Rheumatoid ArthritisNCT05422313
Assessment of Galectin-9 in Rheumatoid Arthritis and Its Correlation With Disease Activity
An observational study of Rheumatoid Arthritis, run by Assiut University.
Trial summary
Rheumatoid arthritis (RA) is an autoimmune disease in which a symmetrical Synovial inflammation, bone destruction occur in both small and big Joints. If left untreated, this illness does not generally cause death, but it does drastically affect the quality of life and life expectancy of patients. Read more about this study
- Who is it for?
- Any age
- Conditions the study is for
- Rheumatoid Arthritis
- How many people
- 86 participants
- Where
- No sites listed yet
- Study dates
- Jun 2022to Dec 2023
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages Any age
- All sexes
- Child, Adult, Older adult
Study population: All hospitalized patients
Who may be able to join
- Patients age is > 20 years old.
- All rheumatoid arthritis patients must fulfill the 2010 ACR/EULAR criteria for RA.
Who cannot join
- Patients age is < 20 years old.
- Patient with evidence of any concomitant inflammatory disease, Acute infection or chronic inflammatory status.
Trial locations and contacts
No sites are listed yet.
About this study
Rheumatoid arthritis (RA) is an autoimmune disease in which a symmetrical Synovial inflammation, bone destruction occur in both small and big Joints. If left untreated, this illness does not generally cause death, but it does drastically affect the quality of life and life expectancy of patients. Although there is no cure for RA, patients are generally on long-term long-acting disease-modifying anti-rheumatic medications (DMARDs) to control joint inflammation, reduce joint damage, maintain joint function, and keep the illness in remission.
RA disease activity could be detected be DAS28 score. The DAS28 is a four-item scale that gives an absolute number reflecting disease activity. It includes the number of swollen and tender joints (SJC, TJC), the visual analogue scale of patients' assessment of their general health (VAS-GH), and the erythrocyte sedimentation rate (ESR) in the first hour.
Read more
In the pathophysiology of RA, cytokine networks play a crucial role. Rheumatoid inflammation has been linked to the generation of proinflammatory cytokines throughout time. Increased cytokine levels, such as tumour necrosis factor (TNF) and interleukin-6 (IL-6), represent rheumatoid synovial inflammation and have been linked to RA disease activity and anti-cytokine therapeutic response. The relationship between circulating cytokine levels and the phenotype of RA illness is, however, poorly understood.
Anti-citrullinated peptide antibodies (ACPA) are effective in the diagnosis of RA and have been linked to joint destruction progression and therapy response in RA patients. However, the relationship between ACPA status and proinflammatory cytokines during the course of RA illness is yet unknown.
Galectins are lectins with carbohydrate recognition domains (CRDs) that are extremely similar in sequence and exclusively bind to β--galactoside carbs. There are at least 15 galectins found in mammals, each having one or two CRDs comprising roughly 130 amino acids. Galectins have a wide range of activities due to their ubiquitous distribution, including mRNA splicing, programmed cell death, cell cycle control, activation, adhesion, migration, and cell differentiation.
Galectin-9 (Gal-9) is abundantly present in lymph nodes, bone marrow, liver, thymus, and spleen. It is expressed by immune cells, endothelial cells, and fibroblasts and plays an important role in regulating inflammation and immune reactions. Gal-9 is a ligand for T cell immunoglobulin and mucin-containing-moleculte-3 (Tim-3) that is expressed on CD4+ T helper (Th) 1 and Th17 and sends inhibitory signals to Tim-3. As a result of its interaction with Tim-3, Gal-9 suppresses pro-inflammatory T cell responses, and the Gal-9/Tim-3 pathway causes apoptosis of CD4+ Th1 or Th17 cells.
Considering that RA is a Th1-polarized autoimmune illness, dysregulated Gal-9 levels may induce an innate/adaptive immunity imbalance, resulting in pathological rheumatoid inflammation. Gal-9 has been demonstrated to mediate angiogenesis and inflammatory cell infiltration in inflammatory arthritis.
These findings show that Gal-9 may have a role in the inflammatory processes of rheumatoid arthritis. As a result, we concentrated on Gal-9 and postulated that it could be involved in the pathogenesis of RA. The levels of serum Gal-9 in individuals with RA were studied in this study, and the results were compared to clinical indicators
- Conditions
- Rheumatoid Arthritis
- Medical subject headings
- Arthritis, Rheumatoid
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| 56 patients with RA. | Patients age is > 20 years old. | |
| : 30 age-matched Healthy | Individual must be without a prior history of chronic inflammation or any form of arthritis. - . |
What is being measured
The primary outcome is the main question the study is designed to answer.
To correlate galectin-9 level with RA disease activity.
use galectin-9 to determine disease activity
Measured: 1.5 years
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted16 Jun 2022
- Study startJun 2022 (estimated)
- Primary completionNov 2023 (estimated)
- Study completionDec 2023 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (12)Papers the sponsor has linked to this study.
- Other trials for Rheumatoid ArthritisStudies of the same condition, open and under way.
- More trials run by Assiut UniversityThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case-control
- Time perspective
- Retrospective
- Enrolment
- 86 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Assiut University
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Norhan mostafa Mohamed Abdelal, Assiut University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05422313
- Sponsor's protocol ID
- VDSF
- Status last verified
- Jun 2022
- First submitted
- 14 Jun 2022
- Last updated
- 22 Jun 2022
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided
Publications
Floudas A, Canavan M, McGarry T, Mullan R, Nagpal S, Veale DJ, Fearon U. ACPA Status Correlates with Differential Immune Profile in Patients with Rheumatoid Arthritis. Cells. 2021 Mar 14;10(3):647. doi: 10.3390/cells10030647.
PubMed 33799480Gieseke F, Kruchen A, Tzaribachev N, Bentzien F, Dominici M, Muller I. Proinflammatory stimuli induce galectin-9 in human mesenchymal stromal cells to suppress T-cell proliferation. Eur J Immunol. 2013 Oct;43(10):2741-9. doi: 10.1002/eji.201343335. Epub 2013 Jul 23.
PubMed 23817958Golden-Mason L, McMahan RH, Strong M, Reisdorph R, Mahaffey S, Palmer BE, Cheng L, Kulesza C, Hirashima M, Niki T, Rosen HR. Galectin-9 functionally impairs natural killer cells in humans and mice. J Virol. 2013 May;87(9):4835-45. doi: 10.1128/JVI.01085-12. Epub 2013 Feb 13.
PubMed 23408620Yap HY, Tee SZ, Wong MM, Chow SK, Peh SC, Teow SY. Pathogenic Role of Immune Cells in Rheumatoid Arthritis: Implications in Clinical Treatment and Biomarker Development. Cells. 2018 Oct 9;7(10):161. doi: 10.3390/cells7100161.
PubMed 30304822McInnes IB, Schett G. Cytokines in the pathogenesis of rheumatoid arthritis. Nat Rev Immunol. 2007 Jun;7(6):429-42. doi: 10.1038/nri2094.
PubMed 17525752Naranjo A, Ojeda S, Francisco F, Erausquin C, Rua-Figueroa I, Rodriguez-Lozano C. Fibromyalgia in patients with rheumatoid arthritis is associated with higher scores of disability. Ann Rheum Dis. 2002 Jul;61(7):660-1. doi: 10.1136/ard.61.7.660. No abstract available.
PubMed 12079919Ogata A, Kato Y, Higa S, Yoshizaki K. IL-6 inhibitor for the treatment of rheumatoid arthritis: A comprehensive review. Mod Rheumatol. 2019 Mar;29(2):258-267. doi: 10.1080/14397595.2018.1546357. Epub 2019 Jan 3.
PubMed 30427250O'Brien MJ, Shu Q, Stinson WA, Tsou PS, Ruth JH, Isozaki T, Campbell PL, Ohara RA, Koch AE, Fox DA, Amin MA. A unique role for galectin-9 in angiogenesis and inflammatory arthritis. Arthritis Res Ther. 2018 Feb 12;20(1):31. doi: 10.1186/s13075-018-1519-x.
PubMed 29433546Li S, Yu Y, Koehn CD, Zhang Z, Su K. Galectins in the Pathogenesis of Rheumatoid Arthritis. J Clin Cell Immunol. 2013 Sep 30;4(5):1000164. doi: 10.4172/2155-9899.1000164.
PubMed 24416634Xia T, Zheng XF, Qian BH, Fang H, Wang JJ, Zhang LL, Pang YF, Zhang J, Wei XQ, Xia ZF, Zhao DB. Plasma Interleukin-37 Is Elevated in Patients with Rheumatoid Arthritis: Its Correlation with Disease Activity and Th1/Th2/Th17-Related Cytokines. Dis Markers. 2015;2015:795043. doi: 10.1155/2015/795043. Epub 2015 Sep 6.
PubMed 26435567Zhu C, Anderson AC, Kuchroo VK. TIM-3 and its regulatory role in immune responses. Curr Top Microbiol Immunol. 2011;350:1-15. doi: 10.1007/82_2010_84.
PubMed 20700701Zhu C, Anderson AC, Schubart A, Xiong H, Imitola J, Khoury SJ, Zheng XX, Strom TB, Kuchroo VK. The Tim-3 ligand galectin-9 negatively regulates T helper type 1 immunity. Nat Immunol. 2005 Dec;6(12):1245-52. doi: 10.1038/ni1271. Epub 2005 Nov 13.
PubMed 16286920
Study at a glance
From the registry record, last updated by the sponsor on 22 Jun 2022. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Assessment of Galectin-9 in Rheumatoid Arthritis and Its Correlation With Disease Activity
- ClinicalTrials.gov ID
- NCT05422313
- Acronym / sponsor ID
- VDSF
- Conditions
- Rheumatoid Arthritis
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 86 participants (estimated)
- Lead sponsor
- Assiut UniversityUniversity, hospital or other
- Study start
- Jun 2022 (estimated)
- Primary completion
- Nov 2023 (estimated)
- Study completion
- Dec 2023 (estimated)
- First posted
- 16 Jun 2022 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Rheumatoid arthritis (RA) is an autoimmune disease in which a symmetrical Synovial inflammation, bone destruction occur in both small and big Joints. If left untreated, this illness does not generally cause death, but it does drastically affect the quality of life and life expectancy of patients. Although there is no cure for RA, patients are generally on long-term long-acting disease-modifying anti-rheumatic medications (DMARDs) to control joint inflammation, reduce joint damage, maintain joint function, and keep the illness in remission.
RA disease activity could be detected be DAS28 score. The DAS28 is a four-item scale that gives an absolute number reflecting disease activity. It includes the number of swollen and tender joints (SJC, TJC), the visual analogue scale of patients' assessment of their general health (VAS-GH), and the erythrocyte sedimentation rate (ESR) in the first hour.
In the pathophysiology of RA, cytokine networks play a crucial role. Rheumatoid inflammation has been linked to the generation of proinflammatory cytokines throughout time. Increased cytokine levels, such as tumour necrosis factor (TNF) and interleukin-6 (IL-6), represent rheumatoid synovial inflammation and have been linked to RA disease activity and anti-cytokine therapeutic response. The relationship between circulating cytokine levels and the phenotype of RA illness is, however, poorly understood.
Anti-citrullinated peptide antibodies (ACPA) are effective in the diagnosis of RA and have been linked to joint destruction progression and therapy response in RA patients. However, the relationship between ACPA status and proinflammatory cytokines during the course of RA illness is yet unknown.
Galectins are lectins with carbohydrate recognition domains (CRDs) that are extremely similar in sequence and exclusively bind to β--galactoside carbs. There are at least 15 galectins found in mammals, each having one or two CRDs comprising roughly 130 amino acids. Galectins have a wide range of activities due to their ubiquitous distribution, including mRNA splicing, programmed cell death, cell cycle control, activation, adhesion, migration, and cell differentiation.
Galectin-9 (Gal-9) is abundantly present in lymph nodes, bone marrow, liver, thymus, and spleen. It is expressed by immune cells, endothelial cells, and fibroblasts and plays an important role in regulating inflammation and immune reactions. Gal-9 is a ligand for T cell immunoglobulin and mucin-containing-moleculte-3 (Tim-3) that is expressed on CD4+ T helper (Th) 1 and Th17 and sends inhibitory signals to Tim-3. As a result of its interaction with Tim-3, Gal-9 suppresses pro-inflammatory T cell responses, and the Gal-9/Tim-3 pathway causes apoptosis of CD4+ Th1 or Th17 cells.
Considering that RA is a Th1-polarized autoimmune illness, dysregulated Gal-9 levels may induce an innate/adaptive immunity imbalance, resulting in pathological rheumatoid inflammation. Gal-9 has been demonstrated to mediate angiogenesis and inflammatory cell infiltration in inflammatory arthritis.
These findings show that Gal-9 may have a role in the inflammatory processes of rheumatoid arthritis. As a result, we concentrated on Gal-9 and postulated that it could be involved in the pathogenesis of RA. The levels of serum Gal-9 in individuals with RA were studied in this study, and the results were compared to clinical indicators
Study design
- Observational model
- Case-control
- Time perspective
- Retrospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| 56 patients with RA. | – | –Patients age is > 20 years old. |
| : 30 age-matched Healthy | – | –Individual must be without a prior history of chronic inflammation or any form of arthritis. - . |
Who may qualify
- Sex
- All
- Age groups
- Child, Adult, Older adult
- Study population
- All hospitalized patients
Key inclusion criteria (2 listed)
- Patients age is > 20 years old.
- All rheumatoid arthritis patients must fulfill the 2010 ACR/EULAR criteria for RA.
Key exclusion criteria (2 listed)
- Patients age is < 20 years old.
- Patient with evidence of any concomitant inflammatory disease, Acute infection or chronic inflammatory status.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
To correlate galectin-9 level with RA disease activity.
Time frame: 1.5 years
use galectin-9 to determine disease activity
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 22 Jun 2022.
- Background: PubMed 33799480Floudas A, Canavan M, McGarry T, Mullan R, Nagpal S, Veale DJ, Fearon U. ACPA Status Correlates with Differential Immune Profile in Patients with Rheumatoid Arthritis. Cells. 2021 Mar 14;10(3):647. doi: 10.3390/cells10030647.
- Background: PubMed 23817958Gieseke F, Kruchen A, Tzaribachev N, Bentzien F, Dominici M, Muller I. Proinflammatory stimuli induce galectin-9 in human mesenchymal stromal cells to suppress T-cell proliferation. Eur J Immunol. 2013 Oct;43(10):2741-9. doi: 10.1002/eji.201343335. Epub 2013 Jul 23.
- Background: PubMed 23408620Golden-Mason L, McMahan RH, Strong M, Reisdorph R, Mahaffey S, Palmer BE, Cheng L, Kulesza C, Hirashima M, Niki T, Rosen HR. Galectin-9 functionally impairs natural killer cells in humans and mice. J Virol. 2013 May;87(9):4835-45. doi: 10.1128/JVI.01085-12. Epub 2013 Feb 13.
- Background: PubMed 30304822Yap HY, Tee SZ, Wong MM, Chow SK, Peh SC, Teow SY. Pathogenic Role of Immune Cells in Rheumatoid Arthritis: Implications in Clinical Treatment and Biomarker Development. Cells. 2018 Oct 9;7(10):161. doi: 10.3390/cells7100161.
- Background: PubMed 17525752McInnes IB, Schett G. Cytokines in the pathogenesis of rheumatoid arthritis. Nat Rev Immunol. 2007 Jun;7(6):429-42. doi: 10.1038/nri2094.
- Background: PubMed 12079919Naranjo A, Ojeda S, Francisco F, Erausquin C, Rua-Figueroa I, Rodriguez-Lozano C. Fibromyalgia in patients with rheumatoid arthritis is associated with higher scores of disability. Ann Rheum Dis. 2002 Jul;61(7):660-1. doi: 10.1136/ard.61.7.660. No abstract available.
- Background: PubMed 30427250Ogata A, Kato Y, Higa S, Yoshizaki K. IL-6 inhibitor for the treatment of rheumatoid arthritis: A comprehensive review. Mod Rheumatol. 2019 Mar;29(2):258-267. doi: 10.1080/14397595.2018.1546357. Epub 2019 Jan 3.
- Background: PubMed 29433546O'Brien MJ, Shu Q, Stinson WA, Tsou PS, Ruth JH, Isozaki T, Campbell PL, Ohara RA, Koch AE, Fox DA, Amin MA. A unique role for galectin-9 in angiogenesis and inflammatory arthritis. Arthritis Res Ther. 2018 Feb 12;20(1):31. doi: 10.1186/s13075-018-1519-x.
- Background: PubMed 24416634Li S, Yu Y, Koehn CD, Zhang Z, Su K. Galectins in the Pathogenesis of Rheumatoid Arthritis. J Clin Cell Immunol. 2013 Sep 30;4(5):1000164. doi: 10.4172/2155-9899.1000164.
- Background: PubMed 26435567Xia T, Zheng XF, Qian BH, Fang H, Wang JJ, Zhang LL, Pang YF, Zhang J, Wei XQ, Xia ZF, Zhao DB. Plasma Interleukin-37 Is Elevated in Patients with Rheumatoid Arthritis: Its Correlation with Disease Activity and Th1/Th2/Th17-Related Cytokines. Dis Markers. 2015;2015:795043. doi: 10.1155/2015/795043. Epub 2015 Sep 6.
- Background: PubMed 20700701Zhu C, Anderson AC, Kuchroo VK. TIM-3 and its regulatory role in immune responses. Curr Top Microbiol Immunol. 2011;350:1-15. doi: 10.1007/82_2010_84.
- Background: PubMed 16286920Zhu C, Anderson AC, Schubart A, Xiong H, Imitola J, Khoury SJ, Zheng XX, Strom TB, Kuchroo VK. The Tim-3 ligand galectin-9 negatively regulates T helper type 1 immunity. Nat Immunol. 2005 Dec;6(12):1245-52. doi: 10.1038/ni1271. Epub 2005 Nov 13.
- Individual participant dataSharing planned: Undecided
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Questions about this trial
What is this clinical trial studying?
An observational study of Rheumatoid Arthritis, run by Assiut University.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 2 inclusion and 2 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 22 Jun 2022. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Sohair K Sayed, professor (0102447771, Ksoher3@yahoo.com), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
To correlate galectin-9 level with RA disease activity. (time frame: 1.5 years). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT05422313, which also lists 12 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 22 Jun 2022; AzTrials last refreshed its copy on 7 Nov 2026.