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

November 25, 2011
December 28, 2011
November 2011
July 2013   (final data collection date for primary outcome measure)
Change from baseline in serum T3 levels at 48 hours [ Time Frame: baseline and 48 hours ] [ Designated as safety issue: No ]
Same as current
Complete list of historical versions of study NCT01501110 on ClinicalTrials.gov Archive Site
Not Provided
Not Provided
Not Provided
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Effects of N-acetylcysteine on Low T3 Syndrome
Evaluation of the Effects of N-acetylcysteine on Thyroid Hormone Levels in the Low T3 Syndrome

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.

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.

Interventional
Phase 4
Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Single Blind (Subject)
Primary Purpose: Treatment
  • Acute Myocardial Infarction
  • Euthyroid Sick Syndrome
  • Ischemic Heart Disease
Drug: N-acetylcysteine
in infusion of 1200 mg of n-acetylcysteine twice a day for 48 hours
Other Names:
  • NAC
  • acetylcysteine
  • Active Comparator: n-acetylcysteine
    intra-venous infusion of 1200 mg of n-acetylcysteine twice a day for 48 hours.
    Intervention: Drug: N-acetylcysteine
  • No Intervention: no intervention

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
60
July 2013
July 2013   (final data collection date for primary outcome measure)

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
Both
18 Years to 80 Years
No
Contact: Josi Vidart 55 51 98472520 josividart@gmail.com
Contact: Ana L Maia almaia@ufrgs.br
Brazil
 
NCT01501110
110061
Yes
Josi Vidart, Federal University of Rio Grande do Sul
Federal University of Rio Grande do Sul
  • Hospital de Clinicas de Porto Alegre
  • Programa de pós-graduação em endocrinologia
Principal Investigator: Josi Vidart Federal University of Rio Grande do Sul
Study Director: Ana maia Federal University of Rio Grande do Sul
Federal University of Rio Grande do Sul
December 2011

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP