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Objective: This study investigates the predictive capacity of LACC1 regarding the response to upadacitinib (UPA) in individuals with rheumatoid arthritis (RA).
Methods: The study involved sixty adult patients with active RA who either did not respond well to or could not tolerate methotrexate. The regimen involved UPA monotherapy at 15 mg/day, while maintaining a fixed dose of glucocorticoids was acceptable. Follow-up was planned for 24 weeks. Treatment response was assessed using Clinical Disease Activity Index, Simplified Disease Activity Index, tender joint count (TJC), swollen joint count, and Health Assessment Questionnaire. Moreover, parameters associated with treatment response to UPA were measured.
Results: Serum LACC1 levels may be protective in predicting response to UPA therapy. Age, prolonged disease duration, increased use of csDMARDs, low neutrophil counts, and higher inflammatory markers were strongly associated with non-good response. Prolonged disease duration, increased TJC/68, low neutrophil count, and high GM-CSF levels were all independent unfavorable predictors of good response to UPA treatment, while higher serum LACC1 levels were more helpful in predicting good response. Patients with an extended disease course, high TJC/68, and significantly increased inflammatory cytokines should be advised of the potential for poor early outcomes.
Conclusion: Higher serum LACC1 levels are associated with better efficacy of UPA, with implications for optimizing clinical individualized dosing strategies.
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http://dx.doi.org/10.1186/s40001-025-02938-0 | DOI Listing |
Eur J Med Res
August 2025
Department of Rheumatology and Immunology, Hainan General Hospital (Hainan Medical University Hainan Hospital), No.19 Xiuhua Road, Xiuying District, Haikou City, 570311, Hainan Province, China.
Objective: This study investigates the predictive capacity of LACC1 regarding the response to upadacitinib (UPA) in individuals with rheumatoid arthritis (RA).
Methods: The study involved sixty adult patients with active RA who either did not respond well to or could not tolerate methotrexate. The regimen involved UPA monotherapy at 15 mg/day, while maintaining a fixed dose of glucocorticoids was acceptable.
Clin Immunol
August 2024
Department of Rheumatology and Immunology, Shenzhen Children's hospital, 7019 Yitian Road, Shenzhen 518038, China. Electronic address:
Objective: Juvenile arthritis caused by loss-of-function LACC1 mutations is characterized by early onset of symmetric and chronic arthritis, associated with an elevation of inflammatory markers. We aimed to describe serum cytokine levels, explore the type I interferon pathway, and evaluate the efficacy of treatment in a patient presenting with polyarthritis and anemia caused by novel compound heterozygous variations in LACC1.
Methods: Clinical data of a patient with compound heterozygous variations in LACC1 was collected.
BMC Gastroenterol
October 2023
Department of Gastroenterology, The Affiliated Shuyang Hospital of Xuzhou Medical University, No.9, Yingbin Avenue, Shuyang County, Suqian, 223600, Jiangsu, China.
Background: The aim of this study was to explore the mechanism whereby LACC1 regulates the intestinal flora in a mouse model of inflammatory bowel disease (IBD).
Methods: C57BL/6 and Lacc1 mice were used to establish a mouse model of IBD induced by dextran sodium sulfate (DSS). The effects of Lacc1 deletion in mice were evaluated.
J Immunol
January 2019
Department of Human Genetics, Genentech, Inc., South San Francisco, CA 94080.
Both common and rare genetic variants of laccase domain-containing 1 (, previously C13orf31) are associated with inflammatory bowel disease, leprosy, Behcet disease, and systemic juvenile idiopathic arthritis. However, the functional relevance of these variants is unclear. In this study, we use LACC1-deficient mice to gain insight into the role of LACC1 in regulating inflammation.
View Article and Find Full Text PDFInflamm Bowel Dis
January 2019
Department of Gastroenterology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Background: Few studies have investigated the blood proteome of inflammatory bowel disease (IBD). We characterized the serum abundance of proteins encoded at 163 known IBD risk loci and tested these proteins for their biomarker discovery potential.
Methods: Based on the Human Protein Atlas (HPA) antibody availability, 218 proteins from genes mapping at 163 IBD risk loci were selected.