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Open-label study of infliximab treatment for psoriatic arthritisClinical and magnetic resonance imaging measurements of reduction of inflammation.

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Arthritis & Rheumatism (Arthritis Care & Research)
Vol. 47, No. 5, October 15, 2002, pp 506 –512
DOI 10.1002/art.10671
© 2002, American College of Rheumatology
Open-Label Study of Infliximab Treatment for
Psoriatic Arthritis: Clinical and Magnetic
Resonance Imaging Measurements of Reduction of
Objective. To evaluate infliximab efficacy and safety in disease-modifying antirheumatic drug– unresponsive psoriatic
arthritis (PsA).
Methods. In a 54-week, open-label, compassionate-use study, 10 patients received intravenous infliximab (5 mg/kg;
weeks 0, 2, 6; individualized dosing after week 10). Patients continued their current therapy (stable dose) until week 10.
Assessments were performed at weeks 2, 6, 10, and 54. Magnetic resonance imaging (MRI) objectively measured joint
inflammation at weeks 0 and 10.
Results. Patients achieved a 20% improvement according to the American College of Rheumatology (ACR) criteria
(ACR20) in all patients by week 2; 8 patients improved 70% (ACR70) at week 10; 6 patients maintained ACR70 after week
54. Week 10 MRI revealed an 82.5% mean reduction in inflammation from baseline, and psoriasis area and severity index
scores were reduced by 71.3% ⴞ 16.7%. There were no significant adverse events, severe infections, or infusion reactions.
Conclusion. Infliximab was effective, safe, and well tolerated in PsA. Arthritis and psoriasis improved in all patients
during the 54-week evaluation. Further investigation of the use of infliximab for PsA and psoriasis is warranted.
KEY WORDS. Infliximab, Magnetic Resonance Imaging, Psoriasis, Psoriatic arthritis, Remicade, Tumor Necrosis Factor ␣
Psoriatic arthritis (PsA) is a spondylarthropathy that occurs in approximately 6 –20% of patients with psoriasis
(1). There is evidence that tumor necrosis factor ␣ (TNF␣)
is linked to the pathogenesis of PsA and psoriasis. This
proinflammatory cytokine upregulates adhesion molecules and triggers an inflammatory cytokine cascade (2– 4),
resulting in inflammation and arthritis. Evidence of the
involvement of TNF␣ in the pathophysiology of PsA is
Christian Antoni, MD, Claudia Dechant, MD, P. D. HannsMartin Lorenz, MD, Joerg Wendler, MD, Alexandra Ogilvie,
MD, Mathias Lueftl, MD, Dolores Kalden-Nemeth, MD, Prof.
Dr. H. C. Joachim R. Kalden, MD, Prof. Bernhard Manger,
MD: Friedrich-Alexander-University, Erlangen, Germany.
Address correspondence and reprint requests to Christian
Antoni, MD, Friedrich-Alexander-University, Department
of Medicine III, Krankenhausstrasse 12 91056 Erlangen,
Germany. E-mail: christian.antoni@med3.imed.uni-erlangen.
Submitted for publication October 20, 2001; accepted in
revised form March 11, 2002.
based on several findings. First, circulating T lymphocytes
and macrophages isolated from PsA patients produce increased TNF␣ compared with healthy controls (5). The
levels of TNF␣ are elevated in patient synovium, (6,7) as
well as in the skin lesions of PsA patients, (8 –10) and
TNF␣ levels correlate with disease activity in psoriasis
(11–14). Second, TNF receptors are elevated in synovial
fluid and their level of expression correlates with clinical
disease severity (15). Finally, a mutation in the promoter
region of TNF␣ is associated with juvenile-onset PsA (16).
The current therapeutic approaches for PsA, similar to
those for rheumatoid arthritis (RA), include nonsteroidal
antiinflammatory drugs and disease-modifying antirheumatic drugs (DMARDs) such as methotrexate (17), sulfasalazine (18), and cyclosporin A (19). Although the exact
mechanism of action of these agents is unknown, they may
directly or indirectly downregulate TNF␣ or other immune
mechanisms associated with PsA and RA. Of the current
therapeutic options, methotrexate and sulfasalazine are
the only 2 agents with well-documented efficacy (20).
However, these agents are associated with significant ad-
Infliximab Treatment of Psoriatic Arthritis
Table 1. DMARD and infliximab treatment history for weeks 10 –50*
ACR score
Treatment after week 10
Week 10
Week 54
No DMARD, discontinued
MTX after week 10 due to side effects
5 mg/kg every 8 weeks
3 mg/kg every 8 weeks
3 mg/kg every 8 weeks
3 mg/kg every 8 weeks
Discontinued month 8; infusion reaction and pregnancy
Discontinued month 5, remission
Discontinued month 8, remission
Discontinued month 7, remission
Discontinued week 10, remission
3 mg/kg every 8 weeks
DMARD ⫽ Disease-modifying antirheumatic drug; ACR score ⫽ American College of Rheumatology criteria; MTX ⫽ Methotrexate.
verse events, and many patients do not respond to these
treatments (17,21).
Because anti⫺TNF␣ antibodies (22–24) and fusion proteins (25) have demonstrated efficacy and safety in the
treatment of RA, another TNF␣–mediated inflammatory
arthritis, it was reasoned that they may have efficacy for
the treatment of PsA as well. Infliximab is a novel chimeric
murine-human monoclonal antibody (cA2, Remicade;
Centocor, Malvern, PA) that blocks TNF␣, neutralizing
both the soluble and membrane-bound forms of the cytokine. In RA patients, it has been demonstrated that, following infliximab therapy, adhesion molecules and inflammatory cytokines known to potentiate inflammation,
such as interleukin-6, are downregulated (26). In a recent
clinical trial evaluating the efficacy and safety of infliximab and methotrexate combination therapy in RA, 50%
of treated patients achieved a 20% or greater improvement
according to the American College of Rheumatology (ACR)
criteria (ACR20) (27) as early as 2 weeks after treatment,
with most patients maintaining an ACR20 response at
week 30 (24). Based on clinical trials in RA, infliximab was
considered safe and well tolerated. Infliximab has US Food
and Drug Administration and European Agency for the
Evaluation of Medicinal Products approval for use in RA
as well as for the treatment of Crohn’s disease (28). However, the potential of infliximab as a treatment for PsA has
been previously evaluated in only 9 patients with a rather
short observation period of 12 weeks (29).
The objective of the current study was to determine the
efficacy and safety of infliximab inhibition of TNF␣ in PsA
patients unresponsive to DMARD therapy. Patient responses to therapy were monitored by magnetic resonance
imaging (MRI), an objective measure of inflammation, as
well as by standard assessments of arthritis and psoriasis.
Patients. Ten patients with a diagnosis of polyarticular
disease with persistent clinical and serologic activity despite DMARD therapy were eligible for study inclusion.
Seven patients were taking methotrexate, 1 patient was
taking sulfasalazine, and 2 patients were not taking
DMARDs at the time of inclusion. All patients had psoriatic skin lesions, joint involvement, and x-ray lesions characteristic of PsA. Patients with ⱖ 6 tender joints and ⱖ 6
swollen joints as well as 1 of 3 baseline criteria (erythrocyte sedimentation rate [ESR] ⱖ 25 mm, C-reactive protein
[CRP] ⱖ 15 mg/L, or morning stiffness ⱖ 45 minutes) were
included. Patients with a prior history of malignancy, ongoing or recent history of severe infection, pregnancy, or
any unstable medical condition were excluded. All patients provided written informed consent. Patients had not
previously received infliximab and had no known sensitivity to its components.
Study design. The study was designed as a single-center, open-label, compassionate-use trial of infliximab. Patients were recruited from the outpatient department of the
Department of Medicine III of the University of ErlangenNurnberg or after referral from a rheumatologist. Patients
were treated within the study center on an outpatient
Infliximab (5 mg/kg) was infused intravenously with
normal saline over a 2-hour period. Infliximab treatments
were administered at the initial visit (week 0 or baseline)
and at weeks 2 and 6, with additional followup evaluation
at weeks 10 and 54. Between weeks 10 and 54, patients
were treated with infliximab (3 mg/kg) every 8 weeks (with
some exceptions; Table 1) on an individual basis determined by their response to infliximab and adverse events
Patients were allowed to continue stable-dose DMARD
(methotrexate [15 to 25 mg/week] or sulfasalazine), steroid
(ⱕ 10 mg/day prednisolone equivalent, stable dose), and
nonsteroidal antiinflammatory drug therapy through week
10. After week 10, doses of concurrent medications were
adjusted (decreased as appropriate), but no new DMARD
or steroid therapy was started. Patients did not receive
topical treatment for their psoriasis lesions between weeks
0 and 10.
Patient evaluation. At weeks 2, 6, 10, and 54, the following assessments were made by the physician: tender
joint count (the number of tender joints of 68 possible),
Antoni et al
swollen joint count (the number of swollen joints of 66
possible), Physician Global Visual Analogue Scale (VAS)
of disease severity (0 –100 mm VAS, with increasing numbers indicating increasing disease severity). Patients also
assessed their pain and disease severity by recording the
Patient Global VAS (0 –100 mm VAS) of disease severity
and the Patient VAS Assessment of Pain (0 –100 mm VAS),
as well as by completing the Stanford Health Assessment
Questionnaire (HAQ, a measure of patient functional disability). Laboratory measurements included CRP and ESR,
both of which increase in proportion to disease severity.
Based on the arthritis measures, the stringent response
criteria established by the ACR (27) and by Clegg et al (30)
were calculated. The ACR criteria for arthritis improvement from baseline are defined as a 20%, 50%, or 70%
improvement (ACR20, ACR50, or ACR70, respectively) in
the number of swollen and tender joints, with a corresponding improvement in 3 of 5 additional categories (Patient Global VAS, Physician Global VAS, HAQ, ESR, or
CRP, and Patient VAS of Pain). Clegg et al (30) defined
response to treatment as improvements in 2 of 4 criteria
with 1 improvement being joint tenderness or swelling.
The 4 criteria are as follows: a 30% improvement in the
tender joint count, a 30% improvement in the swollen
joint count, an improvement in Physician Global VAS, and
an improvement in Patient Global VAS. When applying
the Clegg PsA response criteria, no categories may deteriorate.
MRI of gadolinium-diethylenetriaminepentaacetic acid
(DTPA) uptake (described in detail below) was determined
at baseline and week 10 following infliximab treatment to
document changes in joint inflammation.
Psoriasis skin disease was monitored by calculating the
psoriasis area and severity index (PASI) (31) for 6 out of 10
patients at weeks 0 and 10. The remaining 4 patients had
only very mild skin involvement at baseline and were not
evaluated. The PASI scores measure the extent of psoriasis
disease as well as the morphology and thickness of psoriasis plaques. The PASI is calculated as follows:
PASI⫽0, 1(Eh⫹Ich⫹Dh)Ah⫹0,3(Et⫹It⫹Dt)At⫹
H, t, u, and l represent head, trunk, upper extremities
and lower extremities, respectively. Erythema (E), infiltration (I) and desquamation (D) are measured on a scale of 0
to 4 according to the severity of the skin changes. The area
(A) is recorded as 0 to 6 according to the percentage of the
skin involved. Skin biopsies were obtained from 3 patients
at baseline (before treatment) and at week 10. Biopsies
were subject to routine histopathologic sectioning, staining, and analysis.
Magnetic resonance imaging. Because both the Physician and Patient Global VAS are subjective measures of
disease severity and because placebo effects occur during
DMARD trials for PsA (20), MRI detection of gadoliniumDTPA was employed as an objective measure of inflammation. The amount of gadolinium-DTPA uptake by joints
directly correlates with the severity of inflammatory arthritis (32). MRI of gadolinium-DTPA uptake by inflamed
joints at baseline (week 0) and week 10 was performed on
8 patients who gave consent to the examination. The patient’s inflamed joints were imaged with a 1.5 Tesla magnet (Magneton/Siemens, Erlangen, Germany) as previously
described (32). A dynamic flash 2D gradient echo was
employed in addition to special superficial coils for optimal resolution. Time-dependent signal intensity changes
were measured in 4 defined, enhancing regions of interest
after a bolus injection of 0.1 mg/kg gadolinium-DTPA
(Magnevist/Schering, Berlin, Germany) following 1 prior
unenhanced series. The relative signal intensity (SI) increase (percentage per minute) was calculated at baseline
and at week 10 by the following formula:
[SImax ⫺ SIpre-contrast] ⫻ 100
SIpre-contrast ⫻ Tmax
Safety. Vital signs including blood pressure, pulse, and
temperature were measured every 30 minutes until 1 hour
after the end of the infliximab infusion. Vital sign parameters and laboratory tests (including a blood count with
differential, and biochemical tests including electrolytes,
urea, creatinine, total protein, and liver enzymes [serum
glutamic-pyruvic transaminase, serum glutamic-oxaloacetic transaminase, gamma-glutamyltransferase]) were performed during and after each infusion and again at followup (week 54). Patient-reported adverse events were
monitored at each visit and noted by the study evaluator in
addition to any adverse events occurring during infliximab
Statistical analysis. All data are depicted graphically or
in tabular format. Means and standard deviations were
calculated for global and peripheral arthritis measures.
Two-tailed Mann-Whitney Test (P ⬍ 0.05 considered significant) was applied to determine the significance of
changes in gadolinium-DTPA uptake.
Patients. A total of 10 patients (6 male and 4 female)
with a mean age of 34.8 years (range 23– 43 years) and a
disease duration of 6.6 years (range 1–22 years) were enrolled in the study. All patients exhibited polyarticular
disease with stable clinical and serologic activity despite
DMARD therapy. All patients presented with elevated CRP
and ESR values and experienced morning stiffness for ⬃30
to 120 minutes (with the exception of 1 patient who did
not experience any morning stiffness). All patients completed infusions at weeks 0, 2, and 6, and were included in
the data analysis. Patient treatment was individualized
between weeks 10 and 54, based on patient response to
infliximab and adverse events.
After week 10, treatment with infliximab was continued
or discontinued in 5 patients. Reasons for discontinuation
were infusion reaction and detected pregnancy (1 patient),
and clinical remission (4 patients). Remission was defined
as absence of any active joint inflammation and/or serologic activity (Table 1).
Infliximab Treatment of Psoriatic Arthritis
Table 2. Arthritis assessments*
Response parameter
Week 0
Week 2
Week 6
Week 10
Week 54
Physician Global VAS assessment, mm
Patient Global VAS assessment, mm
VAS Pain, mm
CRP, mg/L
ESR, mm
Tender joint count (68)
Swollen joint count (66)
Morning stiffness, minutes
69.2 (19.0)
72.8 (21.0)
1.05 (0.53)
67.7 (19.6)
37.9 (24.4)
35.2 (16.4)
20.6 (15.7)
14.1 (9.8)
58.5 (45.0)
11.6 (11.4)
19.3 (18.4)
0.5 (0.6)
16.9 (16.2)
2.7 (2.5)
10.7 (8.1)
4.5 (5.9)
2.6 (2.8)
16.5 (37.7)
4.4 (6.9)
17.0 (15.9)
0.28 (0.38)
14.3 (11.6)
3.4 (3.7)
8.6 (6.1)
3.6 (6.6)
2.1 (4.9)
15.5 (37.9)
3.5 (6.9)
12.1 (13.5)
0.28 (0.39)
11.8 (10.1)
1.7 (2.1)
10.7 (12.4)
2.1 (4.3)
1.6 (3.7)
12.0 (14.6)
9.0 (16.5)
20.8 (16.0)
0.39 (0.53)
20.2 (21.4)
9.9 (12.4)
15.0 (14.3)
3.6 (7.5)
2.0 (4.7)
18.1 (24.3)
* Values are mean (SD). VAS ⫽ visual analogue scale; HAQ ⫽ Health assessment questionnaire; CRP ⫽ C-reactive protein; ESR ⫽ erythrocyte
sedimentation rate.
Efficacy. Measures of arthritis severity. Two weeks following infliximab therapy, improvements were seen in the
mean global and peripheral assessments of arthritis severity (Table 2) compared with baseline (week 0). Improvements were noted in Physician Global VAS, Patient Global
VAS, HAQ, Patient VAS Assessment of Pain, ESR, and
CRP. The number of tender and swollen joints decreased,
as did the duration of morning stiffness. Maximum improvements for all global and peripheral assessments were
seen at week 10 following infliximab treatment, with improvements maintained in all categories at week 54 compared with baseline.
The ACR20, ACR50, and ACR70 responses are summarized in Table 3. By week 2 after infliximab treatment, 10
of 10 patients achieved an ACR20 response, with 8 patients achieving ACR50 and 6 patients achieving ACR70
responses. Additionally, all 10 patients demonstrated
ACR50 responses by 6 weeks after the initiation of infliximab therapy. Finally, 8 patients attained ACR70 responses by week 10, with 6 of 10 patients maintaining an
ACR70 response at the 54-week followup. Patient responses calculated according to the PsA response criteria
established by Clegg et al (21) showed similar patient
improvements at week 2 with all patients remaining stable
at week 54 after the initiation of infliximab therapy (Table
3). At week 54, 8 of 10 patients still had no tender or
swollen joints.
Inflammation measures. Prior to infliximab treatment,
the peripheral joints of 8 patients demonstrated marked
inflammation as revealed by MRI detection of gadoliniumDTPA uptake (Figure 1A). The mean gadolinium-DTPA
uptake at week 0 was 114%/min (SD ⫾ 73.0% per minute;
Figure 2). By the week 10 MRI (Figure 1B) the inflammaTable 3. American College of Rheumatology (ACR)
Criteria and Clegg Criteria responses of 10 patients to
infliximab treatment
Response, no. patients
Clegg response
Week 2
Week 6
Week 10
Week 54
tion was substantially reduced as evidenced by decreased
gadolinium-DTPA within the joints (mean, 16.4%/min ⫾
10.4% per minute; Figure 2). Upon quantitation of the
percent reduction in gadolinium-DTPA uptake, it was determined that all patients achieved a reduction in inflammation, with a mean reduction of 82.5% ⫾ 10.3% (P ⫽
0.0071; Table 4).
Psoriasis measures. As summarized in Table 5, PASI
scores improved significantly at week 10 for all 6 evaluated patients, with a mean percent reduction from baseline
of 71.3% ⫾ 16.7% (P ⫽ 0.0321). Prior to infliximab therapy, 6 PsA patients exhibited characteristic sharply circumscribed erythematous psoriasis plaques covered by
silvery scales. By week 10 after infliximab treatment the
plaque was almostly completely clear, a response that was
typical for all of the 6 patients who had significant skin
manifestation at baseline. Upon histopathologic analysis
of psoriasis plaques from patient skin, demonstrated a
reduction in epidermal hyperplasia and inflammation coinciding with the decrease in plaque size by week 10 of
infliximab treatment, as evidenced by the near-normal epidermal structure.
Safety. Infliximab treatment was well tolerated by all
patients, with no significant adverse events, severe infections, or infusion reactions. Nine of 10 patients completed
the 54-week study, with no patient discontinuations due
to adverse events. One patient discontinued infliximab at
month 8 because of a mild infusion reaction (facial flushing and myalgia in the extremities) and a detected pregnancy. The infusion reaction was successfully resolved by
antihistamine treatment. At term, the patient gave birth to
a healthy child. One patient stopped methotrexate therapy
because of combined hyperlipidemia. Infliximab treatment
was continued in this patient and the abnormal values
improved. One patient paused infliximab treatment between months 5 and 12 because of an elective spine operation. There were no reports of dyspnea, urticaria, or headache.
There are few treatment alternatives for patients with progressive PsA who fail to respond to methotrexate. Of the
Antoni et al
Figure 1. Magnetic resonance imaging of gadolinium-diethylenetriaminepentaacetic acid
uptake. A, Representative patient foot before and B, 10 weeks after infliximab treatment.
world’s population, 1–3% is afflicted with psoriasis (1)
and 6 –20% of those patients develop PsA (1,33). In the
present study, infliximab, a chimeric antibody that binds
to and inactivates TNF␣, thereby downregulating inflammatory cytokines and adhesion molecules (26), was administered to PsA patients who had failed to respond to
the standard treatment options. Infliximab treatment resulted in an improvement in all global and peripheral
assessments of arthritis in all treated patients. Furthermore, applying the stringent response criteria established
by the ACR to evaluate RA patient responses to therapy
revealed that by week 6 every patient had achieved a 50%
improvement in arthritis severity (ACR50)—a response
that was sustained by all patients out to week 54 despite
lowering the dose or discontinuing infliximab treatment
due to remission in some patients. Response criteria defined by Clegg et al (21) also demonstrated that all patients
responded to infliximab treatment. Improvements in both
arthritis measures were achieved as early as week 2 following the administration of the antibody, and 6 patients
continued to meet ACR70 criteria at week 54 after the
Table 4. Reduction of magnetic resonance imaging
Gadolinium uptake at week 10
Figure 2. Gadolinium-diethylenetriaminepentaacetic acid (DTPA)
uptake at baseline (week 0) and week 10 after infliximab treatment. Gadolinium-DTPA uptake based on magnetic resonance
imaging, expressed as percentage per minute, was calculated as
described in the Methods section.
* Values are % per minute.
Infliximab Treatment of Psoriatic Arthritis
Table 5. Psoriasis Activity and Severity Index (PASI)*
at Week
10 (%)
* PASI score described in Methods section.
initiation of infliximab therapy. The MRI analysis provided objective confirmation of the patients’ reduced inflammation with a mean reduction in gadolinium-DTPA
uptake of 82.5%. Lastly, infliximab appeared to also resolve other manifestations of psoriasis with improvements
in PASI indices in addition to a visual reduction in psoriatic plaque size that was confirmed by histopathologic
analysis. Within this small cohort we have seen only 1
infusion reaction and no serious adverse events.
The present study was open-label and involved only a
small number of patients and no control group. The conclusions that can be drawn from the results are limited.
However, our observation that the arthritis measures correlated with MRI data (an objective measure of inflammation) suggests that the responses were due to a true therapeutic effect. The rapid response of clinical parameters, as
well as the marked reduction of ESR and CRP, makes a
spontaneous reduction of inflammation due to selection
criteria unlikely. MRI can be used to visualize the soft
tissue abnormalities prior to any further inflammatory
damage and is, therefore, a powerful technique for monitoring patients who may be predisposed to arthritis, such
as psoriasis patients, as well as for monitoring patient
responses to antiinflammatory therapy (34). In the present
study MRI was used to document the decrease in inflammation in the joints of infliximab-treated PsA patients.
These data, and a previous study using MRI to quantitate
the effects of infliximab therapy (32), confirm that MRI, in
addition to its current use in diagnosing inflammatory
arthritis, is a powerful tool for monitoring antiinflammatory therapy responses.
Data from this study are consistent with those of Van
den Bosch et al (29), in which infliximab was used to treat
21 patients with various spondylarthropathies, including
9 patients with PsA. The dose (5 mg/kg infliximab) and
treatment regimens were similar between the 2 studies and
were modeled after the treatment regimens that have
proven efficacious for RA (23). Similar to the current
study, Van den Bosch et al documented significant improvements following the first infliximab infusion, with
treatment responses maintained through 84 days posttreatment. In addition to the global and peripheral assessments,
ESR, CRP, and PASI score measurements presented by Van
den Bosch et al, the current study includes ACR and Clegg
response data that are more stringent measurements of a
drug effect than the individual measures. Additionally, the
MRI data objectively quantify the improvement of PsA in
response to infliximab. Furthermore, in the present study,
patient improvements in psoriasis plaques were observed
and examined by histopathologic techniques, confirming
the concurrent improvements in skin and joint psoriasis.
During a recent double-blind, monocenter study of PsA
treatment with etanercept (a TNF␣ receptor fusion protein), patient improvements according to ACR and Clegg
response criteria were also documented (35). In this study
73% of etanercept-treated patients achieved an ACR20
response by week 12 of treatment compared with 13% of
patients in the placebo group. The ACR50 and ACR70
responses were 50% and 13%, respectively, for the etanercept-treatment group compared with 3% and 0% in the
placebo group. Interpreted together, the present study and
the 2 previously published studies highlight the pathophysiologic role of TNF␣ in PsA and suggest that, similar
to RA patients, PsA patients may benefit from infliximab
In the present study, in the Van den Bosch study (29),
and in the etanercept study (35), improvements in PsA
were accompanied by improvements in psoriatic plaques.
These data suggest that, irrespective of the antigens and
cell types driving disease in the skin and joints, both
manifestations of psoriasis are dependent to some extent
upon TNF␣. Therefore, inhibition of TNF␣ may effectively
treat both aspects of the disease.
In conclusion, based on our analysis of this small study,
infliximab is effective and safe for the treatment of PsA in
patients unresponsive to DMARD therapy. Furthermore,
patients also benefited by an improvement in psoriatic
plaques. Taken together, the improvement in ACR and
Clegg arthritis criteria and the reduction in inflammation
detected by MRI, an objective measure of inflammation,
suggest that infliximab warrants further investigation for
the treatment of psoriatic arthritis.
The authors would like to thank Bettina Raddatz, RN for
her excellent assistance during this study.
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