MM, Sturrock RD, Fogelman I, Smith ML. Whole-body retention of diphosphonate in rheumatoid arthritis. J Rheumatol 1982;9:873-7. 5. Heaney RP, Walch JJ, Steffes P, Skillman TG. Periarticular bone remodelling in rheumatoid arthritis. Calcif Tiss Res 1968; 2(suppl):33-33B. 6. Kennedy AC, Allam BF, Rooney PJ, et al. Hypercalcaemia in rheumatoid arthritis: investigation of its causes and implications. Ann Rheum Dis 1979;38:401-12. 7. Bramble MG, Blake DR, White T, Sly J, Kerr DNS. Ionised calcium in rheumatoid arthritis: effect of non-steroidal anti-inflammatory drugs. Br Med J 1980;281:840-l. 8. Riis BJ, Als OS, Christiansen C, Catherwood BD, Deftos LJ. Bone turnover in rheumatoid arthritis. Calcif Tiss Int 1984;suppl2: S4. 9. Duncan H, Frost HM, Villanueva AR, Sigler JW. The osteoporosis of rheumatoid arthritis. Arthritis Rheum 1965;8(5):943-54. 10. Minaire P, Meunier P, Edouard C, Bernard J, Courpron P, Bourret J. Quantitative histological data on disuse osteoporosis: comparison with biological data. Calcif Tiss Res 1974;17:57-73. 11. Vitiama P, Helela T, Kalliomaki JL. Osteoporosis in rheumatoid arthritis. Acta Rheum Scand 1968;14:276-84. 12. Bjelle AO, Nilsson BE. Osteoporosis in rheumatoid arthritis. Calcif Tiss Res 1970;5:32732. 13. Kennedy AC, Smith DA, Buchanan WW, Anderson JB, Jasani MK. Bone loss in patients with rheumatoid arthritis. Scand J Rheumatol 1975;4:73-9. 14. Wordsworth BP, Vipond S, Woods CG, Mowat AG. Metabolic bone disease among in-patients with rheumatoid arthritis. Br J Rheumatol 1984,23:251-7. 15. Taylor RT, Huskisson EC, Whitehouse GH, Dudley Hart F. Spontaneous fractures of 242 16. 17. 18. 19. 20. 21. 22. BRITISH JOURNAL OF RHEUMATOLOGY VOL. XXV NO. 3 pelvis in rheumatoid arthritis. Br Med J 1971;4:663-4. Maddison PJ, Bacon PA. Vitamin D deficiency, spontaneous fractures, and osteopenia in rheumatoid arthritis. Br MedJ 1974;4:433-5. Stevenson JC, Whitehead MI. Postmenopausal osteoporosis. Br Med J 1982; 285:585-8. McConkey B, Fraser GM, Bligh AS. Osteoporosis and purpura in rheumatoid disease: prevalence and relation to treatment with corticosteroids. Quart J Med 1962;124:419-27. Sambrook PN, Abeyasekera G, Ansell BM, et al. Calcium absorption in rheumatoid arthritis. Ann Rheum Dis 1985;44:585-8. Fogelman I. Osteoporosis, bone mineral measurements and photon absorptiometry. Nucl Med Commun 1985;6:373-5. Riggs BL, Wahner HW, Seeman E, et al. Changes in bone mineral density of the proximal femur and spine with aging. J Clin Invest 1982;70:716-23. Treasure J, Fogelman I, Russell GFM. Osteopenia of the lumbar spine and femoral neck in anorexia nervosa. Scott Med J (in press). 23. Karris JA. Treatment of osteoporotic fracture. Lancet 1984;i:27-33. 24. Stamler J. Coronary heart disease: doing the 'right things'. N Engl J Med 1985;312: 1053-5. 25. Parfitt AM. Dietary risk factors for age-related bone loss and fractures. Lancet 1983;ii: 26. Horsman A, Gallagher JC, Simpson M, Nordin BEC. Prospective trial of oestrogen and calcium in post-menopausal women. Br Med J 1977;2:789-92. 27. Lindsay R, Aitken JM, Anderson JB, Hart DM, MacDonald EB, Clarke AC. Longterm prevention of postmenopausal osteoporosis by oestrogen: evidence for an increased bone mass after delayed onset of oestrogen treatment. Lancet 1976;i:103841. 28. Gordan GS. Osteoporotic bone loss. J Med 1980;ll:203-22. 29. Fardon DF, In: Osteoporosis. New York: Macmillan Publishing Company, 1985;3. EDITORIAL NOTICE IN order to accommodate an increasing demand for publication in the British Journal of Rheumatology, the Editorial Board has decided to increase the space available to contributors. As you can see in the current edition this has been initially achieved by introducing two columns and a slightly reduced type size. In 1987 and thereafter, the journal will be published on six occasions each year. This policy will substantially reduce the waiting period between acceptance and publication of original work. PERFORMANCE New in rheumatoid arthritis ETODOLAC CAPSULES Clinical efficacy with patient acceptability ABBREVIATED PRESCRIBING INFORMATION Presentation iodine capsules contain 200mq etodolac Basic NHS price 60 x 200mg capsules £16 80 Uses Acute or long term in rheumatoid arthntrt Dosage and Administration Oratty 20Omg twice dairy, some patients may requtre 600"Xj daily Safety of doses m excess of 600mq per day not established Elderty - no change m initial dosage required Paediatric dosage not estabfcsned Contra-indications. Warnings, etc Contra •ndkat-nm u.-v-vo--;-*-.—. ac*-v*> peptK ukeration or a history of peptic uker dtsease. patients who experience asthma, rhinitis or urticaria during therapy with asfHnrt or other non steradal anti mftammaton/ drugs Pregnancy, dunng lactation Precautions Although rton itercHdal anti inflammatory drugs do not have the same d^ect effects on platelets as does aspwin aH drugs which .nhib't the twosynthesis of prostagtandms may interfere, to some extent. with platelet function Patients recennng Lodme who may be adversely affected by such actions should be carefully observed There has been no evidence of significant changes in renal or hepatK function with the use of Lodtne tn man However, impairment of renal or hepatK functions due to other causes may alter drug metabotem, patwnn recervmg long term *fw*pv osrw-wHv the etberiv shoutd be observed f c potent^ side effects and their drug Ooses aofuslea di neeoeu. w n*; drug discontinued Drug interactions Highly proteri bound drugs, eg anticoagulants Side-Effects Reported side effects nctude nausea, ep^astrk pan, diarrhoea, rufcgestion. heartburn, natulence. abdominal pam. constipation, headaches, dizztnws. drovvsirw*ss Tmnttus 'ash ^nd *si«que Product Licence Htimber 607/74 For full prescnb*>g mformatton ptease refer to data sheet Date of preparation November 198S international Ayerst Laboratories Ltd South Way, Andover. Hampshire SP10 SLT Telephone Andover (0264) 58711 Lodtne is a Trade Mart