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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.
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http://dx.doi.org/10.1515/jpem.2008.21.12.1179 | DOI Listing |
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.
Int J Mol Sci
May 2025
Department of Otolaryngology-Head and Neck Surgery, National Taiwan University Hospital, Taipei 100225, Taiwan.
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 PDFMol 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 PDFNeurobiol Dis
August 2025
Department of Otorhinolaryngology, Institute of Science Tokyo, Tokyo, Japan. Electronic address:
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.
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