SEARCH

SEARCH BY CITATION

Abstract

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. AUTHOR CONTRIBUTIONS
  8. Acknowledgements
  9. REFERENCES

Objective

To establish the frequency and predictors of minimal disease activity in psoriatic arthritis (PsA) and to investigate the prognostic ability of minimal disease activity criteria to predict future joint damage.

Methods

The study was conducted using an observational PsA cohort. Patients were classified as being in minimal disease activity if they fulfilled the criteria on consecutive visits for >12 months. Predictive factors for minimal disease activity and joint damage were investigated using regression models. Joint damage progression was based on clinically damaged joint counts.

Results

Of the 344 patients, 208 (60%) achieved minimal disease activity at ≥1 visit and 116 (34%) achieved minimal disease activity for ≥12 months (sustained minimal disease activity). The average duration of minimal disease activity was 28 months (range 12–48 months). Twelve patients (10%) experienced a flare of disease after 34 months in minimal disease activity. Low erythrocyte sedimentation rate (ESR) and oligoarthritis were predictors of achieving sustained minimal disease activity (P < 0.03). The mean change in damaged joint counts was 0.931 (range 0–12) in the sustained minimal disease activity group and 2.245 (range 0–17) in the controls (P < 0.001). Of the sustained minimal disease activity group, 69% showed no progression of joint damage, compared with 51% in the control group. Elevated ESR, baseline joint damage, and use of biologic therapies increased the likelihood of damage progression (P < 0.05).

Conclusion

Minimal disease activity was achieved by a significant proportion of patients and was sustained in one-third of the population studied. Patients achieving sustained minimal disease activity had a significant reduction in joint damage progression. Other factors, representing disease activity and disease severity, impact on the likelihood of achieving sustained minimal disease activity and on damage progression.


INTRODUCTION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. AUTHOR CONTRIBUTIONS
  8. Acknowledgements
  9. REFERENCES

Psoriatic arthritis (PsA) is now recognized as an inflammatory arthritis associated with an increased risk of joint damage (1). Cohort studies have suggested the link between inflammation and joint damage, showing that swollen joints are a predictor of a future increase in the clinically damaged joint count (1, 2) and of radiologic progression (3). Studies of new tumor necrosis factor (TNF)–blocking therapies have also supported that link, showing a reduction of disease activity with treatment and subsequent reductions in radiographic damage (4–6). There is a need for accurate assessment of disease activity in patients with PsA.

Measures of disease activity states allow identification of a desired state rather than that of a significant reduction in disease activity that may still represent a considerable burden of disease. Previous studies have assessed the frequency of remission in PsA using nonvalidated definitions (7–9). Two of the published studies assessed remission in the peripheral joints and did not take into account any of the other aspects of the disease (8, 9). Another study included enthesitis in addition to peripheral joint disease, but did not include skin disease (7).

Although remission is considered to be the ultimate goal of therapy in PsA, experts recognize that remission may be difficult to achieve and maintain, and that mild disease activity in 1 domain may be acceptable (10). It has been concluded that near remission or low disease activity could be an appropriate goal (10).

The conceptual definition of minimal disease activity was agreed at the Outcome Measures in Rheumatology Clinical Trials (OMERACT) 6 conference as “that state of disease activity deemed a useful target of treatment by both the patient and physician, given current treatment possibilities and limitations” (11). Minimal disease activity encompasses both remission and low disease activity. Recently, a definition of minimal disease activity in PsA was derived from the opinion of 60 experts in PsA using real-life cases from an observational study (12).

However, these criteria have not previously been applied in any independent population. The aim of this study was to investigate the frequency and duration of minimal disease activity in an independent observational cohort. Potential features that may be associated with achieving minimal disease activity in PsA were investigated. The prognostic ability of these criteria was also investigated to assess their true clinical relevance. The aim of this study was to establish how many patients with PsA achieved minimal disease activity for over 12 months at consecutive clinic visits (sustained minimal disease activity) and whether this was associated with a reduction in the progression of joint damage.

PATIENTS AND METHODS

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. AUTHOR CONTRIBUTIONS
  8. Acknowledgements
  9. REFERENCES

Our study was conducted at the University of Toronto PsA clinic. Patients were evaluated using a standard protocol every 6–12 months. Clinical assessments included a 68 tender/66 swollen joint count, the Spondylarthritis Research Consortium of Canada enthesitis instrument, and dactylitis using the Leeds Dactylitis instrument (13, 14). Skin assessment included both the body surface area and the Psoriasis Area and Severity Index (PASI) (15). A clinically damaged joint count was recorded in addition to tender and swollen joint counts at each visit. Damaged joints were defined as those that had a reduced range of motion >20% of the range that could not be explained by joint effusion, joints that had undergone surgery, or joints showing deformity, subluxation, loosening, or ankylosis. We have previously demonstrated the reliability of this measure in PsA both in our Clinic and across Canada (16, 17). A physician global assessment was completed and patients completed self-reported questionnaires including the Health Assessment Questionnaire (HAQ) and patient global assessments routinely. Blood results, including erythrocyte sedimentation rate (ESR), were recorded at each visit. ESR levels were recorded as a continuous variable and also as normal or raised (>15 for male patients, >20 for female patients).

To achieve the minimal disease activity criteria, patients must have fulfilled ≥5 of the 7 following criteria: tender joint count ≤1, swollen joint count ≤1, PASI score ≤1 or body surface area ≤3%, patient pain visual analog score (VAS) ≤15, patient global disease activity VAS score ≤20, HAQ score ≤0.5, and tender entheseal points ≤1 (12). Being that the minimal disease activity criteria require data on joint counts, enthesitis counts, skin activity, pain, patient's assessment of global disease activity, and HAQ score, the analysis was restricted to those visits occurring after 2003 when all information was available.

Patients were classified as achieving sustained minimal disease activity if they achieved the criteria at consecutive visits for a minimum of 12 months. These patients were compared with controls who had persistently active disease or achieved the criteria for <12 months. The change in the clinically damaged joint count was measured from the first visit in which patients achieved minimal disease activity to the last visit or, for the controls, from the prior visit closest to the median time of achieving minimal disease activity. Progression of clinical damage was said to have occurred if any joint changed from being nondamaged to damaged.

Three time points for data analysis were considered: 1) clinic entry: data from the first clinic visit for each patient (date of clinic entry ranged from January 1978 to December 2007), 2) study entry: data from the first clinic visit on or after January 1, 2003, and 3) followup: data from the last clinic visit prior to or on December 31, 2007.

Statistical analysis.

Patients achieving minimal disease activity and the control group (nonminimal disease activity) were compared using descriptive statistics. Factors affecting the likelihood of patients achieving minimal disease activity were investigated using logistic regression models. Three outcomes were defined based on the change in damaged joint count. We fit regression models for the raw change in damaged joint count, the change standardized by the patient-years at risk, and a binary response indicating whether ≥1 joint became damaged. Linear regression was used for the first 2 outcomes and logistic regression for the latter. The covariate of central interest was minimal disease activity status, age at onset of PsA, and, as measured at the first visit following January 1, 2003, ESR, duration of PsA, and an indicator of having ≥1 damaged joint. In addition, we examined the role of anti-TNF agents both before and after the time of minimal disease activity for those achieving minimal disease activity or, for controls, the median time of minimal disease activity. Univariate and multivariate regression models were fit with backward elimination carried out to identify variables that were independently predictive of joint damage. In order to examine the effect of time-varying covariates, we also fit Cox regression models for the time to first achievement of minimal disease activity. Univariate and multivariate models were fit with backward elimination carried out to identify factors independently associated with minimal disease activity.

RESULTS

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. AUTHOR CONTRIBUTIONS
  8. Acknowledgements
  9. REFERENCES

Full data were available on 344 patients with PsA (59% men, mean age 43 years). At clinic entry they had a mean age at onset of PsA of 36 years; mean joint counts of 10 tender, 4 swollen, 4 clinically damaged, and 5 radiographically damaged joints; and a mean PASI score of 4. Of the subjects, 44% were being treated with disease-modifying antirheumatic drugs (DMARDs) and 2% were being treated with biologic agents at study entry. Of the 344 patients, 208 (60%) achieved minimal disease activity at ≥1 visit. There were a total of 300 visits during which patients achieved minimal disease activity, and of these, 110 visits (37%) were recorded where patients met 5 of the 7 criteria, 114 visits (38%) where patients met 6 criteria, and 76 visits (25%) where patients fulfilled all 7 criteria.

Of the patients, 116 (34%) achieved sustained minimal disease activity on consecutive visits for a minimum duration of 12 months. The median duration of minimal disease activity was 28 months (range 12–48 months). The characteristics of the patients who met and sustained the minimal disease activity criteria are shown in Table 1 and Table 2. Of these patients, 46 (40%) were receiving treatment with conventional disease-modifying therapy alone and 40% were treated with TNF-blocking therapy (with or without concurrent DMARDs) at followup. Of the patients maintaining minimal disease activity, only 15 (12.9%) had escalation of their drug therapy made during their time in minimal disease activity.

Table 1. Characteristics of patients studied at clinic entry*
 Minimal disease activity (n = 116)Nonminimal disease activity (n = 228)
  • *

    Values are the mean (minimum, maximum) unless otherwise indicated. PsA = psoriatic arthritis; ESR = erythrocyte sedimentation rate; DMARD = disease-modifying antirheumatic drug.

Age, years40 (16, 71)44 (19, 79)
Sex, no. (%)  
 Women40 (34)100 (44)
 Men76 (66)128 (56)
Age at PsA onset, years34 (9, 65)37 (13, 75)
Disease duration, years6.6 (0, 39.1)6.8 (0, 37.9)
Arthritis pattern, no. (%)  
 Oligoarthritis (≤4 joints)48 (41)72 (32)
 Polyarthritis (≥5 joints)68 (59)154 (68)
 Axial disease (in addition)15 (13)47 (21)
Disease activity, mean joint count  
 Active joints8.611.0
 Effused joints3.63.7
Disease severity, mean joint count  
 Clinical damage3.63.9
 Radiologic damage4.54.7
ESR  
 Mean value, mm/hour25.625.3
 Normal ESR, no. (%)42 (43)87 (40)
 Elevated ESR, no. (%)56 (57)129 (60)
Treatment, no. (%)  
 No medication65 (56)121 (53)
 DMARD treatment alone49 (42)103 (45)
 Biologic treatment2 (2)4 (2)
Table 2. Characteristics of patients studied at study entry and followup*
 Minimal disease activity (n = 116)Nonminimal disease activity (n = 228)
  • *

    Values are the number (percentage) of patients unless otherwise indicated. PASI = Psoriasis Area and Severity Index. See Table 1 for additional definitions.

Study entry  
 Disease activity, mean joint count  
  Active joints3.49.2
  Effused joints1.32.9
 Disease severity, mean joint count  
  Clinical damage8.49.2
  Radiologic damage88.8
  PASI3.55.7
  Enthesitis count0.10.4
 ESR  
  Mean value, mm/hour16.420.6
  Normal ESR65 (63)95 (48)
  Elevated ESR38 (37)105 (53)
 Medication  
  No medication28 (24)31 (14)
  DMARD treatment alone53 (46)125 (55)
  Biologic treatment35 (30)72 (32)
Followup  
 Disease activity, mean joint count  
  Active joints0.74.3
  Effused joints0.21.3
 Disease severity, mean joint count  
  Clinical damage1011
  Radiologic damage910
  PASI2.74.2
  Enthesitis count0.10.2
 ESR  
  Mean value, mm/hour10.615.8
  Normal ESR88 (79)132 (63)
  Elevated ESR24 (21)78 (37)
 Medication  
  No medication23 (20)31 (14)
  DMARD treatment alone46 (40)125 (55)
  Biologic treatment47 (40)72 (32)

Of those who did not fulfill all 7 criteria, the most common active domain was skin psoriasis (n = 44), followed by patient global VAS (n = 17). None of the patients had a swollen joint count of >1. After the minimum 12-month period required for inclusion, 12 patients (10%) experienced a flare of their disease and ceased to fulfill the minimal disease activity criteria after an average of 34 months in minimal disease activity. The remainder were still in minimal disease activity at their most recent followup, after a mean followup of 37 months.

Demographic, clinical, and therapeutic features of those patients who sustained minimal disease activity were then compared with the features of those who did not. In univariate analysis, the only factor at the time of clinic entry increasing the probability of subsequently achieving minimal disease activity for over 12 months was younger age at disease onset (P = 0.04). However, this did not remain in the final multivariate model.

Similar features at the study entry visit were then analyzed. Univariate logistic regression analyses showed that high ESR, polyarthritis (>4 tender and/or swollen joints), and prior treatment with DMARDs or anti-TNF agents (compared with none) reduced the probability of achieving sustained minimal disease activity (P < 0.03). In multivariate logistic regression analysis, polyarthritis (odds ratio [OR] 0.296, 95% confidence interval [95% CI] 0.171–0.511; P < 0.0001) and elevated ESR (OR 0.546, 95% CI 0.326–0.914; P = 0.02) were associated with lower probability of achieving sustained minimal disease activity (Table 3). Using Cox regression modeling including time-dependent covariates, the outcome being time to first achieving sustained minimal disease activity, polyarthritis (relative risk [RR] 0.255, 95% CI 0.152–0.429; P < 0.0001) was again associated with a lower probability of achieving sustained minimal disease activity. In addition, treatment with DMARDs and/or anti-TNF agents showed a significant effect (P = 0.02 for global covariate effect) (Table 4). Further analysis suggested that treatment was significantly associated with time to achieving sustained minimal disease activity (P = 0.020). Treatment with DMARDs alone (compared with no treatment) was associated with lower probability of achieving sustained minimal disease activity (RR 0.74, 95% CI 0.442–1.239; P = 0.25), whereas treatment with anti-TNF agents with or without DMARDs increased the probability of achieving sustained minimal disease activity, although this was not statistically significant (RR 1.382, 95% CI 0.767–2.489; P = 0.28). Treatment with biologic agents (with or without DMARDs) versus DMARDs alone produced an RR of 1.868 (95% CI 1.197–2.913, P = 0.006).

Table 3. Patients' characteristics at study entry that affect the likelihood of achieving sustained minimal disease activity: results of logistic regression analysis*
CovariateUnivariate modelReduced multivariate model
OR (95% CI)PPOR (95% CI)P
  • *

    OR = odds ratio; 95% CI = 95% confidence interval. See Table 1 for additional definitions.

  • For global test of covariate effect.

Sex: male vs. female1.515 (0.917–2.502)0.11   
Age at PsA onset (1 year increase)0.979 (0.959–0.999)0.04   
Duration of PsA (1 year increase)1.007 (0.983–1.031)0.59   
Polyarthritis vs. oligoarthritis0.299 (0.174–0.514)< 0.0001 0.296 (0.171–0.511)< 0.0001
Axial arthritis vs. no axial arthritis0.58 (0.299–1.125)0.11   
Clinically damaged joint count ≥1 vs. none1.137 (0.685–1.885)0.62   
Radiographically damaged joint count ≥1 vs. none1.381 (0.766–2.491)0.28   
ESR: elevated vs. normal0.557 (0.339–0.915)0.02 0.546 (0.326–0.914)0.02
Medication     
 Treated with DMARDs only vs. none0.432 (0.228–0.817)0.010.03  
 Treated with biologic agents vs. none0.446 (0.218–0.914)0.03   
Table 4. Patients' characteristics over time that affect the time to first achieving sustained minimal disease activity: results of Cox regression analysis*
CovariateRR (95% CI)PPRR (95% CI)PP
  • *

    RR = relative risk; 95% CI = 95% confidence interval. See Table 1 for additional definitions.

  • For global test of covariate effect.

Fixed covariates      
 Sex: male vs. female1.316 (0.891–1.944)0.17    
 Age at PsA onset (1 year increase)0.988 (0.973–1.004)0.16    
 Duration of PsA at study entry (1 year increase)0.993 (0.975–1.012)0.5    
Time-dependent covariates starting from study entry      
 Polyarthritis vs. oligoarthritis0.262 (0.156–0.439)< 0.0001 0.255 (0.152–0.429)< 0.0001 
 Axial arthritis vs. no axial arthritis0.699 (0.405–1.204)0.2    
 Clinically damaged joint count ≥1 vs. none0.934 (0.628–1.391)0.74    
 Radiographically damaged joint count ≥1 vs. none1.082 (0.673–1.741)0.74    
 ESR: elevated vs. normal0.623 (0.42–0.925)0.02    
 Medication      
  Treated with DMARDs only vs. none0.661 (0.395–1.106)0.110.040.74 (0.442–1.239)0.250.02
  Treated with biologic agents vs. none1.125 (0.628–2.016)0.69 1.382 (0.767–2.489)0.28 

Because tender and swollen joint counts are included in the minimal disease activity criteria, the multivariate logistic regression and Cox regression modeling were repeated excluding tender and/or swollen joint count as a covariate. In this second multivariate logistic regression analysis, treatment with DMARDs (OR 0.42, 95% CI 0.22–0.80; P = 0.009), DMARDs and biologic agents (OR 0.40, 95% CI 0.19–0.83; P = 0.01), and an older age at disease onset (OR 0.98 per 1 year increase, 95% CI 0.96–1.00; P = 0.03) were all associated with a lower probability of achieving sustained minimal disease activity. In the second Cox regression model, only elevated ESR was identified as being associated with a lower probability of achieving sustained minimal disease activity (RR 0.623, 95% CI 0.420–0.925; P = 0.02)

When analyzing the prognostic value of the minimal disease activity criteria, the patients in sustained minimal disease activity were compared with 200 controls who did not achieve the minimal disease activity criteria for at least 12 months. The average followup time to assess progression of disease was matched at 34 months for both groups. The mean change in damaged joint counts over the study period was 0.931 (range 0–12) in the sustained minimal disease activity group and 2.245 (range 0–17) in the controls (P < 0.001). Of the patients with sustained minimal disease activity, 69% showed no progression of joint damage, compared with 51% in the control group.

Reduced multivariate regression models for change in damaged joint count revealed that achievement of sustained minimal disease activity was associated with fewer joints developing clinical damage (P = 0.03), whereas the presence of clinical joint damage at study entry (P = 0.01) and use of anti-TNF agents during the study period (P = 0.02) increased the number of joints showing clinical damage progression. Linear regression modeling using the change standardized by patient-years at risk and logistic regression modeling of the binary outcome of joint damage progression (or none) confirmed that the presence of clinical joint damage and use of anti-TNF agents increased joint damage, but additionally found that elevated ESR at study entry was also a predictive factor (P = 0.03).

DISCUSSION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. AUTHOR CONTRIBUTIONS
  8. Acknowledgements
  9. REFERENCES

Until recently, there were no composite disease activity measures available to measure a state of disease in PsA. The proposed criteria for minimal disease activity in PsA encompass different aspects of this heterogeneous disease, and could provide a new outcome measure for future clinical trials in PsA (12).

In the Toronto prospective study, it was shown that 17.6% of patients achieved remission in their peripheral joint activity (no actively inflamed joints) for at least 12 months, but 52% of these patients relapsed during followup (8). In the Swedish early PsA cohort, 17% of subjects were found to be in remission at 2 years (no tender or swollen joints and normal inflammatory markers) (9). A further study of remission in early disease showed a higher frequency of 24% of patients despite more stringent criteria requiring no enthesitis or dactylitis disease activity (7). This may partially represent the changing availability of treatments over the last decade.

The data in the current study show that sustained minimal disease activity occurred in approximately one-third of the population. The higher prevalence is not surprising being that the criteria were less strict than those used for remission in previous studies. Low levels of disease activity were allowed in all domains and only 5 of the 7 cutoffs must have been met. As seen in the previous remission studies, flare of disease occurred after a significant duration of time in minimal disease activity in ∼10% of the patients, demonstrating the variable activity of disease both on and off therapy. The majority of patients in minimal disease activity stayed on stable therapy, but 15 did have an escalation of their treatment. This may represent specific treatment for a certain high domain (e.g., active skin psoriasis only) or an increasing focus by the PsA clinic on the target of remission. Of those patients who did not achieve all 7 of the criteria, the most common high domains were skin and the patient's global assessment of disease activity. The latter may represent the patient's perception of active skin disease. These high domains may indicate that skin psoriasis is harder to control or that patients or physicians are more tolerant of moderate skin activity if other aspects of the disease are well controlled. However, it is important that measures of skin disease and patient-reported outcomes are included in such criteria to ensure a holistic approach to the treatment of psoriatic disease.

Before a new outcome measure can be recommended for routine use, it must prove to be valid in assessment. The OMERACT filter domains of truth, discrimination, and feasibility provide a framework to assess tools for use in clinical trials. The current study provides initial information on the responsiveness of the new minimal disease activity criteria and their prognostic ability. Further research is needed in other independent cohorts to demonstrate that if patients with a bad prognosis are treated to minimal disease activity with effective therapy, joint damage is prevented.

Although there was a marked reduction in the progression of joint damage, there was still evidence of some progression despite patients consistently achieving minimal disease activity. It must be noted that these criteria are not for remission but rather for minimal disease activity, and therefore a small amount of disease activity may be present. The patients achieving the minimal disease activity criteria can have active disease in 1 or 2 domains while still fulfilling the criteria, and even in the other domains low disease activity is considered acceptable by the criteria (e.g., 1 tender joint). This may account for the lower rate of joint damage. We also know that clinical examination does not identify all inflamed joints and that it is particularly insensitive to low levels of inflammation (subclinical disease) (18). Even in patients with rheumatoid arthritis who are in remission (as defined by Disease Activity Score), joint damage progression has been shown to occur and is related to subclinical inflammation seen on imaging (19). In the current study, a clinically damaged joint count was used rather than an assessment of joint damage on conventional radiography. This outcome measure has been validated against conventional radiography (16, 17), but is probably less sensitive to early joint damage and to minor changes than radiography. Therefore, the progression in both groups may be an underestimation of the progression of damage in PsA. Further research with conventional radiography and validated scoring systems needs to be conducted.

The advantage of using observational data from a cohort such as the PsA program in Toronto is that these data provide relevant information on real-life patients all treated according to their clinical need rather than any set trial protocol. However, exactly because of this, there are some limitations on the conclusions that can be drawn from the data. The analyses showed that disease-modifying treatment with standard DMARDs and biologic agents reduced the likelihood of achieving minimal disease activity, and the use of biologic therapies was also found to be associated with an increase in damaged joints. This is despite numerous observational studies and randomized trials showing a benefit with such therapies, and highlights the problems of confounding in data from observational cohorts. Patients presenting with active disease and joint damage are highly likely to be prescribed biologic therapies given their active disease, but also have a more severe disease phenotype and a higher potential for damage progression. It seems likely from this observational data that both treatment and a milder disease phenotype can have an impact on a patient's ability to achieve minimal disease activity. To understand the relative impact of disease phenotype and disease treatment, these new criteria must be tested in an interventional study.

Although we have shown an improved prognosis in those patients achieving a state of minimal disease activity, we cannot be sure what proportion of this is due to the natural history of the disease and what impact successful treatment has on outcome. PsA is known to be a heterogeneous disorder, and the progression of joint damage is highly variable between individuals. In previous publications using data from the same cohort, it has been shown that the presence of tender and/or swollen joints, raised ESR, and preexisting joint damage at the time of referral to the clinic predict future progression of joint damage (3). The association with raised ESR and preexisting joint damage has been confirmed in the current study. Future work, in the form of interventional therapeutic trials, must address the issue of whether achieving minimal disease activity in patients who present with active disease with poor prognostic features can influence the long-term outcome.

Although the Toronto PsA clinic has longitudinal data from over 30 years, full data to assess minimal disease activity using the new criteria were available from 2003 onward. This means that we could not identify which patients were in minimal disease activity prior to 2003, and that the patients included in the study had a maximum followup duration of 5 years. We have demonstrated with our data that patients can move in and out of the minimal disease activity state and that some “control” patients may have been in minimal disease activity prior to 2003. Therefore, the prognostic ability of the criteria is limited to the followup duration of 5 years for which we have full data on the patients. However, this limitation does mean that these data are representative of current practice and treatment opportunities, particularly regarding access to biologic therapies. Over this study period, minimal disease activity was achieved by a significant proportion of patients and was sustained for over 12 months in one-third of the population studied. Achievement of the criteria was associated with an improved prognosis in terms of joint damage progression. As therapeutic advances continue and the target for treatment becomes more ambitious, the proportion of patients achieving minimal disease activity may increase.

AUTHOR CONTRIBUTIONS

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. AUTHOR CONTRIBUTIONS
  8. Acknowledgements
  9. REFERENCES

All authors were involved in drafting the article or revising it critically for important intellectual content, and all authors approved the final version to be submitted for publication. Dr. Gladman had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Study conception and design. Coates, Cook, Lee, Chandran, Gladman.

Acquisition of data. Coates, Cook, Lee, Chandran, Gladman.

Analysis and interpretation of data. Cook, Chandran, Gladman.

Acknowledgements

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. AUTHOR CONTRIBUTIONS
  8. Acknowledgements
  9. REFERENCES

The authors would like to acknowledge the contribution of Catherine T. Schentag toward data collection.

REFERENCES

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. AUTHOR CONTRIBUTIONS
  8. Acknowledgements
  9. REFERENCES
  • 1
    Gladman DD, Shuckett R, Russell ML, Thorne JC, Schachter RK. Psoriatic arthritis (PSA): an analysis of 220 patients. Q J Med 1987; 62: 12741.
  • 2
    Gladman DD, Stafford-Brady F, Chang CH, Lewandowski K, Russell ML. Longitudinal study of clinical and radiological progression in psoriatic arthritis. J Rheumatol 1990; 17: 80912.
  • 3
    Bond SJ, Farewell VT, Schentag CT, Gladman DD, Bond SJ, Farewell VT, et al. Predictors for radiological damage in psoriatic arthritis: results from a single centre. Ann Rheum Dis 2007; 66: 3706.
  • 4
    Mease PJ, Gladman DD, Ritchlin CT, Ruderman EM, Steinfeld SD, Choy EH, et al, for the Adalimumab Effectiveness in Psoriatic Arthritis Trial Study Group. Adalimumab for the treatment of patients with moderately to severely active psoriatic arthritis: results of a double-blind, randomized, placebo-controlled trial. Arthritis Rheum 2005; 52: 327989.
  • 5
    Mease PJ, Kivitz AJ, Burch FX, Siegel EL, Cohen SB, Ory P, et al. Etanercept treatment of psoriatic arthritis: safety, efficacy, and effect on disease progression. Arthritis Rheum 2004; 50: 226472.
  • 6
    Van der Heijde D, Kavanaugh A, Gladman DD, Antoni C, Krueger GG, Guzzo C, et al, for the IMPACT 2 Study Group. Infliximab inhibits progression of radiographic damage in patients with active psoriatic arthritis through one year of treatment: results from the induction and maintenance psoriatic arthritis clinical trial 2. Arthritis Rheum 2007; 56: 2698707.
  • 7
    Cantini F, Niccoli L, Nannini C, Cassara E, Pasquetti P, Olivieri I, et al. Frequency and duration of clinical remission in patients with peripheral psoriatic arthritis requiring second-line drugs. Rheumatology (Oxford) 2008; 47: 8726.
  • 8
    Gladman DD, Hing EN, Schentag CT, Cook RJ. Remission in psoriatic arthritis. J Rheumatol 2001; 28: 10458.
  • 9
    Lindqvist UR, Alenius GM, Husmark T, Theander E, Holmstrom G, Larsson PT. The Swedish early psoriatic arthritis register: 2-year followup. A comparison with early rheumatoid arthritis. J Rheumatol 2008; 35: 66873.
  • 10
    Kavanaugh A, Fransen J. Defining remission in psoriatic arthritis. Clin Exp Rheumatol 2006; 24 Suppl 43: S837.
  • 11
    Wells GA, Boers M, Shea B, Brooks PM, Simon LS, Strand CV, et al. Minimal disease activity for rheumatoid arthritis: a preliminary definition. J Rheumatol 2005; 32: 201624.
  • 12
    Coates LC, Fransen J, Helliwell PS. Defining minimal disease activity in psoriatic arthritis: a proposed target for treatment. Ann Rheum Dis 2010; 69: 4853.
  • 13
    Gladman DD, Inman RD, Cook RJ, Maksymowych WP, Braun J, Davis JC, et al. International spondyloarthritis interobserver reliability exercise: the INSPIRE study. II. Assessment of peripheral joints, enthesitis, and dactylitis. J Rheumatol 2007; 34: 17405.
  • 14
    Healy PJ, Helliwell PS. Measuring dactylitis in clinical trials: which is the best instrument to use? J Rheumatol 2007; 34: 13026.
  • 15
    Chandran V, Gottlieb A, Cook RJ, Duffin KC, Garg A, Helliwell P, et al. International multicenter psoriasis and psoriatic arthritis reliability trial for the assessment of skin, joints, nails, and dactylitis. Arthritis Rheum 2009; 61: 123542.
  • 16
    Gladman DD, Cook RJ, Schentag C, Feletar M, Inman RI, Hitchon C, et al. The clinical assessment of patients with psoriatic arthritis: results of a reliability study of the spondyloarthritis research consortium of Canada. J Rheumatol 2004; 31: 112631.
  • 17
    Gladman DD, Farewell V, Buskila D, Goodman R, Hamilton L, Langevitz P, et al. Reliability of measurements of active and damaged joints in psoriatic arthritis. J Rheumatol 1990; 17: 624.
  • 18
    Wakefield RJ, Green MJ, Marzo-Ortega H, Conaghan PG, Gibbon WW, McGonagle D, et al. Should oligoarthritis be reclassified? Ultrasound reveals a high prevalence of subclinical disease. Ann Rheum Dis 2004; 63: 3825.
  • 19
    Brown AK, Quinn MA, Karim Z, Conaghan PG, Peterfy CG, Hensor E, et al. Presence of significant synovitis in rheumatoid arthritis patients with disease-modifying antirheumatic drug–induced clinical remission: evidence from an imaging study may explain structural progression. Arthritis Rheum 2006; 54: 376173.