Treatment of Hyperuricemia in Patients With Heart Failure

This study has been completed.
Sponsor:
Information provided by:
Tottori University Hospital
ClinicalTrials.gov Identifier:
NCT00422318
First received: January 12, 2007
Last updated: NA
Last verified: January 2007
History: No changes posted
  Purpose

The study aims to assess (I) the contribution of UA itself to the CHF pathophysiology and (II) to test the effect of lowering UA by uricosuric treatment in CHF.


Condition Intervention Phase
Heart Failure
Hyperuricemia
Drug: Benzbromarone (drug)
Phase 4

Study Type: Interventional
Study Design: Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Crossover Assignment
Masking: Double-Blind
Primary Purpose: Treatment
Official Title: Hyperuricemia and the Effects of the Uricosuric Agents Benzbromarone in Patients With Chronic Heart Failure

Resource links provided by NLM:


Further study details as provided by Tottori University Hospital:

Primary Outcome Measures:
  • parameters of echocardiography at 16 weeks
  • BNP levels at 16 weeks

Secondary Outcome Measures:
  • parameters of glucose metabolism at 16 weeks
  • Parameters of lipid metabolism at 16 weeks

Study Start Date: January 2004
Estimated Study Completion Date: December 2005
Detailed Description:

Hyperuricemia is often observed in patients with congestive heart failure (CHF). It has been reported that hyperuricemia is related to exercise capacity, inflammation markers and diastolic dysfunction in such patients. In addition, hyperuricemia in CHF relates to both symptomatic status (i.e. morbidity) as well as impaired prognosis (i.e. mortality). Hyperuricemia is likely to play an important role in the pathophysiology of CHF. Up-regulation of xanthine oxidase (XO) activity in CHF has been shown to contribute to higher uric acid (UA) in CHF and the therapeutic concept of XO inhibition has shown beneficial effects in a number of surrogate markers in these patients. The XO inhibition accounts for substantial decrease in oxygen radical load, the latter is discussed as the main benefit of XO inhibition treatment in hyperuricemic patients. However, whether high uric acid itself is important or merely a marker of XO activity (and hence of increased radical accumulation) is currently under discussion. Therefore, this study aims to assess (I) the contribution of UA itself to the CHF pathophysiology and (II) to test the effect of lowering UA by uricosuric treatment in CHF.

  Eligibility

Genders Eligible for Study:   Both
Criteria

Inclusion Criteria:

  • chronic heart failure
  • hyperuricemia

Exclusion Criteria:

  • renal dysfunction (Cr > 2.0 mg/dl)
  • under treatment with anti-diabetic agents
  Contacts and Locations
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Please refer to this study by its ClinicalTrials.gov identifier: NCT00422318

Locations
Japan
Tottori University Hospital
Yonago, Japan, 683-8504
Sponsors and Collaborators
Tottori University Hospital
Investigators
Principal Investigator: Kazuhide Ogino, MD Tottori University Hospital
  More Information

No publications provided by Tottori University Hospital

Additional publications automatically indexed to this study by ClinicalTrials.gov Identifier (NCT Number):
ClinicalTrials.gov Identifier: NCT00422318     History of Changes
Other Study ID Numbers: #345
Study First Received: January 12, 2007
Last Updated: January 12, 2007
Health Authority: Japan: Ministry of Health, Labor and Welfare

Keywords provided by Tottori University Hospital:
Heart Failure
Insulin
Metabolism
Pharmacology
Uric Acid

Additional relevant MeSH terms:
Heart Failure
Hyperuricemia
Heart Diseases
Cardiovascular Diseases
Pathologic Processes
Benzbromarone
Uricosuric Agents
Gout Suppressants
Antirheumatic Agents
Therapeutic Uses
Pharmacologic Actions
Renal Agents

ClinicalTrials.gov processed this record on July 22, 2014