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Letters

To the Editor:

I read with interest the recent editorial, "The Place of Juvenile Onset Spondyloarthropathy in the Durban 1997 ILAR Classification Criteria of JIA"¹. The Journal previously published proposals for the development of classification criteria for the idiopathic arthritides of childhood in 1995 (Santiago)², and the revision of proposals for classification of juvenile idiopathic arthritis (JIA) from Durban in 1998³.

In the Durban (1997) classification of JIA there are, as summarized in the editorial, 7 subgroups that may be clinically identifiable after 6 months of disease: (1) Systemic arthritis; (2) oligoarthritis; (3) polyarthritis (rheumatoid factor negative); (4) polyarthritis (rheumatoid factor positive); (5) enthesitis related arthritis; (6) psoriatic arthritis; and (7) other arthritis.

Within the discussion the term JIA is used¹, and in addition in the original article defining the Durban criteria³, there is specific reference to "juvenile rheumatoid arthritis" and "juvenile chronic arthritis" as being terms that were major sources of disagreement in the past and which were therefore discarded in favor of the umbrella term "juvenile idiopathic arthritis." The signatories to this revision included respected practitioners in the field of pediatric rheumatology from Canada, the UK, the USA, South Africa, Australia, South America, Central America, and Europe (France). It is accepted that this classification is by no means perfect and does present difficulties in some areas such as the definitive diagnosis of psoriatic arthritis.

In the same issue of The Journal, there is an article⁴ entitled "Preliminary Definition of Disease Flare in Juvenile Rheumatoid Arthritis." The first sentence reads, "Juvenile rheumatoid arthritis (JRA) is a group of inflammatory autoimmune conditions of childhood...." There are 3 key references (numbers 3,4, and 5) that use the term "juvenile rheumatoid arthritis" or "JRA."

The next article in that issue is entitled "Osteopenia in Adults with a History of Juvenile Rheumatoid Arthritis"⁵, and another is "Differences in the Profiles of Circulating Levels of sTNFR and IL-1 Receptor Antagonist Reflect the Heterogeneity of the Subgroups of Juvenile Rheumatoid Arthritis"⁶.

It is disappointing that on page 1079 there is yet another article, "Higher Response rate in the Phase I/II Study of Meloxicam in Juvenile Rheumatoid Arthritis"⁷, which includes among its authors the first author of the Editorial on JIA.

There are therefore no less than 4 articles in that May 2002 edition of The Journal that use the term "juvenile rheumatoid arthritis" as a generic term in the title.

Given that The Journal has seen fit not only to publish the original and revised classification criteria^2,3, and in addition an Editorial in which aspects of the classification are discussed and where the generic term used is clearly "juvenile idiopathic arthritis," it seems inconsistent to include 4 other articles in the same edition that refer to juvenile arthritis in all its forms and allow them to be described as "juvenile rheumatoid arthritis."

Surely the time has come for an international publication of the standing and reputation of The Journal of Rheumatology to take an initiative and a lead in promoting the unification of the concepts and terminology of "juvenile idiopathic arthritis" and to clarify and refine the use of the term "juvenile rheumatoid arthritis."

To many practising pediatric rheumatologists, "juvenile rheumatoid arthritis" refers only to polyarticular arthritis that is rheumatoid factor positive, i.e., group 4 of the revised Durban classification³, and that typically presents in girls in their second decade of life and then evolves into an adult form of RA. In many respects this subgroup could be redefined as "true JRA." This subgroup 4 is further refined, as are all the groups in the Durban classification, in terms of definition, exclusions, and descriptors.

The Journal is in a prime position through the editorial process to effect changes in the use of the term "juvenile rheumatoid arthritis" as a generic term for what is known worldwide as "juvenile idiopathic arthritis" or "juvenile arthritis" or what used to be termed "juvenile chronic arthritis."

While there may be other nonmedical factors that contribute to the continued use of "rheumatoid" as the generic term in the USA, these surely should not stand in the way of standardization.

I would therefore suggest that the Editorial Board should insist that the term "juvenile rheumatoid arthritis" should not be acceptable as a generic term for publications relating to arthritis in children in general.

Many pediatric rheumatologists are of the opinion that the term "juvenile rheumatoid arthritis" should be avoided for the following reasons: (1) The term "rheumatoid" is very evocative and for many parents the use of this term may immediately conjure up a spectre of a very severely affected adult with advanced severe disease. (2) It is inaccurate in terms of the Durban classification. (3) There is some indication that the use of the term "rheumatoid" in insurance applications may result in loading of premiums even though the adult may merely have had oligoarthritis, which was managed with one intraarticular injection that effected a significant improvement, and there was no further disease activity.

I do not understand therefore how the Editorial Board of The Journal can allow this inconsistency to continue to permeate its pages. However, it seems as if old conventions are ingrained, as the publicity for the next eagerly anticipated major international pediatric rheumatology conference, "Pediatric Rheumatology 2003: Park City and Beyond," which is promoted by the American Academy of Pediatrics, Section on Rheumatology, is using the term "juvenile rheumatoid arthritis"⁸.

JOHN A. SILLS, MA, MB, BChir, FRCP, FRCPCH, DCH, Consultant Paediatric Rheumatologist, Royal Liverpool Children's Hospital, Liverpool L12 2AP, UK. E-mail: John.sills@rlch-tr.nwest.nhs.uk

REFERENCES

1. Burgos-Vargas R, Rudwaleit M, Sieper J. The place of juvenile onset spondyloarthropathies in the Durban 1997 ILAR Classification Criteria of juvenile idiopathic arthritis. J Rheumatol 2002;29:869-4.

2. Fink CM and the Task Force for Classification Criteria. Proposal for the development of classification criteria for idiopathic arthritides of childhood. J Rheumatol 1995;22:1566-9.

3. Petty RE, Southwood TR, Baum J, et al. Revision of the proposed classification criteria for juvenile idiopathic arthritis: Durban, 1997. J Rheumatol 1998;25:1991-4.

4. Brunner HI, Lovell DJ, Finck BK, Giannini EH. Preliminary definition of disease flare in juvenile rheumatoid arthritis. J Rheumatol 2002;29:1058-64.

5. French AR, Mason T, Nelson AM, et al. Osteopenia in adults with a history of juvenile rheumatoid arthritis. J Rheumatol 2002;29:1065-70.

6. Muzaffer MA, Dayer J-M, Feldman BM, et al. Differences in the profiles of circulating levels of soluble tumor necrosis factor receptors and interleukin 1 receptor antagonist reflect the hetereogeneity of the subgroups of juvenile rheumatoid arthritis. J Rheumatol 2002;29:1071-8.

7. Foeldvari I, Burgos-Vargas R, Thon A, Tuerck D. High response rate in the phase I/II study of meloxicam in juvenile rheumatoid arthritis. J Rheumatol 2002;29:1079-83.

8. American Academy of Pediatrics. Pediatric Rheumatology 2003: Park City and Beyond. [Cited January 24, 2003] www.aap.org/profed/03rheum.pdf

Neck and Upper Limb Pain

To the Editor:

In a recent interesting study Van der Windt, et al¹ described a relationship between extent of pain in the neck-upper limb area and psychological distress. Patients with generalized pain had significantly higher scores, particularly for depression, on the Hospital Anxiety and Depression Scale¹ versus subjects with localized pain. At issue then is why subjects with generalized pain should be more depressed than subjects with localized pain?

Part of the answer to this problem relates to findings of 2 recent reviews on the relationship between pain and depression. In the first evidence based structured review (not a metaanalysis), Fishbain, et al² showed that: (1) depression is more common in patients with chronic pain than controls; (2) the preponderance of the evidence indicated that depression followed the development of chronic pain; (3) however, depression predisposition predisposed to the development of depression following the development of chronic pain; and (4) most important, there was a relationship between the perceived severity and frequency of pain and development of depression. This last study was recently supported by a metaanalysis performed on studies utilizing patients with rheumatoid arthritis (RA) who were depressed and had pain³ . Here, effect sizes for depression were shown to vary in a linear manner in proportion to the effect size for pain. The authors concluded that depression is more common in patients with RA than in healthy individuals, due in part to the levels of pain experienced³. Thus pain severity can be related to the development of depression^2,3. It is to be noted that Windt, et al¹ found that their generalized pain subjects had significantly greater levels of pain than those with localized pain¹. Thus, these findings would indirectly support the conclusions of the above reviews^2,3. In addition, it is to be noted that 2 previous studies^4,5 have also found an association between pains (multiple pains) and depression.

DAVID A. FISHBAIN, MD, FAPA, Professor of Psychiatry, Neurosurgery and Anesthesiology, University of Miami School of Medicine, and University of Miami Comprehensive Pain and Rehabilitation Center, Miami, Florida, USA.

REFERENCES

1. Van der Windt D, Croft P, Penninx B. Neck and upper limb pain: more pain is associated with psychological distress and consultation rate in primary care. J Rheumatol 2002;29:564-9. 2.

2. Fishbain DA, Cutler R, Rosomoff HL, Rosomoff RS. Chronic pain associated depression: antecedent or consequence of chronic pain? A review. Clin J Pain 1997;13:116-37.

3. Dickens C, McGowan L, Clark-Carter B, Creed F. Depression in rheumatoid arthritis: a systematic review of the literature with a meta-analysis. Psychosom Med 2000;64:52-60.

4. Benjamin S, Morris S, McBeth J, et al. The associations between chronic widespread pain and mental disorder. Arthritis Rheum 2000;43:561-7.

5. Dworkin SF, Von Korff M, LeResche L. Multiple pains and psychiatric disturbance: An epidemiologic investigation. Arch Gen Psychiatry 1990;47:239-44.

Fluvoxamine Therapy for Fibromyalgia

To the Editor:

Pain in patients with fibromyalgia (FM) is difficult to treat, and no single intervention has been universally accepted. Fluvoxamine (FL), a selective serotonin reuptake inhibitor (SSRI), has been used for patients with depressive illness and obsessive-compulsive disorders¹. Since patients with FM often have mild depression/depressive state² or obsessive-compulsive personality disorders, it is reasonable to study FL as a treatment for FM. We describe for the first time a beneficial result of FL therapy for pain in patients with FM.

Sixty-eight Japanese patients with FM were enrolled between 1991 and 2001; all were diagnosed by the American College of Rheumatology 1990 criteria. These patients were divided into 2 groups: 30 patients who were treated with amitriptyline (AM) (mean dose 20 mg/day) and 38 patients with FL (mean dose 25 mg/day). Effectiveness for pain was evaluated by a visual analog scale (VAS) 4 weeks after starting medication. AM or FL was evaluated as effective only when a patient reported that pain decreased by ³ 50%.

Twelve (40%) patients treated with AM and 6 (16%) treated with FL dropped out of the study because of side effects or other reasons. For the remaining respective 18 and 32 patients, mean age, male to female ratio, ratio of primary to secondary FM, disease duration, and number of tender points were not significantly different (Table 1). Side effects in the AM group were drowsiness in 4, and epigastralgia, hypersomnia, dizziness, fatigue, and thirst in one patient each. Adverse effects in the FL group were nausea in 6, and palpitation, constipation, and epigastralgia in one patient each.

Table 1. Mean (standard deviation) respiratory findings at start and after 6 months of treatment in 11 patients with SSc.

Nine (50%) patients of the AM group and 13 (41%) patients of the FL group in the respective groups reported effective pain relief at 4 weeks after medication, and these frequencies did not differ statistically (chi square = 0.411, p = 0.5647). The actual VAS values in each patient and in each group are shown in Figure 1.

Efficacy of AM for pain in FM patients has been established through multiple double-blind controlled studies³. Since FL in relatively low doses was effective for pain in 41% of FM patients, a frequency not different from AM-treated patients, it is likely that FL will be useful for some patients with FM.

MASAHIKO NISHIKAI, MD; KUMIKO AKIYA, MD, Department of Internal Medicine, National Tokyo Medical Center, 2-5-1 Higashigaoka, Meguro-ku, Tokyo 152-8902, Japan.

REFERENCES

1. Hollander E. Treatment of obsessive-compulsive spectrum disorders with SSRIs. Br J Psychiatry 1998;173:7-12.

2. Nishikai M. Fibromyalgia in Japanese. J Rheumatol 1992;19:110-4.

3. Carette S, McCain GA, Bell DA, et al. Evaluation of amitriptyline in primary fibrositis. A double-blind, placebo-controlled study. Arthritis Rheum 1986;29:655-9.

Salicin and Treatment of Rheumatic Diseases

To the Editor:

Buchanan and Kean¹ presented an account of "The Treatment of Acute Rheumatism by Salicin, by T.J. Maclagan — The Lancet, 1876." Unfortunately, the authors seemed to be unaware of the apothecaries' units of mass used in the report of Maclagan. Maclagan² administered to his patient 12 grains (equivalent to a total of 778 milligram) salicin every 3 hours, which Buchanan and Kean mistook for 12 gram (g) every 3 hours. Salicin is in vivo metabolized to salicylic acid³. The administration of 12 g of salicin would be equivalent to the administration of 5.8 g of salicylic acid every 3 hours, which would have led almost certainly to toxic symptoms. Buchanan and Kean¹ also mention a recently published trial⁴ in which, as they say, "salicin has proven better than placebo for low back pain". However, this trial was conducted with willow bark extract, which cannot be equated with salicin. Salicin is just one, although probably the best known, constituent of willow bark extract⁵. Pharmacokinetic studies indicate that the clinical efficacy of willow bark extract cannot be attributed to salicin alone³, since therapeutic doses of willow bark extract lead to much lower serum salicylate concentrations than observed after analgesic doses of synthetic salicylates.

IRMELA WAGNER, MPharm; LUTZ HEIDE, PhD, Pharmaceutical Institute, Tübingen University, Tübingen, Germany. E-mail: heide@uni-tuebingen.de

REFERENCES

1. Buchanan WW, Kean WF. The treatment of acute rheumatism by salicin, by T.J. Maclagan — The Lancet, 1876. J Rheumatol 2002;29:1321-3.

2. Maclagan TJ. The treatment of acute rheumatism by salicin. Lancet 1876;I:342-3.

3. Schmid B, Kotter I, Heide L. Pharmacokinetics of salicin after oral administration of a standardised willow bark extract. Eur J Clin Pharmacol 2001;57:387-91.

4. Chrubasik S, Eisenberg E, Balan E, Weinberger T, Luzzati R, Conradt C. Treatment of low back pain exacerbations with willow bark extract: a randomized double-blind study. Am J Med 2000;109:9-14.

5. European Scientific Cooperative on Phytotherapy. Salicis cortex - Willow bark. In: ESCOP Monographs on the Medicinal Uses of Plant Drugs; Fascicule 4. Exeter, UK: European Scientific Cooperative on Phytotherapy; 1997.