RE: AVS and Laparoscopic Adrenalectomy Cost

[Guest guest]

Mike which one of the specific studies were you on

1. http://clinicalstudies.info.nih.gov/cgi/detail.cgi?A_2000-CH-0180.html

2. http://clinicaltrials.gov/ct2/show/NCT00005927?term=0160 & rank=12

> > > > > > >

> > > > > > > > Hi,

> > > > > > > >

> > > > > > > > What is the typical cost for AVS and the Laparoscopic

> > Adrenalectomy?

> > > > > > > >

> > > > > > > > I am considering doing the operation in US.

> > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

> >

>

[Guest guest]

Mike which one of the specific studies were you on

1. http://clinicalstudies.info.nih.gov/cgi/detail.cgi?A_2000-CH-0180.html

2. http://clinicaltrials.gov/ct2/show/NCT00005927?term=0160 & rank=12

> > > > > > >

> > > > > > > > Hi,

> > > > > > > >

> > > > > > > > What is the typical cost for AVS and the Laparoscopic

> > Adrenalectomy?

> > > > > > > >

> > > > > > > > I am considering doing the operation in US.

> > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

> >

>

[Guest guest]

Hi :The $12000 covered blood tests, cat scans, other doctors fees, AVS and hospital charges for the AVS. If you are referring to surgery by doing an Adrenolectomy, I did not have an adrenolectomy. And yes I was covered by my insurance but had to pay a percentage of it

myself that my insurance did not cover because I live in California and not Minnesota.If you dont have insurance and planning to travel there I think its best you contact Mayo Clinic and ask them how much it will 

cost. Then also look into the option of finding a good travel insurance(may be a possiblilty) and make sure they will cover such tests and costs and not just cover accidents(there are many travel health insurances available and some of them are just there to 

charge you money and not cover anything).Hope this helps.Good health and Happy New Year to all.FarahOn Thu, Dec 31, 2009 at 3:25 AM, <bryanfjohnson@...> wrote:

 

Does the $12,000 cover both operation and without insurance since I am from Jamaica (Caribbean)

>

> >

> >

> > Hi,

> >

> > What is the typical cost for AVS and the Laparoscopic Adrenalectomy?

> >

> > I am considering doing the operation in US.

> >

> >

> >

>

[Guest guest]

Hi :The $12000 covered blood tests, cat scans, other doctors fees, AVS and hospital charges for the AVS. If you are referring to surgery by doing an Adrenolectomy, I did not have an adrenolectomy. And yes I was covered by my insurance but had to pay a percentage of it

myself that my insurance did not cover because I live in California and not Minnesota.If you dont have insurance and planning to travel there I think its best you contact Mayo Clinic and ask them how much it will 

cost. Then also look into the option of finding a good travel insurance(may be a possiblilty) and make sure they will cover such tests and costs and not just cover accidents(there are many travel health insurances available and some of them are just there to 

charge you money and not cover anything).Hope this helps.Good health and Happy New Year to all.FarahOn Thu, Dec 31, 2009 at 3:25 AM, <bryanfjohnson@...> wrote:

 

Does the $12,000 cover both operation and without insurance since I am from Jamaica (Caribbean)

>

> >

> >

> > Hi,

> >

> > What is the typical cost for AVS and the Laparoscopic Adrenalectomy?

> >

> > I am considering doing the operation in US.

> >

> >

> >

>

[Guest guest]

Thanks Farah this helps. There are no state insurance here but employee

insurance coverage. Based on where you work this can be good. I am trying the

clinical trials Mike and Francis indicated first. Failing this, Mayo Clinic is

the next option.

> > >

> > > >

> > > >

> > > > Hi,

> > > >

> > > > What is the typical cost for AVS and the Laparoscopic Adrenalectomy?

> > > >

> > > > I am considering doing the operation in US.

> > > >

> > > >

> > > >

> > >

> >

> >

> >

>

[Guest guest]

Active in the Endocrinology study, with tumor contribution to the tumor study.

Bindner

Web Directory (links to my sites and blogs):

http://www.geocities.com/mikeybdc/index.html

http://mikeybdc.blogspot.com

From: <bryanfjohnson@...>Subject: Re: AVS and Laparoscopic Adrenalectomy Costhyperaldosteronism Date: Thursday, December 31, 2009, 4:02 PM

Mike which one of the specific studies were you on 1. http://clinicalstud ies.info. nih.gov/cgi/ detail.cgi? A_2000-CH- 0180.html2. http://clinicaltria ls.gov/ct2/ show/NCT00005927 ?term=0160 & rank=12> > > > > > >> > > > > > > > Hi,> > > > > > > >> > > > > > > > What is the typical cost for AVS and the Laparoscopic > > Adrenalectomy?> > > > > > > >> > > > > > > > I am considering doing the operation in US.> > > > > > > >> > > > > > > >> > > > > > >> > > > > >> > > >

>> > > >> > >> >> >>

[Guest guest]

Mike,

It seems the Tumor Study would be the better option since it offers the removal

of the adenoma.

> > > > > > > >

> > > > > > > > > Hi,

> > > > > > > > >

> > > > > > > > > What is the typical cost for AVS and the Laparoscopic

> > > Adrenalectomy?

> > > > > > > > >

> > > > > > > > > I am considering doing the operation in US.

> > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> > >

> >

>

[Guest guest]

You get the treatment you need in either study. They will put you in the Endo study to start and give a piece of your tumor to the other.

Bindner

Web Directory (links to my sites and blogs):

http://www.geocities.com/mikeybdc/index.html

http://mikeybdc.blogspot.com

From: <bryanfjohnson@...>Subject: Re: AVS and Laparoscopic Adrenalectomy Costhyperaldosteronism Date: Thursday, December 31, 2009, 6:53 PM

Mike,It seems the Tumor Study would be the better option since it offers the removal of the adenoma. > > > > > > > >> > > > > > > > > Hi,> > > > > > > > >> > > > > > > > > What is the typical cost for AVS and the Laparoscopic > > > Adrenalectomy?> > > > > > > > >> > > > > > > > > I am considering doing the operation in US.> > > > > > > > >> > > > > > > > >> > > > > > > >> > > > > > >> > > > > >> > > > >> > > >> > >> > >>

>>

[Guest guest]

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D2 Dopamine Receptor on Human Aldosterone-Producing Adenoma and Its Role in Aldosterone Secretion and Cell Proliferation

This study is currently recruiting participants.

Verified by National Taiwan University Hospital, August 2005

First Received: September 12, 2005 Last Updated: June 7, 2007 History of Changes

Sponsor:

National Taiwan University Hospital

Information provided by:

National Taiwan University Hospital

ClinicalTrials.gov Identifier:

NCT00173446

Purpose

Dopamine (DA) is one of the main catecholamines in mammals. Its major role as a brain neurotransmitter is well known as well as its contribution to the development of pathologies, mainly arterial hypertension. Traditionally, dopamine receptors are divided into two families according to the stimulation or inhibition they may produce at the adenyl cyclase level. Five dopamine receptors have been identified: D1 (D1a) and D5 (D1b) exist in the D1 family. D2s, D2l, D3 and D4 belong to the D2 family. Formerly, less than 1% of patients with hypertension were believed to have primary hyperaldosteronism; however, recent studies have suggested that primary aldosteronism affects 5-13% of patients with hypertension and aldosteronomas are a more common cause of hypertension than previously thought. At least 2% of patients with hypertension may have an aldosteronoma. The investigators' previous clinical observation found two subtypes of aldosterone-producing adenoma (APA), which were defined according to their responses to metoclopramide during salt manipulation. On a high-salt diet (HS), the nonsuppressible subjects, with less dopaminergic inhibition of aldosterone secretion, had less urinary DA excretion and greater blood pressure (BP) elevation [Wu KD et al. 2002]. The investigators' recent study of six patients with an APA found that the expression of the D2 receptor in APA was not universal. The amounts of D2 receptor messenger ribonucleic acid (mRNA) were more variant in either APA or their remnant adrenal glands. Only two cases of APA expressed the D2 receptors with much weaker signals compared with those in their respective remnant adrenals [Wu KD et al. 2001]. The investigators' current work demonstrates that the D2 receptor negatively regulates AII-stimulated aldosterone secretion and aldosterone synthase mRNA expression in NCI-H295R cells. On the other hand, the D4 receptor counteracts with the effect of the D2 receptor. In a future study, the investigators wish to quantify D2 and D4 receptor mRNA and protein expression in APA and their remnant adrenal glands and correlate them to their clinical metoclopramide test results. The investigators also wish to know whether the difference between the D2 and D4 receptor expression reflect the different effects of dopamine inhibition on AII-stimulated aldosterone secretion and aldosterone synthase transcription. Finally, the investigators will explore the role of D2 and D4 receptors on AII-stimulated adrenal cell proliferation.

Condition

HypertensionAdrenal Aldosterone-Producing Adenoma

Study Type:

Observational

Study Design:

Screening, Cross-Sectional, Defined Population, Retrospective Study

Official Title:

Expression of D2-Like Dopamine Receptor of Human Aldosterone-Producing Adenoma and Its Role in Regulation of Aldosterone Secretion and Cell Proliferation

Resource links provided by NLM:

MedlinePlus related topics: High Blood Pressure

Drug Information available for: Dopamine Aldosterone

U.S. FDA Resources

Further study details as provided by National Taiwan University Hospital:

Estimated Enrollment:

30

Study Start Date:

January 2002

Eligibility

Genders Eligible for Study:

Both

Accepts Healthy Volunteers:

No

Criteria

Inclusion Criteria:

Adrenal aldosterone-producing adenoma

Contacts and Locations

Please refer to this study by its ClinicalTrials.gov identifier: NCT00173446

Contacts

Contact: Hong-Wei Chang

886223123456 ext 5762

chianghongwei@...

Locations

Taiwan

National Taiwan University Hospital

Recruiting

Taipei, Taiwan, 100

Contact: Hong-Wei Chang 886223123456 ext 5762 chianghongwei@...

Sponsors and Collaborators

National Taiwan University Hospital

Investigators

Principal Investigator:

Hong-Wei Chang

National Taiwan University Hospital

More Information No publications provided

Study ID Numbers:

9461700673

Study First Received:

September 12, 2005

Last Updated:

June 7, 2007

ClinicalTrials.gov Identifier:

NCT00173446 History of Changes

Health Authority:

Taiwan: Department of HealthKeywords provided by National Taiwan University Hospital:

Normal part of the adrenal glandAdditional relevant MeSH terms:

NeoplasmsNeoplasms by Histologic TypeVascular DiseasesCardiovascular Diseases

AdenomaNeoplasms, Glandular and EpithelialHypertensionClinicalTrials.gov processed this record on December 30, 2009

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The Therapeutic Effect of Bromocriptin in Patients With Primary Aldosteronism

This study is currently recruiting participants.

Verified by National Taiwan University Hospital, December 2006

First Received: March 22, 2007 No Changes Posted

Sponsor:

National Taiwan University Hospital

Information provided by:

National Taiwan University Hospital

ClinicalTrials.gov Identifier:

NCT00451672

Purpose

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

Condition

Intervention

Phase

HyperaldosteronismHypertension

Drug: bromocriptine

Phase IV

Study Type:

Interventional

Study Design:

Treatment, Non-Randomized, Open Label, Uncontrolled, Single Group Assignment, Safety/Efficacy Study

Resource links provided by NLM:

MedlinePlus related topics: High Blood Pressure

Drug Information available for: Bromocriptine mesylate Bromocriptine

U.S. FDA Resources

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 2007Detailed 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@...

Locations

Taiwan

National Taiwan Univserty Hospital

Recruiting

Taipei, Taiwan

Contact: Pan-Chyr Yang 886-2-2356-2000 pcyang@...

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:

Chang HW, Chu TS, Huang HY, Chueh SC, Wu VC, Chen YM, Hsieh BS, Wu KD. Down-Regulation of D2 Dopamine Receptor and Increased PKC{micro} Phosphorylation in Aldosterone-Producing Adenoma Play Roles in Aldosterone Overproduction. J Clin Endocrinol Metab. 2007 Feb 13; [Epub ahead of print]

Study ID Numbers:

950912

Study First Received:

March 22, 2007

Last Updated:

March 22, 2007

ClinicalTrials.gov Identifier:

NCT00451672 History of Changes

Health Authority:

United States: Food and Drug Administration; Taiwan: Department of HealthKeywords provided by National Taiwan University Hospital:

aldosteronism, bromocriptin, hypertensionAdditional relevant MeSH terms:

HyperaldosteronismBromocriptineNeurotransmitter AgentsMolecular Mechanisms of Pharmacological ActionAnti-Dyskinesia AgentsHormone AntagonistsPhysiological Effects of DrugsHormones, Hormone Substitutes, and Hormone AntagonistsVascular DiseasesAdrenal Gland Diseases

Endocrine System DiseasesAntiparkinson AgentsDopamine AgonistsAdrenocortical HyperfunctionPharmacologic ActionsTherapeutic UsesDopamine AgentsCardiovascular DiseasesCentral Nervous System AgentsHypertensionClinicalTrials.gov processed this record on December 30, 2009

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Diagnosis of Primary Aldosteronism: Comparison of Post Captopril Active Renin Concentration and Plasma Renin Activity

This study is currently recruiting participants.

Verified by National Taiwan University Hospital, June 2009

First Received: June 8, 2009 Last Updated: June 9, 2009 History of Changes

Sponsor:

National Taiwan University Hospital

Collaborator:

Novartis

Information provided by:

National Taiwan University Hospital

ClinicalTrials.gov Identifier:

NCT00917345

Purpose

Background: The most common pharmacologic test for diagnosis of primary aldosteronism (PA) is administration of captopril to examine whether abnormal aldosterone to plasma rennin activity (PRA)(ARR) persists, although active rennin concentration (ARC) in contrast to PRA may offers advantages with regard to processing and standardization.

Objective: To assess whether post captopril ARC offer any additional advantage in screening primary aldosteronism (PA) than PRA and establish thresholds for the diagnosis using ARC.

Condition

Intervention

Primary Aldosteronism

Drug: captopril test

Study Type:

Observational

Study Design:

Case Control, Prospective

Resource links provided by NLM:

Drug Information available for: Captopril

U.S. FDA Resources

Further study details as provided by National Taiwan University Hospital:

Primary Outcome Measures:

Determination of ARC in contrast to PRA offers advantage with regard to processing and standardization, knowing the postcaptopril sensitivity and specificity [ Time Frame: 1 day ] [ Designated as safety issue: Yes ]Biospecimen Retention: Samples Without DNA

Biospecimen Description:

Estimated Enrollment:

150

Study Start Date:

January 2008

Estimated Study Completion Date:

May 2009

Estimated Primary Completion Date:

January 2009 (Final data collection date for primary outcome measure)

Groups/Cohorts

Assigned Interventions

aldosteronism, hypertension

Drug: captopril test The blood samplings were obtained one hour after the administration of 50 mg of captopril.The testing is performed in the morning on a seated ambulatory patient

hypertension

Drug: captopril test The blood samplings were obtained one hour after the administration of 50 mg of captopril.The testing is performed in the morning on a seated ambulatory patient Detailed Description:

Primary aldosteronism (PA), characterized by an inappropriate production of aldosterone, affects 5-13% of patients with hypertension(1, 2). The use of aldosterone-renin ratio (ARR) as screening test contributes to the increased diagnostic rate of this disease(2), but it is not standardized among laboratories. As the incidence of PA has increased since ARR has been used as a screening test (3, 4), the difficulty in establishing a diagnosis of PA may be encountered because of atypical manifestations. Administration of captopril to differentiate the normal renin-angiotensin- aldosterone axis from autonomous secretion of aldosterone has been proved to be a safe and effective test in confirmation of the diagnosis (5-8). Several studies have demonstrated that the ARR after a single dose of captopril is diagnostic (5-8) and as sensitive as the saline loading test for the identification of aldosterone- producing adenoma (APA)(8).

Active rennin concentration (ARC) is considerably easier to perform; being a single immunoradiometric assay as opposed to the initial generation of angiotensin I generated from angiotensinogen followed by radioimmunoassay of PRA(9). It was demonstrated as a reliable and convenient screening tool for ambulatory conditions, independent of body posture (10). Decreased angiotensinogen level is noted in pathological status ( e.g. liver cirrhosis, sever cardiac failure) (11, 12) that results in dissociate of PRA measurement. PAC when used in conjunction with aldosterone to produce an ARRARC , has been reported to classify aldosteronism correctly(13). Although PRA is highly sensitive, the measurement is time-consuming and measured values can vary considerably between laboratories(14). In aldosteronism with suppressed renin, the ratio of ARR is clearly dependent on the variants lower detection limit(15). Though determination of ARC in contrast to PRA offers advantage with regard to processing and standardization, knowing the postcaptopril sensitivity and specificity as well as the optimum cut off value of ARC is paramount (16) help to the diagnosis PA (15, 17, 18) and might serve better performance than ARRPRA.

Eligibility

Ages Eligible for Study:

18 Years to 80 Years

Genders Eligible for Study:

Both

Accepts Healthy Volunteers:

No

Sampling Method:

Non-Probability Sample

Study Population

Patients were referred to the hypertension clinics for suspicious of aldosteronism after an initial evaluation, and recorded in the Taiwan Primary Aldosteronism Investigation (TAIPAI). The initial evaluation included (1) age at onset younger than 35 years, (2) hypertension that is difficult to control after initiating therapy, (3) clinical occurrence of a hypertensive crisis, (4) the presence of hypokaliemia or metabolic alkalosis, or a random aldosterone-renin ration (ARR) >30, and (5) evidence of adrenal incidentaloma and hypertension or hypokalemia. All patients with intention to confirm and received captopril test were recruited and data were prospectively collected.

Criteria

Inclusion Criteria:

age at onset younger than 35 years,

hypertension that is difficult to control after initiating therapy,

clinical occurrence of a hypertensive crisis,

the presence of hypokaliemia or metabolic alkalosis, or a random aldosterone-renin ration (ARR) >30, and

evidence of adrenal incidentaloma and hypertension or hypokalemia.

Exclusion Criteria:

chronic kidney disease with elevated estimated glomerular filtration rate (< 60, mL/min/1.73 m2)

liver disease with elevated GPT (> 35)

heart failure

classified as more than NYHA II,

hyperthyroidism

malignancy with metastasis

Contacts and Locations

Please refer to this study by its ClinicalTrials.gov identifier: NCT00917345

Contacts

Contact: VinCent Wu, MD

+886927223278

q91421028@...

Locations

Taiwan

National Taiwan University Hospital

Recruiting

Taipei, Taiwan, 100

Contact: VinCent Wu, MD +886937223278

Sponsors and Collaborators

National Taiwan University Hospital

Novartis

More Information No publications provided

Responsible Party:

National Taiwan University Hospital ( Yang PC )

Study ID Numbers:

200904076R

Study First Received:

June 8, 2009

Last Updated:

June 9, 2009

ClinicalTrials.gov Identifier:

NCT00917345 History of Changes

Health Authority:

Taiwan: Department of HealthKeywords provided by National Taiwan University Hospital:

ARCPRAprimary aldosteronism

captopril testaldosterone-renin ratioPrimary aldosteronism (PA) than PRA and establish thresholds for the diagnosis using ARC.Additional relevant MeSH terms:

HyperaldosteronismCaptoprilMolecular Mechanisms of Pharmacological ActionAdrenal Gland DiseasesEndocrine System DiseasesEnzyme InhibitorsCardiovascular Agents

Antihypertensive AgentsAdrenocortical HyperfunctionPharmacologic ActionsProtease InhibitorsTherapeutic UsesAngiotensin-Converting Enzyme InhibitorsClinicalTrials.gov processed this record on December 30, 2009

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Kallikrein-Kinin (KKS) and Renin-Angiotensin-Aldosterone System (RAAS) in Primary Aldosteronism

This study is currently recruiting participants.

Verified by National Taiwan University Hospital, July 2002

First Received: September 9, 2005 Last Updated: December 19, 2005 History of Changes

Sponsor:

National Taiwan University Hospital

Information provided by:

National Taiwan University Hospital

ClinicalTrials.gov Identifier:

NCT00155064

Purpose

The tissue kallikrein-kinin (KKS) and renin-angiotension-aldosterone system (RAAS) had been implicated in regulating blood pressure and electrolyte homeostasis. Both of the KKS and RAAS may work coordinately to regulate salt metabolism, local blood flow. Thus, we conducted this study to elucidate, first, whether some alterations in components of the kallikrein-kinin system could do effect on aldosterone secretion.

Previous study has shown the post captopril plasma aldosterone concentration (PAC)/ plasma rennin activity (PRA) ration (ARR) was a reliable method for diagnosis of primary aldosteronism (PA). The ARR change by angiotensin II receptor blockade was reported to be significantly higher than that by ACE inhibitor. This study assessed whether angiotensin II receptor blockade offers any additional advantage in the diagnosis of PA. Clinically we evaluated the sensitivity and specificity of captopril (angiotensin-converting enzyme inhibition) and losartan (angiotensin II type 1 receptor blocker) test in PA patient. This interaction mechanism, in term, could further explain the interaction of KKS and RAAS.

Condition

Intervention

Phase

Hyperaldosteronism

Drug: captopril, Losartan (drug)

Phase IV

Study Type:

Interventional

Study Design:

Diagnostic, Randomized, Open Label, Uncontrolled, Single Group Assignment, Safety/Efficacy Study

Resource links provided by NLM:

Drug Information available for: Aldosterone Captopril Losartan Kallidinogenase

U.S. FDA Resources

Further study details as provided by National Taiwan University Hospital:

Primary Outcome Measures:

Diagnosis of primary aldosteronism

Secondary Outcome Measures:

Subgroup analysis of primary aldosteronism

Estimated Enrollment:

100

Study Start Date:

July 2002

Estimated Study Completion Date:

July 2007Detailed Description:

Hypertension affects 20% to 25% of adult population. Most patients are diagnosed as having essential or primary hypertension. Up to 10% to 15 % have an identifiable cause and many of those have an adrenal basis [Miroslava H. et al., 2002]. The tissue kallikrein-kinin (KKS) and renin-angiotension-aldosterone system (RAAS) had been implicated in regulating blood pressure and electrolyte homeostasis. Recent studies in humans indicate that the vasodilator tissue KKS, the counterpart of the tissue RAAS, is also expressed in the adrenal gland. The adrenal gland regulates sodium and water excretion and reabsorption through the release of aldosterone and corticosterone. Previous study reveals an anatomical linkage between the tissue KKS and sodium and water metabolism. Both of the KKS and RAAS may work coordinately to regulate salt metabolism, local blood flow. In contrast, although many investigators have supported the notion that Ang II and BK physiologically antagonize each other's effects on blood pressure, there are many instances where the two peptides exert common actions. For example, the Bradykinin also stimulates aldosterone release from adrenocortical cells through B2 receptors. Furthermore, the AT1 receptor and the bradykinin (B2) receptor form stable heterodimers, the two major signaling proteins triggered by AT1. In vitro studies (Margolius 1995) have shown that kallikrein acts as a prorenin-activating enzyme, and that tissue kallikrein can generate angiotensin II.

However, the interactions between both systems are complex and not always simply antagonistic. The interactions of the two systems on aldosterone secretion are not examined Thus, we conducted this study to elucidate, first, whether some alterations in components of the kallikrein-kinin system could do effect on aldosterone secretion.

Our study provides evidence that bradykinin contributes substantially to the aldosterone secretion with or without the effects of angiotensin. The data also could confirm whether ATR2-Bradykinin-B2-aldosterone really works. We want to realize the expression of angiotensin and bradykinin in the adrenal gland and hypertension related to these systems.

Previous study has showed the post captopril plasma aldosterone concentration (PAC)/ plasma rennin activity (PRA) ration (ARR) was a reliable method for diagnosis of primary aldosteronism (PA). The ARR change by angiotensin II receptor blockade was reported to be significantly higher than that by ACE inhibitor. This study assessed whether angiotensin II receptor blockade offers any additional advantage in the diagnosis of PA. Clinically we evaluated the sensitivity and specificity of captopril (angiotensin-converting enzyme inhibition) and losartan (angiotensin II type 1 receptor blocker) test in PA patient. This interaction mechanism, in term, could further explain the interaction of KKS and RAAS.

Eligibility

Ages Eligible for Study:

18 Years to 80 Years

Genders Eligible for Study:

Both

Accepts Healthy Volunteers:

No

Criteria

Inclusion Criteria:

Patients with hypertension admitted for the diagnosis of primary aldosteronism

Exclusion Criteria:

Pregnant or lactating women. (Pre-menopause women, capable of bearing children will undergo pregnancy test), hypertension without discontinuous b-blocker, ACEI or ARB for more than 10 days.

Contacts and Locations

Please refer to this study by its ClinicalTrials.gov identifier: NCT00155064

Contacts

Contact: Kwan-Dun Wu, MD, PhD

+886-2-23562082

kdw@...

Locations

Taiwan

National Taiwan University Hospital

Recruiting

Taipei, Taiwan

Contact: Wu, MD +886-2-23562082 walt-wu@...

Sponsors and Collaborators

National Taiwan University Hospital

Investigators

Study Chair:

Kwan-Dun Wu, Md, PhD

National Taiwan University Hospital

Study Director:

Vin-Cent Wu, MD

National Taiwan University Hospital

More Information Publications:

Agharazii M, Douville P, Grose JH, Lebel M. Captopril suppression versus salt loading in confirming primary aldosteronism. Hypertension. 2001 Jun;37(6):1440-3.

Dendorfer A, Wolfrum S, Dominiak P. Pharmacology and cardiovascular implications of the kinin-kallikrein system. Jpn J Pharmacol. 1999 Apr;79(4):403-26. Review.

Hesse B, Rasmussen S, Lund JO, Christensen P, Damkjaer Nielsen M. Urinary excretion of kallikrein before and after operation for aldosterone-producing adenoma. Acta Med Scand. 1985;217(5):501-5.

Study ID Numbers:

9361700632

Study First Received:

September 9, 2005

Last Updated:

December 19, 2005

ClinicalTrials.gov Identifier:

NCT00155064 History of Changes

Health Authority:

Taiwan: Department of HealthKeywords provided by National Taiwan University Hospital:

Primary aldosteronismkallikreinaldosteronecaptoprilAdditional relevant MeSH terms:

HyperaldosteronismCaptoprilCoagulantsMolecular Mechanisms of Pharmacological ActionPhysiological Effects of DrugsHematologic AgentsAdrenal Gland DiseasesEndocrine System DiseasesEnzyme InhibitorsReproductive Control Agents

Cardiovascular AgentsAntihypertensive AgentsAdrenocortical HyperfunctionFertility Agents, MalePharmacologic ActionsProtease InhibitorsKallikreinsTherapeutic UsesFertility AgentsAngiotensin-Converting Enzyme InhibitorsClinicalTrials.gov processed this record on December 30, 2009

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Related Studies

Metabolic Syndrome and Insulin Resistance in Primary Aldosteronism

This study is currently recruiting participants.

Verified by National Taiwan University Hospital, November 2007

First Received: September 12, 2005 Last Updated: November 28, 2007 History of Changes

Sponsor:

National Taiwan University Hospital

Information provided by:

National Taiwan University Hospital

ClinicalTrials.gov Identifier:

NCT00173082

Purpose

Primary aldosteronism (PA) is occasionally associated with impaired glucose tolerance. Glucose intolerance, in general metabolic syndrome is caused by suppression of insulin release from the pancreas and suppression of insulin sensitivity of the target tissues. Several studies have suggested that impaired glucose tolerance in primary aldosteronism is due to an inability of the beta cells to release insulin by potassium depletion. It was suggested glucose intolerance in PA is caused by the suppression of insulin release related to hypopotassemia and compensatory increase of insulin sensitivity is observed in PA. The increased insulin secretory capacity associated with correction of negative potassium balance may account for the increase in plasma leptin after curing primary aldosteronism. The conclusion with respect to the possible causal relationship between diabetes mellitus (DM) and PA, however, can be obtained after the evaluation of the effect of surgical /pharmacological treatment of PA.

Condition

Intervention

Primary Aldosteronism

Procedure: Glucose tolerance test

Study Type:

Observational

Study Design:

Prospective

Official Title:

Metabolic Syndrome and Insulin Resistance in Primary Aldosteronism

Resource links provided by NLM:

Drug Information available for: Insulin

U.S. FDA Resources

Further study details as provided by National Taiwan University Hospital:

Estimated Enrollment:

100

Study Start Date:

June 2005

Estimated Study Completion Date:

July 2008Detailed Description:

Primary aldosteronism (PA) is occasionally associated with impaired glucose tolerance. Glucose intolerance, in general metabolic syndrome is caused by suppression of insulin release from the pancreas and suppression of insulin sensitivity of the target tissues. Several studies have suggested that impaired glucose tolerance in primary aldosteronism is due to an inability of the beta cells to release insulin by potassium depletion. It was suggested glucose intolerance in PA is caused by the suppression of insulin release related to hypopotassemia and compensatory increase of insulin sensitivity is observed in PA. The increased insulin secretory capacity associated with correction of negative potassium balance may account for the increase in plasma leptin after curing primary aldosteronism. The conclusion with respect to the possible causal relationship between DM and PA, however, can be obtained after the evaluation of the effect of surgical /pharmacological treatment of PA. From July 2005 to July 2008, patients with primary aldosteronism, hospitalized for a comprehensive study of the subtypes of primary aldosteronism before operation will receive informed consent about the insulin sensitivity test. In the present study, we measured insulin sensitivity via the ability to release insulin by the 75 g oral glucose tolerance test (OGTT) in PA to clarify the mechanisms of glucose intolerance in PA. Seventy-five gram OGTT was performed in PA before and after adrenalectomy. Within one minute, 75 g of glucose dissolved in 200 cc water was ingested. Venous blood samples were drawn at 0, 60, 120 minutes for determination of plasma glucose and plasma insulin levels. Serum potassium levels were measures at 0 minutes. Furthermore, the adipokines, HOMA, QUICKI, leptin, adiponectin, homocystine, C-reactive protein, proinflammatory cytokine and adhesion molecules were also measured.

Eligibility

Ages Eligible for Study:

18 Years to 80 Years

Genders Eligible for Study:

Both

Accepts Healthy Volunteers:

No

Criteria

Inclusion Criteria:

Age more than 18 years old

Aldosteronism patients

Exclusion Criteria:

Patients with pregnancy

Contacts and Locations

Please refer to this study by its ClinicalTrials.gov identifier: NCT00173082

Contacts

Contact: Vin-cent Wu, MD

+886-2-23562082

kdw@...

Locations

Taiwan

National Taiwan University Hospital

Recruiting

Taipei, Taiwan

Contact: Wu, MD +886-2-23562082 walt-wu@...

Sponsors and Collaborators

National Taiwan University Hospital

Investigators

Study Chair:

Kwan-Dun Wu, MD, PhD

National Taiwan University Hospital

Study Director:

Vin-cent Wu, MD

National Taiwan University Hospital

More Information Publications:

Corry DB, Tuck ML. The effect of aldosterone on glucose metabolism. Curr Hypertens Rep. 2003 Apr;5(2):106-9. Review.

Widimsky J Jr, Strauch B, Sindelka G, Skrha J. Can primary hyperaldosteronism be considered as a specific form of diabetes mellitus? Physiol Res. 2001;50(6):603-7.

Kreze A Sr, Kreze-Spirova E, Mikulecky M. Diabetes mellitus in primary aldosteronism. Bratisl Lek Listy. 2000;101(4):187-90.

Study ID Numbers:

9461700402

Study First Received:

September 12, 2005

Last Updated:

November 28, 2007

ClinicalTrials.gov Identifier:

NCT00173082 History of Changes

Health Authority:

Taiwan: Department of HealthKeywords provided by National Taiwan University Hospital:

primary aldosteronismInsulin resistanceMetabolic syndromeOGTTAdditional relevant MeSH terms:

HyperaldosteronismMetabolic DiseasesDiseasePhysiological Effects of DrugsAdrenal Gland DiseasesEndocrine System DiseasesAdrenocortical HyperfunctionPharmacologic Actions

InsulinHyperinsulinismPathologic ProcessesHypoglycemic AgentsSyndromeInsulin ResistanceGlucose Metabolism DisordersClinicalTrials.gov processed this record on December 30, 2009

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> > > > > > > > >> > > > > > > > > > Hi,> > > > > > > > > >> > > > > > > > > > What is the typical cost for AVS and the Laparoscopic > > > > Adrenalectomy?> > > > > > > > > >> > > > > > > > > > I am considering doing the operation in US.> > > > > > > > > >> > > > > > > > > >> > > > > > > > >> > > > > > > >> > > > > > >> > > > > >> > > > >> > > >> > > >> > >> >>