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.
We read with interest the editorial of Ritchlin and Tausk1 about psoriasiform lesions developed in patients receiving tumour necrosis factor (TNF)α antagonists. We would like to provide additional information. Indeed, we have recently reported 6 cases of psoriasiform lesions during TNFα antagonist therapy and described common characteristics of this paradoxical reaction with 40 cases already pu...
We read with interest the editorial of Ritchlin and Tausk1 about psoriasiform lesions developed in patients receiving tumour necrosis factor (TNF)α antagonists. We would like to provide additional information. Indeed, we have recently reported 6 cases of psoriasiform lesions during TNFα antagonist therapy and described common characteristics of this paradoxical reaction with 40 cases already published in literature.2
To date, with our series1 and recent reports3-7 pooled together, 55 cases have been described, including one case in a patient with juvenile idiopathic arthritis 2 years after initiation of etanercept.5
One of these cases concerns psoriatic arthritis.6 Interestingly, after an initial resolution of plaque psoriasis with infliximab, the
patient developed an inverse psoriasis (axillae and groin). In this context of pre-existing psoriasis, other cases have been reported: exacerbation of plaque psoriasis treated with infliximab8, development of a guttate psoriasis and a worsening of psoriasis in 2 patients with plaque psoriasis treated with etanercept9, exacerbation of underlying psoriasis (asymptomatic for many years) in 3 patients with rheumatoid arthritis (RA)receiving etanercept or infliximab10, exacerbation of palmoplantar pustulosis (PPP) and apparition of erythematopapular scaly lesions in a patient with RA treated with infliximab.11 These cases of exacerbation
thus highlight that a change in clinical aspects of psoriasis can occur.
We also observed this characteristic in a woman with spondylarthropathy with Crohn’s disease but without a personal history of psoriasis. She developed follicular skin lesions over the trunk, back, pubis, buttocks,
and scalp with infliximab, and then inflammatory lesions over the upper eyelids, neck, and inner thighs with etanercept.2
Finally, we could compare these cases with PPP relapse described recently in 2 out of 4 cases of SAPHO treated with infliximab without active cutaneous manifestations before its initiation12. The latter support the specificity of this cutaneous manifestation for TNF antagonist-induced psoriasis.
Moreover, it is difficult to establish the prevalence of the phenomenon according to diagnosis. Admittedly, RA is the most common etiology in the case reports. Nevertheless, the hypothesis that this is due to the fact that more patients receive TNF antagonists for this
condition could not explain the low representativeness of Crohn’s disease.
This last remark contributes to the mystery of this paradoxical reaction.
REFERENCES
1 Ritchlin C, Tausk F. A medical conundrum: onset of psoriasis in patients receiving anti-tumour necrosis factor agents. Ann Rheum Dis 2006;65:1541-44.
2 Cohen JD, Bournerias I, Buffard V, Paufler A, Chevalier X, Bagot M, et al. Psoriasis induced by tumor necrosis factor-α antagonist therapy: a case series. J Rheumatol 2006 Oct 1; [Epub ahead of print]
3 Sari I, Akar S, Birlik M, Sis B, Onen F, Akkoc N. Anti-tumor necrosis factor-α-induced psoriasis. J Rheumatol 2006;33:1411-4.
4 Aslanidis S, Pyrpasopoulou A, Leontsini M, Zamboulis C. Anti-TNF-α-induced psoriasis: Case report of an unusual adverse event. Int J Dermatol 2006;45:982-3.
5 Peek R, Scott-Jupp R, Strike H, Clinch J, Ramanan AV. Psoriasis after treatment of juvenile idiopathic arthritis with etanercept. Ann Rheum Dis 2006;65:1259.
6 Matthews C, Rogers S, FitzGerald O. Development of new-onset psoriasis while on anti-TNFα treatment. Ann Rheum Dis 2006;65:1529-30.
7 Pirard D, Arco D, Debrouckere V, Heenen M. Anti-tumor necrosis factor alpha-induced psoriasiform eruptions: Three further cases and current overview. Dermatol 2006;213:182-6.
8 Bovenschen HJ, Van De Kerkhof PC, Gerritsen WJ, Seyger MM. The role of lesional T cells in recalcitrant psoriasis during infliximab therapy. Eur J Dermatol 2005;15:454-8.
9 Gottlieb AB, Matheson RT, Lowe N, Krueger GG, Kang S, Goffe B, et al. A randomized trial of etanercept as monotherapy for psoriasis. Arch Dermatol 2003;139:1627-32.
10 Kary S, Worm M, Audring H, Husher D, Renelt M, Soerensen H, et al. New onset or exacerbation of psoriatic skin lesions in patients with definite rheumatoid arthritis receiving TNF-α antagonists. Ann Rheum
Dis 2006;65:405-7.
11 Michaëlsson G, Kajermo U, Michaëlsson A, Hagforsen E. Infliximab can precipitate as well as worsen palmoplantar pustulosis: possible linkage to the expression of tumour necrosis factor-α in the normal
palmar eccrine sweat duct? Br J Dermatol 2005;153:1243-4.
12 Massara A, Cavazzini PL, Trotta F. In SAPHO syndrome anti-TNF-alpha may induce persistent amelioration of osteoarticular complaints, but may exacerbate cutaneous manifestations. Rheumatol 2006;45:730-3.
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...
Dear Editor,
We read with interest the editorial of Ritchlin and Tausk1 about psoriasiform lesions developed in patients receiving tumour necrosis factor (TNF)α antagonists. We would like to provide additional information. Indeed, we have recently reported 6 cases of psoriasiform lesions during TNFα antagonist therapy and described common characteristics of this paradoxical reaction with 40 cases already pu...
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