Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

We report a young woman with genetically confirmed Pendred syndrome and discuss the current therapeutic strategies of dyshormonogenetic goitre. A small diffuse thyroid enlargement developed during infancy and although substitution therapy with L-thyroxine was adequate, it progressed and underwent multinodular transformation. Cervical ultrasound at the age of 22 years demonstrated three solid nodules and fine-needle aspiration biopsy showed a finding typical of follicular adenoma. It is known that dyshormonogenetic goitres have a tendency to grow despite appropriate treatment with L-thyroxine. Management of a patient with Pendred syndrome requires careful follow-up and regular imaging of the thyroid. Although the therapeutic approach to dyshormonogenetic goitres is still controversial, in our patient we chose total thyroidectomy as the most advantageous method to prevent the development of malignancies that may arise more frequently from dyshormonogenetic goitres than from goitres of other aetiologies.

Download full-text PDF

Source
http://dx.doi.org/10.1515/jpem.2008.21.12.1179DOI Listing

Publication Analysis

Top Keywords

pendred syndrome
12
dyshormonogenetic goitres
12
dyshormonogenetic
5
thyroidectomy patient
4
patient multinodular
4
multinodular dyshormonogenetic
4
dyshormonogenetic goitre--a
4
goitre--a case
4
case pendred
4
syndrome confirmed
4

Similar Publications

Novel SLC26A4 variant in Pendred syndrome with non-classical inheritance: a case report.

Eur Arch Otorhinolaryngol

August 2025

School of Medicine, Southeast University, 87 Dingjiaqiao, Hunan Road, Nanjing, 210009, Jiangsu, China.

Purpose: To evaluate the clinical and diagnostic implications of identifying only a single heterozygous SLC26A4 variant in a patient with the full clinical phenotype of Pendred syndrome.

Methods: A 20‑year‑old woman with lifelong deaf‑mutism developed progressive retrosternal goitre with dysphagia and dyspnoea. Pure-tone audiometry demonstrated profound bilateral sensorineural hearing loss.

View Article and Find Full Text PDF

Recessive variants of are a common cause of hereditary hearing impairment and are responsible for non-syndromic enlarged vestibular aqueducts and Pendred syndrome. Patients with bi-allelic variants often suffer from fluctuating hearing loss and recurrent vertigo, ultimately leading to severe to profound hearing impairment. However, there are currently no satisfactory prevention or treatment options for this condition.

View Article and Find Full Text PDF

Genetic heterogeneity in patients with enlarged vestibular aqueduct and Pendred syndrome.

Mol Med

May 2025

Diabgene Laboratory, Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Dubravska cesta 9, Bratislava, 845 05, Slovakia.

Background: Pathogenic variants in the SLC26A4 gene, encoding for Cl/HCO and I anion transporter pendrin, are associated with non-syndromic hearing loss with enlarged vestibular aqueduct (NSEVA) and Pendred syndrome (PDS). In the Caucasian population, up to 75% of patients fail to identify a genetic cause through biallelic mutations in the SLC26A4 gene. The CEVA haplotype could therefore play an important role in the diagnostics of NSEVA.

View Article and Find Full Text PDF

Hearing loss associated with SLC26A4 mutations exhibits diverse phenotypes, including congenital, acquired, progressive, and fluctuating impairments. This study investigates how pigmentation influences auditory dysfunction and immune responses in the stria vascularis using albino and pigmented Slc26a4 knockout (Slc26a4) mice. We found that albino Slc26a4 mice exhibited significantly less severe hearing loss along with reduced macrophage activation than their pigmented counterpart did.

View Article and Find Full Text PDF