1505
In patients with acute low back pain (LBP), Meade et al showed superiority for chiropractic intervention, a finding consistent with spontaneous regression of acute LBP in more than 80% of patients.2 Patients with acute LBP are frequently offered year-long no
prevention by chiropractors, a practice not justified by work or based on experience with conventional treatment. On the contrary, these manipulations may turn the "person into a patient". We believe that strengthening the back is the correct means of preventing recurrent LBP, and prefer active to passive therapy.3 In patients with chronic LBP, Meade et al observed an effect with prolonged therapy, in accordance with the present interpretation of this disease as a mixture of physical and psychological problems.’ However, chiropractic intervention lasted longer than control, and failure to equalise the number and duration recurrence
published
of treatments in treatment and control groups is a drawback to studies in this field.’ We interpret the study by Meade et al as showing that chiropractic manipulation may be superior to the mixture of treatments that the medical profession is in the process of doing away with. It is increasingly evident that the answer to chronic LBP is usually active training. The emphasis of modem physical therapy is on exercise with behavioural support.6-9 The background to this development is knowledge of the complicated pathogenesis of LBP, with pain-coping problems involved in most cases. We now have means of treating the spine with cautious techniques in order to avoid the complications of chiropractic manipulations, which may, albeit rarely, lead to severe disablement.9 Thus, we do not agree that chiropractic manipulation be given higher priority. The trend toward a wide perspective on the issues of therapy of LBP should continue.
the absence of binding to zwitterion phospholipids. This has been shown by the Ouchterlony procedure,z inhibition studies,3.4 and ELISA tests.4,s The preferential binding of aPL to negatively charged phospholipids rather than to zwitterion phospholipids or to other antigens containing phosphodiester groups (eg, DNA 3’) has persuaded most investigators that anionic phospholipids are the true antigen for aPL antibodies. These antigens may be presented alone or possibly as a protein-phospholipid complex (c). Division of
Department of Rheumatology, State University Hospital, Copenhagen 2100 Ø, Denmark
HENNING BLIDDAL TOM BENDIX
1. Meade TW, Dyer S, Browne W, Townsend J, Frank AO. Low back pain of mechanical origin, randomised comparison of chiropractic and hospital outpatient treatment. Br Med 1990; 300: 1431-37. J 2. Quebec Task Force on Spinal Disorders Scientific approach to the assessment of activity-related spinal disorders Spine 1987; 12 (suppl 1). 3. Biering-Sørensen F. Physical measurements as risk indicators for low-back trouble over a one-year period Spine 1984; 9: 106-19. 4. Waddell G. A new clinical model for the treatment for low-back pain Spine 1987; 12: 632-44. 5 Coxhead CE, Inskip H, Meade TW, North WRS, Troup JDG Multicentre trial of physiotherapy in the management of sciatic symptoms Lancet 1981; i: 1065-68. 6 Manniche C, Hesselsøe G, Bentzen L, Christensen I, Lundberg E. Clinical trial of intensive muscle training for chronic low back pain. Lancet 1988; ii: 1473-76 7 Mayer TG, Gatchel RJ, et al. Objective assessment of spine function following industrial injury. Spine 1985; 10: 482-93. 8 Hazard RG, Fenwick JW, et al Functional restoration with behavioural support. Spine 1989, 14: 157-61. 9. Povlsen UJ, Kjaer L, Arlien-Søborg P Locked-in syndrome following cervical manipulation Acta Neurol Scand 1987, 76: 486-88.
What is the "true"
antigen for
antiphospholipid antibodies? SIR,-We wish to clarify the issues in the debate about the "true" antigen of antiphospholipid antibodies (aPL) (Aug 25, p 505; Oct 13, p 952). The three possible antigens, expressed
diagrammatically, are: Dr Galli and co-workers (June 30, p 1544) state that aPL bind &bgr;2-glycoprotein I only (a). McNeil et all claim that the antibodies bind anionic phospholipids (such as cardiolipin) only when they are linked to &bgr;z-glycoprotein I (c). We have stated, on the basis of our own and other data, that aPL bind anionic phospholipids (b) with or without &bgr;2-glycoprotein 1. It may be that &bgr;2-glycoprotein I alters the conformation of anionic phospholipids (c) so that they are more avidly bound by aPL, but we find little experimental basis for Galli and colleagues’ view that the protein alone is the antigen. Bevers and Galli (Oct 13 letter) now seem to argue more in favour of structure (c) being the antigen. Dr Matsuura and colleagues (July 21, p 177) also seem to suggest that autoimmune aPL antibodies, in contrast to syphilis antibodies, bind the phospholipid-glycoprotein complex. Bevers and Galli state correctly that any experiment which shows that aPL bind negatively charged phospholipids should also show
Rheumatology, Department of Medicine, University of Louisville, Louisville, Kentucky 40292,
NIGEL E. HARRIS SILVIA PIERANGELI
USA
1. McNeil HP, Simpson RJ, Chesterman CN, Krillis SA. Antiphospholipid antibodies are directed against a complex antigen that includes a lipid-binding inhibitor of coagulation &bgr;2 glycoprotein I(apo H). Proc Natl Acad Sci (USA)1990; 87: 4120-24. 2. Thiagarajan P, Shapiro SS, DeMarco L A monoclonal immunoglobulin M coagulation inhibitor with phospholipid specificity mechanism of a lupus anticoagulant. J Clin Invest 1980; 66: 397-405. 3. Harris EN, Gharavi AE, Loizou S, Derue G, Chan JK. Crossreactivity of anti-phospholipid antibodies. J Clin Lab Invest 1985; 66: 397-405. 4 Pengo V, Thiagarajan P, Shapiro SS, Haine MJ. Immunological specificity and mechanism of action of IgG lupus anticoagulants. Blood 1987; 70: 69-76. 5. Harris EN, Gharavi AE, Tincani A, et al. Affinity purified anticardiolipin antibodies and anti-DNA antibodies. J Clin Lab Immunol 1985, 17: 155-62.
Cholecystectomy in Saudi Arabia SiR,—Iread with dismay the first sentence of Professor Tamimi and colleagues’ summary of their report (Nov 17, p 1235), which stated: "Gallstones have become increasingly prevalent in Saudi Arabia ...". Could I possibly have missed the epidemiological data despite close attention to published work? The answer is no, because there is no such published information and nor do Tamimi and colleagues’ article provide any. The increased surgical activity they report probably reflects investment of oil revenues in health care, so that diagnostic ultrasonography and operations are available at a much higher level than before. It would indeed be very interesting, and compatible with evidence from the UK, Japan, and Norway, if gallstone prevalence had increased in Saudi Arabia lately, but this would depend on proper population-based surveys or necropsy reviews. Cholecystectomy rates might give quite false impressions about changes in gallstone prevalence. Rates have fallen strikingly in Sweden and Scotland at a time when gallstone disease is known to remain very common. General
Hospital, Bishop Auckland, County Durham DL14 6AD, UK 1 Bateson MC Gallstone variable. Lancet 1984;
prevalence ii:
521-25
M. C. BATESON and
cholecystectomy
rate are
independently
In patients with acute low back pain (LBP), Meade et al showed superiority for chiropractic intervention, a finding consistent with spontaneous regression of acute LBP in more than 80% of patients.2 Patients with acute LBP are frequently offered year-long no
prevention by chiropractors, a practice not justified by work or based on experience with conventional treatment. On the contrary, these manipulations may turn the "person into a patient". We believe that strengthening the back is the correct means of preventing recurrent LBP, and prefer active to passive therapy.3 In patients with chronic LBP, Meade et al observed an effect with prolonged therapy, in accordance with the present interpretation of this disease as a mixture of physical and psychological problems.’ However, chiropractic intervention lasted longer than control, and failure to equalise the number and duration recurrence
published
of treatments in treatment and control groups is a drawback to studies in this field.’ We interpret the study by Meade et al as showing that chiropractic manipulation may be superior to the mixture of treatments that the medical profession is in the process of doing away with. It is increasingly evident that the answer to chronic LBP is usually active training. The emphasis of modem physical therapy is on exercise with behavioural support.6-9 The background to this development is knowledge of the complicated pathogenesis of LBP, with pain-coping problems involved in most cases. We now have means of treating the spine with cautious techniques in order to avoid the complications of chiropractic manipulations, which may, albeit rarely, lead to severe disablement.9 Thus, we do not agree that chiropractic manipulation be given higher priority. The trend toward a wide perspective on the issues of therapy of LBP should continue.
the absence of binding to zwitterion phospholipids. This has been shown by the Ouchterlony procedure,z inhibition studies,3.4 and ELISA tests.4,s The preferential binding of aPL to negatively charged phospholipids rather than to zwitterion phospholipids or to other antigens containing phosphodiester groups (eg, DNA 3’) has persuaded most investigators that anionic phospholipids are the true antigen for aPL antibodies. These antigens may be presented alone or possibly as a protein-phospholipid complex (c). Division of
Department of Rheumatology, State University Hospital, Copenhagen 2100 Ø, Denmark
HENNING BLIDDAL TOM BENDIX
1. Meade TW, Dyer S, Browne W, Townsend J, Frank AO. Low back pain of mechanical origin, randomised comparison of chiropractic and hospital outpatient treatment. Br Med 1990; 300: 1431-37. J 2. Quebec Task Force on Spinal Disorders Scientific approach to the assessment of activity-related spinal disorders Spine 1987; 12 (suppl 1). 3. Biering-Sørensen F. Physical measurements as risk indicators for low-back trouble over a one-year period Spine 1984; 9: 106-19. 4. Waddell G. A new clinical model for the treatment for low-back pain Spine 1987; 12: 632-44. 5 Coxhead CE, Inskip H, Meade TW, North WRS, Troup JDG Multicentre trial of physiotherapy in the management of sciatic symptoms Lancet 1981; i: 1065-68. 6 Manniche C, Hesselsøe G, Bentzen L, Christensen I, Lundberg E. Clinical trial of intensive muscle training for chronic low back pain. Lancet 1988; ii: 1473-76 7 Mayer TG, Gatchel RJ, et al. Objective assessment of spine function following industrial injury. Spine 1985; 10: 482-93. 8 Hazard RG, Fenwick JW, et al Functional restoration with behavioural support. Spine 1989, 14: 157-61. 9. Povlsen UJ, Kjaer L, Arlien-Søborg P Locked-in syndrome following cervical manipulation Acta Neurol Scand 1987, 76: 486-88.
What is the "true"
antigen for
antiphospholipid antibodies? SIR,-We wish to clarify the issues in the debate about the "true" antigen of antiphospholipid antibodies (aPL) (Aug 25, p 505; Oct 13, p 952). The three possible antigens, expressed
diagrammatically, are: Dr Galli and co-workers (June 30, p 1544) state that aPL bind &bgr;2-glycoprotein I only (a). McNeil et all claim that the antibodies bind anionic phospholipids (such as cardiolipin) only when they are linked to &bgr;z-glycoprotein I (c). We have stated, on the basis of our own and other data, that aPL bind anionic phospholipids (b) with or without &bgr;2-glycoprotein 1. It may be that &bgr;2-glycoprotein I alters the conformation of anionic phospholipids (c) so that they are more avidly bound by aPL, but we find little experimental basis for Galli and colleagues’ view that the protein alone is the antigen. Bevers and Galli (Oct 13 letter) now seem to argue more in favour of structure (c) being the antigen. Dr Matsuura and colleagues (July 21, p 177) also seem to suggest that autoimmune aPL antibodies, in contrast to syphilis antibodies, bind the phospholipid-glycoprotein complex. Bevers and Galli state correctly that any experiment which shows that aPL bind negatively charged phospholipids should also show
Rheumatology, Department of Medicine, University of Louisville, Louisville, Kentucky 40292,
NIGEL E. HARRIS SILVIA PIERANGELI
USA
1. McNeil HP, Simpson RJ, Chesterman CN, Krillis SA. Antiphospholipid antibodies are directed against a complex antigen that includes a lipid-binding inhibitor of coagulation &bgr;2 glycoprotein I(apo H). Proc Natl Acad Sci (USA)1990; 87: 4120-24. 2. Thiagarajan P, Shapiro SS, DeMarco L A monoclonal immunoglobulin M coagulation inhibitor with phospholipid specificity mechanism of a lupus anticoagulant. J Clin Invest 1980; 66: 397-405. 3. Harris EN, Gharavi AE, Loizou S, Derue G, Chan JK. Crossreactivity of anti-phospholipid antibodies. J Clin Lab Invest 1985; 66: 397-405. 4 Pengo V, Thiagarajan P, Shapiro SS, Haine MJ. Immunological specificity and mechanism of action of IgG lupus anticoagulants. Blood 1987; 70: 69-76. 5. Harris EN, Gharavi AE, Tincani A, et al. Affinity purified anticardiolipin antibodies and anti-DNA antibodies. J Clin Lab Immunol 1985, 17: 155-62.
Cholecystectomy in Saudi Arabia SiR,—Iread with dismay the first sentence of Professor Tamimi and colleagues’ summary of their report (Nov 17, p 1235), which stated: "Gallstones have become increasingly prevalent in Saudi Arabia ...". Could I possibly have missed the epidemiological data despite close attention to published work? The answer is no, because there is no such published information and nor do Tamimi and colleagues’ article provide any. The increased surgical activity they report probably reflects investment of oil revenues in health care, so that diagnostic ultrasonography and operations are available at a much higher level than before. It would indeed be very interesting, and compatible with evidence from the UK, Japan, and Norway, if gallstone prevalence had increased in Saudi Arabia lately, but this would depend on proper population-based surveys or necropsy reviews. Cholecystectomy rates might give quite false impressions about changes in gallstone prevalence. Rates have fallen strikingly in Sweden and Scotland at a time when gallstone disease is known to remain very common. General
Hospital, Bishop Auckland, County Durham DL14 6AD, UK 1 Bateson MC Gallstone variable. Lancet 1984;
prevalence ii:
521-25
M. C. BATESON and
cholecystectomy
rate are
independently
