Evidence map›Paper›PMID 27730079›Full record

ArticleIndian journal of endocrinology and metabolism

Oxidative stress in hypothyroid patients and the role of antioxidant supplementation.

Sumit Kumar Chakrabarti, Sujoy Ghosh, Sandip Banerjee, Satinath Mukherjee, Subhankar Chowdhury

Open access · diamondAbstract read
In one paragraph

Article in Indian journal of endocrinology and metabolism. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Sumit Kumar ChakrabartiDepartment of General Medicine, NRS Medical College and Hospital, Jadavpur, Kolkata, West Bengal, India.
Sujoy GhoshDepartment of Endocrinology, IPGME & R and SSKM Hospital, Jadavpur, Kolkata, West Bengal, India.
Sandip BanerjeeDepartment of Biochemistry, KPC Medical College, Jadavpur, Kolkata, West Bengal, India.
Satinath MukherjeeDepartment of Endocrinology, IPGME & R and SSKM Hospital, Jadavpur, Kolkata, West Bengal, India.
Subhankar ChowdhuryDepartment of Endocrinology, IPGME & R and SSKM Hospital, Jadavpur, Kolkata, West Bengal, India.
Medical College and Hospital, Kolkata · INInstitute of Post Graduate Medical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextThe available data concerning oxidant stress and antioxidant capacity in hypothyroidism are scanty and inconclusive. While some authors suggest that tissues may be protected from oxidant damage because of a hypometabolic state in hypothyroidism, others report increased oxidative stress in hypothyroidism. Selenium acts as a cofactor for the thyroid hormone (TH) deiodinases that activate and then deactivate various THs and their metabolites. Selenium may inhibit thyroid autoimmunity.

aimsThe study was designed, first, to study the impact of oxidative stress in patients of primary hypothyroidism due to autoimmune thyroiditis, by estimation of serum malondialdehyde (MDA) as a biomarker of oxidative stress. Second, to study the change in MDA level pre- and post-L-thyroxine treatment. Finally, to look into the possible role of selenium supplementation on oxidative stress in autoimmune hypothyroidism. SUBJECTS AND

methodsPatients attending endocrine outpatient department (OPD) services of IPGMER and SSKM hospital were considered for the study. Sixty treatment-naive adult patients (age > 18 years) with hypothyroidism were included in the study. The patients were divided into two groups, each comprised thirty patients. One group was treated with L-thyroxine and placebo (Group A). The other group received L-thyroxine replacement along with selenium (100 mcg twice a day) as antioxidant supplementation (Group B). The patients were blinded about selenium and placebo. The study duration for both groups was 6 months. The starting dose of L-thyroxine was 1.6 mcg/kg body weight free thyroxine (FT4), and thyroid-stimulating hormone (TSH) was repeated after 12 weeks. L-thyroxine dose adjustments were done if needed. MDA was assessed at the beginning and at the end of the study, i.e., after 6 months of treatment. The control cohort was composed of thirty healthy adults. Only overt hypothyroidism (OH) cases were included in the study. STATISTICAL ANALYSIS USED: Normality of data was determined using Anderson-Darling test, Shapiro-Wilk test, and QQ plot.

resultsAfter treatment in Group A patients, FT4 showed a significant increment while TSH value decreased. MDA level reduced after treatment, (

conclusionsOxidative stress compounds hypothyroidism. Hypothyroidism is a state of increased oxidative stress. In this study, biomarker, MDA level is high in treatment-naive primary hypothyroid patients. After treatment with L-thyroxine, the stress marker is reduced to a significant extent. MDA can be used as a useful biomarker to measure and monitor oxidative stress. The role of the addition of antioxidant in the form of selenium remained inconclusive.

Indexed as

Antioxidant supplementationovert hypothyroidismoxidative stressserum malondialdehyde

Identifiers

PMID27730079
PMCPMC5040049
OpenAlexW2519832108

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.