Investigation Center
Vadhana, Bangkok, 10110, Thailand
Location contact
Nathaphong Dejthida, Medical Degree
CONTACT
Nathaphong Dejthida, Medical Degree
PRINCIPAL_INVESTIGATOR
CONTACT
NCT Number: NCT07748975
Clinical outcome to identify and analyze the epigenetic, phenotypic, protein variation, metabolites of CYP450 Family 11 Subfamily B, both 1 and 2, human-associated aldosterone protein release, and signaling inhibitory pathways post-aldosterone-mineralocorticoid interaction.
We will include clinical studies (RCTs, cohort, case-control/series/report) from fresh human specimens. We will exclude animal studies, studies generated from cell culture, and aldosterone synthesis.
To systematically review and synthesize the literature on the main 2 questions Question 1: Which environment induces CYP11B1 or CYP11B2 activation causing hyperaldosteronemia in hypertension patients? Question 2: Which intracellular signal silences aldosterone-MR activity? For Individual Participant Data Meta-analysis, data will be extracted from final analysis articles from the framework of the data selection process only; the effect measurement and multi-variable model meta-analysis will be performed.
Primary Objective1: to identify CYP450 Family 11 Subfamily B and Aldosterone in hypertension patients following; By structure ● Evidence confirms Epigenetic profile of CYP450 Family 11 Subfamily B, Aldosterone, Signal in hypertension patients, both random and treated from any DNA sequencing method Protein synthesis evidence of aldosterone protein induces hypertension from Western blot or LC-MS By function Metabolomic profile: the substrate or product refers to aldosterone interaction causing end-organ cell line dysfunction or impaired structure.
Inhibitory signaling profiling of hypertension patients compared to non-hypertension patients, which negatively feedback to CYP450 Family 11 Subfamily B or Aldosterone
Secondary Objective 2:
Sub-group analysis effect measurement following;
* Proposed mechanisms, biological markers, or pathways that contribute to failure to regulate aldosteronemia * Treatment-related permanent normotensive post-hyperaldosteronemia. Primary Objective 2: Identify possible intracellular signal inhibit aldosterone action * Analyze possible mechanisms of signal that are silent aldosterone-MR activity * Differentiation of free aldosterone and attached aldosterone
Secondary Objective 2:
● Sensitivity and specificity of outcomes of hypertension patients who underwent estimate substrate associated aldosterone circulation Plasma CYP450 Family 11 Subfamily B Urine CYP450 Family 11 Subfamily B Plasma Aldosterone (active form) Plasma Aldosterone (metabolite form) Urine Aldosterone
Trial opening soon.
Get Notified18 year–100 year
All sexes
Interventional
Not applicable
Vadhana, Bangkok, 10110, Thailand
Nathaphong Dejthida, Medical Degree
CONTACT
Nathaphong Dejthida, Medical Degree
PRINCIPAL_INVESTIGATOR
CONTACT
Primary Objective1: to identify CYP450 Family 11 Subfamily B and Aldosterone in hypertension patients following; By structure ● Evidence confirms Epigenetic profile of CYP450 Family 11 Subfamily B, Aldosterone, Signal in hypertension patients, both random and treated from any DNA sequencing method Protein synthesis evidence of aldosterone protein induces hypertension from Western blot or LC-MS By function Metabolomic profile: the substrate or product refers to aldosterone interaction causing end-organ cell line dysfunction or impaired structure.
Inhibitory signaling profiling of hypertension patients compared to non-hypertension patients, which negatively feedback to CYP450 Family 11 Subfamily B or Aldosterone
Secondary Objective 2:
Sub-group analysis effect measurement following;
Secondary Objective 2:
● Sensitivity and specificity of outcomes of hypertension patients who underwent estimate substrate associated aldosterone circulation Plasma CYP450 Family 11 Subfamily B Urine CYP450 Family 11 Subfamily B Plasma Aldosterone (active form) Plasma Aldosterone (metabolite form) Urine Aldosterone Axin-CK1-GSK3-APC-Beta-catenin complex
Healthy volunteers accepted: No
Only the study team can determine whether someone qualifies for participation.
Inclusion criteria
Exclusion criteria
Evidence of synthesis of aldosterone and/or degradation of inactive forms of aldosterone, which focuses on
Medical treatment that interferes with free aldosterone levels and reports systolic blood pressure deviation
The non-medical intervention includes MIS, Open surgery, and intravascular guide treatment aim to treat hypetension and lower aldosterone level.
Time frame: 12 months
The result, both qualitative and quantitative, from aldosterone synthesis to degradation and elimination via urine.
Time frame: 12 months
Focus on both quantitative and qualitative evidence of aldosterone, CYP11B1, andand CYP11B2 protein
Time frame: 12 months
Focus on the ratio of degradation activity of the inactive form of aldosterone and the inhibitory competitor inhibits the cell product from the aldosterone-mineralocorticoid receptor. Axin-CK1-GSK3-APC complex profile is indicated
Contact information is provided by the study sponsor or research team.
DejthidaNathaphong
Other
Acronym: DETAIL
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View the official ClinicalTrials.gov record (opens in a new tab)This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.
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