Abstract
Objectives
Obesity and psoriatic arthritis (PsA) have a complicated relationship. While weight alone does not cause PsA, it is suspected to cause worse symptoms. Neutrophil gelatinase-associated lipocalin (NGAL) is secreted through various cell types. Our objective was to assess the changes and trajectories in serum NGAL and clinical outcomes in patients with PsA during 12 months of anti-inflammatory treatment.
Method
This exploratory prospective cohort study enrolled PsA patients initiating conventional synthetic or biological disease-modifying anti-rheumatic drugs (csDMARDs/bDMARDs). Clinical, biomarker, and patient-reported outcome measures were retrieved at baseline, and 4 and 12 months. Control groups at baseline were psoriasis (PsO) patients and apparently healthy controls. The serum NGAL concentration was quantified by a high-performance singleplex immunoassay.
Results
In total, 117 PsA patients started a csDMARD or bDMARD, and were compared indirectly at baseline with a cross-sectional sample of 20 PsO patients and 20 healthy controls. The trajectory in NGAL related to anti-inflammatory treatment for all included PsA patients showed an overall change of −11% from baseline to 12 months. Trajectories in NGAL for patients with PsA, divided into treatment groups, showed no clear trend in clinically significant decrease or increase following anti-inflammatory treatment. NGAL concentrations in the PsA group at baseline corresponded to the levels in the control groups. No correlation was found between changes in NGAL and changes in PsA outcomes.
Conclusion
Based on these results, serum NGAL does not add any value as a biomarker in patients with peripheral PsA, either for disease activity or for monitoring.
Acknowledgements
We wish to acknowledge all patients participating in the current study, as well as the patient research partners. We also would like to thank the clinical departments for assisting with recruitment of the participants. Furthermore, we thank data manager Christian Cato Holm, the Parker Institute, for assistance during the collection and retrieval of data to conduct the study.
Disclosure statement
MS has received research funding from Eli Lilly and Pfizer; and speaker fees from Janssen-Cilag. AE has received research funding from Pfizer, Eli Lilly, Novartis, Bristol-Myers Squibb, AbbVie, Janssen Pharmaceuticals, Boehringer Ingelheim, the Danish National Psoriasis Foundation, the Simon Spies Foundation, and the Kgl Hofbundtmager Aage Bang Foundation; and honoraria as a consultant and/or speaker from AbbVie, Almirall, Leo Pharma, Zuellig Pharma, Galápagos NV, Sun Pharmaceuticals, Samsung Bioepis Co., Pfizer, Eli Lilly and Company, Novartis, Union Therapeutics, Galderma, Dermavant, UCB, Mylan, Bristol-Myers Squibb, McNeil Consumer Healthcare, Horizon Therapeutics, Boehringer Ingelheim, and Janssen Pharmaceuticals. TSJ has received fees as a speaker and consultant for AbbVie, Pfizer, Roche, Novartis, UCB, Biogen, Gilead, and Eli Lilly. LD has received research funding from BMS outside the present work; and honoraria as a speaker from Galderma, Eli Lilly, and Janssen Pharmaceuticals. LEK reports speakers’ bureaux for Pfizer, AbbVie, Amgen, UCB, Gilead, Biogen, BMS, MSD, Novartis, Eli Lilly, and Janssen Pharmaceuticals; and is a consultant for Pfizer, AbbVie, Amgen, UCB, Gilead, Biogen, BMS, MSD, Novartis, Eli Lilly, and Janssen Pharmaceuticals. The remaining authors report no conflicts of interest.
Data availability
The underlying data for this article cannot be shared publicly to protect the privacy of the individuals who participated in the study. Data may be shared as part of research collaborations between participating institutions in line with GDPR and if approved by the Parker Institute and the Danish authorities.
Supplementary material
Supplemental data for this article can be accessed online at https://doi.org/10.1080/03009742.2023.2216046