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On-Label Treatment Persistence Through 24 Months Among Patients with Active Psoriatic Arthritis Initiating Guselkumab or Subcutaneous Tumor Necrosis Factor Inhibitors
There is limited prior literature comparing long-term treatment persistence between guselkumab and subcutaneous (SC) tumor necrosis factor inhibitors (TNFi) in biologic-naïve and biologic-experienced patients with active psoriatic arthritis (PsA). This study compared on-label persistence through 24 months between patients with active PsA newly initiating guselkumab or SC TNFi.
Methods
IQVIA PharMetrics® Plus database was used to identify adults with active PsA initiating guselkumab or an SC TNFi (adalimumab or biosimilar, certolizumab pegol, etanercept or biosimilar, SC golimumab) between 07/14/2020 and 12/31/2022 (index date: first treatment claim for one of these medications). Patients were further stratified as biologic-naïve (no pre-index biologic disease-modifying antirheumatic drug [bDMARD] claim) or biologic-experienced (≥ 1 pre-index bDMARD claim). The guselkumab and SC TNFi cohorts were balanced using overlap propensity score weighting. Treatment persistence with on-label therapy (absence of dose modification or therapy exposure gap of twice the duration between consecutive administrations, i.e., 112 days for guselkumab or 56 days for SC TNFi) was estimated using weighted Kaplan–Meier analysis through 24 months. On-label persistence rates were compared between cohorts using weighted Cox proportional hazards models.
Results
In the guselkumab cohort (N = 804), 361 (44.9%) were biologic-naïve and 443 (55.1%) were biologic-experienced; in the SC TNFi cohort (N = 2490), 2171 (87.2%) were biologic-naïve and 319 (12.8%) were biologic-experienced. At 24 months post index, on-label persistence rates were 45.5% (guselkumab) versus 28.5% (SC TNFi; P < 0.001). Patients initiating guselkumab were 2.24 times more likely to be persistent with on-label therapy through 24 months than patients initiating an SC TNFi (hazard ratio [95% confidence interval] 2.24 [1.90, 2.64]; P < 0.001). Results were consistent among biologic-naïve (2.36 [1.88, 2.98]; P < 0.001) and biologic-experienced patients (1.86 [1.46, 2.37]; P < 0.001).
Conclusion
Patients with active PsA initiating guselkumab were significantly (approximately two times) more likely to remain persistent with on-label therapy through 24 months versus SC TNFi, overall and among biologic-naïve and biologic-experienced subgroups.
Prior Presentation: Part of the material in this manuscript was presented at the Congress of Clinical Rheumatology-West held September 26–29, 2024 in San Diego, California, USA, as a poster presentation, and at Maui Derm Hawaii 2025 held January 20–24, 2025 in Maui, Hawaii, USA, as a poster presentation.
Key Summary Points
Why carry out this study?
Disease and symptom control in chronic conditions such as psoriatic arthritis (PsA) is contingent upon long-term persistent use of therapy
A prior study found that patients with active PsA initiating guselkumab were three times more likely than those initiating subcutaneous (SC) tumor necrosis factor inhibitors (TNFi) to remain persistent with on-label treatment through 12 months
This study was conducted to extend the prior follow-up by comparing on-label persistence through 24 months between patients with active PsA newly initiating guselkumab or SC TNFi, overall and among biologic-naïve and biologic-experienced patients
What was learned from the study?
Overall, patients initiating guselkumab were 2.24 times more likely to be persistent with on-label therapy through 24 months than patients initiating an SC TNFi (hazard ratio [95% confidence interval] 2.24 [1.90, 2.64]; P < 0.001), with consistent results among biologic-naïve (2.36 [1.88, 2.98]; P < 0.001) and biologic-experienced patients (1.86 [1.46, 2.37]; P < 0.001), thus corroborating and extending the findings from the 12-month analysis
Given that treatment persistence may serve as a proxy for effectiveness and safety, higher on-label persistence associated with guselkumab may reflect an associated improvement in disease management outcomes
Introduction
Psoriatic arthritis (PsA) is a chronic, progressive, inflammatory, musculoskeletal and skin disease that develops in up to 30% of patients with psoriasis, with an estimated prevalence of 182 per 100,000 in the USA [1, 2]. PsA has a heterogeneous presentation involving multiple tissues and can include manifestations like peripheral arthritis, skin and nail psoriasis, enthesitis, dactylitis, and axial disease [1, 3]. The persistent inflammation of PsA can lead to joint destruction and considerable disability over time, negatively impacting physical function and patient quality of life [1, 3].
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The goals of PsA management are to minimize disease activity and complications, prevent structural damage, optimize functional status, and improve quality of life [4]. As noted in current treatment guidelines from the American College of Rheumatology (ACR) [5], the European Alliance of Associations for Rheumatology (EULAR) [6], and the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) [4], pharmacotherapy for PsA typically follows a “step-up” approach. Nonsteroidal anti-inflammatory drugs and glucocorticoids are recommended for initial symptom control, followed by treatment with conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), biologic disease-modifying antirheumatic drugs (bDMARDs), or targeted synthetic disease-modifying antirheumatic drugs (tsDMARDs) depending on the disease domains affected [4‐6]. The introduction of tumor necrosis factor inhibitors (TNFi) revolutionized the therapeutic landscape of PsA over the past 2 decades, with several classes of bDMARDs now indicated for the treatment of active PsA, including interleukin (IL)-17A inhibitors, an IL-17A/F inhibitor, an IL-12/23 inhibitor, and IL-23 inhibitors [1, 4].
Guselkumab was the first and only fully human IL-23p19-subunit inhibitor approved by the US Food and Drug Administration (FDA) in July 2020 for the treatment of adult patients with active PsA, on the basis of the results of the double-blind, randomized, placebo-controlled phase 3 clinical trials DISCOVER-1 and DISCOVER-2 [7‐9]. In both trials, 24 weeks of guselkumab treatment was associated with a significantly higher response rate for achieving ≥ 20% improvement in the American College of Rheumatology response criteria (ACR20) compared with placebo among patients with active PsA, including those with prior exposure to TNFi [7, 8]. Improvements in joint and psoriatic skin symptoms, physical function, and health-related quality of life were sustained through up to 2 years with continued guselkumab treatment [10‐13].
As with any long-term therapy used to treat chronic conditions, disease and symptom control is contingent on continued and persistent use of the drug [14]. However, there are limited data to evaluate the treatment persistence of guselkumab in comparison with other bDMARDs, such as TNFi, among patients with PsA. Walsh et al. previously conducted a claims-based analysis of on-label treatment persistence in patients with PsA and found that those initiating guselkumab were three times more likely than those initiating subcutaneous (SC) TNFi to remain persistent on treatment through 12 months [15]. Given the chronic nature of PsA, there is a need for longer-term data in routine clinical practice, particularly among groups of patients with or without prior exposure to biologics. The current study was conducted to compare on-label persistence through 24 months between patients with active PsA newly initiating guselkumab or SC TNFi, overall and stratified by prior biologic exposure.
Methods
Data Source
This analysis used data from January 1, 2011 to June 30, 2023 in the IQVIA PharMetrics® Plus database. The database comprises fully adjudicated claims for inpatient and outpatient services, prescriptions, and outpatient-administered treatments for more than 215 million unique enrollees in the USA. Additionally, information on dates of service, demographic variables (age, gender, geography), and monthly indicators of health plan enrollment are available. Data contributors to the database are largely commercial health plans, and the database was considered representative of the commercially insured US national population for patients under 65 years of age.
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The IQVIA PharMetrics® Plus database was used under license. All data were de-identified in compliance with the Health Insurance Portability and Accountability Act (HIPAA); therefore, institutional review board review was not required.
Study Design
A retrospective cohort design was used to compare on-label persistence up to 24 months following treatment initiation between patients with active PsA initiating guselkumab or SC TNFi (i.e., adalimumab or its biosimilars; certolizumab pegol; etanercept or its biosimilars; SC golimumab) (Fig. 1). The index date was the date of the first claim for either guselkumab or the first SC TNFi during the intake period: July 14, 2020 (the day after US FDA approval of guselkumab for active PsA) to December 31, 2022 (6 months prior to the end of data availability). The baseline period for each patient was defined as the 12 months of continuous insurance eligibility prior to the index date, while the follow-up period spanned from the index date until the earliest of end of continuous insurance eligibility or end of data availability. Patients who reached the end of continuous insurance eligibility were censored.
Fig. 1
IQVIA PharMetrics® Plus database (1/1/2011–6/30/2023)a study designb−d. bDMARD biologic disease-modifying antirheumatic drug, GUS guselkumab, ICD-10-CM International Classification of Disease, Tenth Revision, Clinical Modification, PsA psoriatic arthritis, SC subcutaneous, TNFi tumor necrosis factor inhibitor. aThe IQVIA Pharmetrics® Plus database comprises fully adjudicated claims for inpatient and outpatient services, and outpatient prescription drugs, offering a diverse representation of geographic zones, employers, payers, providers, and therapy areas. bA validated algorithm for identifying patients with PsA in US claims data was used: ≥ 2 claims with a PsA diagnosis (ICD-10-CM, L40.5x) ≥ 30 days apart and ≥ 1 prescription claim for a PsA-related medication (i.e., guselkumab or SC TNFi). cPatients could be biologic-naïve or biologic-experienced during baseline but were naïve to treatment with guselkumab or SC TNFi agents. dPatients in the SC TNFi cohort were newly initiated within the class. eDiagnoses for PsA include claims on the index date
Patients were included in the study if they met the following criteria: (1) first observed medical or pharmacy claim for an index agent during the intake period; (2) ≥ 12 months of continuous health plan eligibility before the index date; (3) ≥ 2 claims with a diagnosis code for PsA ≥ 30 days apart during the baseline period or on the index date; (4) ≥ 18 years of age on the index date; (5) medical or pharmacy claims for only one index agent on the index date; (6) no claims for any of the index agents (i.e., guselkumab; adalimumab or its biosimilars; certolizumab pegol; etanercept or its biosimilars; SC golimumab), intravenous (IV) infliximab or its biosimilars, or IV golimumab during the most recent period of continuous eligibility and before the index date; and (7) no claims for ankylosing spondylitis, other inflammatory arthritides, other spondylopathies, rheumatoid arthritis, systemic connective tissue disorders, relapsing polychondritis, unclassified connective tissue disease, hidradenitis suppurativa, inflammatory bowel disease, or uveitis during the baseline period (to ensure that index agents were prescribed specifically for PsA). Biologic agents need prior authorization to be covered by a commercial health plan, ensuring they are prescribed for the approved indication. Thus, because the biologics studied in this analysis are FDA-approved for active PsA, a claim for these drugs was considered an indicator of active disease.
Patients were included in the guselkumab or SC TNFi cohorts (mutually exclusive) in accordance with their index agent. Within each cohort, patients were further classified as biologic-naïve (i.e., no medical or pharmacy claims for other bDMARDs any time during the period of continuous eligibility before the index date) or biologic-experienced (i.e., ≥ 1 medical or pharmacy claim for any other bDMARD any time during the period of continuous eligibility before the index date). The purpose of the biologic-naïve and biologic-experienced subgroup analyses was to assess the comparative effectiveness of guselkumab vs SC TNFi among patients with and without prior use of medications in the same class.
Days of Supply Imputations
As discrepancies may exist between days of supply values and interval between claims in administrative claims databases [16], the days of supply were imputed for both medical and pharmacy claims. Days of supply for the first guselkumab medical claim were imputed to 28 days (per label) and all subsequent guselkumab medical claims were imputed to 56 days (per label) [9]. For adalimumab and certolizumab pegol medical claims, days of supply were imputed to 28 days (i.e., adalimumab and certolizumab pegol are each indicated every 2 weeks, per respective labels, but imputations were based on mode days of supply typically observed in pharmacy claims, which was 28 days, as each claim contains 2 doses and covers 4 weeks of treatment) [17, 18]. For etanercept medical claims, days of supply were imputed to 28 days (i.e., etanercept is indicated every week, per label, but imputations were based on mode days of supply typically observed in pharmacy claims, which was 28 days, as each dispensing contains 4 doses and covers 4 weeks of treatment) [19]. For SC golimumab medical claims, days of supply were imputed to 28 days, per label [20].
For pharmacy claims, imputations were informed by the FDA-approved dosing regimens, as well as the mode of days of supply and distribution of time between consecutive claims observed in the data. Days of supply of guselkumab were imputed as 28 days for the first pharmacy claim with days of supply > 30 days. For subsequent pharmacy claims with missing days of supply or days of supply < 56 days, days of supply were imputed as 28 days if time to next claim was < 42 days, 56 days if it was 42–70 days, or 84 days if it was > 70 days; if there was no next claim, days of supply of the previous claim were carried forward, or the per-label number of days of supply (i.e., 56 days) was imputed if the original value was missing. No imputations were made for subsequent guselkumab pharmacy claims with days of supply of 56–60 days or > 60 days. For days of supply of adalimumab, certolizumab pegol, etanercept, and SC golimumab, no imputations were made because days of supply typically observed in claims data for these agents are generally consistent with the respective drug labels [15, 21].
Study Outcomes
On-label treatment persistence with the index agent was evaluated in the overall guselkumab and SC TNFi cohorts and in the respective biologic-naïve and biologic-experienced subgroups, separately, during the follow-up period. On-label treatment persistence was defined as no treatment discontinuation, dose escalation, or dose reduction during the follow-up period. Treatment discontinuation was defined as an exposure gap twice the longest duration of time between consecutive administrations per the FDA-approved dosing regimen for each index agent and/or mode of days of supply observed in the data; that is, 112 days (56 days × 2) for guselkumab [9] and 56 days (28 days × 2) for adalimumab, certolizumab pegol, etanercept, and SC golimumab (all based on mode days of supply and each claim covering 4 weeks of treatment) [17‐20]. On-label persistence was assessed for the index treatment (i.e., guselkumab or SC TNFi) specifically, independent of other PsA-related agents that may have been initiated following the index date, while on treatment with guselkumab or SC TNFi.
The discontinuation date was the last day of supply (date of the last claim plus the days of supply) preceding the therapy exposure gap. Patients with any dose change (i.e., any dose escalation or reduction relative to the dosing instructions in the label) were censored on the date of the first observed dose change. If discontinuation was not observed, patients were censored on the last day of supply for the index agent before the end of the follow-up period.
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Statistical Analysis
To balance potential confounders between the guselkumab and SC TNFi cohorts, overlap propensity score weighting was used [22, 23]. Propensity scores were generated using probability estimates from a logistic regression model in which guselkumab treatment (yes/no) was the binary dependent variable, and baseline demographic and clinical characteristics were the independent variables. Each patient was attributed a weight that was defined as the probability of that patient being assigned to the opposite treatment group. Weights were normalized using the mean of weights in each individual cohort. Overlap propensity score weighting was performed separately for the overall cohorts and the biologic-naïve and biologic-experienced subgroups. As a result, it was possible for different baseline characteristics to be included in each propensity score model. Standardized differences were used to assess the balance of baseline characteristics between the guselkumab and SC TNFi cohorts (i.e., < 10% was considered well balanced) [24].
The proportion of patients remaining persistent on treatment was evaluated using weighted Kaplan–Meier (KM) survival analysis (overall and within the biologic-naïve and biologic-experienced subgroups) up to 24 months post-index. Weighted Cox proportional hazards models were used to compare on-label persistence rates between the guselkumab and SC TNFi cohorts, with hazard ratios (HRs) and 95% confidence intervals (CIs). Any baseline characteristics that remained imbalanced after weighting were included as covariates in the weighted Cox proportional hazards models.
All analyses were conducted using SAS Enterprise Guide 7.1.
Sensitivity Analyses
Two sensitivity analyses were conducted. The first utilized a therapy exposure gap of the longest duration of time between administrations, per the FDA-approved dosing regimen for each index agent and/or mode of days of supply observed in the data; that is, 56 days for guselkumab and 28 days for adalimumab, certolizumab pegol, etanercept, and SC golimumab [9, 17‐20]. A second sensitivity analysis was conducted using a fixed therapy exposure gap of 112 days to define discontinuation for all agents.
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Results
Patient Characteristics
Among 804 patients included in the guselkumab cohort, 361 (44.9%) were biologic-naïve and 443 (55.1%) were biologic-experienced (Fig. 2). Among 2490 patients included in the SC TNFi cohort, 2171 (87.2%) were biologic-naïve and 319 (12.8%) were biologic-experienced.
Fig. 2
Identification of the study population of patients with PsA initiated on guselkumab or an SC TNFi agent. GUS guselkumab, IV intravenous, PsA psoriatic arthritis, SC subcutaneous, TNFi tumor necrosis factor inhibitor. aFirst claim for guselkumab or SC TNFi during intake period July 14, 2020 to December 31, 2022. bThe SC TNFi cohort was defined as patients with an index claim for an SC TNFi (i.e., adalimumab, certolizumab pegol, etanercept, or SC golimumab). cSpecific conditions assessed during the 12-month baseline period included ankylosing spondylitis, other inflammatory arthritis, other spondylopathies, rheumatoid arthritis, systemic connective tissue disorders, relapsing polychondritis, unclassified connective tissue disease, hidradenitis suppurativa, inflammatory bowel disease, or uveitis
In the overall analysis population, weighted characteristics during the baseline period were well-balanced between the guselkumab and SC TNFi cohorts, except for use of bDMARDs (47.6% and 14.0%, respectively) and csDMARDs (22.4% and 48.3%, respectively), which were included as covariates in the weighted Cox proportional hazards model (Table 1). The average age on the index date was 49.4 years in the guselkumab cohort and 49.5 years in the SC TNFi cohort, while 60.3% were female in both cohorts. The mean time between the latest observed PsA diagnosis and the index date was 1.2 months in both cohorts. Most patients (86.3%) in both cohorts had a psoriasis diagnosis code during the baseline period, and the most common comorbidities were hypertension (guselkumab: 37.5%; SC TNFi: 37.7%), hyperlipidemia (34.7% in both cohorts), obesity (guselkumab: 32.1%; SC TNFi: 32.0%), and osteoarthritis (30.3% in both cohorts). A similar proportion of patients in the guselkumab cohort (21.1%) and SC TNFi cohort (23.4%) received tsDMARDs during the baseline period. The mean follow-up duration was 15.4 months in the guselkumab cohort and 15.2 months in the SC TNFi cohort.
Table 1
Baseline demographic and clinical characteristics
Mean ± SD [median] or n (%)
Guselkumab
SC TNFi
Std. diff., %
Guselkumab weighteda,b
SC TNFi weighteda,b
Std. diff., %
N = 804
N = 2490
N = 804
N = 2490
Age at start of continuous insurance eligibility (years)
46.3 ± 11.4 [47.5]
44.1 ± 11.4 [45.3]
19.4
45.4 ± 11.3 [45.9]
45.4 ± 11.1 [46.5]
0.0
Age at index date (years)
50.2 ± 11.2 [51.3]
48.3 ± 11.4 [49.4]
16.8
49.4 ± 11.2 [50.3]
49.5 ± 11.2 [51.0]
0.8
Female
487 (60.6)
1496 (60.1)
1.0
485 (60.3)
1502 (60.3)
0.0
Male
317 (39.4)
994 (39.9)
1.0
319 (39.7)
988 (39.7)
0.0
Region of residence at index date
South
425 (52.9)
1113 (44.7)
16.4
408 (50.8)
1264 (50.8)
0.0
Midwest
175 (21.8)
614 (24.7)
6.9
184 (22.9)
571 (22.9)
0.0
Northeast
124 (15.4)
429 (17.2)
4.9
126 (15.7)
391 (15.7)
0.0
West or unknown
80 (10.0)
334 (13.4)
11.2
85 (10.6)
264 (10.6)
0.0
Insurance type at index date
PPO
616 (76.6)
1846 (74.1)
5.8
612 (76.2)
1896 (76.2)
0.0
HMO
100 (12.4)
344 (13.8)
4.1
100 (12.4)
327 (13.1)
2.3
Otherc
88 (10.9)
300 (12.0)
3.5
93 (11.4)
266 (10.7)
2.9
Medicare Advantage
24 (3.0)
37 (1.5)
10.2
19 (2.4)
48 (1.9)
3.1
Relationship of patient to primary beneficiary
Self
471 (58.6)
1486 (59.7)
2.2
472 (58.7)
1523 (61.2)
5.1
Spouse or child
193 (24.0)
576 (23.1)
2.1
193 (24.0)
570 (22.9)
2.6
Unknown
140 (17.4)
428 (17.2)
0.6
139 (17.3)
397 (15.9)
3.7
Year of index date
2020
88 (10.9)
426 (17.1)
17.8
94 (11.7)
292 (11.7)
0.0
2021
338 (42.0)
1131 (45.4)
6.8
349 (43.4)
1080 (43.4)
0.0
2022
378 (47.0)
933 (37.5)
19.4
361 (44.9)
1118 (44.9)
0.0
Time between latest observed PsA diagnosis to index date (months)d
1.4 ± 1.7 [0.8]
0.9 ± 1.2 [0.6]
31.2
1.2 ± 1.4 [0.7]
1.2 ± 1.6 [0.7]
0.0
Quan-CCI
0.6 ± 1.3 [0.0]
0.5 ± 1.1 [0.0]
8.8
0.6 ± 1.3 [0.0]
0.6 ± 1.2 [0.0]
0.6
PsA-related comorbidities
Hypertension
316 (39.3)
869 (34.9)
9.1
302 (37.5)
938 (37.7)
0.3
Hyperlipidemia
306 (38.1)
780 (31.3)
14.2
279 (34.7)
864 (34.7)
0.0
Obesity
264 (32.8)
742 (29.8)
6.6
258 (32.1)
797 (32.0)
0.2
Osteoarthritis
226 (28.1)
891 (35.8)
16.5
243 (30.3)
754 (30.3)
0.0
Coronary artery disease
59 (7.3)
105 (4.2)
13.4
52 (6.5)
162 (6.5)
0.0
Stroke including transient ischemic attack
12 (1.5)
50 (2.0)
3.9
13 (1.6)
40 (1.6)
0.0
Psoriasis
719 (89.4)
1706 (68.5)
53.1
693 (86.3)
2148 (86.3)
0.0
Any prior PsA treatment
583 (72.5)
1665 (66.9)
12.3
572 (71.2)
1772 (71.2)
0.0
bDMARDse
391 (48.6)
282 (11.3)
89.1
383 (47.6)
350 (14.0)
78.0
Number of prior bDMARDs
0
413 (51.4)
2208 (88.7)
89.1
421 (52.4)
2140 (86.0)
78.0
1
338 (42.0)
254 (10.2)
77.8
331 (41.2)
314 (12.6)
68.0
≥ 2
53 (6.6)
28 (1.1)
29.3
52 (6.4)
36 (1.4)
26.7
csDMARDsf
177 (22.0)
1201 (48.2)
57.1
180 (22.4)
1202 (48.3)
56.3
tsDMARDsg
180 (22.4)
472 (19.0)
8.5
170 (21.1)
583 (23.4)
5.5
JAK inhibitors
42 (5.2)
54 (2.2)
16.2
33 (4.1)
103 (4.1)
0.0
Prior NSAID use
321 (39.9)
1186 (47.6)
15.6
343 (42.7)
1063 (42.7)
0.0
Prior topical corticosteroid use
436 (54.2)
1022 (41.0)
26.6
405 (50.4)
1256 (50.4)
0.0
Prior systemic (oral/IV) corticosteroid use
302 (37.6)
1188 (47.7)
20.6
319 (39.7)
989 (39.7)
0.0
Prior opioid use
265 (33.0)
655 (26.3)
14.6
245 (30.5)
758 (30.5)
0.0
Continuous opioid treatmenth
51 (6.3)
76 (3.1)
15.6
38 (4.7)
117 (4.7)
0.0
bDMARD biologic disease-modifying antirheumatic drug, CCI Charlson comorbidity index, csDMARD conventional synthetic disease-modifying antirheumatic drug, CTLA cytotoxic T lymphocyte-associated protein, HMO health maintenance organization, IL interleukin, IV intravenous, JAK Janus kinase, NSAID nonsteroidal anti-inflammatory drug, PPO preferred provider organization, PS propensity score, PsA psoriatic arthritis, SC subcutaneous, SD standard deviation, Std. diff. standardized difference, TNFi tumor necrosis factor inhibitor, tsDMARD targeted synthetic disease-modifying antirheumatic drug
aTo balance potential confounders between the 2 cohorts, overlap PS weighting was used. PSs were generated using probability estimates from a logistic regression model in which guselkumab treatment (yes/no) was the dependent variable and baseline demographic and clinical characteristics were the independent variables. Each patient was attributed a weight that was defined as the probability of that patient being assigned to the opposite treatment group; for the guselkumab cohort, the weight was assigned as 1 − PS, and for the SC TNFi cohort, the weight was assigned as PS. Weights were normalized using the mean of weights in each individual cohort (i.e., Hajek estimator). Baseline covariates included all demographic and clinical characteristics reported in this table with the exception of Medicare Advantage enrollment, relationship of patient to primary beneficiary, hypertension, obesity, and prior PsA treatment with bDMARDs, csDMARDs, and tsDMARDs. Prior PsA treatment with bDMARDs and csDMARDs were included in the adjusted Cox proportional hazard models
bOf note, the number of patients reported in this weighted population represents the sum of weights for the corresponding non-weighted patients, rounded to the nearest integer. The proportions displayed were calculated prior to the rounding and may be slightly different than if they were calculated on the basis of rounded numbers
cPoint-of-service, consumer directed health care, indemnity/traditional, and unknown plan type
gApremilast and JAK inhibitors (tofacitinib, upadacitinib, baricitinib)
hCumulative days of opioid use is calculated as a sum of unique days of supply in opioid pharmacy claims during the 12-month baseline period
In the biologic-naïve subgroup, weighted baseline characteristics were well-balanced between the guselkumab and SC TNFi cohorts, except for use of csDMARDs (25.5% and 35.1%, respectively) and tsDMARDs (31.7% and 22.6%, respectively), which were included as covariates in the weighted Cox proportional hazards model (Supplementary Table S1). The average age on the index date was 48.8 years in the guselkumab cohort and 49.0 years in the SC TNFi cohort, while 60.2% were female in both cohorts. The mean follow-up duration was 15.5 months in the guselkumab cohort and 15.0 months in the SC TNFi cohort.
In the biologic-experienced subgroup, weighted baseline characteristics were generally well-balanced between the guselkumab and SC TNFi cohorts (Supplementary Table S2). In both cohorts, the average age on the index date was 49.5 years and 62.3% were female. The mean follow-up duration was 15.4 months in the guselkumab cohort and 15.8 months in the SC TNFi cohort.
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On-Label Persistence
Overall Cohorts
The median time to discontinuation of the index agent was 22.0 months in the guselkumab cohort and 9.2 months in the SC TNFi cohort. KM rates of on-label persistence in the guselkumab versus SC TNFi cohort were 82.1% versus 63.8%, respectively, at 6 months, 65.9% versus 43.8% at 12 months, 58.1% versus 35.4% at 18 months, and 45.5% versus 28.5% at 24 months (all P < 0.001; Table 2). Patients initiating guselkumab were 2.24 times more likely to be persistent with on-label therapy through 24 months than patients initiating an SC TNFi (HR [95% CI] 2.24 [1.90, 2.64]; P < 0.001; Fig. 3).
Table 2
Kaplan–Meier rates for on-label persistence in weighted guselkumab and SC TNFi cohorts: primary analysis (gap of twice the duration of time between administrations as per FDA label)
6 months
12 months
18 months
24 months
Overall
Guselkumab, Kaplan–Meier rate (95% CI)
82.1 (76.3, 86.6)
65.9 (59.2, 71.8)
58.1 (49.5, 65.7)
45.5 (26.9, 62.1)
SC TNFi, Kaplan–Meier rate (95% CI)
63.8 (60.1, 67.3)
43.8 (39.3, 48.2)
35.4 (30.0, 40.8)
28.5 (21.5, 35.9)
Log-rank test P value
< 0.001
< 0.001
< 0.001
< 0.001
Biologic-naïve
Guselkumab, Kaplan–Meier rate (95% CI)
86.2 (76.6, 92.1)
73.1 (63.2, 80.7)
62.9 (50.2, 73.1)
48.9 (24.9, 69.3)
SC TNFi, Kaplan–Meier rate (95% CI)
63.8 (59.3, 68.0)
43.8 (38.0, 49.4)
35.3 (28.4, 42.3)
28.4 (19.6, 37.9)
Log-rank test P value
< 0.001
< 0.001
< 0.001
< 0.001
Biologic-experienced
Guselkumab, Kaplan–Meier rate (95% CI)
76.9 (68.3, 83.4)
57.7 (47.1, 67.0)
50.6 (36.3, 63.2)
39.5 (3.6, 63.0)
SC TNFi, Kaplan–Meier rate (95% CI)
58.1 (47.0, 67.6)
40.3 (27.7, 52.4)
31.1 (15.3, 48.5)
23.3 (5.2, 48.2)
Log-rank test P value
< 0.001
< 0.001
< 0.001
< 0.001
CI confidence interval, FDA Food and Drug Administration, SC subcutaneous, TNFi tumor necrosis factor inhibitor
Fig. 3
Kaplan–Meier analysis of on-label persistence in weighted guselkumab and SC TNFi cohorts among the overall population (gap of twice the duration of time between administrations as per FDA label)a,b. bDMARD biologic disease-modifying antirheumatic drug, CI confidence interval, csDMARD conventional synthetic disease-modifying antirheumatic drug, FDA Food and Drug Administration, GUS guselkumab, HR hazard ratio, SC subcutaneous, TNFi tumor necrosis factor inhibitor. aTreatment discontinuation was defined as having a gap in treatment of more than twice the duration of days of supply for a claim (i.e., 2 × 56 = 112 days for guselkumab or 2 × 28 = 56 days for SC TNFi). bPatients with dose changes inconsistent with FDA-approved dosing were censored as of the first dose change. cA weighted Cox proportional hazards model, further adjusted for baseline bDMARD and csDMARD use, was used to compare on-label persistence between cohorts
Among biologic-naïve patients, the median time to discontinuation of the index agent was 22.4 months in the guselkumab cohort and 9.2 months in the SC TNFi cohort. KM rates of on-label persistence in the guselkumab versus SC TNFi cohort were 86.2% versus 63.8%, respectively, at 6 months, 73.1% versus 43.8% at 12 months, 62.9% versus 35.3% at 18 months, and 48.9% versus 28.4% at 24 months (all P < 0.001; Table 2). Patients initiating guselkumab were 2.36 times more likely to be persistent with on-label therapy through 24 months than patients initiating an SC TNFi (HR [95% CI] 2.36 [1.88, 2.98]; P < 0.001; Fig. 4).
Fig. 4
Kaplan–Meier analysis of on-label persistence in weighted guselkumab and SC TNFi cohorts among biologic-naïve patients (gap of twice the duration of time between administrations as per FDA label)a,b. CI confidence interval, csDMARD conventional synthetic disease-modifying antirheumatic drug, FDA Food and Drug Administration, GUS guselkumab, HR hazard ratio, SC subcutaneous, TNFi tumor necrosis factor inhibitor, tsDMARD targeted synthetic disease-modifying antirheumatic drug. aTreatment discontinuation was defined as having a gap in treatment of more than twice the duration of days of supply for a claim (i.e., 2 × 56 = 112 days for guselkumab or 2 × 28 = 56 days for SC TNFi). bPatients with dose changes inconsistent with FDA-approved dosing were censored as of the first dose change. cA weighted Cox proportional hazards model, further adjusted for baseline csDMARD and tsDMARD use, was used to compare on-label persistence between cohorts
For biologic-experienced patients, the median time to discontinuation of the index agent was 18.4 months in the guselkumab cohort and 7.4 months in the SC TNFi cohort. KM rates of on-label persistence in the guselkumab versus SC TNFi cohort were 76.9% versus 58.1%, respectively, at 6 months, 57.7% versus 40.3% at 12 months, 50.6% versus 31.1% at 18 months, and 39.5% versus 23.3% at 24 months (all P < 0.001; Table 2). Patients initiating guselkumab were 1.86 times more likely to be persistent with on-label therapy through 24 months than patients initiating an SC TNFi (HR [95% CI] 1.86 [1.46, 2.37]; P < 0.001; Fig. 5).
Fig. 5
Kaplan–Meier analysis of on-label persistence in weighted guselkumab and SC TNFi cohorts among biologic-experienced patients (gap of twice the duration of time between administrations as per FDA label)a,b. CI confidence interval, FDA Food and Drug Administration, GUS guselkumab, HR hazard ratio, SC subcutaneous, TNFi tumor necrosis factor inhibitor. aTreatment discontinuation was defined as having a gap in treatment of more than twice the duration of days of supply for a claim (i.e., 2 × 56 = 112 days for guselkumab or 2 × 28 = 56 days for SC TNFi). bPatients with dose changes inconsistent with FDA-approved dosing were censored as of the first dose change. cA weighted Cox proportional hazards model was used to compare on-label persistence between cohorts
Therapy Exposure Gap of Once the Longest Duration of Time Between Administrations
When a therapy exposure gap of once, as opposed to twice, the longest duration of time between administrations was used, on-label persistence results were consistent with those of the main analyses (Supplementary Table S3). The KM rates for on-label persistence were higher in the guselkumab cohort than in the SC TNFi cohort in the overall population through 24 months, at which time the KM rate of on-label persistence was 27.6% versus 18.1% (HR [95% CI] 1.90 [1.65, 2.19]; P < 0.001) (Supplementary Fig. S1). Similar results were observed regardless of prior biologic experience. Patients in the guselkumab group were more likely to remain persistent with on-label treatment compared with those in the SC TNFi group in both the biologic-naïve subgroup (30.7% versus 18.3%; HR [95% CI] 1.87 [1.55, 2.27]; P < 0.001) and biologic-experienced subgroup (25.0% versus 18.2%; HR [95% CI] 1.73 [1.39, 2.16]; P < 0.001) (Supplementary Figs. S2 and S3).
Fixed Therapy Exposure Gap
When a fixed therapy exposure gap of 112 days was used, on-label persistence results were also consistent with those of the main analyses (Supplementary Table S4). The KM rates for on-label persistence were higher in the guselkumab cohort than in the SC TNFi cohort through 24 months, at which time the KM rates of on-label persistence were 45.5% versus 39.1% (HR [95% CI] 1.80 [1.52, 2.13]; P < 0.001) for the overall population, 48.9% versus 40.9% (HR [95% CI] 1.76 [1.39, 2.22]; P < 0.001) for the biologic-naïve cohort, and 39.5% versus 27.9% (HR [95% CI] 1.65 [1.28, 2.11]; P < 0.001) for the biologic-experienced cohort (Supplementary Figs. S4–S6).
Discussion
In this real-world study of patients with active PsA, guselkumab was associated with significantly higher on-label persistence than SC TNFi through 24 months, regardless of prior exposure to bDMARDs. Patients receiving guselkumab were more than twice as likely to remain persistent with on-label therapy through 24 months relative to those receiving an initial SC TNFi. Similarly, biologic-naïve and biologic-experienced patients were approximately 2.4 and 1.9 times more likely, respectively, to remain persistent with on-label therapy through 24 months when initiating guselkumab versus SC TNFi. Moreover, results were robust when different therapy exposure gaps were used to define treatment discontinuation in sensitivity analyses. These real-world findings complement the phase 3, randomized, placebo-controlled trials, DISCOVER-1 and DISCOVER-2, in which guselkumab demonstrated efficacy in improving the signs and symptoms of PsA, including achievement of almost clear or clear skin, resolution of enthesitis and dactylitis, and minimal disease activity [7, 8].
The study conducted by Walsh et al. was the first to evaluate guselkumab and SC TNFi on-label persistence rates in a similar patient population through 12 months of treatment [15]. We now report findings through 24 months among patients with active PsA initiating guselkumab or SC TNFi in real-world clinical practice in the USA. The current study is consistent with the 12-month data from Walsh et al., in which on-label persistence rates were 71.5% among patients initiating guselkumab and 43.7% among those initiating SC TNFi, with the former being three times more likely to remain persistent on treatment at 12 months (P < 0.001). As such, the current study builds upon the prior analysis by confirming these first-year trends and providing evidence of sustained persistence for guselkumab over an extended follow-up of 24 months. Furthermore, the current analysis also evaluated persistence by previous biologic exposure and found that treatment persistence was observed to be consistently higher for guselkumab than SC TNFi in both patient subgroups.
Limited data are available on treatment persistence with on-label guselkumab. A previous retrospective analysis evaluated treatment effectiveness and persistence among patients with PsA in the CorEvitas Psoriatic Arthritis/Spondyloarthritis Registry who initiated guselkumab. Nearly 80% of those who initiated on-label guselkumab, 73% of whom had received at least one prior TNFi, were persistent with on-label therapy through 6 months [25]. Consistent with the previous analysis, the on-label persistence rate observed for guselkumab at 6 months in the current study was 82.1%, although patients did not have prior TNFi treatment by design. Notably, the high guselkumab persistence rates seen in the present study are also consistent with retention rates of guselkumab-randomized participants reported in the phase 3 DISCOVER-1 (94% at 48 weeks) and DISCOVER-2 trials (90% at 100 weeks) [26, 27]. With regards to TNFi, treatment persistence in PsA is well characterized in the literature, with recent studies evaluating biologic-naïve [28, 29] and biologic-experienced [30, 31] patients separately. Among biologic-naïve patients with PsA, persistence rates for TNFi (including IV agents) ranged from 37.1% (using a therapy exposure gap of 30 days) [28] to 72.3% (using a gap of 60 days) [29] at 1 year in two insurance claims-based studies, which is a range that encompasses the rate of 43.8% observed for biologic-naïve patients in the current study. Among biologic-experienced patients with PsA, the present on-label persistence rates of 40.3% at 12 months and 23.3% at 24 months are aligned with two prior observational studies estimating TNFi persistence rates of 36.8% (using a gap of 60 days) to approximately 60% (no gap defined) at 1 year and 21.3% to approximately 50% at 2 years [30, 31]. While comparability between these prior studies and the current analysis is limited by different persistence definitions, TNFi evaluated, and patient populations, the findings were generally consistent.
Despite the lack of comparative PsA literature, prior studies have shown higher persistence with guselkumab relative to TNFi among patients with psoriasis [21, 32, 33], thus reinforcing similar trends observed in the treatment of PsA in the present study. In one claims-based study including both biologic-naïve and biologic-experienced patients with psoriasis, the median time to discontinuation was 26.2 months with guselkumab and 9.9 months with adalimumab [21], which is aligned with the current study estimates of 22.0 and 9.2 months (for SC TNFi overall), respectively. Of note, IL-23p19-subunit inhibitors have demonstrated efficacy in achieving high levels of response in patients with psoriasis [34, 35]. In phase 3 studies of participants with plaque psoriasis, guselkumab was superior to adalimumab in achieving almost clear/clear skin at week 16 [36, 37]. As such, the longer persistence with guselkumab observed in the current study may have been influenced by the efficacy of guselkumab specifically in treating skin symptoms of PsA.
Given the scarcity of head-to-head comparisons between guselkumab and SC TNFi to guide PsA treatment decisions, the present analysis contributes important insights using treatment persistence, a key clinical measure that informs both effectiveness and safety of therapy. Indeed, the most common reasons for discontinuing bDMARDs among patients with psoriasis and PsA are lack of effectiveness and occurrence of adverse effects, suggesting that long-term treatment persistence may reflect positive health outcomes and optimal disease control [14, 38]. In support of this line of thought, on-label persistence with guselkumab for 6 months in the CorEvitas analysis was accompanied by significant improvements in joint, skin, and pain symptoms among patients with PsA [25]. The ability of guselkumab to improve PsA symptoms across multiple domains indicates a broad applicability for guselkumab in the treatment of PsA, based on current guidelines that recommend a domain-based approach to treatment selection [4]. Additional analysis is warranted to confirm the link between guselkumab persistence and disease management outcomes in real-world patients with PsA.
Despite high rates of on-label persistence at 6 months, persistence with both guselkumab and SC TNFi did steadily decrease by 24 months. Although reasons for treatment discontinuation were not available in the claims data, predictors of low bDMARD persistence in PsA have been identified in the literature, including female sex, smoking, comorbidities commonly associated with PsA (e.g., obesity, cardiac conditions), and prior bDMARD/systemic treatment [28, 29, 31, 39, 40]. Consistently, persistence outcomes tended to be better in biologic-naïve than biologic-experienced patients in this study, and other patient characteristics may have also influenced persistence in both cohorts. Future research may evaluate the impact of comorbidities and prior exposure to different bDMARD classes on guselkumab persistence in patients with PsA.
Strengths and Limitations
The strengths of the study include its large sample size and the use of real-world data, which enhance the generalizability of the findings. The study utilized rigorous statistical methods, including overlap propensity score weighting, to balance the cohorts and address potential confounding variables. Additionally, the analysis spanned 24 months, providing a robust assessment of long-term treatment persistence outcomes.
Some limitations of the study design should be noted. Imputation of days of supply is a valid approach commonly used for claims-based persistence analysis [15, 21, 41]; however, it may occasionally lead to misclassification of treatment discontinuation. For instance, a filled prescription observed in the claims data does not necessarily ensure that the treatment was taken as prescribed. Additionally, treatment effectiveness and reasons for discontinuation (e.g., lack of effectiveness, adverse effects, inconvenient dosing, worsening of related conditions) could not be assessed using claims data. While patients could initiate other treatments following the index date, combination therapy (if any) was not considered in the persistence analysis. Patients with exposure to TNFi prior to initiating guselkumab were not included in this study. Moreover, SC TNFi were evaluated collectively rather than individually, consistent with how these therapies are addressed in current treatment guidelines [4].
While the two cohorts were balanced using overlap propensity score weighting, variables that were underreported or not available in the database, such as psoriasis severity, disease activity, domain involvement, and clinical manifestations, may have led to residual confounding. As there was only limited information on provider specialty available in the database, this was not included in the analysis. Some baseline characteristics remained imbalanced after weighting (e.g., use of bDMARDs and csDMARDs); however, their inclusion as covariates in the weighted persistence analysis minimized any confounding effects. Additionally, although speculative, the exclusion criterion of a prior diagnosis code for ankylosing spondylitis may have inadvertently prevented inclusion of some patients with PsA and axial disease in the analysis population. Conversely, patients with prior or active exposure to treatments indicated only for plaque psoriasis at the time of study conduct (e.g., tildrakizumab, brodalumab) were included in the analysis, and their effects on guselkumab or SC TNFi persistence are unknown. As with all claims-based studies, there may have been billing inaccuracies or omissions in coded procedures, diagnoses, and pharmacy claims, and the extent of these factors is unknown. Lastly, as this study included patients with commercial health plans, the results may not be generalizable to patients with no or other health insurance coverage, or patients outside of the USA.
Conclusions
In this real-world, claims data analysis of long-term, on-label treatment persistence, patients with active PsA initiating guselkumab were significantly (approximately two times) more likely to remain persistent with on-label therapy through 24 months compared to those initiating SC TNFi. These findings were consistent in both biologic-naïve and biologic-experienced patients. Given that treatment persistence may serve as a proxy for effectiveness and long-term disease control, higher on-label persistence associated with guselkumab may reflect an associated improvement in disease management outcomes.
Medical Writing/Editorial Assistance
Medical writing support was provided by Christine Tam, MWC, an employee of Analysis Group, Inc., under the direction of the authors in accordance with Good Publication Practice guidelines (Ann Intern Med 2022;175:1298–1304) and was funded by Johnson & Johnson (study sponsor).
Declarations
Conflict of Interest
Philip J Mease has received research grants from AbbVie, Acelyrin, Amgen, Bristol Myers Squibb, Eli Lilly, Johnson & Johnson, Novartis, and UCB; consulting fees from AbbVie, Acelyrin, Amgen, Bristol Myers Squibb, Century, Cullinan, Eli Lilly, Inmagene, Johnson & Johnson, Novartis, Pfizer, Spyre, Takeda, and UCB; and speaker fees from AbbVie, Amgen, Eli Lilly, Johnson & Johnson, Novartis, Pfizer, and UCB. Jessica Walsh received research funding from AbbVie, Merck, and Pfizer; and consulting fees from AbbVie, Eli Lilly, Johnson & Johnson, Novartis, and UCB. Timothy P Fitzgerald, Soumya D Chakravarty, and Elizabeth Adamson are employees of and own stock in Johnson & Johnson. Bruno Emond, Carmine Rossi, Samuel Schwartzbein, Kana Yokoji, Yuxi Wang, Patrick Lefebvre, and Dominic Pilon are employees of Analysis Group, Inc., a consulting company that has provided paid consulting services to Johnson & Johnson, which funded the development and conduct of this study. Shikha Singla received research funding from Eli Lilly and consulting fees from AbbVie, Janssen and UCB; and speaker fees from Johnson & Johnson. Joseph F Merola is a consultant and/or investigator for AbbVie, Amgen, Astra Zeneca, Biogen, Boehringer Ingelheim, Bristol Myers Squibb, Dermavant, Eli Lilly, Incyte, Johnson & Johnson Leo Pharma, Moonlake, Novartis, Pfizer, Sanofi-Regeneron, Sun Pharma, and UCB.
Ethical Approval
The IQVIA PharMetrics® Plus database was used under license. All data were de-identified in compliance with the Health Insurance Portability and Accountability Act (HIPAA); therefore, institutional review board review was not required.
Open Access This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc/4.0/.
On-Label Treatment Persistence Through 24 Months Among Patients with Active Psoriatic Arthritis Initiating Guselkumab or Subcutaneous Tumor Necrosis Factor Inhibitors
Verfasst von
Philip J. Mease
Jessica A. Walsh
Timothy P. Fitzgerald
Soumya D. Chakravarty
Elizabeth Adamson
Bruno Emond
Carmine Rossi
Samuel Schwartzbein
Kana Yokoji
Yuxi Wang
Patrick Lefebvre
Dominic Pilon
Shikha Singla
Joseph F. Merola
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Nicht nur eine ausschließliche, sondern auch eine ergänzende Nutzung von Komplementär- und Alternativmedizin erhöht bei Brustkrebs das 5-Jahres-Mortalitätsrisiko. Dafür spricht zumindest eine große retrospektive Analyse von US-Daten.
8% der Personen mit DOAK-Therapie haben noch erhöhte Blutwerte der Substanzen, wenn sie sich einer elektiven Operation unterziehen. Besonders häufig sind Ausreißer unter Apixaban. Auf den intraoperativen Blutverlust hatten sie in einer Analyse jedoch keinen Einfluss.
Das Risiko, erstmals an einer Pankreatitis zu erkranken, ist für Personen mit einer Zöliakie um über 40% erhöht. Besonders hoch ist es kurz nach der Diagnose. Auf das Rezidivrisiko hat eine Zöliakie aber keinen Einfluss, legt eine Langzeitanalyse aus Schweden nahe.
Schützt eine verlängerte Vancomycin-Therapie über insgesamt vier Wochen besser vor Rezidiven einer Clostridioides-difficile-Infektion (CDI) als ein kürzeres Behandlungsschema? Dieser Frage ist ein Team aus Kanada nachgegangen.
