Evidence map›Paper›PMID 18250610›Full record

ArticleJournal of endocrinological investigation2007

Two common and three novel PDS mutations in Thai patients with Pendred syndrome.

T Snabboon, W Plengpanich, S Saengpanich, S Sirisalipoch, S Keelawat, S Sunthornyothin, W Khovidhunkit, S Suwanwalaikorn, V Sridama, V Shotelersuk

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Article in Journal of endocrinological investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 41% 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

8 citing papers in PubMed, 22 citations in OpenAlex.

  1. A UniqueInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. Article
  4. Genetic susceptibility to hereditary non-medullary thyroid cancer.Hereditary cancer in clinical practice · 2022
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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

10 authors at 1 institution in 1 country.

T SnabboonDepartment of Internal Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand. thiti.s@chula.ac.th
W Plengpanich
S Saengpanich
S Sirisalipoch
S Keelawat
S Sunthornyothin
W Khovidhunkit
S Suwanwalaikorn
V Sridama
V Shotelersuk
Chulalongkorn University · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pendred syndrome is an autosomal recessive disorder characterized by congenital sensorineural deafness, goiter, and impaired iodide organification. It is caused by mutations in the PDS gene. Most published mutation studies of Pendred syndrome have dealt with Western populations. In this study, we examined clinical and molecular characteristics of 16 affected individuals in 6 unrelated Thai families. Of all the affected, 100% (16/16) had bilateral deafness, 68.8% (11/16) goiters, and 25% (4/16) hypothyroidism. Follicular thyroid carcinoma and Hürthle cell adenoma were found in affected members of a family, raising the possibility of an increased risk of thyroid carcinoma in Pendred syndrome patients. Sequence analysis of the entire coding region of the PDS gene successfully identified all 12 mutant alleles in these 6 families. The 12 identified mutant alleles constituted 6 distinct mutations including 3 splice site mutations (IVS4-1G>A, IVS7-2A>G, IVS9- 1G>A), one frame shift mutation (1548insC) and 2 missense mutations (T67S, H723R). Eight mutations out of 12 were constituted by IVS7- 2A>G and 1548insC, each one being present in 4 distinct alleles in our studied group. The identification of these two frequent PDS mutations will facilitate the molecular diagnosis of Pendred syndrome in Thai populations. In addition, three newly identified mutations, T67S, IVS4-1G>A, and IVS9-1G>A, were not observed in 50 unrelated healthy Thai controls.

Indexed as

Adenoma, OxyphilicAdultAllelesDeafnessFemaleGoiterHumansHypothyroidismIodidesMaleMembrane Transport ProteinsMiddle AgedMutation, MissensePedigreeRisk FactorsSulfate TransportersIodidesMembrane Transport ProteinsSLC26A4 protein, humanSulfate Transporters

Identifiers

PMID18250610
OpenAlexW2051664345

What OpenQuestion holds

Textmetadata
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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.