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IL-6, IL-12, IL-15 and IL-23 Expression Levels in Rheumatoid Arthritis Patients

Effect of cDMARD and Baricitinib Therapy on IL-6, IL-12, IL-15 and IL-23 Expression Levels in Rheumatoid Arthritis Patients

Status
Not yet recruiting
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT06558305
Enrollment
80
Registered
2024-08-16
Start date
2024-09-30
Completion date
2025-04-30
Last updated
2024-08-16

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Rheumatoid Arthritis

Brief summary

Rheumatoid Arthritis (RA) is a systemic autoimmune disease characterized by chronic inflammation and articular damage. Continuous medical research has dramatically improved the outcomes for patients with RA. Traditional therapeutic approaches have relied on glucocorticoids, nonsteroidal anti-inflammatory drugs (NSAIDs) and disease modifying antirheumatic drugs (DMARDs) such as methotrexate, sulfasalazine or leflunomide. Glucocorticoids and NSAIDs interfere with the inflammatory cascades while DMARDs impede both the inflammatory and the destructive processes of RA. These drugs, although efficient, are not specifically directed against inflammatory cells or cytokines and are associated with significant toxicity. The development of biologic DMARDs (bDMARDs), has been an important step forward. Their ability to neutralize specific cytokines or target distinct immune cells filled a gap in existing treatment options for RA. \[3\]. However, some patients still have only partial or no response to bDMARDs. More recently, a group of drugs has been developed that inhibit the janus kinase (JAK) family of intracellular tyrosine kinases, which transmit cytokine- mediated signals via the JAK-signal transducer and activator of transcription (STAT) pathway \[4\]. Baricitinib, with a selectivity to inhibit JAK1 and 2, has been FDA approved for RA in 2018 \[5\]. Many cytokines such IL-6, IL-12, IL-15, IL-23, (GM-CSF) and (IFNs) are associated with the pathogenesis of RA. These cytokines transduce signals via the JAK-STAT pathway.

Interventions

OTHERblood sample

Total RNA will be extracted from the whole blood using a commercial extraction kit (RNA Extraction Kit, applied biotechnology Co.Ltd, Egypt) according to the manufacturer's instructions. RNA will be stored at -80°C.The extracted RNA will be used for cDNA synthesis using commercial kits (cDNA Synthesis Kit, applied biotechnology Co.Ltd, Egypt), according to the manufacturer's instruction.

Sponsors

Assiut University
Lead SponsorOTHER

Study design

Observational model
CASE_CONTROL
Time perspective
CROSS_SECTIONAL

Eligibility

Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
Yes

Inclusion criteria

* Age is at leasr18 years old, * established RA diagnosis according to 2010 the American College of Rheumatology/European League against Rheumatism classification criteria

Exclusion criteria

* Associated autoimmune diseases, * connective tissue diseases, * chronic liver or kidney diseases or * genetic diseases

Design outcomes

Primary

MeasureTime frameDescription
assess the effect of cDMARD and Baricitinib (JAKi) therapy on gene expressions of IL-6, IL-12, IL-15 and, IL-23 in patients with RA relative to the healthy controls.6 monthsassess the effect of cDMARD and Baricitinib (JAKi) therapy on gene expressions of IL-6, IL-12, IL-15 and, IL-23 in patients with RA relative to the healthy controls.

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026