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It is with great interest that I read the study entitled "A novel gene variation of TNF associated with ankylosing spondylitis: a reconfirmed study" by Zhu et al(1). In treating AS in Los Angeles, California, I see many Hispanic patients especially from Mexican descent.
This is very different from the Chinese population presented in this article and may explain some of the difficulties in looking for SNP'...
It is with great interest that I read the study entitled "A novel gene variation of TNF associated with ankylosing spondylitis: a reconfirmed study" by Zhu et al(1). In treating AS in Los Angeles, California, I see many Hispanic patients especially from Mexican descent.
This is very different from the Chinese population presented in this article and may explain some of the difficulties in looking for SNP's in AS.
Zhu et al reported on 79 ankylosing spondylitis (AS) patients and 132 unrelated healthy blood donors. He found that specific haplotype covering TNF gene mutant was strongly associated with AS and speculated that a recombination between HLA-B27 and TNF might have taken place. In studies on Mexican patients, Vargas-Alarcon et al stated that TNF-alpha - 308 polymorphism appears to be associated with the genetic susceptibility U-SpA. which was independent of the susceptibility conferred by HLA-
B27(2). Previously this group had also reported that a significant association of HLA-DR1 and HLA-B15 with SpA existed in Mexicans which is independent of B27(3).
Others have looked onto the role of HSP-2 and B60 as well with varying results.
In my practice, I find that spondylarthropathy patients of varying genetic backgrounds share many clinic features. Even amongst Latino's, there is much genetic variability based on their country of origin. In searching for a molecular basis for the etiology of AS and other rheumaticdisorders it may be necessary to investigate different ethnic populations more accurately to look for SNP associations.
References
1. Xiaoquan Zhu, Yawen Wang, Liang Sun, Yuguo Song, Fei Sun, Lei Tang, Zhenghao Huo, Jianxin Li, and Ze Yang
A novel gene variation of TNF associated with ankylosing spondylitis: a reconfirmed study. Ann Rheum Dis 2007;66:1419-1422.
2. Vargas-Alarcón G, Casasola-Vargas J, Rodríguez-Pérez JM, Huerta-Sil G, Pérez-Hernández N, Londoño J, Pacheco-Tena C, Cardiel MH, Granados J, Burgos-Vargas R. Tumor necrosis factor-alpha promoter polymorphisms in Mexican patients with spondyloarthritis. Hum Immunol 2006;6710):826-32.
3. Vargas-Alarcón G, Londoño JD, Hernández-Pacheco G, Pacheco-Tena C, Castillo E, Cardiel MH, Granados J, Burgos-Vargas R. Effect of HLA-B and HLA-DR genes on susceptibility to and severity of spondyloarthropathies in
Mexican patients. Ann Rheum Dis 2002;61:714-7.
Dear Editor,
We read with great interest the article by Voulgari et al, recently published in the Journal, reporting a series of patients with Rheumatoid arthritis (RA) who developed Granuloma annulare (GA) under anti-TNF therapy [1]. We would like to bring attention to some key points and shed
light on a specific differential diagnoses associated with RA the authors did not discuss.
Dear Editor,
We read with great interest the article by Voulgari et al, recently published in the Journal, reporting a series of patients with Rheumatoid arthritis (RA) who developed Granuloma annulare (GA) under anti-TNF therapy [1]. We would like to bring attention to some key points and shed
light on a specific differential diagnoses associated with RA the authors did not discuss.
GA is a benign, asymptomatic, self-limited, difficult to treat, papular eruption of unknown etiology. The possible role of immune dysregulation induced by immunosuppressive drugs in the pathogenesis of GA has been pointed out [2]. According to a prospective study, cutaneous manifestations occur under TNF-alpha blocking therapy in 25% of all cases:
(i) infection (11%), (ii) eczema (7%) and (iii) drug-related eruptions (5%) [3]. As mentionned by the authors, GA has been formerly reported under TNF-alpha blocker [4]. However, a successful treatment of generalized GA by infliximab rises controversy [5].
Drug-induced eruption diagnosis is based on several criteria : (i) development after the onset of the treatment and persistence throughout the exposure, (ii) clearance after drug withdrawal, (iii) relapse in case
of rechallenge and (iv) elimination of other potential causes for the eruption [6]. Here, the authors barely succeeded in fulfilling one to two criteria. Indeed, in only 2 cases, GA disappeared after drug withdrawal, while a local corticosteroid therapy was applied. In the 7 remaining cases, treatment was maintained and GA resolved under corticosteroid ointment. In our own experience, drug-induced GA is difficult to treat if the culprit treatment is maintained [7]. In the absence of withdrawal of
the anti-TNF therapy, Flendrie et al observed that the lesions usually recur in most cases [3]. Moreover, the authors never reintroduced the therapy to confirm whether or not it was truly involved [1,3]. In their series, Flendrie et al observed that drug-induced eruption mostly occurredduring the first 5 months [3]. Others have reported reaction with longer delays [8]. Here, eruption always occurred within 1 to 2 years. Besides, none of the patients under anti-TNF therapy for ankylosing spondylitis
developed GA. Such restriction to one disease is rather unusual and is notin favour of a drug-induced reaction. For instance, a methotrexate-inducedcutaneous eruption was described in patients with various rheumatic disease [9].
At last, the authors did not discuss a potential differential diagnosis called palisaded neutrophilic granulomatous dermatitis (PNGD). This disease, with a broad spectrum of clinical lesions and histological
patterns, has been described mostly in patients with underlying RA [10,11]. Clinical lesions include: papules, nodules, annular lesions, linear bands or urticarial lesions. They commonly occur on the extensor surfaces of the extremities but may also affect other parts of the body.
The histology may also disclose variable changes ranging from urticaria like infiltrates to leucocytoclastic vasculitis and granulomas annulare [10]. SPA has never been associated to date with GA or PNGD, which may
explain the lack of "drug-induced GA" in the present series.
We believe that most of the reported cases of so-called “anti-TNF induced GA” might be PNGD associated with RA [10,11]. In two cases, anti-TNF was withdrawn with efficiency. Rechallenge of the therapy may give the final
answer, whether or not the drug was implicated in theses eruptions.
References
1. Voulgari PV, Markatseli TE, Exarchou SA, Zioga A, Drosos AA. Granuloma annulare induced by anti-tumor necrosis factor therapy. Ann Rheum Dis 2007 Aug 29.
2. Paul M, Cribier B, Heid E, Grosshans E, Lipsker D. Generalized granuloma annulare and drug-induced immunodeficiency. Ann Dermatol Venereol 2004;131:1051-1054.
3. Flendrie M, Vissers WH, Creemers MC, de Jong EM, van de Kerkhof PC, van Riel PL. Dermatological conditions during TNF-alpha-blocking therapy in patients with rheumatoid arthritis: a prospective study. Arthritis Res
Ther 2005;7(3):R666-676.
4. Devos SA, Van Den Bossche N, De Vos M, Naeyaert JM. Adverse skin reactions to anti-TNF-alpha monoclonal antibody therapy. Dermatology 2003;206(4):388-390.
5. Hertl MS, Haendle I, Schuler G, Hertl M. Rapid improvement of recalcitrant disseminated granuloma annulare upon treatment with the tumour necrosis factor-alpha inhibitor, infliximab. Br J Dermatol 2005;152:552-555.
6. Begaud B, Evreux JC, Jouglard J, Lagier G. Imputation of the unexpected or toxic effects of drugs. Actualization of the method used in France. Thérapie 1985;40:111-118.
7. Kluger N, Moguelet P, Chaslin-Ferbus D, Khosrotehrani K, Aractingi S. Generalized interstitial granuloma annulare induced by pegylated interferon-alpha. Dermatology 2006;213:248-249.
8. Lebas D, Staumont-Sallé D, Solau-Gervais E, Flipo RM, Delaporte E. Cutaneous manifestations during treatment with TNF-alpha blockers: 11 cases. Ann Dermatol Venereol 2007;134:337-342.
9. Goerttler E, Kutzner H, Peter HH, Requena L. Methotrexate-induced papular eruption in patients with rheumatic diseases: a distinctive adverse cutaneous reaction produced by methotrexate in patients with
collagen vascular diseases. J Am Acad Dermatol 1999;40:702-707.
10. Sangueza OP, Caudell MD, Mengesha YM, Davis LS, Barnes CJ, Griffin JE, Fleischer AB, Jorizzo JL. Palisaded neutrophilic granulomatous dermatitis in rheumatoid arthritis. J Am Acad Dermatol 2002;47:251-257.
11. Bremner R, Simpson E, White CR, Morrison L, Deodhar A. Palisaded neutrophilic and granulomatous dermatitis: an unusual cutaneous manifestation of immune-mediated disorders. Semin Arthritis Rheum 2004;34:610-616.
In a study recently published in Annals of the Rheumatic Diseases involving 79 ankylosing spondylitis (AS) patients and 132 unrelated healthy blood donors, Zhu and colleagues report association of a TNFA SNP, rs1799724, with AS [1]. I have many concerns with this paper and its conclusions.
The authors state that only SNP rs1799724 is not in Hardy-Weinberg equilibrium. However, inspection of the ge...
In a study recently published in Annals of the Rheumatic Diseases involving 79 ankylosing spondylitis (AS) patients and 132 unrelated healthy blood donors, Zhu and colleagues report association of a TNFA SNP, rs1799724, with AS [1]. I have many concerns with this paper and its conclusions.
The authors state that only SNP rs1799724 is not in Hardy-Weinberg equilibrium. However, inspection of the genotypes presented in table 2 reveals that rs2284178 is also not in Hardy-Weinberg equilibrium in the controls (P=1.3x10-5). This can occur because of hidden relationship between genotyped individuals, disease-association or selection, but most commonly occurs because of genotyping error.
The two SNPs not in Hardy-Weinberg equilibrium are critical to the findings of the study. The authors suggest that as no linkage disequilibrium was observed between HLA-B27 and rs2284178, which lies between rs1799724 and HLA-B27, or between rs2284178 and rs1799724, that the association of rs1799724 with AS is not due to linkage disequilibrium with HLA-B27. There are three concerns regarding this assertion.
Firstly, the SNP involved, rs2284178, is itself not in Hardy-Weinberg equilibrium, raising the concerns outlined above.
Secondly, the argument assumes that linkage disequilibrium is continuous, which is known not to be the case. It is quite possible for strong linkage disequilibrium to exist between to markers, where an
intervening marker shows no linkage disequilibrium with either. For example, using the HapMap data for Chinese (build 35, www.hapmap.org), marker rs2284178 is not in linkage disequilibrium with either markers rs11752262 (r2=0.06) or rs11757602 (r2=0.017) which lie on either side of rs2284178. However, rs11752262 and rs11757602 are themselves in quite strong linkage disequilibrium (r2=1).
Lastly, to calculate Lewontin’s D’ statistic (used by Zhu et al) requires that the marker genotypes are known, rather than simply carriage of an allele, to determine the haplotypic phase of the alleles of interest [2]. Although it is not absolutely clear, the HLA-B27 genotyping method
employed by Zhu and colleagues for the control samples does not appear to provide the requisite data [3], appearing only to determine if samples carry HLA-B27 rather than the HLA-B genotype i.e. it does not distinguish between HLA-B27 heterozygotes and homozygotes. It is also not clear, but likely, that the case genotyping is similarly limited. If so, then how did the authors calculate D’? Indeed the markedly different frequency of
rs1799724 in B27-positive and -negative AS cases (47.9% vs 62.5%) suggests significant linkage disequilibrium between HLA-B27 and this SNP. However, as only 9 HLA-B27 positive cases were studied, the sample size is inadequate to make any meaningful conclusion about linkage disequilibrium
with HLA-B27.
The association findings are also reported uncorrected for the number of SNPs studied, and none of the SNPs remain associated following appropriate Bonferroni-correction.
Whilst there is strong evidence of the existence on non-B27 MHC genes in AS, notably of HLA-B60 [4-6], but also probably others [7], identification of those genes will require much larger studies with complete control for linkage disequilibrium with HLA-B27. Linkage
disequilibrium across the MHC is extreme and complex [8, 9], and failure to control for it properly leads to an inability to differentiate true association from linkage disequilibrium.
References
[1] Zhu X, Wang Y, Sun L, Song Y, Sun F, Tang L, et al. A novel gene variation of TNFalpha associated with ankylosing spondylitis: a reconfirmed study. Ann Rheum Dis 2007;66:1419-22.
[2] Lewontin RC. The Interaction of Selection and Linkage. I. General Considerations; Heterotic Models. Genetics 1964;49(1):49-67.
[3] Steffens-Nakken HM, Zwart G, van den Bergh FA. Validation of allele-
specific polymerase chain reaction for DNA typing of HLA-B27. Clin Chem 1995;41(5):687-92.
[4] Robinson WP, van der Linden SM, Khan MA, Rentsch HU, Cats A, Russell A, et al. HLA-Bw60 increases susceptibility to ankylosing spondylitis in HLA-B27+ patients. Arthritis Rheum 1989;32:1135-41.
[5] Wei JC, Tsai WC, Lin HS, Tsai CY, Chou CT. HLA-B60 and B61 are strongly associated with ankylosing spondylitis in HLA-B27-negative Taiwan Chinese patients. Rheumatology (Oxford) 2004;43:839-42.
[6] Brown MA, Pile KD, Kennedy LG, Calin A, Darke C, Bell J, et al. HLA class I associations of ankylosing spondylitis in the white population in the United Kingdom. Ann Rheum Dis 1996;55(4):268-70.
[7] Sims AM, Barnardo M, Herzberg I, Bradbury L, Calin A, Wordsworth BP, et al. Non-B27 MHC associations of ankylosing spondylitis. Genes Immun 2007;8(2):115-23.
[8] de Bakker PI, McVean G, Sabeti PC, Miretti MM, Green T, Marchini J, et al. A high-resolution HLA and SNP haplotype map for disease association studies in the extended human MHC. Nat Genet 2006;38(10):1166-72.
[9] Miretti MM, Walsh EC, Ke X, Delgado M, Griffiths M, Hunt S, et al. A high-resolution linkage-disequilibrium map of the human major histocompatibility complex and first generation of tag single-nucleotide polymorphisms. Am J Hum Genet 2005;76:634-46.
We do thank Maarten Boers for his complement. We did not employ the composite indices DAS or DAS28 to report clinical efficacy of the two strategy groups in our study, because we had used joint counts not
including shoulder joints, which precludes calculating these indices. In our view, shoulder joints are seldom involved in early rheumatoid arthritis and are in addition difficult to score for swelling....
We do thank Maarten Boers for his complement. We did not employ the composite indices DAS or DAS28 to report clinical efficacy of the two strategy groups in our study, because we had used joint counts not
including shoulder joints, which precludes calculating these indices. In our view, shoulder joints are seldom involved in early rheumatoid arthritis and are in addition difficult to score for swelling.
For remission and minimal disease activity, the DAS and DAS28 have been investigated; and were found to underestimate disease activity,(1,2) especially the DAS28.(3) We therefore explained clearly in our report why we used our specific definition of remission. We are aware of ongoing processes to improve the definition and criteria of remission, and perhapswe will be able in the near future to report our present results using that new definition.
References
1. Khanna D, Oh M, Furst DE, Ranganath V, Gold RH, Sharp JT, et al. Evaluation of the preliminary definitions of minimal disease activity and remission in an early seropositive rheumatoid arthritis cohort. Arthritis
Rheum 2007;57:440-7.
2. Smolen JS, Aletaha D, Koeller M, Weisman MH, Emery P. New therapies for treatment of rheumatoid arthritis. Lancet 2007.
3. Landewe R, van der HD, van der LS, Boers M. Twenty-eight-joint counts invalidate the DAS28 remission definition owing to the omission of the lower extremity joints: a comparison with the original DAS remission.
Ann Rheum Dis 2006;65:637-41.
We have read the comments of Zsolt Balogh on our cross sectional study of cytokine profiles in JIA (1). Indeed a good point arises that patient selection in these kinds of studies are critical. In this case however, a printing error is the cause of the confusion.
During the review process of this paper several brief communications took place with the editing office due to printing errors in table 1. In...
We have read the comments of Zsolt Balogh on our cross sectional study of cytokine profiles in JIA (1). Indeed a good point arises that patient selection in these kinds of studies are critical. In this case however, a printing error is the cause of the confusion.
During the review process of this paper several brief communications took place with the editing office due to printing errors in table 1. In the final print proofs table 1 was correct.
However now we noticed that patient characteristics of poly articular and systemic onset JIA again were switched in the final published version.
The numbers are correct in the methods section (20 poly articular JIA of which 3 are RF positive, and 15 systemic onset JIA patients) as well as the results and discussion.
We agree it is interesting to study the differences between RF positive and RF negative poly arthritis. However due to low numbers present (n=3) in this study, the RF positive patients were included in the polyarthritis
group.
Reference List
1. de Jager W., Hoppenreijs E.P., Wulffraat N.M., Wedderburn L.R., Kuis W., and Prakken B.J. Blood and synovial fluid cytokine signatures in patients with juvenile idiopathic arthritis: a cross-sectional study. Ann Rheum Dis 2007;66:589-598.
I read with interest the importance you place in the role of psoriasis support groups in assisting patient understanding of treatment-and compliance. Our organisation maintains a very large database of patient groups worldwide.
In a recent exercise in October 2007, we updated details of psoriasisself-help groups in the UK, but were surprised to discover that many had shutdown, or been disbanded te...
I read with interest the importance you place in the role of psoriasis support groups in assisting patient understanding of treatment-and compliance. Our organisation maintains a very large database of patient groups worldwide.
In a recent exercise in October 2007, we updated details of psoriasisself-help groups in the UK, but were surprised to discover that many had shutdown, or been disbanded temporarily.
As you are aware the support groups are primarily financed by hospital dermatological departments. One nurse reported to us that the self-group was closed due to recent cutbacks incurred by her hospital.
Another psoriasis patient reported low attendance figures as the reason, suggesting the emergence of internet chat-rooms may have played a role in the diminishing status of self-help groups. I wonder if any of your readers in other countries could report a similar experience and how the
problem may be overcome?
We read with expectations the study on cytokine signatures in patients with juvenile idiopathic arthritis (JIA) [1]. The widespread investigation of cytokines and chemokines, the smart and spectacular presentation of the results (especially Fig. 2.) are impressive. Even so,
we must make a remark that the alignment of the patients has not been done the most fortunate way.
We read with expectations the study on cytokine signatures in patients with juvenile idiopathic arthritis (JIA) [1]. The widespread investigation of cytokines and chemokines, the smart and spectacular presentation of the results (especially Fig. 2.) are impressive. Even so,
we must make a remark that the alignment of the patients has not been done the most fortunate way.
As the authors state, the patients were classified according to the International League Against Rheumatism (ILAR) criteria, referring to the first revision (Durban, 1997 [2]) and the second revision (Edmonton, 2001 [3]) of the 7 category of JIA (first published in 1995 [4]). The primary aims of these ILAR proposals for classification were „to delineate, for research purposes, relatively homogenous, mutually exclusive categories of JIA” [3]. It is hardly possible to follow the instructions of both
revisions at the same time as there are a lot of differences between them. (In one of our studies, where we classified 445 children with JIA according firstly to the Durban than to the Edmonton criteria, the classification of 57 patiens was affected by these differences.) We do not
think that the second revision in Edmonton was the final one. We tend to agree with other authors, who suggest, that history of psoriasis in a first-degree relative as an exclusion criterion for all the categories but the psoriatic arthritis should not be taken that seriously [5,6], or that „arthritis in an HLA-B27 positive male beginning after the 6th birthday” should not be an exclusion criterion for psoriatic arthritis. The importance of the antinuclear antibodies (ANA) and the difficulties of distinction between rheumatoid factor negative polyarthritis and extended oligoarthritis may lead to the union and repartition of these groups, as
Ravelli A. et al. suggest [7].
However, the ILAR categories are rather homogeneous and very well definied which enables their comparison. As rheumatoid arthritis, psoriatic arthritis, spondyloarthropathies are separate entities in adulthood, they should not be jumbled up in childhood either. Obviously, systemic arthritis is easy to detach, nevertheless, confusing the other JIA classes can be an explanation for the general conclusion that there was no relevant difference in the cytokine profiles of the oligoarticular and the polyarticular group. It is worth to mention that rheumatoid factor positive polyarthritis was not represented at all, hence it is hard to confirm that there is a contrast between JIA and adult rheumatoid
arthritis regarding the cytokine pattern. (On the other hand, 3 out of 20 systemic arthritis patient were rheumatoid factor positive, but this is an exclusion criterion for systemic arthritis.)
As the new technology of multiplex immunoassay offers a special opportunity for mapping mediators, hereby for discovering novel therapeutic agents, it would be fairly beneficial to continue with this kind of examinations – with accurate patient selection for the more convincing results.
References
1. de Jager W, Hoppenreijs,Esther P A H., Wulffraat NM, Wedderburn LR, Kuis W, Prakken BJ. Blood and synovial fluid cytokine signatures in patients with juvenile idiopathic arthritis: a cross-sectional study. Ann of the Rheum Dis 2007;66(5):589-598.
2. Petty RE, Southwood TR, Baum J, Bhettay E, Glass DN, Manners P, et al. Revision of the proposed classification criteria for juvenile idiopathic arthritis: Durban, 1997. Journal of Rheumatology 1998;25(10):1991-1994.
3. Petty RE, Southwood TR, Manners P, Baum J, Glass DN, Goldenberg J, et al. International League of Associations for Rheumatology classification of juvenile idiopathic arthritis: second revision, Edmonton, 2001. J Rheum 2004;31(2):390-392.
4. Fink CW, Baum J, Bhettay E, Goldenberg J, He X, Maldonado-Coco J, et al. Proposal for the development of classification criteria for idiopathicarthritides of childhood. J Rheum 1995;22(8):1566-1569.
5. Berntson L, Fasth A, Andersson-Gare B, Herlin T, Kristinsson J, Lahdenne P, et al. The influence of heredity for psoriasis on the ILAR classification of juvenile idiopathic arthritis. J Rheum 2002;29(11):2454-2458.
6. Manners P, Lesslie J, Speldewinde D, Tunbridge D. Classification of juvenile idiopathic arthritis: should family history be included in the criteria? J Rheum 2003;30(8):1857-1863.
7. Ravelli A, Felici E, Magni-Manzoni S, Pistorio A, Novarini C, Bozzola E, et al. Patients with antinuclear antibody-positive juvenile idiopathic arthritis constitute a homogeneous subgroup irrespective of the course of
joint disease. Arthritis Rheum 2005;52(3):826-832.
Dear Editor, Even though the data may be difficult to obtain, it is important that sleep apnea be identified as a gout comorbidity. It actually is a causal factor for gout, and it is known to be strongly associated with all the other gout comorbidities listed in the above article. The hypoxic episodes of sleep apnea have two effects which can lead to a gout attack in short order. The first effect is the catabolic process initi...
Dear Editor, Even though the data may be difficult to obtain, it is important that sleep apnea be identified as a gout comorbidity. It actually is a causal factor for gout, and it is known to be strongly associated with all the other gout comorbidities listed in the above article. The hypoxic episodes of sleep apnea have two effects which can lead to a gout attack in short order. The first effect is the catabolic process initiated in the cells, which culminates irreversibly in their generation of excess uric acid. The second effect is hypercapnia and acidosis which increases the likelihood of serum uric acid precipitation in the form of monosodium urate crystals, which cause a gout attack when they are deposited in synovial fluid. These two effects were both described in pulmonology journal literature as early as 1987. [1,2,3]
Sleep apnea is far more prevalent than gout, and far more dangerous. Those who are subject to gout attacks have an unignorable warning of sleep apnea which, if they and/or their doctors knew what it meant, could lead
to the diagnosis and treatment of their sleep apnea before its long-term life-threatening consequences were to begin to develop. The resolution of their sleep apnea would probably cure their gout as well, as it did for me.
The question now is what the physicians who treat gout patients should do after reading this correspondence. My hope is that they will adjust their protocols to learn to effectively screen their gout patients for sleep apnea, and then refer those that they suspect of having it for
further diagnosis and treatment. My own primary care physician has been doing that with results showing very high sensitivity. When that becomes common practice, patients will be better served, and the epidemiological
data on this missing gout comorbidity will be readily obtainable.
References
[1] Hasday JD, Grum CM. "Nocturnal Increase of Urinary Uric Acid:Creatine Ratio: a Biological Correlate of Sleep-Associated Hypoxemia," American Review of Respiratory Diseases 1987;135:534-38.
[2] Saito, H., et al, "Tissue Hypoxia in Sleep Apnea Syndrome as Assessed by Uric Acid and Adenosine," Chest 2002;121 (55):1686-1694.
[3] Ruiz Garcia, A., et al, "Blood Uric Acid Levels in Patients with Sleep-Disordered Breathing." Archivos de Bronconeumologia 2006;42 (10):492-500.
Dear Editor, Verstappen et al are to be congratulated on their 'CAMERA' strategy trial. However, they have chosen not to report the results expressed in the Disease Activity Score (DAS or DAS28). In addition, the international RA core set agreed to in 1992 was not fully applied because physician global assessment was not measured. This is a pity because it precludes
calculation of ACR reponse. The lack of both DAS and ACR re...
Dear Editor, Verstappen et al are to be congratulated on their 'CAMERA' strategy trial. However, they have chosen not to report the results expressed in the Disease Activity Score (DAS or DAS28). In addition, the international RA core set agreed to in 1992 was not fully applied because physician global assessment was not measured. This is a pity because it precludes
calculation of ACR reponse. The lack of both DAS and ACR response in the report hinders comparisons between this and other trials, including systematic reviews, and in my view unnecessarily downgrades the value of this report.
Finally, the key finding of substantial remission rates is hard to interpret because the measure of remission chosen is nonstandard and unvalidated.
I urge the authors to at least report the DAS/DAS28 results, because they have the data available. They should also report the proportion of patients in DAS-remission or in minimal disease activity state (DAS28 <2.85).
Sincerely,
Maarten Boers
Dear Editor, It is with great interest that I read the article "Effective treatment of a colchicine-resistant familial Mediterranean fever patient with anakinra" by Kuijk et al. Previously, our group reported on the
successful treatment of FMF with secondary AA amyloid with the monoclonal anti-TNF agent Infliximab(reference 1). In this case, there was an additional benefit of complete resolution of proteinuria as well as resol...
Dear Editor, It is with great interest that I read the article "Effective treatment of a colchicine-resistant familial Mediterranean fever patient with anakinra" by Kuijk et al. Previously, our group reported on the
successful treatment of FMF with secondary AA amyloid with the monoclonal anti-TNF agent Infliximab(reference 1). In this case, there was an additional benefit of complete resolution of proteinuria as well as resolution of fevers and joint pains. This article confirms that further
investigation into FMF pathophysiology as it is related to the role of TNF and other cytokines is neccessary to decide which biological option could be of increased benefit. Controlled and blinded studies based on Genetic
subsets in FMF with assessment of potential SNP's may give us a better road map in choosing a treatment option.
Reference
Metyas S, Arkfeld DG, Forrester DM, Ehresmann GR. Infliximab Treatment of Familiar Mediterranean Fever and its Effect on Secondary AA
Amyloidosis. J Clin Rheumatol 2004;10(3):134-137.
Dear Editor,
It is with great interest that I read the study entitled "A novel gene variation of TNF associated with ankylosing spondylitis: a reconfirmed study" by Zhu et al(1). In treating AS in Los Angeles, California, I see many Hispanic patients especially from Mexican descent. This is very different from the Chinese population presented in this article and may explain some of the difficulties in looking for SNP'...
Dear Editor, We read with great interest the article by Voulgari et al, recently published in the Journal, reporting a series of patients with Rheumatoid arthritis (RA) who developed Granuloma annulare (GA) under anti-TNF therapy [1]. We would like to bring attention to some key points and shed light on a specific differential diagnoses associated with RA the authors did not discuss.
GA is a benign, asymptomatic, sel...
Dear Editor,
In a study recently published in Annals of the Rheumatic Diseases involving 79 ankylosing spondylitis (AS) patients and 132 unrelated healthy blood donors, Zhu and colleagues report association of a TNFA SNP, rs1799724, with AS [1]. I have many concerns with this paper and its conclusions.
The authors state that only SNP rs1799724 is not in Hardy-Weinberg equilibrium. However, inspection of the ge...
Dear Editor,
We do thank Maarten Boers for his complement. We did not employ the composite indices DAS or DAS28 to report clinical efficacy of the two strategy groups in our study, because we had used joint counts not including shoulder joints, which precludes calculating these indices. In our view, shoulder joints are seldom involved in early rheumatoid arthritis and are in addition difficult to score for swelling....
Dear Editor,
We have read the comments of Zsolt Balogh on our cross sectional study of cytokine profiles in JIA (1). Indeed a good point arises that patient selection in these kinds of studies are critical. In this case however, a printing error is the cause of the confusion. During the review process of this paper several brief communications took place with the editing office due to printing errors in table 1. In...
Dear Editor,
I read with interest the importance you place in the role of psoriasis support groups in assisting patient understanding of treatment-and compliance. Our organisation maintains a very large database of patient groups worldwide.
In a recent exercise in October 2007, we updated details of psoriasisself-help groups in the UK, but were surprised to discover that many had shutdown, or been disbanded te...
Dear Editor,
We read with expectations the study on cytokine signatures in patients with juvenile idiopathic arthritis (JIA) [1]. The widespread investigation of cytokines and chemokines, the smart and spectacular presentation of the results (especially Fig. 2.) are impressive. Even so, we must make a remark that the alignment of the patients has not been done the most fortunate way.
As the authors state,...
Dear Editor, Even though the data may be difficult to obtain, it is important that sleep apnea be identified as a gout comorbidity. It actually is a causal factor for gout, and it is known to be strongly associated with all the other gout comorbidities listed in the above article. The hypoxic episodes of sleep apnea have two effects which can lead to a gout attack in short order. The first effect is the catabolic process initi...
Dear Editor, Verstappen et al are to be congratulated on their 'CAMERA' strategy trial. However, they have chosen not to report the results expressed in the Disease Activity Score (DAS or DAS28). In addition, the international RA core set agreed to in 1992 was not fully applied because physician global assessment was not measured. This is a pity because it precludes calculation of ACR reponse. The lack of both DAS and ACR re...
Dear Editor, It is with great interest that I read the article "Effective treatment of a colchicine-resistant familial Mediterranean fever patient with anakinra" by Kuijk et al. Previously, our group reported on the successful treatment of FMF with secondary AA amyloid with the monoclonal anti-TNF agent Infliximab(reference 1). In this case, there was an additional benefit of complete resolution of proteinuria as well as resol...
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