Dear Editor, this is the most up-to-dated, complete, holistic and informative article on AOSD existed contemporaneously.
My only addition/suggestion would be to indicate suggested average duration of treatment (for steroids and immunosuppressive drugs) when symptoms are controlled. What it should be an average duration of giving for example methotrexate or plaqueline when laboratory tests are within the norm, symptoms...
Dear Editor, this is the most up-to-dated, complete, holistic and informative article on AOSD existed contemporaneously.
My only addition/suggestion would be to indicate suggested average duration of treatment (for steroids and immunosuppressive drugs) when symptoms are controlled. What it should be an average duration of giving for example methotrexate or plaqueline when laboratory tests are within the norm, symptoms are no longer exist and patient is in full remission.
Thank you again for this comprehensive and useful information and wish you success.
We have read the interesting paper of Clements PJ et al (1) as well as their previous article “Cyclophosphamide versus placebo in scleroderma lung disease” (2).
We think the Authors should give information about the autoantibody status of the patients; the recent analysis of the very large EUSTAR cohort of scleroderma cases demonstrated that autoantibody specificity is more closely related to or...
We have read the interesting paper of Clements PJ et al (1) as well as their previous article “Cyclophosphamide versus placebo in scleroderma lung disease” (2).
We think the Authors should give information about the autoantibody status of the patients; the recent analysis of the very large EUSTAR cohort of scleroderma cases demonstrated that autoantibody specificity is more closely related to organ involvement than systemic sclerosis cutaneous subset (3). Concerning pulmonary evaluation this study (3) did not consider alveolitis, as in “Scleroderma lung study” (1, 2), but both pulmonary fibrosis and lung restrictive defect were about three times morefrequent in patients carrying anti-Scl70 antibody in comparison with anticentromere positive patients; comparing diffuse and limited cutaneous subsets of disease the difference in percentage of lung involvement was less pronounced. In particular we are interested in knowing how many patients affected by limited systemic sclerosis were anti-Scl70 autoantibody positive. In our experience, alveolitis rarely complicates
the course of patients with limited systemic sclerosis harbouring anticentromere antibody.
Moreover we would like to know the Authors opinion about the worse DLCO decline in patients with limited systemic sclerosis treated with cyclophosphamide in comparison with placebo group, as presented in table 3. The trend of this parameter was different in respect to the other pulmonary function tests: was the incidence of pulmonary hypertension similar in the two subgroups?
References
1) Clements PJ, Roth MD, Elashoff R, Tashkin PD, Goldin J, Silver RM,et al. Scleroderma Lung Study (SLS): Differences in the presentation and course of patients with limited versus diffuse systemic sclerosis. Ann
Rheum Dis 2007 May 7; [Epub ahead of print]
2) Tashkin PD, Elashoff R, Clements PJ, Goldin J, Roth MD, Furst DE, et al. Cyclophosphamide versus placebo in scleroderma lung disease. N EnglJ Med 2006;354:2655-66.
3) Walker UA, Tyndall A, czirjak L, Denton CP, Farge Baucel D, Kowal-Bielecka O, et al. Clinical risk assessment of organ manifestations in systemic sclerosis - a report from the EULAR Scleroderma Trials And Research (EUSTAR) group data base. Ann Rheum Dis 2007 Feb 1; [Epub ahead of print]
The issue that mutations in genes responsible for autoinflammatory syndromes could explain also some inflammatory or rheumatological disorders has been raised in recent researches. In particular, Mevalonate Kinase Deficiency (MKD) can occasionally overlap clinically and
genetically with Behcet's disease. A clinical overlap could be observed also between episodes of MKD and Henoch Schönlein Purpura (HSP):...
The issue that mutations in genes responsible for autoinflammatory syndromes could explain also some inflammatory or rheumatological disorders has been raised in recent researches. In particular, Mevalonate Kinase Deficiency (MKD) can occasionally overlap clinically and
genetically with Behcet's disease. A clinical overlap could be observed also between episodes of MKD and Henoch Schönlein Purpura (HSP): fever, arthritis, abdominal involvement are common to the two disorders; the rash
of MKD often shows an HSP-like aspect; nephritis could also be present in MKD. As a matter of fact, some MVK crisis are not distinguishable from HSP. For this reason we analyzed MKD in a series of patients affected by
HSP, whose DNA was previously collected in order to evaluate the association of vascular endothelial growth factor haplotypes with renal lesions in HSP. MVK gene was analyzed by PCR amplification of exons 2-11 followed by direct sequencing. We identified no mutation in MVK in this series, but only 5 Single Nucleotide Plymorphisms (SNPs) previously described. Moreover, the allelic frequence of these SNPs did not differ significantly from that one observed in normal population.
We conclude
that it is very unlikely that MVK mutations play a role in the pathogenesis of HSP.
We have read with interest the article recently published by Matsui et al (1). They study a large cohort of patients with rheumatoid arthritisfrom 33 hospitals in Japan and conclude that the modified Disease Activity Score including 28-joint count and using C-reactive protein (DAS28-CRP) gives mean values lower than the same index using ESR (DAS28-ESR). They find a mean difference of 0.72 and state that DAS...
We have read with interest the article recently published by Matsui et al (1). They study a large cohort of patients with rheumatoid arthritisfrom 33 hospitals in Japan and conclude that the modified Disease Activity Score including 28-joint count and using C-reactive protein (DAS28-CRP) gives mean values lower than the same index using ESR (DAS28-ESR). They find a mean difference of 0.72 and state that DAS28-CRP underestimates thedisease activity if the criteria of evaluation for DAS28-ESR are applied.
The patients included in clinical trials and multicentre studies may be not representative of the usual patients attended in clinical practice. Since 2002 we have registered all the data from all our patients directly
into computers using software that calculates different clinical indexes and also enables reports to be given to them when they are still at the office. The analysis of the data from the 266 patients with rheumatoid arthritis treated by one of us in 2006 confirms the same findings reportedby Matsui. In the 242 patients with complete data available, DAS28-CRP waslower than DAS28-ESR (mean difference 0.49). Our results are also similar to those recently published by Inoue, from another large Japanese data base (2). Table I shows the characteristics of our patients and the results of the statistical analysis. It includes a regression line that strongly correlates DAS28-ESR and DAS28-CRP, as well as the proposed cut-off points of DAS28-CRP values that correspond to DAS28-ESR scores of 2'6, 3'2 and 5'1, obtained by means of Receiver Operating Characteristic (ROC) curves and defining remission, low disease activity and high disease activity, respectively. Unlike Matsui, we have not observed larger differences between DAS28-ESR and DAS28-CRP when DAS28 increases. However, the correlation of both indexes is stronger at high values of DAS28, a finding also reported by Inoue.
Our results support the conclusions of Matsui and Inoue that DAS28-CRP should be evaluated using different criteria from that for DAS28-ESR and extend them to daily practice.
REFERENCES
1. Matsui T, Kuga Y, Kaneko A, Nishino J, Eto Y, Chiba N et al. Disease activity score (DAS28) using CRP underestimates the disease activity and overestimates the EULAR response criteria compared with DAS28 using ESR in a large observational cohort of rheumatoid arthritis patients
in Japan. Ann Rheum Dis published online 16 mar 2007.
2. Inoue E, Yamanaka H, Hara M, Tomatsu T, Kamatani N. Comparison of Disease Activity Score (DAS)28-erythrocyte sedimentation rate and DAS28-C-reactive protein threshold values. Ann Rheum Dis 2007;66:407-409.
Dear Editor,
The recent retrospective study by Kaul et al(1) on the assessment of the 2006 revised classification criteria for definite antiphospholipid syndrome (2) sets the ground for at least three issues. a) The inclusion of “non-criteria aPL features” in the revised APS criteria is indeed a step
forward, but it appears that it requires revaluation, particularly with regards to the addition of thrombocytopenia as a dist...
Dear Editor,
The recent retrospective study by Kaul et al(1) on the assessment of the 2006 revised classification criteria for definite antiphospholipid syndrome (2) sets the ground for at least three issues. a) The inclusion of “non-criteria aPL features” in the revised APS criteria is indeed a step
forward, but it appears that it requires revaluation, particularly with regards to the addition of thrombocytopenia as a distinct clinical criteria. As known, this hematological manifestation was amongst the first clinical features recognized as part of the syndrome (3), it is actually more frequent than pregnancy morbidity in large series of APS patients (4,5) and, aCL and anti-ß2-glycoprotein-I antibodies (anti-ß2GP-I) bind strongly to activated platelets in vitro via ß2GP-I (6).
In Kaul’s series, 16 patients with aPL had thrombocytopenia (11 had a vascular event and 5 were classified as being “asymptomatic”) while 9 patients fulfilled the
pregnancy morbidity as the only criteria for APS. b) Four patients (10%) had APS according to the 2006 criteria, but not by the 1998 criteria, due to the fact that those patients fulfilled the IIc serological criteria, that is, they had anti-ß2GP-I as the only antibody. This is in agreement with earlier papers that reported the existence of aCL-negative, anti-ß2GP -I-positive patients, with or without systemic lupus erythematosus (SLE), but with otherwise clinical manifestations of the APS (7,8). Kaul´s finding also confirms that aCL (-), LAC (-), anti-ß2GP-I (+) patients account for 5-10% of patients with antiphospholipid syndrome (9,10). c) Kaul´s et al studied 82 “asymptomatic” patients, 39 of them met at least one
serological criteria for APS; assuming that the remainder 43 patients were asymptomatic and aPL negative, the sensitivity and specificity of aCL alone for APS is 0.28 and 0.67, 0.09 and 0.98 for anti-ß2GP-I alone, 0.28 and 0.59 for more than one aPL and 0.52 and 0.52 for all serological criteria, respectively. This finding confirms previous data showing that aCL have high sensitivity and low specificity for APS while anti-ß2GP-I have higher specificity and lower sensitivity than aCL for APS.
More than a decade ago, it has been our contention that antibodies toß2GP-I are comprised by at least two subpopulations, one directed against a cryptic epitope (detected by the conventional aCL ELISA) and another one
reactive with the native protein (detected by the modified ELISA with purified ß2GP-I as antigen). Thus, both immunoassays detect antibodies to ß2GP-I, while the conventional aCL ELISA also detects antibodies reactive
with cardiolipin proper (authentic aCL). This latter phenomenon may thus explain the low specificity of aCL for APS (In Kual´s series, 54% of asymptomatic patients had aCL).
The Sapporo APS criteria were developed by the experts’ opinions on the subject, while the amended criteria were born after an appraisal of the existing evidence on clinical and laboratory features of APS 1. What it is clearly needed is a large multinational study to objectively and prospectively validate the revised criteria and, why not, to challenge them with those developed 15 years ago after the systematic study of 667
patients with SLE 4
References
1. Kaul MS, Erkan D, Sammaritano L, Lockshin MD. Assessment of the 2006 revised antiphospholipid syndrome classification criteria. Ann Rheum Dis 2007.
2. Miyakis S, Lockshin MD, Atsumi T, Branch DW, Brey RL, Cervera R et al. International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS). J Thromb Haemost 2006;4:295-306.
3. Hughes GRV. Hughes' syndrome: the antiphospholipid syndrome. A historical view. Lupus 1998;2:1-4.
4. Alarcón-Segovia D, Pérez-Vázquez ME, Villa AR, Drenkard C, Cabiedes J. Preliminary classification criteria for the antiphospholipid syndrome within systemic lupus erythematosus. Semin Arthritis Rheum 1992;21:275-86.
5. Cervera R, Piette JC, Font J, Khamashta MA, Shoenfeld Y, Camps MTet al. Antiphospholipid syndrome. Clinical and immunologic manifestations and patterns of disease expression in a cohort of 1000 patients. Arthritis
Rheum 2002;46:1019-27.
6. Vázquez-Mellado J, Llorente L, Alarcón-Segovia D. Exposure of anionic phospholipids upon platelet activation permits binding of ß2-glycoprotein-I and through it IgG antiphospholipid antibodies. Studies in platelets from patients with antiphospholipid syndrome and normal
subjects. J Autoimmunity 1994;7:335-48.
7. Cabral AR, Amigo MC, Cabiedes J, Alarcón-Segovia D. The antiphospholipid/cofactor syndromes. A primary variant with antibodies to ß2-glycoprotein-I but no antibodies detectable in standard antiphospholipid assays. Am J Med 1996;101:472-81.
8. Alarcón-Segovia D, Mestanza M, Cabiedes J, Cabral AR. The antiphospholipid/cofactor syndromes. II. A variant in patients with systemic lupus erythematosus with antibodies to ß2-glycoprotein-I but no antibodies detectable in standard antiphospholipid assays. J Rheumatol 1997;24:1545-51.
9. Damoiseaux J, Wijffels M, Willems GM, Bevers EM, Spaanderman ME, van Pampus EC et al. The antiphospholipid/cofactor syndrome: results of routine screening for antibodies to ß2-GPI upon suspicion of the
antiphospholipid syndrome. Scand J Rheumatol 2004;33(6):441-2.
10. Galli M, Luciani D, Bertolini G, Barbui T. Anti-b2-glycoprotein I, antiprothrombin antibodies, and the risk of thrombosis in the antiphospholipid syndrome. Blood 2003;102:2717-23.
Dear Editor,
W Zhang and al. in their fourth recommendation for hand osteoarthritis consider that their proposition is based on expert opinion alone.
In France, and probably other European country, spa therapy (with hot mud, water or cloud) is often used for treating hand osteoarthritis.
A French spa centre supported two randomised clinical trial: One showed positive and equivalent effect between two different types of mud...
Dear Editor,
W Zhang and al. in their fourth recommendation for hand osteoarthritis consider that their proposition is based on expert opinion alone.
In France, and probably other European country, spa therapy (with hot mud, water or cloud) is often used for treating hand osteoarthritis.
A French spa centre supported two randomised clinical trial: One showed positive and equivalent effect between two different types of mud and thermal cloud [1] (which remain unpublished but is cited in the review of
E Maheu et al[2]). The other shows superiority of thermal cloud application on topical NSAI (ibuprofen) [3].
Even if they have some methodological limitation, we propose that these two trials (in French language) could be analysed by ESCISIT, in future recommendations, for determining if level of evidence could be improved by
their conclusion.
References
[1] Collin JF, Constant F, Herbeth B. Evaluation of comparative efficacy of mud and Berthollet on hand osteoarthritis [evaluation de l’efficacité compare de la boue et du Berthollet sur l’arthrose des mains]. Journée pratique s”hydrologie thérapeutique, MEDEC 1993.
[2] Trèves R, Maheu E, Dreiser RL. Clinical trials in hand osteoarthritis. Critical review.[les essais thérapeutiques dans l’arthrose digitale, revue
critique] Rev Rhum 1995, 62:119S-128S.
[3] Graber Duvernay B, Forestier R, Françon A. Efficacy of the Berthollet technique at Aix Les Bains spa on fuctionnal inpairment in hand osteoarthritis. A controlled therapeutic study [Efficacité du Berthollet d’Aix Les bains sur les manifestations fonctionnelles de l’arthrose des mains - Essai thérapeutique contrôlé.]Rhumatologie 1997;49(4):151-6.
Dear Editor, 1977 was the year in which U Lanz described 4 median nerve variants. All of them could be detected by ultrasonography. As this classification was surgical dependent it did not represent the real
distribution of the variants in the community. Bifid median nerve was 2.8% only. This percent is not coping with our practical or research findings.
As a radiologist interested in this new field of neurosonography the m...
Dear Editor, 1977 was the year in which U Lanz described 4 median nerve variants. All of them could be detected by ultrasonography. As this classification was surgical dependent it did not represent the real
distribution of the variants in the community. Bifid median nerve was 2.8% only. This percent is not coping with our practical or research findings.
As a radiologist interested in this new field of neurosonography the median nerve was on the top of my research. In contrast to EULAR strategy {teach the teachers} my strategy is {teach your self} so all my cases
undergo what I call ultrasonographic median nerve print. Indeed this ultrasonographic study on 308 median nerves support my findings =Bifid median nerve is not uncommon condition=. In this present study The median nerve was divided in 11.7% of the hands and this agree with our practical finding by using ultrasonography as a screening modality. From a radiological point of view the median nerve subdivision may be equal or show a variation in size, and may be adjacent to each other or separated
with presence or absent of a persistent median artery. The unequal subdivisions that occur in the proximal forearm attract more my interest.
The median nerve fibers show a very interesting phenomenon at the proximal part of CT. The fascicles change their direction by 180 degrees so the right fascicles at the forearm are located at left side at the CT area and the upper fascicles at the forearm are located inferiorly at the CT area.
We can follow the small and large subdivision of the median nerve at the forearm to the CT area and see this reposition directly. It's more interesting to notice that this redirection of the fascicles returns back to the forearm arrangement with strong flexion of the wrist. From surgical point of view direct apposition of the fascicles at median nerve repair may miss this redirection so the microscopic surgical repair gives a higher rate of success. Another point the bifid median with separated
subdivisions when suspected to an injury to the wrist one subdivision may be only affected. So examination of the median nerve should be started from the upper part of the forearm. The effect of this variant on nerve conduction study should be put in consideration. Another practical finding is that the bifid median nerve are more present at the left side and runs in families i.e. find a case usually denote presence of other cases at the
same family.
The role of sonography in rheumatology has been
increased in the last decade. The frequent question is [can US simulate other investigatory methods in this branch], for example can US simulate the nerve conduction studies in detection of nerve abnormalities? The research directed to answer this question is limited and misses the fact that the ultrasonography has two components, the static and dynamic compo...
The role of sonography in rheumatology has been
increased in the last decade. The frequent question is [can US simulate other investigatory methods in this branch], for example can US simulate the nerve conduction studies in detection of nerve abnormalities? The research directed to answer this question is limited and misses the fact that the ultrasonography has two components, the static and dynamic components. Nerve visualization and characterization of the deviation of the normality can be easily detected by the static examination. The detected abnormality can be also graded to different stages according to the degree of affection. For long time the increase cross section area was taken as the stander for the nerve affection. According to our anatomical and biomechanical knowledge about the median nerve the ultrasonography has more powerful diagnostic value in cases of CTS. Ultrasonography can detect the direct signs of nerve pathological changes, the sonographic signs of
entrapment, with the ability to predict the further outcome of the examined cases. The normal nerve as seen by high resolution ultrasonography is:
1- oval shaped or round with high ability to change its shape in response to applied pressure easily seen by dynamic study during flexion and extension of the limbs
2- the nerve according to the number of fascicles has a normal fascicular pattern
3- it has the ability to change its position according to the force applied on it during limb movement this excursion can be calculated by the dynamic study
4- in response to exercise it reacts in the form of increase its cross section area and increase signals from its blood vessels
5- in response to the applied pressure the cross section area is reduced by 20-30% with flattening of the contour so by applying all these parameters the subtle
changes can be detected....
first = the loss of fascicular pattern which seen with long standing pathology can be detected and its length can be measured
second = the loss of compressibility by applied pressure [most probably due to fibrosis and new short nerve fiber growth] can be easily measured and the less the compressibility the poorer the outcome of treatment
third = loss of normal nerve excursion during limb movement on the dynamic study due either intrinsic changes or surrounding fibrosis fourth the focal nerve changes can be estimated and the change in the volume by measuring the affected segment length and the cross section area can
calculated and used for follow up.
So the cross section area as single criterion do not explain the recurrent cases of the operated carpal tunnel
syndrome or the poor response to the operation in conservative cases.
Finally to use the gray ultrasound alone the echotexture of the nerve with applied stress compressibility test together with the cross sectional areain rest and on dynamic stress condition should be used in all examined
cases.
Maradit-Kremers and colleagues raise several important issues in their excellent paper on heart failure in rheumatoid arthritis (RA) (1), but at least two important questions as well. Although, as they point out,
there have been previous links suggested between ESR and heart failure (2) many other factors can interfere with ESR. C-reactive protein (CRP), a much 'cleaner' measure of inflammation, and is...
Maradit-Kremers and colleagues raise several important issues in their excellent paper on heart failure in rheumatoid arthritis (RA) (1), but at least two important questions as well. Although, as they point out,
there have been previous links suggested between ESR and heart failure (2) many other factors can interfere with ESR. C-reactive protein (CRP), a much 'cleaner' measure of inflammation, and is also linked with heart failure (3). Do they have figures for CRP in these patients, or why did
they choose ESR?
Second, they admit that no allowance is made in the figures for NSAID use, which are known to trigger heart failure. Does the increase in inflammatory markers before the onset of heart failure, and the development of anaemia (a side-effect of NSAID treatment) in the six months afterwards, not suggest that NSAIDs might have an important role to play in the development of cardiac failure? Although figures for NSAID use were not available, were there any surrogate markers to suggest an
influence, for example, correlation between the duration or degree of the inflammatory response (perhaps requiring increased NSAID use), and the extent of the anaemia?
References
1. Maradit-Kremers H, Nicola PJ, Crowson CS, Ballman KV, Jacobsen SJ, Roger VL et al. Raised erythrocyte seimentation rate signals heart failure in patients with rheumatoid arthritis. Ann Rheum Dis 2007;66:76-80.
2. Sharma R, Rauchhaus M, Ponikowski PP, Varney S, Poole-Wilson PA, Mann DL et al. The relationship of the erythrocyte sedimentation rate to inflammatory cytokines and survival in patients with chronic heart failure
treated with angiotensin-converting enzyme inhibitors. J Am Coll Cardiol 2000;36:523-8.
3. Kardys I, Knetsch AM, Bleumink GS, Deckers JW, Hofman A, Stricker BH et al. C-reactive protein and risk of heart failure. The Rotterdam Study. Am Heart J 2006;152:514-20.
I read with great interest the recently published EULAR recommendations for the management of early arthritis.(1) However, I would like to add a few words of comment regarding the use of analgesicsin patients with cardiovascular (CV) and gastrointestinal (GI) risk
factors. In my opinion the rational choice for such patients is the use ofaspirin combined with a proton-pump inhibitor.
I read with great interest the recently published EULAR recommendations for the management of early arthritis.(1) However, I would like to add a few words of comment regarding the use of analgesicsin patients with cardiovascular (CV) and gastrointestinal (GI) risk
factors. In my opinion the rational choice for such patients is the use ofaspirin combined with a proton-pump inhibitor.
First, both coxibs and traditional NSAIDs should not be prescribed in patients at higher CV risk. On the contrary, there is good evidence that analgesic doses of aspirin (up to 1500mg) are associated with protection
from CV events.(2,3) Furthermore, aspirin dose or its higher lifetime use is not significantly associated with hypertension(4) or renal toxicity.(5,6) Importantly, a recent meta- analysis of 24 randomised controlled trials found no evidence of dose- responsiveness for bleeds
over a wide range of doses (50 to 1500 mg/day).(7) Indeed, aspirin in doses commonly used in practice, seems to have an excellent safety profile.(8)
Second, recent evidence suggest that not only NSAIDs but also acetaminophen can raise cardiovascular risk.(9) High acetaminophen use may also increase the risk of hypertension(4) and a decrease of renal function.(5) Interestingly, increased acetaminophen use has now been linked to increased prevalence of asthma and chronic obstructive pulmonarydisease, and with lowered lung function.(10) Surprisingly, a recent case-control study showed that acetaminophen (>2 g per day) was ssociated
with a greater risk of GI perforation or bleed(11) and one cohort study reported a dose-response relationship between acetaminophen and dyspepsia.(12) It appears that regular use of acetaminophen is also associated with symptoms of severe diverticular disease, particularly bleeding.(13)
Lastly, compelling evidence suggests that both aspirin and other NSAIDs are superior to acetaminophen for improving moderate-to-severe painin patients with osteoarthritis(14,15,16) and rheumatoid arthritis.(17)
Likewise, in acute pain states aspirin provides significant and more rapidanalgesia than acetaminophen.(18)
References
1. Combe B, Landewe R, Lukas C, Bolosiu HD, Breedveld F, Dougados M, et al. EULAR recommendations for the management of early arthritis: report of a task force of the European Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis 2007;66:34-45. Epub 2006 Jan 5.
2. Antithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ
2002;324:71-86.
3. Johnson ES, Lanes SF, Wentworth CE 3rd, Satterfield MH, Abebe BL, Dicker LW.A metaregression analysis of the dose-response effect of aspirin on stroke. Arch Intern Med 1999;159:1248-53.
4. Forman JP, Stampfer MJ, Curhan GC. Non-narcotic analgesic dose andrisk of incident hypertension in US women. Hypertension 2005;46:500-7.
5. Curhan GC, Knight EL, Rosner B, Hankinson SE, Stampfer MJ. Lifetime nonnarcotic analgesic use and decline in renal function in women. Arch Intern Med 2004;164:1519-24.
6. Dubach UC, Rosner B, Sturmer T. An epidemiologic study of abuse of analgesic drugs. Effects of phenacetin and salicylate on mortality and cardiovascular morbidity (1968 to 1987) N Engl J Med 1991;324:155-60.
7. Derry S, Loke YK. Risk of gastrointestinal haemorrhage with long term use of aspirin: meta-analysis. BMJ 2000;321:1183-7.
8. Fries JF, Ramey DR, Singh G, Morfeld D, Bloch DA, Raynauld JP. A reevaluation of aspirin therapy in rheumatoid arthritis. Arch Intern Med 1993;153:2465-71.
9. Chan AT, Manson JE, Albert CM, Chae CU, Rexrode KM, Curhan GC, et al. Nonsteroidal antiinflammatory drugs, acetaminophen, and the risk of cardiovascular events. Circulation 2006;113:1578-87.
10. McKeever TM, Lewis SA, Smit HA, Burney P, Britton JR, Cassano PA. The association of acetaminophen, aspirin, and ibuprofen with respiratory disease and lung function. Am J Respir Crit Care Med 2005;171:966-71.
11. Garcia Rodriguez LA, Hernandez-Diaz S. Relative risk of upper gastrointestinal complications among users of acetaminophen and nonsteroidal anti-inflammatory drugs. Epidemiology 2001;12:570-6.
12. Rahme E, Pettitt D, LeLorier J. Determinants and sequelae associated with utilization of acetaminophen versus traditional nonsteroidal antiinflammatory drugs in an elderly population. Arthritis Rheum 2002;46:3046-54.
13. Aldoori WH, Giovannucci EL, Rimm EB, Wing AL, Willett WC. Use of acetaminophen and nonsteroidal anti-inflammatory drugs: a prospective study and the risk of symptomatic diverticular disease in men. Arch Fam Med 1998;7:255-60.
14. Lee C, Straus WL, Balshaw R, Barlas S, Vogel S, Schnitzer TJ. A comparison of the efficacy and safety of nonsteroidal antiinflammatory agents versus acetaminophen in the treatment of osteoarthritis: a meta-analysis. Arthritis Rheum 2004;51:746-54.
15. Towheed TE, Maxwell L, Judd MG, Catton M, Hochberg MC, Wells G. Acetaminophen for osteoarthritis. Cochrane Database Syst Rev 2006;(1):CD004257.
16. Zhang W, Jones A, Doherty M. Does paracetamol (acetaminophen) reduce the pain of osteoarthritis? A meta-analysis of randomised controlled trials. Ann Rheum Dis 2004;63:901-7.
17. Wienecke T, Gotzsche PC. Paracetamol versus nonsteroidal anti-inflammatory drugs for rheumatoid arthritis. Cochrane Database Syst Rev 2004;(1):CD003789.
18. Seymour RA, Hawkesford JE, Sykes J, Stillings M, Hill CM. An investigation into the comparative efficacy of soluble aspirin and solid paracetamol in postoperative pain after third molar surgery. Br Dent J 2003;194:153-7.
Conflict of Interest:
Dr. Pijak has received speaker fees and travel assistance from Fournier.
Dear Editor, this is the most up-to-dated, complete, holistic and informative article on AOSD existed contemporaneously.
My only addition/suggestion would be to indicate suggested average duration of treatment (for steroids and immunosuppressive drugs) when symptoms are controlled. What it should be an average duration of giving for example methotrexate or plaqueline when laboratory tests are within the norm, symptoms...
Dear Sir,
We have read the interesting paper of Clements PJ et al (1) as well as their previous article “Cyclophosphamide versus placebo in scleroderma lung disease” (2).
We think the Authors should give information about the autoantibody status of the patients; the recent analysis of the very large EUSTAR cohort of scleroderma cases demonstrated that autoantibody specificity is more closely related to or...
Dear Editor,
The issue that mutations in genes responsible for autoinflammatory syndromes could explain also some inflammatory or rheumatological disorders has been raised in recent researches. In particular, Mevalonate Kinase Deficiency (MKD) can occasionally overlap clinically and genetically with Behcet's disease. A clinical overlap could be observed also between episodes of MKD and Henoch Schönlein Purpura (HSP):...
Dear Editor,
We have read with interest the article recently published by Matsui et al (1). They study a large cohort of patients with rheumatoid arthritisfrom 33 hospitals in Japan and conclude that the modified Disease Activity Score including 28-joint count and using C-reactive protein (DAS28-CRP) gives mean values lower than the same index using ESR (DAS28-ESR). They find a mean difference of 0.72 and state that DAS...
Dear Editor, The recent retrospective study by Kaul et al(1) on the assessment of the 2006 revised classification criteria for definite antiphospholipid syndrome (2) sets the ground for at least three issues. a) The inclusion of “non-criteria aPL features” in the revised APS criteria is indeed a step forward, but it appears that it requires revaluation, particularly with regards to the addition of thrombocytopenia as a dist...
Dear Editor, W Zhang and al. in their fourth recommendation for hand osteoarthritis consider that their proposition is based on expert opinion alone. In France, and probably other European country, spa therapy (with hot mud, water or cloud) is often used for treating hand osteoarthritis. A French spa centre supported two randomised clinical trial: One showed positive and equivalent effect between two different types of mud...
Dear Editor, 1977 was the year in which U Lanz described 4 median nerve variants. All of them could be detected by ultrasonography. As this classification was surgical dependent it did not represent the real distribution of the variants in the community. Bifid median nerve was 2.8% only. This percent is not coping with our practical or research findings. As a radiologist interested in this new field of neurosonography the m...
Dear Editor
The role of sonography in rheumatology has been increased in the last decade. The frequent question is [can US simulate other investigatory methods in this branch], for example can US simulate the nerve conduction studies in detection of nerve abnormalities? The research directed to answer this question is limited and misses the fact that the ultrasonography has two components, the static and dynamic compo...
Dear Editor,
Maradit-Kremers and colleagues raise several important issues in their excellent paper on heart failure in rheumatoid arthritis (RA) (1), but at least two important questions as well. Although, as they point out, there have been previous links suggested between ESR and heart failure (2) many other factors can interfere with ESR. C-reactive protein (CRP), a much 'cleaner' measure of inflammation, and is...
Dear Editor,
I read with great interest the recently published EULAR recommendations for the management of early arthritis.(1) However, I would like to add a few words of comment regarding the use of analgesicsin patients with cardiovascular (CV) and gastrointestinal (GI) risk factors. In my opinion the rational choice for such patients is the use ofaspirin combined with a proton-pump inhibitor.
First...
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