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Giant cell arteritis (GCA) is a chronic inflammatory vasculitis in large and medium-sized arteries. Glucocorticoids (GCs) remain the cornerstone of treatment but carry significant long-term adverse effects. Tocilizumab (TCZ), an interleukin (IL)-6 receptor inhibitor, has become a GC-sparing agent, yet optimal treatment duration remains uncertain.
Methods
This retrospective cohort study evaluated treatment patterns, clinical outcomes, and GC burden in patients (N = 121) with GCA treated at a specialized clinic in Montreal, Canada, between January 2017 and February 2025. Patients were stratified by initial treatment: GC only, GC + TCZ, and GC + other immunosuppressants (OIS). The primary endpoint was sustained remission at 12 months, defined by symptom resolution and normalization of inflammatory markers maintained for ≥ 6 months.
Results
Overall, two-thirds of patients (83, 68.6%) (95% confidence interval [CI] 60.3–76.9%) achieved sustained remission, with similar rates in GC only (35, 72.9%) and GC + TCZ (44, 69.8%) groups, but lower in the GC + OIS group (4, 40.0%). Most patients remained on GCs after 1 year, highlighting the difficulty of achieving steroid-free remission. Relapses occurred in nearly half of patients (58, 47.9%), with a median time to first relapse of 283.5 days (95% CI 206–326). Methotrexate showed limited GC-sparing efficacy, with several patients relapsing (6, 60%). TCZ-treated patients had the lowest cumulative GC exposure (mean 3431 mg (standard deviation [SD] = 1049) vs. 4690 mg (SD 969) in GC only), though a quarter of patients (16, 25.4%) relapsed after TCZ discontinuation.
Conclusion
The current 1-year TCZ treatment limit in Canada may be inadequate for long-term disease control. Adverse events were generally low, though hypertension, hyperglycemia, and infections were common. Two bowel perforations occurred in the TCZ group. These findings underscore the need for individualized, long-term treatment in GCA to minimize steroid exposure and maintain disease control. Future research should explore optimal therapy durations and support policy changes to expand access to steroid-sparing agents to improve long-term GCA outcomes.
Giant cell arteritis (GCA) affects adults over 50 and leads to major morbidity, frequent relapses, and a high healthcare burden driven by limited steroid-sparing options and toxicities from prolonged glucocorticoid (GC) use.
This study examined real-world relapse, remission, and GC burden in Canadian patients treated with methotrexate (MTX) and tocilizumab (TCZ), to assess whether current management achieves sustained disease control.
What was learned from the study?
Nearly half of patients relapsed. MTX provided limited benefit in reducing relapse or steroid exposure, while TCZ lowered cumulative GC exposure but still had substantial relapse rates, especially after treatment discontinuation.
Relapses commonly occurred after treatment was stopped, often due to reimbursement limits rather than disease activity. This underscores the need for more steroid-sparing options, patient-centered management, and policies that support flexible long-term therapy.
Introduction
Giant cell arteritis (GCA), also known as temporal arteritis, is a chronic inflammatory disease predominantly targeting large and medium-sized arteries, particularly the cranial branches of the carotid artery [1]. This condition most commonly afflicts individuals over the age of 50, with a higher prevalence among women and those of Northern European, particularly Scandinavian, descent [2]. GCA is characterized by a range of symptoms including severe headaches, scalp tenderness, jaw claudication, and visual disturbances, which can lead to irreversible blindness and stroke if not promptly and effectively treated [3, 4].
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Glucocorticoids (GCs) are the cornerstone of GCA treatment, typically resulting in rapid amelioration of symptoms and inflammation control, thereby preventing further ischemic complications [5]. Despite their efficacy, nearly half of patients experience disease relapse, necessitating prolonged GC treatment [6]. This extended GC therapy is associated with significant adverse effects (AEs), including osteoporosis, hypertension, hyperglycemia, myopathy, easy bruising, cushingoid features, fatigue, and cataracts, which collectively compromise quality of life [5, 7, 8].
Methotrexate (MTX) is used as an immunosuppressant and anti-inflammatory in the treatment of GCA and is commonly used as a GC-sparing adjunct. However, its efficacy in managing GCA remains inadequately supported by robust clinical evidence [9]. Tocilizumab (TCZ) is an interleukin-6 (IL-6) receptor inhibitor and was the only biologic agent approved for GCA treatment in Canada during the study period. Its efficacy was demonstrated in the landmark phase 3 randomized clinical trial GiACTA, in which patients receiving TCZ alongside a corticosteroid taper achieved higher rates of sustained remission and required lower cumulative steroid doses compared to those treated with corticosteroids alone [10]. A 2-year multicenter retrospective study in Japan confirmed TCZ’s overall effectiveness in managing GCA, even in populations with lower disease prevalence and different clinical presentations [2, 11]. TCZ has shown significant effectiveness in the treatment of GCA by reducing disease activity, maintaining remission, and minimizing corticosteroid exposure.
Despite these advances, significant evidence gaps persist regarding treatment patterns and clinical outcomes. Addressing these gaps is crucial to better understanding GC usage and steroid-tapering agents, as well as their impact on GCA clinical outcomes and disease relapses.
This comprehensive, single-center, non-interventional, retrospective cohort study aimed to describe the clinical outcomes and treatment patterns for patients with GCA treated in a specialized GCA clinic in Canada.
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Methods
Study Design
A cohort analysis was conducted of a specialized GCA clinic in Montreal, QC, Canada, from January 01, 2017 to February 28, 2025, providing a comprehensive perspective on treatment patterns and clinical outcomes in Canada. This clinic leveraged a web-based referral system allowing physicians to refer patients with suspected GCA (new or relapsing) and include the relevant signs and symptoms within the referral. If the signs and symptoms indicated a moderate to high risk for GCA, a 3-day prescription of GCs was automatically issued to provide bridging symptomatic coverage until the patient’s appointment at the clinic. Patients identified as having moderate to high suspicion of GCA were seen within 48 h of referral; otherwise, they were seen within 7 days. The confirmation of GCA was conducted during the initial clinic visit by ultrasound or alternative diagnostic methods such as biopsy and was considered the “index event”.
Patient demographics, clinical characteristics, GCA diagnosis and treatment details, as well as any treatment-related adverse events (AEs), were retrospectively extracted by the treating physician through the review of 121 patient records. Diagnostic assessments and clinical observations routinely performed as part of standard care were entered into a clinical database by the physician or delegated staff under their supervision, who were also responsible for completing the case report forms.
Definitions of Selected Terms
For this study, standardized definitions were applied to ensure consistency of classification. New-onset GCA was defined as the first occurrence of symptoms leading to a diagnosis of GCA. Active disease referred to new, persistent, or worsening clinical signs or symptoms attributed to GCA and not related to prior damage. Remission was defined as the absence of clinical signs or symptoms attributed to active GCA, whether or not patients were receiving immunosuppressive therapy. Sustained remission required the absence of GCA-related clinical symptoms and normalization of inflammatory markers (C-reactive protein ≤ 10 mg/L and erythrocyte sedimentation rate ≤ 30 mm/h), maintained continuously for at least six months following the index date. Relapse was defined as the recurrence of active disease after a period of remission. Treatments were categorized as follows: IV pulse GCs (IV methylprednisolone 500–1000 mg/day for 3–5 days); high-dose oral GCs (prednisone 1 mg/kg/day up to 80 mg or equivalent); moderate-dose oral GCs (prednisone 0.5 mg/kg/day, generally 10–40 mg/day in adults, or equivalent); and low-dose oral GCs (prednisone ≤ 10 mg/day or equivalent). Non-GC nonbiologic immunosuppressive therapies included azathioprine, leflunomide (LEF), MTX, mycophenolate mofetil, and cyclophosphamide (Cyclo). Biologic agents encompassed abatacept, tumor necrosis factor inhibitors, and TCZ. Surgical interventions included angioplasty, stent placement, vascular bypass, or vascular grafting procedures.
Inclusion and Exclusion Criteria
Eligible participants were adults with a confirmed diagnosis of new-onset or relapsing GCA established either prior to, or within 1 month after, the index event, defined as the baseline visit to the clinic, which had to occur between January 1, 2017 and February 28, 2024. Inclusion required compatible clinical symptoms together with at least one positive diagnostic test, including color Doppler ultrasound (halo sign, stenosis, or occlusion), temporal artery biopsy, magnetic resonance imaging (MRI), computed tomography angiography (CTA), or positron emission tomography (PET) showing findings consistent with GCA. PET/CT scans were conducted using a standardized protocol: patients fasted for at least 6 h; blood glucose levels were verified prior to radiotracer injection. A weight-based dose of 18F-FDG was administered (approximately 3–5 MBq/kg), and image acquisition began approximately 60 min after tracer injection. All studies were performed on a GE Discovery PET/CT scanner.
Participants were also required to have a minimum of 1 year of follow-up. Patients were excluded if the index event occurred while they were participating in a randomized controlled clinical trial, if they had large-vessel vasculitis associated with autoinflammatory or infectious diseases, or if they had isolated polymyalgia rheumatica (PMR) or isolated aortitis without cranial or branch artery involvement. However, cases of isolated extracranial GCA were eligible if the arterial distribution was compatible with the disease.
Statistical Analysis
All statistical analyses were conducted in accordance with the pre-specified Statistical Analysis Plan (SAP v1.0, dated 21 March 2025) and aligned with the study protocol (SA-004897, version 11 March 2024). Analyses were descriptive in nature, reflecting the retrospective and non-interventional design of the study. No formal hypothesis testing or multiplicity adjustments were performed.
The full analysis set (FAS) included all patients with a confirmed diagnosis of new-onset or relapsing GCA, who initiated treatment for the index event within the defined study window (01 January 2017–28 February 2024) and had at least one follow-up visit. The safety analysis set (SS) consisted of all patients in the FAS who received at least one dose of therapy for the index event. All efficacy and safety analyses were conducted using these respective analysis sets.
Descriptive statistics were used throughout. Continuous variables were summarized using mean, standard deviation (SD), median, interquartile range (IQR; Q1–Q3), minimum, and maximum. Categorical variables were summarized as counts and percentages. Analyses were stratified by initial treatment group: GC only, GC + TCZ, and GC + other immunosuppressive therapies (OIS). Missing data were summarized and handled as observed; no imputation was applied unless otherwise specified in sensitivity analyses.
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The primary endpoint was the proportion of patients achieving sustained remission at 12 months following therapy initiation for the index event.
Unadjusted sustained remission rates were reported for the overall population and each treatment group, with corresponding 95% confidence intervals (CI). Adjusted remission rates were estimated using logistic regression models, accounting for covariates such as baseline Vasculitis Damage Index (VDI), initial GC dose category, GCA duration, number of prior relapses, and year of index event. Odds ratios (ORs) and 95% CIs were reported. Sensitivity analyses included multiple imputations for missing remission status and alternative definitions of remission (e.g., stricter inflammatory marker thresholds or extended duration of remission).
Time-to-remission and duration of sustained remission were estimated using Kaplan–Meier methods, with censoring applied for death, loss to follow-up, or study withdrawal. Kaplan–Meier curves were presented by treatment group. Time-to-event endpoints, such as time to first relapse post-treatment discontinuation (GC, TCZ, or other immunosuppressants (OIS)), were analyzed using Kaplan–Meier methods. Median time to relapse and corresponding 95% CIs were estimated. Patients discontinuing therapy were identified using predefined algorithmic criteria based on medication stop flags and dose plateauing.
Treatment-related AEs were extracted from physician documentation and classified by system organ class. Frequencies of AEs were summarized by treatment group and GC exposure. Time to first adverse event was estimated using Kaplan–Meier methods.
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Data Source and Ethics Approval
This study was conducted in accordance with the Helsinki Declaration of 1964 and its later amendments. Data collection began after the study received approval, from the institution’s Research Ethics Board (Certificate number is 2025–2884; REB: CIUSSS NIM—Hôpital du Sacré-Coeur de Montréal). This study was a retrospective cohort design using non-identifiable data from patients’ medical records and therefore patient consent was not required. All data were anonymized before analysis to ensure confidentiality.
Results
A total of 255 patients were assessed for eligibility (Fig. 1 and Table 1). Of these, 134 were excluded for the following reasons: patients were seen for opinions/consultations only with insufficient follow-up time as they were actively followed at other centers (69, 27.1%), patients did not experience an index event during the study period (42, 16.5%), and misdiagnosis of GCA (23, 9.0%) including cases of isolated PMR (12, 4.7%), isolated aortitis (9, 3.5%) (isolated aortitis was not classified as GCA unless the large vessel phenotype was compatible), and VEXAS syndrome (2, 0.8%) (not target population). Ultimately, patients (121, 47.5%) fulfilling the inclusion and exclusion criteria were included in the final analysis and all patients (121, 100%) met the 2022 American College of Rheumatology (ACR)/European Alliance of Associations for Rheumatology (EULAR) classification criteria for GCA. All patients in the GC + OIS group were treated with MTX as the primary steroid-sparing agent. A few patients switched from GC + MTX to GC + LEF (3, 3%) or from GC only to GC + Cyclo (1, 1%) when other treatments were not possible. No other conventional synthetic disease-modifying antirheumatic drugs (DMARDs), biologic agents, or JAK inhibitors were used within this subgroup during the study period.
FAS full analysis set, GC glucocorticoid, GCA giant cell arteritis, N number of patients in treatment arm, n number of patients in specified population or group, SS safety analysis set, TCZ tocilizumab, OIS other immunosuppressant
aFAS population Includes all patients who meet the eligibility criteria as specified. Confirmed diagnosis of new-onset or relapsing GCA, either prior to or within 1 month of the index event. Index event occurring between January 1, 2017 and February 28, 2024 (inclusive). Initiation of treatment for the index event within the defined study period
bSS population consists of all FAS patients who received at least one dose of therapy for the index event
Baseline Characteristics
The GCA study population included 121 patients living with GCA, predominantly female (83, 68.6%) and white (111, 91.7%) (Table 2). The GCA diagnoses were either new-onset (104, 86.0%) or relapsing (17, 14.0%) at index date (Table 3). The proportion of new-onset cases was similar across treatment groups (42 or 87.5% in the GC only group, 55 or 87.3% in the GC combined with TCZ group (GC + TCZ), and 7 or 70.0% in the GC combined with OIS group (GC + OIS).
Table 2
Baseline demographic characteristics
GC (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
Sex, n (%)
Male
18 (37.5%)
16 (25.4%)
4 (40.0%)
38 (31.4%)
Female
30 (62.5%)
47 (74.6%)
6 (60.0%)
83 (68.6%)
Age, years
Mean (SD)
77.6 (8.07)
75.0 (8.65)
72.7 (8.90)
75.9 (8.52)
Median
79
75
74
76
Q1, Q3
73, 83
68, 81
69, 80
69, 82
Min, max
61, 93
54, 91
53, 85
53, 93
Age groups (years), n (%)
50–64
4 (8.3%)
10 (15.9%)
1 (10.0%)
15 (12.4%)
65–74
11 (22.9%)
21 (33.3%)
4 (40.0%)
36 (29.8%)
≥ 75
33 (68.8%)
32 (50.8%)
5 (50.0%)
70 (57.9%)
Race, n (%)
White
42 (87.5%)
60 (95.2%)
9 (90.0%)
111 (91.7%)
Black
1 (2.1%)
1 (1.6%)
0
2 (1.7%)
Asian
2 (4.2%)
2 (3.2%)
1 (10.0%)
5 (4.1%)
Unknown
3 (6.3%)
0
0
3 (2.5%)
Baseline weight (kg)
n*
47
63
10
120
Mean (SD)
66.7 (12.53)
64.7 (10.20)
65.2 (10.90)
65.5 (11.17)
Median
64
65
66
65
Q1, Q3
58, 74
58, 71
58, 72
58, 71
Min, max
48, 100
43, 90
43, 80
43, 100
Median
1.62
1.67
1.64
1.65
Q1, Q3
1.59, 1.70
1.60, 1.70
1.60, 1.72
1.59, 1.70
Min, max
1.54, 1.80
1.51, 1.79
1.50, 1.75
1.50, 1.80
Baseline BMI (kg/m2)
n*
45
60
10
115
Mean (SD)
24.76 (3.854)
23.69 (3.355)
23.86 (2.349)
24.12 (3.502)
Median
24
22.9
23.7
23.5
Q1, Q3
22.1, 26.0
21.5, 24.7
22.7, 26.4
21.7, 25.5
Min, max
18.8, 36.1
18.5, 34.2
19.1, 27.0
18.5, 36.1
Based on full analysis set
n* indicates the number of patients with available data; for any baseline characteristic where n is not specified, data are available for all patients
BMI body mass index, GC glucocorticoid, min minimum, max maximum, N number of patients in treatment arm, n number of patients with given characteristic, Q1 first quartile (25%), Q3 third quartile (75%), SD standard deviation, TCZ tocilizumab, OIS other immunosuppressants
Table 3
Giant cell arteritis relapse vs. new onset
Category
GC (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
Patients with new onset GCAa
42 (87.5%)
55 (87.3%)
7 (70.0%)
104 (86.0%)
Relapse GCA
6 (12.5%)
8 (12.7%)
3 (30.0%)
17 (14.0%)
Based on full analysis set
GC glucocorticoid, GCA giant cell arteritis, N number of patients in treatment arm, TCZ tocilizumab, OIS other immunosuppressant
aProportions per treatment group = (n/N) × 100
The median age (76 years, IQR 69–82) showed that more than half of the patients were aged 75 years or older (70, 57.9%); the median weight (65 kg, IQR 58–71) and the median BMI (23.5 kg/m2, IQR 22.1–26.0) were also recorded. Many patients had comorbid conditions, including hypertension (76, 62.8%), diabetes (21, 17.4%), and coronary artery disease (16, 13.2%). Smoking history showed that over half of patients had never smoked (63, 52.1%), while some were former smokers (52, 43.0%), or current smokers (6, 5.0%). The mean erythrocyte sedimentation rate (ESR) (49.7 mm/h, SD 18.6, median 49, IQR 36–60), and the mean C-reactive protein (CRP) (88.9 mg/L, SD 71.4, median 66, IQR 36–120) were reported at baseline.
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All (121, 100%) patients received oral GCs, with several (19, 15.7%) also receiving GCs intravenously (Tables 4 and 5). Intravenous GCs were administered to patients during the diagnostic workup, prior to confirmation of GCA diagnosis. The mean daily oral dose was 54.3 mg (SD 11.1), with a median of 60 mg (IQR 50–60) across treatment groups.
Table 4
Baseline clinical characteristics
GC (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
ESR (mm/h)
n*
43
60
10
113
Mean (SD)
48.4 (21.30)
50.3 (17.88)
52.2 (8.18)
49.7 (18.58)
Median
47
49
51
49
Q1, Q3
31, 60
40, 61
48, 60
36, 60
Min, max
15, 120
14, 96
36, 63
14, 120
CRP (mg/L)
Mean (SD)
83.4 (66.51)
99.1 (75.58)
51.4 (54.54)
88.9 (71.35)
Median
65
77
37
66
Q1, Q3
36, 117
41, 131
12, 64
36, 120
Min, max
5, 300
4, 300
4, 189
4, 300
History of hypertension, n (%)
Yes
30 (62.5%)
42 (66.7%)
4 (40.0%)
76 (62.8%)
No
18 (37.5%)
21 (33.3%)
6 (60.0%)
45 (37.2%)
History of diabetes, n (%)
Yes
10 (20.8%)
11 (17.5%)
0
21 (17.4%)
No
38 (79.2%)
52 (82.5%)
10 (100.0%)
100 (82.6%)
History of coronary artery disease, n (%)
Yes
8 (16.7%)
7 (11.1%)
1 (10.0%)
16 (13.2%)
No
40 (83.3%)
56 (88.9%)
9 (90.0%)
105 (86.8%)
Smoking status, n (%)
Never
24 (50.0%)
33 (52.4%)
6 (60.0%)
63 (52.1%)
Past
23 (47.9%)
25 (39.7%)
4 (40.0%)
52 (43.0%)
Current
1 (2.1%)
5 (7.9%)
6 (5.0%)
History of prior GC use, n (%)
Yes
32 (66.7%)
50 (79.4%)
7 (70.0%)
89 (73.6%)
No
16 (33.3%)
13 (20.6%)
3 (30.0%)
32 (26.4%)
History of prior TCZ use, n (%)
Yes
0
0
0
0
No
48 (100.0%)
63 (100.0%)
10 (100.0%)
121 (100.0%)
History of prior OIS use, n (%)
Yes
0
0
0
0
No
48 (100.0%)
63 (100.0%)
10 (100.0%)
121 (100.0%)
Number of previous relapses
n*
42 (87.5%)
55 (87.3%)
7 (70.0%)
104 (86.0%)
Mean (SD)
0.1 (0.41)
0.1 (0.34)
0.4 (0.70)
0.2 (0.41)
Median
0
0
0
0
Q1, Q3
0, 0
0, 0
0, 1
0, 0
Min, max
0, 2
0, 1
0, 2
0, 2
Time since GCA diagnosis (days)
Mean (SD)
101.2 (287.20)
84.0 (224.07)
541.6 (963.10)
128.6 (378.64)
Median
0
0
0
0
Q1, Q3
0, 0
0, 0
0, 806
0, 0
Min, max
0, 1397
0, 904
0, 2358
0, 2358
GC use (IV), n (%)
Yes
7 (14.6%)
9 (14.3%)
3 (30.0%)
19 (15.7%)
No
41 (85.4%)
54 (85.7%)
7 (70.0%)
102 (84.3%)
GC daily oral dose (mg)a
Mean (SD)
53.0 (12.45)
55.7 (8.88)
52.0 (16.19)
54.3 (11.10)
Median
60
60
60
60
Q1, Q3
50, 60
50, 60
40, 60
50, 60
Min, max
20, 80
30, 75
30, 80
20, 80
Cumulative GC exposure prior to index date (mg)b
Mean (SD)
609.2 (1143.0)
417.4 (739.9)
1163.3 (1477.1)
550.0 (993.5)
Median
120
120
360
120
Q1, Q3
0, 320
60, 360
50, 1500
0, 380
Min, max
0, 5020
0, 4274
0, 4000
0, 5020
TCZ use, n (%)
Yes
0
63 (100.0%)
0
63 (52.1%)
No
48 (100.0%)
0
10 (100.0%)
58 (47.9%)
OIS use, n (%)c
Yes
0
0
10 (100.0%)
10 (8.3%)
No
48 (100.0%)
63 (100.0%)
0
111 (91.7%)
MTX use, n (%)
Yes
0
0
10 (100.0%)
10 (8.3%)
No
48 (100.0%)
63 (100.0%)
0
111 (91.7%)
LEF use, n (%)
Yes
0
0
0
0
No
48 (100.0%)
63 (100.0%)
10 (100.0%)
121 (100.0%)
OIS combination use, n (%)
Yes
0
0
10 (100.0%)
10 (8.3%)
No
48 (100.0%)
63 (100.0%)
0
111 (91.7%)
Prior GC use, n (%)
Yes
48 (100.0%)
63 (100.0%)
9 (90.0%)
120 (99.2%)
No
0
0
1 (10.0%)
1 (0.8%)
Prior TCZ use, n (%)
Yes
0
0
0
0
No
48 (100.0%)
63 (100.0%)
10 (100.0%)
121 (100.0%)
Prior OIS use, n (%)
Yes
0
0
0
0
No
48 (100.0%)
63 (100.0%)
10 (100.0%)
121 (100.0%)
Time from GCA diagnosis to treatment initiation (days)d
n*
42
55
7
104
Mean (SD)
0.0 (0.00)
0.6 (4.72)
0.0 (0.00)
0.3 (3.43)
Median
0
0
0
0
Q1, Q3
0, 0
0, 0
0, 0
0, 0
Min, max
0, 0
0, 35
0, 0
0, 35
Based on full analysis set
n* indicates the number of patients with available data; for any baseline characteristic where n is not specified, data are available for all patients
CRP C-reactive protein, ESR erythrocyte sedimentation rate, GC glucocorticoid, GCA giant cell arteritis, IV intravenous, LEF leflunomide, max maximum, MTX methotrexate, min minimum, N number of patients in treatment arm, n number of patients with given characteristic, Q1 first quartile (25%), Q3 third quartile (75%), SD standard deviation, TCZ tocilizumab, OIS other immunosuppressants
aGC use includes any glucocorticoid treatment at index
bCumulative GC exposure prior to index date
cOIS use includes methotrexate, leflunomide, or other immunosuppressants
dPatients who were experiencing a relapse at the index event were excluded from this analysis, as their initial diagnosis and corresponding treatment occurred prior to the index event. This resulted in 6 patients in the GC only group, 8 patients in the GC + TCZ group, and 3 patients in the GC + OIS group being included in the table
Table 5
Proportion of patients receiving glucocorticoids, tocilizumab, or other immunosuppressants at baseline
Therapy type
GC (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
Glucocorticoid (IV)
7 (14.6%)
9 (14.3%)
3 (30.0%)
19 (15.7%)
Glucocorticoid (oral)
48 (100.0%)
63 (100.0%)
10 (100.0%)
121 (100.0%)
Tocilizumab
0
63 (100.0%)
0
63 (52.1%)
Methotrexate
0
0
10 (100.0%)
10 (8.3%)
Leflunomide
0
0
0
0
Other immunosuppressant
0
0
0
0
Based on full analysis set. % = Proportion of group receiving therapy
CI confidence interval, GC glucocorticoid, IV intravenous, N number of patients in treatment arm, n number of patients in specified population or group, TCZ tocilizumab, OIS other immunosuppressant
PMR without cranial symptoms was observed in a small proportion of patients (5, 4.1%), with similar proportions across treatment groups (2 or 4.2% in the GC group, 3 or 4.8% in the GC + TCZ group, and none in the GC + OIS group) (Table 6).
Table 6
Polymyalgia rheumatica without cranial symptoms
PMR without cranial symptomsa
GC (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
Yesb
2 (4.2%)
3 (4.8%)
0
5 (4.1%)
Nob
46 (95.8%)
60 (95.2%)
10 (100.0%)
116 (95.9%)
Based on full analysis set
GC glucocorticoid, N number of patients in treatment arm, TCZ tocilizumab, OIS other immunosuppressant, PMR polymyalgia rheumatica
aDerived using logical AND of symptom absence and PMR presence
b% = n/N per group
Treatment Patterns
The mean time from GCA diagnosis to initiation of therapy was 128.6 days (SD 378.6) across all patients (Table 7). Subgroup analysis revealed shorter mean initiation times for patients treated with GC only (48, 101.2 days (SD 287.2)) and those receiving GC + TCZ (63, 84.0 days (SD 224.1)). In contrast, patients treated with GC + OIS experienced a later start (10, 514.6 days (SD 963.1)) after trying other treatments first.
Table 7
Time from giant cell arteritis diagnosis to therapy initiation
Statisticsa
GC (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
Patientsb
48
63
10
121
Mean (SD) time to therapy initiation (days)c
101.2 (287.20)
84.0 (224.07)
541.6 (963.10)
128.6 (378.64)
Median time to therapy initiation (days)d
0.0
0.0
0.0
0.0
95% CI for median (days)d
0.0–786.0
0.0–724.0
0.0–2358.0
0.0–904.0)
Based on full analysis set
CI confidence interval, GC glucocorticoid, GCA giant cell arteritis, N number of patients in treatment arm, n number of patients with given characteristic, TCZ tocilizumab, SD standard deviation, OIS other immunosuppressant
aContinuous endpoint presented by group
bN = patients with valid diagnosis and index dates
cDerived variable: index_date–date_gca_dx
dMedian (95% CI) time from GCA diagnosis to therapy initiation was calculated using descriptive statistics. No censoring was present
The median cumulative GC exposure prior to the index date (120 mg, IQR 0–380), the mean exposure (550 mg, SD 993.5), and the range (up to 5020 mg) were reported (Table 4). None of the patients had prior exposure to TCZ or OIS, and no OIS were used at baseline.
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At index date treatment regimens varied and included GC only (48, 40.0%), GC + TCZ (63, 52.1%), and GC + MTX (10, 8.3%). In the group taking GC only, most were treated orally (40, 83.3%), while a smaller number received GC intravenously (8, 16.7%) (Table 5). Those receiving GC only intravenously were subsequently transitioned to orally administered prednisone.
Figure 2 presents a Sankey diagram illustrating the treatment patterns among patients with GCA, highlighting the frequent transitions between therapies. At baseline (index event), treatment was distributed between GC monotherapy (48, 40%), GC + TCZ (63, 52%), and GC + MTX (10, 8%) (Table 5). By 1 year, GC monotherapy increased by 33 patients and became the predominant regimen (81, 67%), while GC + TCZ decreased by 41 patients (22, 18%), GC + MTX increased by 5 patients (15, 12%), two patients (2, 2%) started LEF, and one patient (1, 1%) discontinued treatment. At 2 years, GC monotherapy remained dominant (86, 71%), GC + TCZ declined further (14, 12%), GC + MTX treatment remained relatively stable (14, 12%), one patient was on LEF (1, 1%) and treatment discontinuation increased (6, 5%). These changes were often driven by factors such as adverse side effects, disease relapse, or in the case of TCZ, the expiration of provincial coverage after 1 year.
Fig. 2
Sankey diagram showing giant cell arteritis treatment patterns. Cyclo cyclophosphamide, GC glucocorticoid, LEF leflunomide, MTX methotrexate, TCZ tocilizumab. Red = GC only, Blue = GC + TCZ, Green = GC + MTX, Yellow = GC + Cyclo, Orange = GC + LEF, Purple = END (end of patient study participation, no subsequent follow-up visits), Dark blue = STOP (patient stopped all treatment). One month visit occurred within ± 2 weeks, 3 month visit within ± 1 month, 6 month visit within ± 2 months, 1–3 year visits within ± 2.5–4 months
Of the 121 patients included in the study, approximately two-thirds (83, 68.6%) were in unadjusted sustained remission at 12 months (Table 8). The unadjusted sustained remission rate was similar in the GC only (35, 72.9%) and the GC + TCZ (44, 69.8%) groups, while the GC + OIS group rate was lower (4, 40.0%) (Table 8). Adjusted logistic regression analysis for sustained remission at 12 months can be found in the Supplementary Material, Table S1.
Table 8
Primary analysis: unadjusted sustained remission rates at 12 months
Sustained remission at 12 months, n (%)a
GC only (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
Yes
35 (72.9%)
44 (69.8%)
4 (40.0%)
83 (68.6%)
No
13 (27.1%)
19 (30.2%)
6 (60.0%)
38 (31.4%)
95% CI
60.3–85.5%
58.5–81.2%
9.6–70.4%
60.3–76.9%
Based on full analysis set
CRP C-reactive protein, ESR erythrocyte sedimentation rate, GCA giant cell arteritis, N number of participants in treatment arm, n number of participants achieving sustained remission, CI confidence interval, GC glucocorticoids, OIS other immunosuppressant, TCZ tocilizumab
aSustained remission defined as absence of GCA symptoms, ESR = 30 mm/h, CRP = 10 mg/L, maintained for 6 months within 12 months of index event
Despite treatment, relapse was prevalent with close to half of patients (58, 47.9%) experiencing at least one relapse. The median time to first relapse was under 1 year (283.5 days, 95% CI for median = 206.0–326.0) (Table 9). Just under two-thirds (6, 60.0%) of patients in the GC + OIS group experienced a relapse (Table 9). Patients who relapsed after initial GC only therapy were clinically evaluated, and either TCZ or MTX was introduced on the basis of individual risk assessment and guideline-aligned practice, with adjunctive therapy added when relapse risk or steroid toxicity was a concern.
Table 9
Time from index event (first remission) to first relapse (full analysis set)
Statistics
GC (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
Patients with ≥ 1 relapsea
21 (43.8%)
31 (49.2%)
6 (60.0%)
58 (47.9%)
Median time to first relapse (days)b
314
242
303.5
283.5
95% CI for median (days)b
114.0–372.0
175.0–314.0
133.0–NE*
206.0–326.0
Median time to first relapse (days)c
NE*
1118.0
528.0
1129.0
95% CI for median (days)c
631–NE*
636–NE*
133.0–NE*
683.0–NE*
Based on full analysis set
CI confidence interval, GC glucocorticoid, N number of patients in treatment arm, n number of patients with given characteristic, OIS other immunosuppressant, SD standard deviation, TCZ tocilizumab
*Not estimable because of insufficient events or data censoring
aCount of patients who experienced ≥ 1 relapse
bMedian (95% CI) time from first remission to first relapse was calculated using descriptive statistics. No censoring was present
cMedian time to relapse and corresponding 95% confidence interval were estimated using the Kaplan–Meier method, based on the time at which the survival probability reaches 50%. Estimates are derived from observed relapse times, with censoring appropriately accounted for
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Among patients who discontinued TCZ (47, 74.6%), a quarter (16, 25.4%) experienced a relapse, with a median time to relapse of 254.0 days (95% CI for median was not estimable as a result of insufficient events or data censoring) (Table 10). Patients in the GC-only treatment group who discontinued GC (27, 56.3%) saw fewer relapses following GC discontinuation (6, 4.9%) (Table 11). Similarly, among patients in the GC + OIS group who discontinued OIS (7, 70%), a small number of patients relapsed (2, 20%) (Table 12). In the first year, a third (22, 35.0%) of patients still on TCZ relapsed, and additional (12, 19.0%), though fewer, relapses occurred in the second year (Table 13).
Table 10
Time from tocilizumab discontinuation to first relapse
Statistic
GC (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
Patients discontinued TCZ [n (%)]a
8 (16.7%)
57 (90.5%)
3 (30.0%)
68 (56.2%)
Relapsed post-discontinuation
3 (6.3%)
16 (25.4%)
2 (20.0%)
21 (17.4%)
Median time to relapse (days)b
344.0
254.0
458.5
344.0
95% CI for median (days)
NE*
NE*
499.0 (418.0–NE*)
NE*
Based on full analysis set
CI confidence interval, GC glucocorticoid, N number of patients in treatment arm, n number of patients with given characteristic, TCZ tocilizumab, OIS other immunosuppressant
*Not estimable because of insufficient events or data censoring
aMedian was calculated using descriptive statistics. No censoring was present
bMedian time to relapse and corresponding 95% confidence interval were estimated using the Kaplan–Meier method, based on the time at which the survival probability reaches 50%. Estimates are derived from observed relapse times, with censoring appropriately accounted for
Table 11
Time from glucocorticoid discontinuation to first relapse
Statistic
GC (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
Patients discontinued GC [n (%)]
27 (56.3%)
43 (68.3%)
7 (70.0%)
77 (63.6%)
Relapsed post-discontinuation
2 (4.2%)
4 (6.3%)
0
6 (4.9%)
Median time to relapse (days)a
521.0
756.5
NE*
756.5
95% CI for median (days)b
NE*
NE*
NE*
NE*
Based on full analysis set
CI confidence interval, GC glucocorticoid, N number of patients in treatment arm, n number of patients with given characteristic, TCZ tocilizumab, OIS other immunosuppressant
*Not estimable because of insufficient events or data censoring
aMedian was calculated using descriptive statistics. No censoring was present
bMedian time to relapse and corresponding 95% confidence interval were estimated using the Kaplan–Meier method, based on the time at which the survival probability reaches 50%. Estimates are derived from observed relapse times, with censoring appropriately accounted for
Table 12
Time from other immunosuppressant discontinuation to first relapse
Statistic
GC (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
Patients discontinued OIS [n (%)]
3 (6.3%)
4 (6.3%)
7 (70.0%)
14 (11.6%)
Relapsed post-discontinuation
0
1 (1.6%)
2 (20.0%)
3 (2.5%)
Median time to relapse (days)a
NE*
NE*
636.5
505.0
95% CI for median (days)b
NE*
NE*
NE*
NE*
Based on full analysis set
CI confidence interval, GC glucocorticoid, N number of patients in treatment arm, n number of patients with given characteristic, TCZ tocilizumab, OIS other immunosuppressant
*Not estimable because of insufficient events or data censoring
aMedian was calculated using descriptive statistics. No censoring was present
bMedian time to relapse and corresponding 95% confidence interval were estimated using the Kaplan–Meier method, based on the time at which the survival probability reaches 50%. Estimates are derived from observed relapse times, with censoring appropriately accounted for
Table 13
Number of relapse events by year
Follow-up perioda
GC (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
0–12 months
15
22
6
43
> 12–24 months
9
12
1
22
> 24–36 months
3
6
1
10
Based on full analysis set
GC glucocorticoid, N number of patients in treatment arm, TCZ tocilizumab, OIS other immunosuppressant
aTotal number of relapse events recorded within each 12-month interval after index event
Glucocorticoid Use
The cumulative GC exposure over the first 12 months varied among treatment groups, with GC + TCZ group experiencing the lowest overall GC burden (Table 14). The mean cumulative GC dose was the highest in the GC only group (4690 mg, SD 969), followed by the GC + OIS group (4539 mg, SD 1289), and lowest in the GC + TCZ group (3431 mg, SD 1049). While the range of cumulative doses spanned all groups, the GC + TCZ group exhibited both the lowest minimum (1985 mg) and a lower maximum (6948 mg). MTX use, however, was associated with higher overall GC exposure, indicating a less pronounced steroid-sparing effect. These results are further corroborated by annualized dosing trends illustrated in Fig. 3, showing consistently lower GC use in the TCZ-treated cohort. However, despite TCZ’s role as a steroid-sparing agent, all participating1 patients (120, 99.2%) were still receiving GCs at week 52, highlighting the persistent difficulty in achieving steroid-free remission. This underscores the complexity of disease management and the limitations of current therapeutic strategies in fully eliminating GC dependence.
Table 14
Cumulative glucocorticoid dose over first 12 months
Statistics
GC (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
Mean (SD) cumulative GC dose (mg)
4690 (969)
3431 (1049)
4539 (1289)
4027 (1202)
Median GC dose (mg)
4380.0
3100.0
4395.0
3990.0
Range (min–max)
2860–7350
1985–6948
2115–6330
1985–7350
Based on full analysis set
GC glucocorticoid, max maximum, min minimum, N number of patients in treatment arm, SD standard deviation, TCZ tocilizumab, OIS other immunosuppressants
Fig. 3
Annualized dosing trends by treatment group (full analysis set). GC glucocorticoid, mg milligram, TCZ tocilizumab, OIS other immunosuppressant. Histogram of final cumulative GC dose (mg, prednisone equivalent) over 12 months. Colored bars represent number of patients in each treatment group by dose range. Overlaid lines represent kernel density estimates (smoothed distribution) for each group
Treatment-related AEs were documented across all groups, with hypertension (31, 25.6%) and hyperglycemia (10, 8.3%) representing the most frequently reported events (Table 15). Infections (21, 17.4%) occurred with slightly higher rates in the GC + TCZ group (13, 20.6%) compared to the GC only group (7, 14.6%). A small number of gastrointestinal upset events (7, 5.8%) as well as psychiatric (5, 4.1%) AEs were reported. Notably, a few patients (2, 1.7%) in the GC + TCZ group experienced bowel perforation, a known potential side effect of TCZ therapy. Osteoporosis was reported in patients (2, 3.2%) receiving GC + TCZ with no documented cases in other groups.
Table 15
Treatment-related adverse effects
Adverse effecta
GC (N = 48)
GC + TCZ (N = 63)
GC + OIS (N = 10)
Total (N = 121)
Osteoporosis
0
2 (3.2%)
0
2 (1.7%)
Hyperglycemia
4 (8.3%)
6 (9.5%)
0
10 (8.3%)
Hypertension
14 (29.2%)
17 (27.0%)
0
31 (25.6%)
Infections
7 (14.6%)
13 (20.6%)
1 (10.0%)
21 (17.4%)
Psychiatric AEs
2 (4.2%)
2 (3.2%)
1 (10.0%)
5 (4.1%)
GI upset
2 (4.2%)
4 (6.3%)
1 (10.0%)
7 (5.8%)
Bowel perforations
0
2 (3.2%)
0
2 (1.7%)
Based on full analysis set
AE adverse event, GC glucocorticoid, GI gastrointestinal, N number of patients in treatment arm, TCZ tocilizumab, OIS other immunosuppressant
aEvent categories manually curated. Frequencies are raw counts by treatment group
Discussion
Interpretation of Results
This study highlights the ongoing unmet need for effective therapeutics and long-term treatment strategies in GCA. Findings from our cohort, as well as data from large registry studies, confirm that GCA is a relapsing–remitting disease in most cases, with relapse rates approaching 45% within 3–4 years, and cumulative rates as high as 45% at 4 years [12]. This is consistent with other studies, where the rate of achieving sustained drug-free remission is only about 25% by year 4 [13]. In our cohort, despite the use of GCs and adjunctive therapies such as TCZ and MTX, relapse rates remained high. Nearly half of the patients (58, 47.9%) experienced at least one relapse, with a median time to first relapse of 283.5 days (95% CI for median 206–326). Notably, 60% of patients in the GC + OIS group relapsed, a rate comparable to GC monotherapy, echoing the limited GC-sparing efficacy of MTX seen in real-world studies [14]. This is further reinforced by recent findings that conventional immunosuppressants like MTX have not demonstrated consistent benefit in preventing relapse or reducing steroid burden compared to GCs alone [7].
In this cohort, time to first relapse was shorter among patients who stopped TCZ in the GC + TCZ group compared with those who stopped GC in the GC only group. This observation likely reflects differences in tapering strategies: patients treated with TCZ underwent a shorter glucocorticoid taper, typically completed within 6–7 months, which was associated with earlier relapses. In contrast, monotherapy patients followed a more gradual tapering schedule (approximately 12–18 months), with relapses generally occurring at lower prednisone doses (approximately 7.5–10 mg/day) and often beyond the first year of treatment. These findings suggest that while TCZ may enable faster steroid reduction, relapses will occur once off of the treatment, underscoring the need for individualized therapies lasting more than the current 12-month treatment duration. In this study, patients treated with GC + TCZ experienced lower cumulative GC exposure over 12 months (mean 3431 mg (SD 1049) compared to 4690 mg (SD 969) in the GC only group), confirming TCZ’s established GC-sparing effect as demonstrated in GiACTA [10] and large observational studies [15]. However, despite this benefit, relapse rates remained substantial: 22 (35.0%) patients relapsed within the first year of TCZ therapy, and a further 12 patients (19.0%) relapsed in the second year. These findings from our and other cohorts suggest that, for a subset of patients, while TCZ reduces cumulative steroid exposure, extended treatment durations or additional therapeutic options may be necessary to sustain remission [12].
Our observations align closely with published literature: for example, a Spanish multicenter cohort found that 15.5% of TCZ-treated patients relapsed after a median follow-up of 2 years, with about half of those relapses occurring while still on therapy [15]. Furthermore, even after extended follow-up, multiple studies have reported relapse rates of 25–50% following TCZ withdrawal [13, 15]. In our study, ceasing TCZ after 1 year led to relapse in more than a quarter of patients, mirroring these international results.
A case study from this cohort further illustrates this point: a patient receiving TCZ experienced repeated flares and hospitalizations each time treatment was discontinued after 1 year. In Quebec, as in most Canadian provinces, reimbursement for TCZ in patients with GCA is restricted to 1 year. This limitation may lead to premature treatment discontinuation and increase the risk of disease relapse, as median relapse times after treatment discontinuation tend to cluster around 6–9 months [13, 15]. In our dataset, 25.4% patients relapsed after discontinuing TCZ, with a median time to relapse of 254.0 days (95% CI for median was not estimable because of insufficient events or data censoring), reinforcing the need for extended treatment in select patients.
Clinical Implications
These findings have important implications for the management of GCA. The high relapse rates and steroid burden observed in this cohort emphasize the need for longer-term pharmacologic support and highly individualized treatment plans to determine both the duration and intensity of therapy.
While TCZ has demonstrated a clear GC-sparing effect, its discontinuation was frequently followed by relapse, indicating that treatment duration should be individualized on the basis of disease activity rather than constrained by fixed reimbursement timelines. Furthermore, patients who require an oral therapeutic, or are unable to take TCZ because of contraindications, as well as those who experience a relapse while on TCZ, underscore a broader unmet need for additional therapeutic options in GCA, highlighting the importance of expanding the treatment landscape beyond currently available agents. Long-term monitoring and proactive management of AEs are essential to optimize outcomes and reduce the risk of complications associated with both disease and treatment in some patients.
Limitations
This study has several limitations. All patients were treated at a single center under the care of 12 physicians, which may limit generalizability. AEs were based on physician assessment and patient memory, introducing potential recall bias. This was mitigated by regular follow-up with an experienced clinician, particularly during the first-year post-diagnosis or relapse. The retrospective nature of the analysis may have led to underreporting of AEs, and the absence of a GC-free comparator group limits interpretation of GC-specific effects. Additionally, small sample sizes within treatment subgroups reduce the statistical power of adjusted analyses, and results should be interpreted with caution.
Future Directions
Future research should focus on prospective, multicenter studies to validate these findings and explore optimal treatment durations for TCZ and other emerging therapies. There is a critical need to develop and evaluate additional steroid-sparing agents that can provide durable remission, particularly for patients who are unable to tolerate TCZ or who relapse despite treatment. The limited therapeutic arsenal for GCA underscores the urgency of identifying novel agents with distinct mechanisms of action to address the heterogeneity of disease presentation and treatment response. Emerging therapies include JAK inhibitors, IL-17 inhibitors, and selective glucocorticoid receptor modulators, but long-term safety and efficacy data are limited [7]. Importantly, policy changes that allow for flexible, patient-centered treatment durations, particularly for advanced therapies, may improve long-term outcomes in GCA and reduce the burden of GC-related toxicity in this population.
Conclusion
This study provides a comprehensive evaluation of treatment patterns, GC burden, relapse rates, and AEs in a cohort of patients with GCA. Key findings include the high rate of relapse across all treatment groups, with close to half of all patients (58, 47.9%) experiencing at least one relapse within the first year. TCZ demonstrated a GC-sparing effect, with lower cumulative steroid exposure compared to other regimens; however, relapse following its discontinuation was common, particularly in settings where reimbursement limits treatment duration to 1 year. MTX did not show evidence of reducing the GC burden or improving remission rates. AEs were generally low, though gastrointestinal complications, including bowel perforation, were observed in the TCZ group.
Clinically, these findings underscore the need for individualized, long-term treatment strategies in GCA, with particular attention to minimizing steroid exposure and maintaining disease control beyond the first year. The recurrent nature of GCA and the pattern of flares following treatment cessation highlight the importance of sustained pharmacologic support and close monitoring. From a research perspective, future studies should aim to validate these findings in larger, multicenter cohorts and explore novel therapeutic options that offer durable remission. Policy adjustments to support extended access to GC-sparing therapies may be critical in improving long-term outcomes for patients living with GCA.
Acknowledgements
The authors sincerely thank all patients whose participation made this study possible.
Medical Writing/Editorial Assistance
The authors thank Michelle Dennehy of Calian Health for providing medical writing and editorial assistance in the preparation of this manuscript. Funding for this assistance was provided by AbbVie. The authors used Microsoft Copilot to support editing, language, and grammar during manuscript development. The authors have reviewed and taken full responsibility for any edits made using AI tools.
Declarations
Conflict of Interest
The research was conducted independently by the investigator at Hôpital du Sacré-Coeur de Montréal and the sponsor (AbbVie Corporation) had no role in the data collection. Jean-Paul Makhzoum reports consultancies, research grants, and speaker fees from the following: AbbVie, Otsuka, Amgen, Sanofi, Kabi Fresenius and AstraZeneca. He received a salary award from Fonds de Recherche du Québec and research funding from the Canadian Institutes of Health Research. Miriam Avadisian and Dalinda Liazoghli are employees of AbbVie Corporation.
Ethical Approval
This study was conducted in accordance with the Helsinki Declaration of 1964 and its later amendments. Data collection began after the study received approval, from the institution’s Research Ethics Board (Certificate number is 2025–2884; REB: CIUSSS NIM—Hôpital du Sacré-Coeur de Montréal). This study was a retrospective cohort design using non-identifiable data from patients’ medical records and therefore patient consent was not required. All data were anonymized before analysis to ensure confidentiality. Only data specified in the protocol was submitted to AbbVie. Neither AbbVie nor any agents acting on behalf of AbbVie completed the case report forms.
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