Lymphadenitis, TuberculousNCT05202548
Immunology Dysregulation in Lymphadenitis Tuberculosis : An Observational Study Using Patient' Block Paraffins 2019 Until 2021
An observational study of Lymphadenitis, Tuberculous and Immune Defect, run by Universitas Katolik Widya Mandala Surabaya at 1 site in Indonesia.
Trial summary
Mycobacterium tuberculosis (M. tuberculosis) infection is still a problem that cannot be overcome in Indonesia. In 2018 the number of tuberculosis (TB) sufferers in Indonesia reached more than 850/100,000 population, an increase around 20% from the previous year's incidence. Read more about this study
- Who is it for?
- Any age
- Conditions the study is for
- Lymphadenitis, Tuberculous, Immune Defect
- What is being tested?
- Immuno-histochemical staining
- How many people
- 45 participants
- Where
- 1 siteIndonesia
- Study dates
- 1 May 2021to 25 Jun 2021
- How long will I take part?
- 1 Year
- 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
- No healthy volunteers
- Child, Adult, Older adult
Study population: The population in this study was blocked paraffin that diagnosed with lymphadenitis TB by pathologist and confirmed with MPT64 staining
Who may be able to join
- Lymphadenitis TB blocked paraffin that already confirmed by the Pathologist and MPT64 staining
Who cannot join
- broken blocked paraffin due to the storage process
Trial locations and contacts
1 site in 1 country.
Indonesia1 site
Vincentius A Paulo Surabaya Hospital
Surabaya, East Java, 60264
About this study
Mycobacterium tuberculosis (M. tuberculosis) infection is still a problem that cannot be overcome in Indonesia. In 2018 the number of tuberculosis (TB) sufferers in Indonesia reached more than 850/100,000 population, an increase around 20% from the previous year's incidence. One of the highest number of cases is in East Java Province, which is 38% of the total number of new TB cases in Indonesia.
Extrapulmonary tuberculosis (EPTB) according to WHO classification criteria is an M. tuberculosis infection that occurs in tissues and organs outside the lung parenchyma. The incidence rate in Indonesia reaches 1-5% of the incidence of TB thus EPTB may often be forgotten. However, the diagnosis, therapy and monitoring post treatment in EPTB remains difficult to do.
Read more
The focus of this research is tuberculous lymphadenitis (TB), due to 50% of EPTB cases in Indonesia was lymphadenitis TB. The risk factors for EPTB are immunocompromised conditions, such as HIV infection or comorbid conditions such as chronic kidney disease (CKD) and diabetes mellitus, but the mechanism of EPTB homing is still unclear. The mechanism of EPTB homing, especially TB lymphadenitis, really needs to be known for the development of diagnostics and therapy as well as preventing the occurrence of TB lymphadenitis.
The importance of this research is to obtain compounds from the human immune response that can be developed as diagnostic markers and therapeutic targets for tuberculosis infection, especially TB lymphadenitis. Activated macrophages containing M. tuberculosis are carried by lymph flow to lymph nodes, where there is deposition of antigen-antibody complexes which then activate CC Chemokine Receptor-2 (CCR2) on lymphocytes, which are the primary receptors for Chemokine (CC motif) ligands ( CCL)-8 and CCL5, proteins expressed on macrophages containing M. tuberculosis. Activation of CCR2 increases the production of IL-10(10). IL-10 has been responsible for decreasing the secretion of TNF-, IFN-γ, and IL-1β (11). IFN-γ affects the process of M. tuberculosis elimination and the success of TB therapy, so that IL-10 is responsible for the failure of macrophages to eliminate M. tuberculosis. IL-10 also binds to Signal Transducer and Activator of Transcription 3 (STAT3) and STAT3 increases the release of Suppressor of Cytokine Signaling 3 (SOCS3). SOCS3 interferes with IFN-γ signaling for CCR2 recognition of M. tuberculosis-containing macrophages. On the other hand, the mechanism of T lymphocytes and macrophages that activate pro-inflammatory mediators (TNF-, IFN-γ, and IL-1β) and the association of IL-10 activation on STAT3, SOCS3 and CCR2 expression in the incidence of EPTB, especially TB lymphadenitis without TB infection remains unknown.
Read the detailed description
Mycobacterium tuberculosis (M. tuberculosis) infection is still a problem that cannot be overcome in Indonesia. In 2018 the number of tuberculosis (TB) sufferers in Indonesia reached more than 850/100,000 population, an increase around 20% from the previous year's incidence. One of the highest number of cases is in East Java Province, which is 38% of the total number of new TB cases in Indonesia.
Extrapulmonary tuberculosis (EPTB) according to WHO classification criteria is an M. tuberculosis infection that occurs in tissues and organs outside the lung parenchyma. The incidence rate in Indonesia reaches 1-5% of the incidence of TB thus EPTB may often be forgotten. However, the diagnosis, therapy and monitoring post treatment in EPTB remains difficult to do.
The focus of this research is tuberculous lymphadenitis (TB), due to 50% of EPTB cases in Indonesia was lymphadenitis TB. The risk factors for EPTB are immunocompromised conditions, such as HIV infection or comorbid conditions such as chronic kidney disease (CKD) and diabetes mellitus, but the mechanism of EPTB homing is still unclear. The mechanism of EPTB homing, especially TB lymphadenitis, really needs to be known for the development of diagnostics and therapy as well as preventing the occurrence of TB lymphadenitis.
The importance of this research is to obtain compounds from the human immune response that can be developed as diagnostic markers and therapeutic targets for tuberculosis infection, especially TB lymphadenitis. Activated macrophages containing M. tuberculosis are carried by lymph flow to lymph nodes, where there is deposition of antigen-antibody complexes which then activate CC Chemokine Receptor-2 (CCR2) on lymphocytes, which are the primary receptors for Chemokine (CC motif) ligands ( CCL)-8 and CCL5, proteins expressed on macrophages containing M. tuberculosis. Activation of CCR2 increases the production of IL-10(10). IL-10 has been responsible for decreasing the secretion of TNF-, IFN-γ, and IL-1β (11). IFN-γ affects the process of M. tuberculosis elimination and the success of TB therapy, so that IL-10 is responsible for the failure of macrophages to eliminate M. tuberculosis. IL-10 also binds to Signal Transducer and Activator of Transcription 3 (STAT3) and STAT3 increases the release of Suppressor of Cytokine Signaling 3 (SOCS3). SOCS3 interferes with IFN-γ signaling for CCR2 recognition of M. tuberculosis-containing macrophages. On the other hand, the mechanism of T lymphocytes and macrophages that activate pro-inflammatory mediators (TNF-, IFN-γ, and IL-1β) and the association of IL-10 activation on STAT3, SOCS3 and CCR2 expression in the incidence of EPTB, especially TB lymphadenitis without TB infection remains unknown.
In this study, Lymphadenitis TB paraffin blocks from patients were collected and screened for immunological responses that TB patients have potential as targets for diagnosis and therapy. The paraffin block samples came from the Anatomical Pathology Laboratory of St. Catholic Hospital. Vincentius A Paulo (RKZ) Surabaya. Existing samples were taken and performed immuno-histochemical (IHC) to define theimmune dysregulation in TB lymphadenitis.
- Conditions
- Lymphadenitis, Tuberculous, Immune Defect
- Being tested
- Immuno-histochemical staining
- Keywords
- Lymphadenitis tuberculosis, C-C Chemokines receptor - 2 (CCR-2), C-C Chemokines ligand - 5 (CCL-5), Cytokines inflammatory
- Medical subject headings
- Tuberculosis, Lymph Node
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Immuno-histochemical stainingOther
blocked paraffin that suit with inclusion and exclusion criteria proceed with immuno-histochemical staining to define immune dysregulation in lymphadenitis TB
| Study group | Role | What they receive |
|---|---|---|
| Lymphadenitis TB | The group study was blocked paraffin from lymphadenitis tuberculosis patient that already confirmed diagnosis histopathological anatomy (PA histopathology) Receives: Other: Immuno-histochemical staining |
What is being measured
The primary outcome is the main question the study is designed to answer.
IHC slides
Histopathology slides stained by immuno-histochemical substrates
Measured: 15 November 2021
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted21 Jan 2022
- Study start1 May 2021
- Primary completion25 Jun 2021
- Study completion25 Jun 2021
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (1)Papers the sponsor has linked to this study.
- Other trials for Lymphadenitis, TuberculousStudies of the same condition, open and under way.
- 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 only
- Time perspective
- Other
- Enrolment
- 45 participants (actual)
- Target duration
- 1 Year
Sponsor and investigators
- Lead sponsor
- Universitas Katolik Widya Mandala Surabaya
- Sponsor type
- University, hospital or other
- Collaborators
- Kementerian Riset dan Teknologi / Badan Riset dan Inovasi Nasional, Indonesia
- Responsible party
- Principal investigator, Bernadette Dian Novita, MD.,PhD, Universitas Katolik Widya Mandala Surabaya
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05202548
- Sponsor's protocol ID
- 002/AMD-SP2H/LT-MULTIPDPK/LL7
- Status last verified
- Jan 2022
- First submitted
- 8 Jan 2022
- Last updated
- 21 Jan 2022
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided: Study protocol share
Publications
Novita BD, Tjahjono Y, Wijaya S, Theodora I, Erwin F, Halim SW, Hendrawan B, Jaya DK, Tahalele PL. Characterization of chemokine and cytokine expression pattern in tuberculous lymphadenitis patient. Front Immunol. 2022 Nov 10;13:983269. doi: 10.3389/fimmu.2022.983269. eCollection 2022.
PubMed 36439164
Study at a glance
From the registry record, last updated by the sponsor on 21 Jan 2022. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Immunology Dysregulation in Lymphadenitis Tuberculosis : An Observational Study Using Patient' Block Paraffins 2019 Until 2021
- ClinicalTrials.gov ID
- NCT05202548
- Acronym / sponsor ID
- 002/AMD-SP2H/LT-MULTIPDPK/LL7
- Conditions
- Lymphadenitis, Tuberculous, Immune Defect
- Keywords
- Lymphadenitis tuberculosis, C-C Chemokines receptor - 2 (CCR-2), C-C Chemokines ligand - 5 (CCL-5), Cytokines inflammatory
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 45 participants (actual)
- Lead sponsor
- Universitas Katolik Widya Mandala SurabayaUniversity, hospital or other
- Collaborators
- Kementerian Riset dan Teknologi / Badan Riset dan Inovasi Nasional, Indonesia
- Study start
- 1 May 2021 (actual)
- Primary completion
- 25 Jun 2021 (actual)
- Study completion
- 25 Jun 2021 (actual)
- First posted
- 21 Jan 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.
Mycobacterium tuberculosis (M. tuberculosis) infection is still a problem that cannot be overcome in Indonesia. In 2018 the number of tuberculosis (TB) sufferers in Indonesia reached more than 850/100,000 population, an increase around 20% from the previous year's incidence. One of the highest number of cases is in East Java Province, which is 38% of the total number of new TB cases in Indonesia.
Extrapulmonary tuberculosis (EPTB) according to WHO classification criteria is an M. tuberculosis infection that occurs in tissues and organs outside the lung parenchyma. The incidence rate in Indonesia reaches 1-5% of the incidence of TB thus EPTB may often be forgotten. However, the diagnosis, therapy and monitoring post treatment in EPTB remains difficult to do.
The focus of this research is tuberculous lymphadenitis (TB), due to 50% of EPTB cases in Indonesia was lymphadenitis TB. The risk factors for EPTB are immunocompromised conditions, such as HIV infection or comorbid conditions such as chronic kidney disease (CKD) and diabetes mellitus, but the mechanism of EPTB homing is still unclear. The mechanism of EPTB homing, especially TB lymphadenitis, really needs to be known for the development of diagnostics and therapy as well as preventing the occurrence of TB lymphadenitis.
The importance of this research is to obtain compounds from the human immune response that can be developed as diagnostic markers and therapeutic targets for tuberculosis infection, especially TB lymphadenitis. Activated macrophages containing M. tuberculosis are carried by lymph flow to lymph nodes, where there is deposition of antigen-antibody complexes which then activate CC Chemokine Receptor-2 (CCR2) on lymphocytes, which are the primary receptors for Chemokine (CC motif) ligands ( CCL)-8 and CCL5, proteins expressed on macrophages containing M. tuberculosis. Activation of CCR2 increases the production of IL-10(10). IL-10 has been responsible for decreasing the secretion of TNF-, IFN-γ, and IL-1β (11). IFN-γ affects the process of M. tuberculosis elimination and the success of TB therapy, so that IL-10 is responsible for the failure of macrophages to eliminate M. tuberculosis. IL-10 also binds to Signal Transducer and Activator of Transcription 3 (STAT3) and STAT3 increases the release of Suppressor of Cytokine Signaling 3 (SOCS3). SOCS3 interferes with IFN-γ signaling for CCR2 recognition of M. tuberculosis-containing macrophages. On the other hand, the mechanism of T lymphocytes and macrophages that activate pro-inflammatory mediators (TNF-, IFN-γ, and IL-1β) and the association of IL-10 activation on STAT3, SOCS3 and CCR2 expression in the incidence of EPTB, especially TB lymphadenitis without TB infection remains unknown.
Detailed description
Mycobacterium tuberculosis (M. tuberculosis) infection is still a problem that cannot be overcome in Indonesia. In 2018 the number of tuberculosis (TB) sufferers in Indonesia reached more than 850/100,000 population, an increase around 20% from the previous year's incidence. One of the highest number of cases is in East Java Province, which is 38% of the total number of new TB cases in Indonesia.
Extrapulmonary tuberculosis (EPTB) according to WHO classification criteria is an M. tuberculosis infection that occurs in tissues and organs outside the lung parenchyma. The incidence rate in Indonesia reaches 1-5% of the incidence of TB thus EPTB may often be forgotten. However, the diagnosis, therapy and monitoring post treatment in EPTB remains difficult to do.
The focus of this research is tuberculous lymphadenitis (TB), due to 50% of EPTB cases in Indonesia was lymphadenitis TB. The risk factors for EPTB are immunocompromised conditions, such as HIV infection or comorbid conditions such as chronic kidney disease (CKD) and diabetes mellitus, but the mechanism of EPTB homing is still unclear. The mechanism of EPTB homing, especially TB lymphadenitis, really needs to be known for the development of diagnostics and therapy as well as preventing the occurrence of TB lymphadenitis.
The importance of this research is to obtain compounds from the human immune response that can be developed as diagnostic markers and therapeutic targets for tuberculosis infection, especially TB lymphadenitis. Activated macrophages containing M. tuberculosis are carried by lymph flow to lymph nodes, where there is deposition of antigen-antibody complexes which then activate CC Chemokine Receptor-2 (CCR2) on lymphocytes, which are the primary receptors for Chemokine (CC motif) ligands ( CCL)-8 and CCL5, proteins expressed on macrophages containing M. tuberculosis. Activation of CCR2 increases the production of IL-10(10). IL-10 has been responsible for decreasing the secretion of TNF-, IFN-γ, and IL-1β (11). IFN-γ affects the process of M. tuberculosis elimination and the success of TB therapy, so that IL-10 is responsible for the failure of macrophages to eliminate M. tuberculosis. IL-10 also binds to Signal Transducer and Activator of Transcription 3 (STAT3) and STAT3 increases the release of Suppressor of Cytokine Signaling 3 (SOCS3). SOCS3 interferes with IFN-γ signaling for CCR2 recognition of M. tuberculosis-containing macrophages. On the other hand, the mechanism of T lymphocytes and macrophages that activate pro-inflammatory mediators (TNF-, IFN-γ, and IL-1β) and the association of IL-10 activation on STAT3, SOCS3 and CCR2 expression in the incidence of EPTB, especially TB lymphadenitis without TB infection remains unknown.
In this study, Lymphadenitis TB paraffin blocks from patients were collected and screened for immunological responses that TB patients have potential as targets for diagnosis and therapy. The paraffin block samples came from the Anatomical Pathology Laboratory of St. Catholic Hospital. Vincentius A Paulo (RKZ) Surabaya. Existing samples were taken and performed immuno-histochemical (IHC) to define theimmune dysregulation in TB lymphadenitis.
Study design
- Observational model
- Case only
- Time perspective
- Other
- Target follow-up
- 1 Year
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Lymphadenitis TB | – | Other: Immuno-histochemical stainingThe group study was blocked paraffin from lymphadenitis tuberculosis patient that already confirmed diagnosis histopathological anatomy (PA histopathology) |
Who may qualify
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult, Older adult
- Study population
- The population in this study was blocked paraffin that diagnosed with lymphadenitis TB by pathologist and confirmed with MPT64 staining
Key inclusion criteria (1 listed)
- Lymphadenitis TB blocked paraffin that already confirmed by the Pathologist and MPT64 staining
Key exclusion criteria (1 listed)
- broken blocked paraffin due to the storage process
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Immuno-histochemical stainingblocked paraffin that suit with inclusion and exclusion criteria proceed with immuno-histochemical staining to define immune dysregulation in lymphadenitis TB | Other | Lymphadenitis TB |
Primary outcome
IHC slides
Time frame: 15 November 2021
Histopathology slides stained by immuno-histochemical substrates
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 21 Jan 2022.
- Derived from this study: PubMed 36439164Novita BD, Tjahjono Y, Wijaya S, Theodora I, Erwin F, Halim SW, Hendrawan B, Jaya DK, Tahalele PL. Characterization of chemokine and cytokine expression pattern in tuberculous lymphadenitis patient. Front Immunol. 2022 Nov 10;13:983269. doi: 10.3389/fimmu.2022.983269. eCollection 2022.
- Individual participant dataSharing planned: Undecided. Study protocol share
Related trials for Lymphadenitis, Tuberculous
Not yet recruiting
Diagnostic Performance and Safety of Endobronchial Ultrasound-guided Transbronchial Mediastinal Cryobiopsy in Diagnosing Tuberculous Mediastinal Lymphadenitis: a Randomised Controlled Trial
Tuberculosis, Mediastinal and Hilar Lymph Node Enlargement
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.
The record lists no contact. Use the official record to reach the sponsor.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Lymphadenitis, Tuberculous and Immune Defect, run by Universitas Katolik Widya Mandala Surabaya at 1 site in Indonesia.
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 1 inclusion and 1 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: finished, as of the sponsor's last update on 21 Jan 2022. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Indonesia. Whether a site is taking part right now should be confirmed with that site. See every site.
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?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
IHC slides (time frame: 15 November 2021). 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 NCT05202548, which also lists 1 linked publication.
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 21 Jan 2022.