Effects of N-acetylcysteine on Low T3 Syndrome

The recruitment status of this study is unknown because the information has not been verified recently.
Verified December 2011 by Federal University of Rio Grande do Sul.
Recruitment status was  Recruiting
Sponsor:
Collaborators:
Hospital de Clinicas de Porto Alegre
Programa de pós-graduação em endocrinologia
Information provided by (Responsible Party):
Josi Vidart, Federal University of Rio Grande do Sul
ClinicalTrials.gov Identifier:
NCT01501110
First received: November 25, 2011
Last updated: December 28, 2011
Last verified: December 2011
  Purpose

The propose of this study is to determine whether N-acetylcysteine is effective in reversing the changes in thyroid hormones seen in critical illness, known as the low T3 syndrome.


Condition Intervention Phase
Acute Myocardial Infarction
Euthyroid Sick Syndrome
Ischemic Heart Disease
Drug: N-acetylcysteine
Phase 4

Study Type: Interventional
Study Design: Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Single Blind (Subject)
Primary Purpose: Treatment
Official Title: Evaluation of the Effects of N-acetylcysteine on Thyroid Hormone Levels in the Low T3 Syndrome

Resource links provided by NLM:


Further study details as provided by Federal University of Rio Grande do Sul:

Primary Outcome Measures:
  • Change from baseline in serum T3 levels at 48 hours [ Time Frame: baseline and 48 hours ] [ Designated as safety issue: No ]

Estimated Enrollment: 60
Study Start Date: November 2011
Estimated Study Completion Date: July 2013
Estimated Primary Completion Date: July 2013 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Active Comparator: n-acetylcysteine
intra-venous infusion of 1200 mg of n-acetylcysteine twice a day for 48 hours.
Drug: N-acetylcysteine
in infusion of 1200 mg of n-acetylcysteine twice a day for 48 hours
Other Names:
  • NAC
  • acetylcysteine
No Intervention: no intervention

Detailed Description:

The low T3 syndrome or nonthyroidal illness is characterized by low levels of T3, normal or high normal levels of rT3, low or normal levels of T4 and inappropriately normal or low levels of TSH. These changes affect up to 75% of patients and have prognostic implications.

Interleukin-6 (IL6) seems to have a causative role in the pathogenesis of nonthyroidal illness. There is evidence that the reduction in serum T3 was inversely associated with serum IL-6, while the rT3 have a positive association. The mechanism of action of cytokines on the metabolism of thyroid hormones has not been determined and the potential role of cytokines on the deiodases has been the focus of research.

In a cell culture model study, IL-6 was able to suppress the conversion of T4 to T3 by deiodases type 1 and 2 and stimulate the inactivation of T3 by deiodase type 3, a situation similar to nonthyroidal illness. The use of N-acetylcysteine prevented this alterations, been consistent with the hypothesis that IL6 inhibits the function of the deiodases by increasing the oxygen reactive species and by consuming gluthathione or some gluthathione dependent cofactor.

Considering the absence of human studies evaluating the use of N-acetylcysteine in nonthyroidal illness, the aim of this study is to investigate whether NAC has in vivo effect on changes of thyroid hormones.

  Eligibility

Ages Eligible for Study:   18 Years to 80 Years
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Criteria

Inclusion Criteria:

  • diagnosis of acute myocardial infarction with less than 12 hours of evolution
  • reperfusion therapy (primary angioplasty)

Exclusion Criteria:

  • Thyroid disease
  • Chronic renal disease with renal replacement therapy
  • hepatic insufficiency
  • immunosuppression
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT01501110

Contacts
Contact: Josi Vidart 55 51 98472520 josividart@gmail.com
Contact: Ana L Maia almaia@ufrgs.br

Locations
Brazil
Hospital de Clínicas de Porto Alegre Recruiting
Porto Alegre, Rio Grande do Sul, Brazil, 90540001
Contact: Josi Vidart       josividart@gmail.com   
Principal Investigator: Josi Vidart         
Instituto de Cardiologia Recruiting
Porto Alegre, Rio Grande do Sul, Brazil, 90540001
Contact: Josi Vidart       josividart@gmail.com   
Sponsors and Collaborators
Federal University of Rio Grande do Sul
Hospital de Clinicas de Porto Alegre
Programa de pós-graduação em endocrinologia
Investigators
Principal Investigator: Josi Vidart Federal University of Rio Grande do Sul
Study Director: Ana maia Federal University of Rio Grande do Sul
  More Information

Additional Information:
Publications:
Responsible Party: Josi Vidart, Principal Investigator, Federal University of Rio Grande do Sul
ClinicalTrials.gov Identifier: NCT01501110     History of Changes
Other Study ID Numbers: 110061
Study First Received: November 25, 2011
Last Updated: December 28, 2011
Health Authority: Brazil: National Committee of Ethics in Research

Keywords provided by Federal University of Rio Grande do Sul:
Euthyroid Sick Syndrome
low T3 syndrome
deiodases
oxidative stress
ischemic heart disease

Additional relevant MeSH terms:
Coronary Artery Disease
Myocardial Ischemia
Euthyroid Sick Syndromes
Heart Diseases
Infarction
Ischemia
Myocardial Infarction
Coronary Disease
Cardiovascular Diseases
Arteriosclerosis
Arterial Occlusive Diseases
Vascular Diseases
Thyroid Diseases
Endocrine System Diseases
Pathologic Processes
Necrosis
Acetylcysteine
N-monoacetylcystine
Antiviral Agents
Anti-Infective Agents
Therapeutic Uses
Pharmacologic Actions
Expectorants
Respiratory System Agents
Free Radical Scavengers
Antioxidants
Molecular Mechanisms of Pharmacological Action
Protective Agents
Physiological Effects of Drugs
Antidotes

ClinicalTrials.gov processed this record on August 28, 2014