Idiopathic Pulmonary Arterial HypertensionNCT01884051
Hormonal, Metabolic, and Signaling Interactions in PAH
An observational study of Idiopathic Pulmonary Arterial Hypertension and Heritable Pulmonary Arterial Hypertension, run by Vanderbilt University Medical Center at 1 site in United States.
Trial summary
Our hypothesis is that optimal treatment of the dysfunctional metabolic pathways which underlie PAH will improve pulmonary vascular function and consequences of the disease. Read more about this study
- Who is it for?
- Ages Up to 90 yearsHealthy volunteers can take part
- Conditions the study is for
- Idiopathic Pulmonary Arterial Hypertension, Heritable Pulmonary Arterial Hypertension, Scleroderma Associated Pulmonary Arterial Hypertension
- How many people
- 1,899 participants
- Where
- 1 siteUnited States
- Study dates
- Sep 2012to Jul 2032
- Phase
- Observational
- Are there results?
- Not yet: the study is under way
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 Up to 90 years
- All sexes
- Healthy volunteers accepted
- Child, Adult, Older adult
Study population: Cohort 1 subjects will be recruited from our adult and pediatric pulmonary vascular disease clinics. Cohort 2-healthy controls will be recruited form patients families and the general public in middle Tennesssee.
Who may be able to join
- Project 1
- Diagnosis of IPAH (idiopathic pulmonary arterial hypertension), HPAH (heritable pulmonary arterial hypertension), or APAH (associated pulmonary arterial hypertension), family members of affected persons
- Age 0-90, age 12-90 for skin biopsy
- Diagnosis of IPAH, HPAH, or APAH, family members of affected persons
- 0-90
- Subjects with reasonably easy access to clinic for blood collection and other testing
Show all 9Show fewer
- Subject able to tolerate fasting state prior to sample collection and EndoPAT (endothelial function assessment) testing
- Diagnosis of IPAH, HPAH, or APAH, family members of affected persons
- 7-90
Who cannot join
- Other diagnosis
- Age greater than 90, age less than 12 or greater than 90 for skin biopsy
- Project 2
- Other diagnosis
- 0-90
- Subjects with difficulty reaching clinic for blood collection and other testing
Show all 12Show fewer
- Subjects unable to tolerate fasting state
- Project 3
- Other diagnosis
- Age less than 7 or greater than 90
- -
- -
Trial locations and contacts
1 site in 1 country. Contact the study team or a site near you to ask about taking part.
United States1 site, 1 recruiting
- Recruiting
Vanderbilt University Medical Center
Nashville, Tennessee, 37232
About this study
Official title: Hormonal, Metabolic, and Signaling Interaction in Pulmonary Arterial Hypertension
Our hypothesis is that optimal treatment of the dysfunctional metabolic pathways which underlie PAH will improve pulmonary vascular function and consequences of the disease.
Read the detailed description
Project 1: This project will work to understand why women are affected by pulmonary arterial hypertension (PAH) so much more often than men. This observation is true in heritable, idiopathic and associated forms of PAH. While males and females have some similar hormone levels, certain hormones exist at higher levels in each gender. For example, estrogen levels are much higher in females, and thus seemed the most sensible place to start looking for differences that may be affecting disease. In a small, early study of our heritable patients, we found differences in how patients break down estrogens as compared to healthy control subjects. Now, we want to confirm that what we found is true in a much larger group of patients that includes idiopathic and associated forms of PAH. We will also look to see if testosterone and other androgenic hormones are somehow protective for males. If the observation holds true in the larger group of patients, then we may try to "fix" the hormone imbalance in a mouse model of PAH with a drug therapy, and see if it helps improve the mouse pulmonary hypertension without bad side effects to the animals. If the animal drug studies work, then we may be able to try this drug in patients to see if it will work as a human treatment.
Project 2: Despite major advances in understanding PAH in recent decades, safe, effective and tolerable therapies remain elusive. The metabolic syndrome (central obesity, insulin resistance, high blood pressure and hyperlipidemia-fats in the blood) has been implicated in PAH. Treating the downstream consequences of insulin resistance in the pulmonary vasculature is a new approach to effective intervention against this highly mortal disease. This project will study the role of insulin resistance in pulmonary arterial hypertension and determine if therapies to treat insulin resistance will improve pulmonary arterial hypertension.
Project 3: In Project 3, we are working on the theory that PAH can be treated by fixing cell-cell junctions in blood vessels with a drug called recombinant ACE2(angiotensin converting enzyme 2). This is the only approach so far that has worked to reverse disease in mouse models of heritable PAH, but we need to better understand how it is working and make sure it has long term safety in animal models before starting human trials, hopefully within a few years. Definition: Cell-cell junctions-all of our organs and body structures are made from cells. Normally, these cells (think of a balloon filled with water) line up right next to each other so that the cell membranes touch each other. Materials can flow from one cell to the next. In PAH patients it is believed that the cells in the linings of the small arteries are not able to line up together as they should.
- Conditions
- Idiopathic Pulmonary Arterial Hypertension, Heritable Pulmonary Arterial Hypertension, Scleroderma Associated Pulmonary Arterial Hypertension, Appetite Suppressant Associate PAH
- Keywords
- Pulmonary arterial hypertension
- Medical subject headings
- Familial Primary Pulmonary Hypertension, Pulmonary Arterial Hypertension
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 |
|---|---|---|
| PAH patients | Patients diagnosed with WHO Group 1 PAH | |
| Healthy subjects | Subjects who have been evaluated for heart and lung disease and found to be healthy |
What is being measured
The primary outcome is the main question the study is designed to answer.
Ratio of sex hormone metabolites
The primary outcome measure is the ratio of 2-hydroxyestrogens to 16-hydroxyestrogens among patients compared to both controls and at risk but well subjects.
Measured: 5 years
Evaluation of insulin resistance in pulmonary arterial hypertension patients/Clinical trial of Metformin in Pulmonary Arterial Hypertension
We will assess various measures of insulin resistance among patients, compared to healthy control subjects as well as at risk but well subjects. The primary measure will be assessed using the glucose clamp technique to quantify insulin secretion and resistance.
Measured: 5 years
Mechanism, safety, and efficacy of ACE-2 (Angiotensin Converting Enzyme 2) in the treatment of PAH.
We will assess the safety and efficacy of ACE-2 for the treatment of established PAH. The primary objective of the study is to determine safety of rhACE2 when administered as a single dose or multiple doses intravenously to subjects with PAH receiving background PAH-specific therapy.
Measured: 5 years
Clinical Trial of Metformin in Pulmonary Arterial Hypertension
Specific Aim 1. To test the hypothesis that metformin will ameliorate oxidant stress in pulmonary arterial hypertension Primary safety endpoint: absence of lactic acidosis, withdrawal from the study if attributed to metformin Primary efficacy endpoint: change in urinary and plasma oxidant stress measures (F2 isoprostanes and metabolites, isofurans, and nitrotyrosine)
Specific Aim 2. To test the hypothesis that metformin will decrease myocardial lipid content, increase oxidative metabolism and decrease glucose uptake.
Primary Endpoints: change in myocardial percent triglycerides (%TGs), kmono/RPP of C11 acetate, and uptake of FDG before and after metformin.
Measured: 3 years
Secondary outcomes (2)
Mechanism, safety, and efficacy of ACE-2 in the treatment of PAH.
The secondary objective of the study is to evaluate changes in biomarkers of disease (BNP, AngII/Ang (1-7, serum soluble IDH, serum NO, cardiac troponin I, SOD2 activity, urine isoprostanes and isofuranes) in subjects with PAH receiving rhACE2. We will also evaluate changes in pulmonary and systemic hemodynamics and echocardiographic markers of right heart function in patients receiving rhACE2.
Measured: 5-year
Clinical Trial of Metformin in Pulmonary Arterial Hypertension
Specific Aim 1. To test the hypothesis that metformin will ameliorate oxidant stress in pulmonary arterial hypertension
Secondary Endpoints: lung cellular proliferation as measured by FDG avidity, change in the markers of insulin resistance and sensitivity, BMPR2 expression in peripheral blood mononuclear cells, and change in glucose and lipid metabolites.
Specific Aim 2. To test the hypothesis that metformin will decrease myocardial lipid content, increase oxidative metabolism and decrease glucose uptake.
Secondary Endpoints: change in RVEF, RV mass index, insulin resistance and sensitivity indices, glucose and lipid metabolites, and six-minute walk distance (6MWD)
Measured: 3 years
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted21 Jun 2013 (estimated)
- Study startSep 2012
- Primary completionJul 2032 (estimated)
- Study completionJul 2032 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (8)Papers the sponsor has linked to this study.
- Other trials for Idiopathic Pulmonary Arterial HypertensionStudies of the same condition, open and under way.
- More trials run by Vanderbilt University Medical CenterThe 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
- Cohort
- Time perspective
- Prospective
- Enrolment
- 1,899 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Vanderbilt University Medical Center
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Anna Hemnes, Vanderbilt University Medical Center
- Investigators
- James E Loyd, MD, Principal investigator, Vanderbilt University Medical Center
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01884051
- Sponsor's protocol ID
- 9401
- Status last verified
- Sep 2026
- First submitted
- 15 Jan 2013
- Last updated
- 25 Sep 2026
- Results posted
- No
- Data monitoring committee
- No
Publications
Austin ED, Cogan JD, West JD, Hedges LK, Hamid R, Dawson EP, Wheeler LA, Parl FF, Loyd JE, Phillips JA 3rd. Alterations in oestrogen metabolism: implications for higher penetrance of familial pulmonary arterial hypertension in females. Eur Respir J. 2009 Nov;34(5):1093-9. doi: 10.1183/09031936.00010409. Epub 2009 Apr 8.
PubMed 19357154Robbins IM, Newman JH, Johnson RF, Hemnes AR, Fremont RD, Piana RN, Zhao DX, Byrne DW. Association of the metabolic syndrome with pulmonary venous hypertension. Chest. 2009 Jul;136(1):31-36. doi: 10.1378/chest.08-2008. Epub 2009 Feb 2.
PubMed 19188551Ferreira AJ, Shenoy V, Yamazato Y, Sriramula S, Francis J, Yuan L, Castellano RK, Ostrov DA, Oh SP, Katovich MJ, Raizada MK. Evidence for angiotensin-converting enzyme 2 as a therapeutic target for the prevention of pulmonary hypertension. Am J Respir Crit Care Med. 2009 Jun 1;179(11):1048-54. doi: 10.1164/rccm.200811-1678OC. Epub 2009 Feb 26.
PubMed 19246717Pugh ME, Robbins IM, Rice TW, West J, Newman JH, Hemnes AR. Unrecognized glucose intolerance is common in pulmonary arterial hypertension. J Heart Lung Transplant. 2011 Aug;30(8):904-11. doi: 10.1016/j.healun.2011.02.016. Epub 2011 Apr 13.
PubMed 21493097West J. Cross talk between Smad, MAPK, and actin in the etiology of pulmonary arterial hypertension. Adv Exp Med Biol. 2010;661:265-78. doi: 10.1007/978-1-60761-500-2_17.
PubMed 20204736Brittain EL, Niswender K, Agrawal V, Chen X, Fan R, Pugh ME, Rice TW, Robbins IM, Song H, Thompson C, Ye F, Yu C, Zhu H, West J, Newman JH, Hemnes AR. Mechanistic Phase II Clinical Trial of Metformin in Pulmonary Arterial Hypertension. J Am Heart Assoc. 2020 Nov 17;9(22):e018349. doi: 10.1161/JAHA.120.018349. Epub 2020 Nov 10.
PubMed 33167773Hemnes AR, Rathinasabapathy A, Austin EA, Brittain EL, Carrier EJ, Chen X, Fessel JP, Fike CD, Fong P, Fortune N, Gerszten RE, Johnson JA, Kaplowitz M, Newman JH, Piana R, Pugh ME, Rice TW, Robbins IM, Wheeler L, Yu C, Loyd JE, West J. A potential therapeutic role for angiotensin-converting enzyme 2 in human pulmonary arterial hypertension. Eur Respir J. 2018 Jun 21;51(6):1702638. doi: 10.1183/13993003.02638-2017. Print 2018 Jun.
PubMed 29903860Shenoy V, Kwon KC, Rathinasabapathy A, Lin S, Jin G, Song C, Shil P, Nair A, Qi Y, Li Q, Francis J, Katovich MJ, Daniell H, Raizada MK. Oral delivery of Angiotensin-converting enzyme 2 and Angiotensin-(1-7) bioencapsulated in plant cells attenuates pulmonary hypertension. Hypertension. 2014 Dec;64(6):1248-59. doi: 10.1161/HYPERTENSIONAHA.114.03871. Epub 2014 Sep 15.
PubMed 25225206
Study at a glance
From the registry record, last updated by the sponsor on 25 Sep 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Hormonal, Metabolic, and Signaling Interaction in Pulmonary Arterial Hypertension
- ClinicalTrials.gov ID
- NCT01884051
- Acronym / sponsor ID
- 9401
- Conditions
- Idiopathic Pulmonary Arterial Hypertension, Heritable Pulmonary Arterial Hypertension, Scleroderma Associated Pulmonary Arterial Hypertension, Appetite Suppressant Associate PAH
- Keywords
- Pulmonary arterial hypertension
- Study type
- Observational
- Recruitment status
- Recruiting
- Enrolment
- 1,899 participants (estimated)
- Lead sponsor
- Vanderbilt University Medical CenterUniversity, hospital or other
- Study start
- Sep 2012
- Primary completion
- Jul 2032 (estimated)
- Study completion
- Jul 2032 (estimated)
- First posted
- 21 Jun 2013 (estimated)
- 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.
Our hypothesis is that optimal treatment of the dysfunctional metabolic pathways which underlie PAH will improve pulmonary vascular function and consequences of the disease.
Detailed description
Project 1: This project will work to understand why women are affected by pulmonary arterial hypertension (PAH) so much more often than men. This observation is true in heritable, idiopathic and associated forms of PAH. While males and females have some similar hormone levels, certain hormones exist at higher levels in each gender. For example, estrogen levels are much higher in females, and thus seemed the most sensible place to start looking for differences that may be affecting disease. In a small, early study of our heritable patients, we found differences in how patients break down estrogens as compared to healthy control subjects. Now, we want to confirm that what we found is true in a much larger group of patients that includes idiopathic and associated forms of PAH. We will also look to see if testosterone and other androgenic hormones are somehow protective for males. If the observation holds true in the larger group of patients, then we may try to "fix" the hormone imbalance in a mouse model of PAH with a drug therapy, and see if it helps improve the mouse pulmonary hypertension without bad side effects to the animals. If the animal drug studies work, then we may be able to try this drug in patients to see if it will work as a human treatment.
Project 2: Despite major advances in understanding PAH in recent decades, safe, effective and tolerable therapies remain elusive. The metabolic syndrome (central obesity, insulin resistance, high blood pressure and hyperlipidemia-fats in the blood) has been implicated in PAH. Treating the downstream consequences of insulin resistance in the pulmonary vasculature is a new approach to effective intervention against this highly mortal disease. This project will study the role of insulin resistance in pulmonary arterial hypertension and determine if therapies to treat insulin resistance will improve pulmonary arterial hypertension.
Project 3: In Project 3, we are working on the theory that PAH can be treated by fixing cell-cell junctions in blood vessels with a drug called recombinant ACE2(angiotensin converting enzyme 2). This is the only approach so far that has worked to reverse disease in mouse models of heritable PAH, but we need to better understand how it is working and make sure it has long term safety in animal models before starting human trials, hopefully within a few years. Definition: Cell-cell junctions-all of our organs and body structures are made from cells. Normally, these cells (think of a balloon filled with water) line up right next to each other so that the cell membranes touch each other. Materials can flow from one cell to the next. In PAH patients it is believed that the cells in the linings of the small arteries are not able to line up together as they should.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| PAH patients | – | –Patients diagnosed with WHO Group 1 PAH |
| Healthy subjects | – | –Subjects who have been evaluated for heart and lung disease and found to be healthy |
Who may qualify
- Ages
- Up to 90 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Child, Adult, Older adult
- Study population
- Cohort 1 subjects will be recruited from our adult and pediatric pulmonary vascular disease clinics. Cohort 2-healthy controls will be recruited form patients families and the general public in middle Tennesssee.
Key inclusion criteria (9 listed)
- Project 1
- Diagnosis of IPAH (idiopathic pulmonary arterial hypertension), HPAH (heritable pulmonary arterial hypertension), or APAH (associated pulmonary arterial hypertension), family members of affected persons
- Age 0-90, age 12-90 for skin biopsy
- Diagnosis of IPAH, HPAH, or APAH, family members of affected persons
- 0-90
Key exclusion criteria (12 listed)
- Other diagnosis
- Age greater than 90, age less than 12 or greater than 90 for skin biopsy
- Project 2
- Other diagnosis
- 0-90
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
Ratio of sex hormone metabolites
Time frame: 5 years
The primary outcome measure is the ratio of 2-hydroxyestrogens to 16-hydroxyestrogens among patients compared to both controls and at risk but well subjects.
Evaluation of insulin resistance in pulmonary arterial hypertension patients/Clinical trial of Metformin in Pulmonary Arterial Hypertension
Time frame: 5 years
We will assess various measures of insulin resistance among patients, compared to healthy control subjects as well as at risk but well subjects. The primary measure will be assessed using the glucose clamp technique to quantify insulin secretion and resistance.
Mechanism, safety, and efficacy of ACE-2 (Angiotensin Converting Enzyme 2) in the treatment of PAH.
Time frame: 5 years
We will assess the safety and efficacy of ACE-2 for the treatment of established PAH. The primary objective of the study is to determine safety of rhACE2 when administered as a single dose or multiple doses intravenously to subjects with PAH receiving background PAH-specific therapy.
Clinical Trial of Metformin in Pulmonary Arterial Hypertension
Time frame: 3 years
Specific Aim 1. To test the hypothesis that metformin will ameliorate oxidant stress in pulmonary arterial hypertension Primary safety endpoint: absence of lactic acidosis, withdrawal from the study if attributed to metformin Primary efficacy endpoint: change in urinary and plasma oxidant stress measures (F2 isoprostanes and metabolites, isofurans, and nitrotyrosine) Specific Aim 2. To test the hypothesis that metformin will decrease myocardial lipid content, increase oxidative metabolism and decrease glucose uptake. Primary Endpoints: change in myocardial percent triglycerides (%TGs), kmono/RPP of C11 acetate, and uptake of FDG before and after metformin.
2 secondary outcomes
Mechanism, safety, and efficacy of ACE-2 in the treatment of PAH.
Time frame: 5-year
Clinical Trial of Metformin in Pulmonary Arterial Hypertension
Time frame: 3 years
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 25 Sep 2026.
- Background: PubMed 19357154Austin ED, Cogan JD, West JD, Hedges LK, Hamid R, Dawson EP, Wheeler LA, Parl FF, Loyd JE, Phillips JA 3rd. Alterations in oestrogen metabolism: implications for higher penetrance of familial pulmonary arterial hypertension in females. Eur Respir J. 2009 Nov;34(5):1093-9. doi: 10.1183/09031936.00010409. Epub 2009 Apr 8.
- Background: PubMed 19188551Robbins IM, Newman JH, Johnson RF, Hemnes AR, Fremont RD, Piana RN, Zhao DX, Byrne DW. Association of the metabolic syndrome with pulmonary venous hypertension. Chest. 2009 Jul;136(1):31-36. doi: 10.1378/chest.08-2008. Epub 2009 Feb 2.
- Background: PubMed 19246717Ferreira AJ, Shenoy V, Yamazato Y, Sriramula S, Francis J, Yuan L, Castellano RK, Ostrov DA, Oh SP, Katovich MJ, Raizada MK. Evidence for angiotensin-converting enzyme 2 as a therapeutic target for the prevention of pulmonary hypertension. Am J Respir Crit Care Med. 2009 Jun 1;179(11):1048-54. doi: 10.1164/rccm.200811-1678OC. Epub 2009 Feb 26.
- Background: PubMed 21493097Pugh ME, Robbins IM, Rice TW, West J, Newman JH, Hemnes AR. Unrecognized glucose intolerance is common in pulmonary arterial hypertension. J Heart Lung Transplant. 2011 Aug;30(8):904-11. doi: 10.1016/j.healun.2011.02.016. Epub 2011 Apr 13.
- Background: PubMed 20204736West J. Cross talk between Smad, MAPK, and actin in the etiology of pulmonary arterial hypertension. Adv Exp Med Biol. 2010;661:265-78. doi: 10.1007/978-1-60761-500-2_17.
- Derived from this study: PubMed 33167773Brittain EL, Niswender K, Agrawal V, Chen X, Fan R, Pugh ME, Rice TW, Robbins IM, Song H, Thompson C, Ye F, Yu C, Zhu H, West J, Newman JH, Hemnes AR. Mechanistic Phase II Clinical Trial of Metformin in Pulmonary Arterial Hypertension. J Am Heart Assoc. 2020 Nov 17;9(22):e018349. doi: 10.1161/JAHA.120.018349. Epub 2020 Nov 10.
- Derived from this study: PubMed 29903860Hemnes AR, Rathinasabapathy A, Austin EA, Brittain EL, Carrier EJ, Chen X, Fessel JP, Fike CD, Fong P, Fortune N, Gerszten RE, Johnson JA, Kaplowitz M, Newman JH, Piana R, Pugh ME, Rice TW, Robbins IM, Wheeler L, Yu C, Loyd JE, West J. A potential therapeutic role for angiotensin-converting enzyme 2 in human pulmonary arterial hypertension. Eur Respir J. 2018 Jun 21;51(6):1702638. doi: 10.1183/13993003.02638-2017. Print 2018 Jun.
- Derived from this study: PubMed 25225206Shenoy V, Kwon KC, Rathinasabapathy A, Lin S, Jin G, Song C, Shil P, Nair A, Qi Y, Li Q, Francis J, Katovich MJ, Daniell H, Raizada MK. Oral delivery of Angiotensin-converting enzyme 2 and Angiotensin-(1-7) bioencapsulated in plant cells attenuates pulmonary hypertension. Hypertension. 2014 Dec;64(6):1248-59. doi: 10.1161/HYPERTENSIONAHA.114.03871. Epub 2014 Sep 15.
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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.
James E Loyd, MD principal investigator
Vanderbilt University Medical Center
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 Idiopathic Pulmonary Arterial Hypertension and Heritable Pulmonary Arterial Hypertension, run by Vanderbilt University Medical Center at 1 site in United States.
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 9 inclusion and 12 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: looking for participants now, as of the sponsor's last update on 25 Sep 2026. 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 United States. 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?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Kelly L Fox (800-288-0378, Kelly.Burke@vumc.org), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Ratio of sex hormone metabolites (time frame: 5 years). The study lists 4 primary outcomes in all. 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 NCT01884051, which also lists 8 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 25 Sep 2026.