The Therapeutic Effect of Bromocriptin in Patients With Primary Aldosteronism

The recruitment status of this study is unknown because the information has not been verified recently.
Verified December 2006 by National Taiwan University Hospital.
Recruitment status was  Recruiting
Sponsor:
Information provided by:
National Taiwan University Hospital
ClinicalTrials.gov Identifier:
NCT00451672
First received: March 22, 2007
Last updated: NA
Last verified: December 2006
History: No changes posted
  Purpose

we propose that bromocriptine may be an alternative treatment of primary aldosteronism, both APA and BAH.


Condition Intervention Phase
Hyperaldosteronism
Hypertension
Drug: bromocriptine
Phase 4

National Taiwan University Hospital has indicated that access to an investigational treatment associated with this study is available outside the clinical trial.  

Study Type: Interventional
Study Design: Allocation: Non-Randomized
Endpoint Classification: Safety/Efficacy Study
Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Treatment

Resource links provided by NLM:


Further study details as provided by National Taiwan University Hospital:

Primary Outcome Measures:
  • tumor size, blood pressure

Secondary Outcome Measures:
  • serum potassium, aldosterone, renine

Estimated Enrollment: 25
Study Start Date: January 2007
Estimated Study Completion Date: December 2007
Detailed Description:

Primary aldosteronism (PA), a common curable disease of hypertension, is characterized by inappropriate production of aldosterone, which is at least partially autonomous of the renin-angiotensin system. A recent clinical study reported that patients with PA experience a higher sate of a higher rate of cardiovascular events than those with essential hypertension(Corry and Tuck 2003; Milliez, Girerd et al. 2005). The prevalence of metabolic syndrome was higher in primary aldosteronism than in essential hypertension was also reported (Fallo, Veglio et al. 2006). The wide applying of the plasma aldosterone/plasma rennin activity (ARR) as a screening test among hypertensive patients have reported a much higher prevalence of this disease, up to 12% of hypertensive patients. In the past decade, an increase in diagnosis rate of PA has been observed in National Taiwan University Hospital, with an average of 15-20 newly diagnosis cases every year.

Idiopathic bilateral adrenal hyperplasia (BAH) and aldosterone-producing adenoma (APA) are the leading causes of primary aldosteronism. Unilateral adrenalectomy is the reasonable therapeutic option of APA and aldosterone antagonists usually brings about well blood pressure (BP) control in BAH. Not every APA patient would accept operation because of other medical conditions, or the cure rate of hypertension in APA after adrenalectomy is 50-70% in most studies. For patients with BAH, aldosterone antagonists are the first choice of treatment, however, intolerance to high dose of these medications is not uncommon. To our best knowledge, there is no alternative treatment for these patients.

Dopaminergic regulation of aldosterone secretion has been well demonstrated in normal subjects as well as patients with PA. We have shown that D2 receptor can down-regulate the transcription of aldosterone synthase (CYP11B2) via a specific PKC isoform and probably intracellular calcium level. Furthermore, there is a reciprocal change of the mRNA of D2 receptor and CYP11B2 in APA. D2 receptor has also been demonstrated in other neuroendocrine tumors, eg., pheochromocytoma, prolactinoma, GH-secreting adenoma ect. [Camacho & Mazzone 1999] Administration of D2 agonist, bromocriptin (BMC), is a standard treatment of prolactinoma, either for pre-operative reduction of the tumors or for non-surgical patients [Chattopadhyay et al., 2005]. Reduction or shrinkage of prolactinoma has been observed in patients treated with BMC [Biswas et al., 2005]. Anti-proliferative effect and apoptosis of BMC have been demonstrated in several cell lines [Wasko et al., 2004]. Recently, we also demonstrated that BMC, in addition to decrease aldosterone secretion and expression of CYP11B2, could inhibit cell proliferation of H295 cells, an adrenocortical carcinoma cell line, with a down-regulation of ERK. In this context, we propose that BMC may be an alternative treatment of PA, both APA and BAH.

  Eligibility

Ages Eligible for Study:   20 Years to 60 Years
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Criteria

Inclusion Criteria:

  • 20-60y/o hyperaldosteronsim patients

Exclusion Criteria:

  • Malignancy
  • Bed-ridden
  • Psychological disease
  Contacts and Locations
Please refer to this study by its ClinicalTrials.gov identifier: NCT00451672

Contacts
Contact: Kwan-Dun Wu, MD, PhD +886-2-23562082 walt-wu@yahoo.com.tw

Locations
Taiwan
National Taiwan Univserty Hospital Recruiting
Taipei, Taiwan
Contact: Pan-Chyr Yang    886-2-2356-2000    pcyang@ha.mc.ntu.edu.tw   
Sponsors and Collaborators
National Taiwan University Hospital
Investigators
Principal Investigator: Kwan-Dun Wu, MD, PhD Internal Medicine, Natinal Taiwan University Hospital
Study Director: Vin-Cent Wu, MD Internal Medicine, National Taiwan University Hospital
  More Information

Publications:
ClinicalTrials.gov Identifier: NCT00451672     History of Changes
Other Study ID Numbers: 950912
Study First Received: March 22, 2007
Last Updated: March 22, 2007
Health Authority: United States: Food and Drug Administration
Taiwan: Department of Health

Keywords provided by National Taiwan University Hospital:
aldosteronism, bromocriptin, hypertension

Additional relevant MeSH terms:
Hyperaldosteronism
Hypertension
Adrenocortical Hyperfunction
Adrenal Gland Diseases
Endocrine System Diseases
Vascular Diseases
Cardiovascular Diseases
Bromocriptine
Antiparkinson Agents
Anti-Dyskinesia Agents
Central Nervous System Agents
Therapeutic Uses
Pharmacologic Actions
Hormone Antagonists
Hormones, Hormone Substitutes, and Hormone Antagonists
Physiological Effects of Drugs
Dopamine Agonists
Dopamine Agents
Neurotransmitter Agents
Molecular Mechanisms of Pharmacological Action

ClinicalTrials.gov processed this record on April 17, 2014