Dear Editor, Sokka et al reported results of a survey of rheumatoid arthritis (RA) patients from 15 countries in 2005-2006, the QUEST-RA study.[1] A similar cross sectional survey was performed in 2004 in Hungary by rheumatologists involving 257 consecutive patients with RA attending routine visits to 6 hospital based outpatient rheumatology centres. Detailed description of the study and certain disease parameters has been publ...
Dear Editor, Sokka et al reported results of a survey of rheumatoid arthritis (RA) patients from 15 countries in 2005-2006, the QUEST-RA study.[1] A similar cross sectional survey was performed in 2004 in Hungary by rheumatologists involving 257 consecutive patients with RA attending routine visits to 6 hospital based outpatient rheumatology centres. Detailed description of the study and certain disease parameters has been published elsewhere.[2]
Although our research was not part of the QUEST-RA, it focussed also on quantitative clinical characteristics and drug therapy use of the patients. Therefore, our results can offer some additional information to the QUEST-RA presenting the situation in Hungary. We highlight some
methodological issues as well.
Demographic characteristics of our sample was similar to the median QUEST-RA results but functional status was worse at a shorter disease duration and disease activity was higher (DAS28≤3.2: 9%, DAS28>5.1: 48.6%) ranking Hungary to the group of countries with severe
disease. Poland’s results were the most similar.(Table 1)
Methotrexate was the most frequently ever used DMARD in Hungary likewise in nearly all QUEST-RA countries. Leflunomide was more common in our survey, only France, Spain and Italy had higher rates. Regular reimbursement of the biological drugs was introduced in 2006 in Hungary so
thus explains their low rate.
The QUEST-RA presented the delay of the first DMARD in months. Recall bias is suspected in a retrospective survey involving patients with disease duration median 9-13.5 years. Furthermore, calculating the delay based on the start of the first symptoms is very uncertain and difficult to standardise, especially in a retrospective international study.
Symptoms to consider (erosions? swollen joints? morning stiffness?) must be very well defined and no literature background for that. Countries with early RA registries (that is not the case of Hungary) are more likely to
offer correct information than others wherein inputs are based on patients’ interviews and documentation reviews. Therefore, we asked for the data on a year level and considered the establishment of the diagnosis by ACR criteria. In our survey, the majority (51.3%) of the
patients started a DMARD in the year of the diagnosis, mean delay was 1.79(SD3.96) years, which is similar to the QUEST-RA results and 5.3% have already had a DMARD before having established RA.
The rate of patients that has never taken any DMARD is also a relevant aspect. In Hungary, 31(18%) patients have never experienced a DMARD.
The overall drug history of a sample does not necessarily reflect thecurrent therapy use.[3-5] Analysis of current rates (and doses) of DMARDs is essential for the evaluation as these, especially biologicals, can
strongly influence the actual clinical status. In Hungary, methotrexate was the most frequently taken DMARD also at the time of the survey (49%) and the rate of leflunomide was still substantial (27.6%), but sulfasalazine and hydroxychloroquin were less used (11.3% and 7.3%,
respectively), gold injections decreased robustly (2.7%) and even less patients (0.7%) were just taking biologics.
Our results present the recent past in Hungary, registries are of primary importance to follow up the changes.
References
1. Sokka T, Kautiainen H, Toloza S et al. QUEST-RA: Quantitative clinical assessment of patients with rheumatoid arthritis seen in standardrheumatology care in 15 countries. Ann Rheum Dis Published Online First: 5
April 2007. doi: 10.1136/ard.2006.069252.
2. Péntek M, Kobelt G, Czirjak L et al. Costs of RA in Hungary. J Rheumatol 2007;34:1437-8.
3. Jobanputra P, Wilson J, Douglas K et al. A survey of British rheumatologists’ DMARD preferences for rheumatoid arthritis. Rheumatology 2004;43:206-210.
4. Edwards CJ, Arden NK, Fisher D et al. The changing-use of disease-modifying anti-rheumatc drugs in individuals with rheumatoid arthritis from the United Kingdom General Practice Research Database. Rheumatology
2005;44:1394-1398.
5. Le Loet X, Berthelot JM, Cantragel A et al. Clinical practice decision tree for the choice of the first disease modifying antirheumatic drug for very early rheumatoid arthritis: a 2004 proposal of the French
Society of Rheumatology. Ann Rheum Dis 2006;65:45-50.
Table 1 Clinical characteristics and drug therapy use in Hungary (year 2004) in comparison with results of a survey performed in 15 countries (years 2005-2006), one of them is Poland.
Dear Editor, we read with interest the editorial by Schett et al. on structural remodeling in ankylosing spondylitis. [1] We acknowledge the effort to
highlight potential differences between ankylosing spondylitis and rheumatoid arthritis but would like to underline a number of critical issues. Most importantly, the authors did not distinguish the process of new cartilage and bone formation at the enthesis as seen in the di...
Dear Editor, we read with interest the editorial by Schett et al. on structural remodeling in ankylosing spondylitis. [1] We acknowledge the effort to
highlight potential differences between ankylosing spondylitis and rheumatoid arthritis but would like to underline a number of critical issues. Most importantly, the authors did not distinguish the process of new cartilage and bone formation at the enthesis as seen in the different forms of spondyloarthritis from osteophyte formation in osteoarthritis that typically occurs at the borderzone between articular cartilage and bone. [2,3] The enthesis and its residing cell populations appear to be
the primary anatomical target site in spondyloarthritis but in their editorial, Schett et al seem to pay little attention to the specific anatomic localization of tissue formation and remodeling. [4,5] We believe this may have important consequences for the molecular pathways involved in these processes and the therapeutic targeting thereof. We haveused an animal model of joint ankylosis starting from the enthesis to investigate the cell and molecular biology of this process. [6] We have demonstrated that new bone formation in this model is predominantly endochondral ossification. In addition, inhibition of bone orphogenetic
proteins (BMP) using overexpression of noggin, a BMP antagonist, has a profound effect on both incidence and severity of arthritis and ankylosingenthesitis in preventive and therapeutic experiments. Biopsy specimens
from ankylosing enthesitis in patients seem to support these molecular findings. [7] Based on these data, we have put forward the hypothesis that inflammation and structural remodeling of the joint in diseases such as
ankylosing spondylitis and psoriatic arthritis are likely to be at least partially independent events. [7,8,9] This was confirmed by the lack of effect of tumour necrosis factor inhibition in this model.[10] Indeed, we demonstrated that etanercept did not inhibit structural changes at the enthesis, findings that now appear to be supported by preliminary human cohort data.[11]
We agree with the authors that WNT signaling may also be an importantpathway in these processes. However, the presence of DKK-1 in erosions in man and mice suggests that DKK-1 inhibits WNT-stimulated direct, not endochondral, bone formation and erosion repair.[12] The data in the TNF-transgenic model also show that DKK-1 has an inhibitory effect on osteophyte formation.[13] However, in our view, the role of Wnt signaling in entheseal changes remains to be studied. In particular it is noteworthy that WNT signaling also has inhibitory effects on chondrogenesis and chondrocyte maturation and may therefore favor membranous rather than endochondral bone formation.[14,15] In addition, differences in serum
DKK-1 levels between rheumatoid arthritis and ankylosing spondylitis patients may reflect differences in systemic inflammation. Establishing a hierarchy of tissue formation pathways in this context and their interactions with inflammatory and tissue destructive mechanisms therefore
remains a major challenge to better understand mechanisms of disease in spondyloarthritis.
References
(1) Schett G, Landewe R, van der HD. Tumour necrosis factor blockersand structural remodelling in ankylosing spondylitis: what is reality and what is fiction? Ann Rheum Dis 2007;66:709-711.
(2) Benjamin M, McGonagle D. The anatomical basis for disease localisation in seronegative spondyloarthropathy at entheses and related sites. J Anat 2001;199:503-526.
(3) Lories RJ, Luyten FP. Bone morphogenetic proteins in destructive and remodeling arthritis. Arthritis Res Ther 2007;9:207.
(4) Ball J. Enthesopathy of rheumatoid and ankylosing spondylitis. Ann Rheum Dis 1971;30:213-223.
(5) McGonagle D, Gibbon W, Emery P. Classification of inflammatory arthritis by enthesitis. Lancet 1998;352:1137-1140.
(6) Lories RJ, Matthys P, Derese I, De Vlam K, Luyten FP. Ankylosing enthesitis, dactylitis and onychoperiostitis in a mouse model of psoriatic
arthritis. Ann Rheum Dis 2004;63:595-598.
(7) Lories RJU, Derese I, Luyten FP. Modulation of Bone Morphogenetic Protein signaling inhibits the onset and progression of ankylosing enthesitis. J Clin Invest 2005;115:1571-1579.
(8) Luyten FP, Lories RJ, Verschueren P, De Vlam K, Westhovens R. Contemporary concepts of inflammation, damage and repair in rheumatic diseases. Best Pract Res Clin Rheumatol 2006;20:829-848.
(9) De Vlam K, Lories RJ, Luyten FP. Mechanisms of Pathologic New Bone Formation. Curr Rheumatol Rep 2006;8:332-337.
(10) Lories RJ, Derese I, De Bari C, Luyten FP. Evidence for uncoupling of inflammation and joint remodeling in a mouse model of Spondyloarthritis. Arthritis Rheum 2006;56:489-497.
(11) van der Heijde DM, Landewe R, Ory P, Vosse D, Zhou L, Tsuji W et al. Two-year etanercept therapy does not inhibit radiographic progression in patients with ankylosing spondylitis. Ann Rheum Dis 2006;65[Suppl. II]: 81.
(12) Walsh NC, Manning CA, Boch JA, Iwata K, Condon KW, McHugh KP et al. Wnt Signaling Antagonists Are Candidates For The Suppression Of Osteoblast Differentiation In Inflammatory Arthritis. Arthritis Rheum 2006;54[9]:S511.
(13) Diarra D, Stolina M, Polzer K, Zwerina J, Ominsky MS, Dwyer D et al. Dickkopf-1 is a master regulator of joint remodeling. Nat Med 2007;13:156-163.
(14) Day TF, Guo X, Garrett-Beal L, Yang Y. Wnt/beta-catenin signaling in mesenchymal progenitors controls osteoblast and chondrocyte differentiation during vertebrate skeletogenesis. Dev Cell 2005;8:739-750.
(15) Lories RJ, Peeters J, Bakker A, Derese I, Tylzanowski P, Schrooten J, Thomas JT, Luyten FP. Deletion of Frzb affects articular cartilage and biomechanical properties of the long bones Arthritis Rheum (in press).
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.
Dear Editor, Sokka et al reported results of a survey of rheumatoid arthritis (RA) patients from 15 countries in 2005-2006, the QUEST-RA study.[1] A similar cross sectional survey was performed in 2004 in Hungary by rheumatologists involving 257 consecutive patients with RA attending routine visits to 6 hospital based outpatient rheumatology centres. Detailed description of the study and certain disease parameters has been publ...
Dear Editor, we read with interest the editorial by Schett et al. on structural remodeling in ankylosing spondylitis. [1] We acknowledge the effort to highlight potential differences between ankylosing spondylitis and rheumatoid arthritis but would like to underline a number of critical issues. Most importantly, the authors did not distinguish the process of new cartilage and bone formation at the enthesis as seen in the di...
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...
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