Congenital Laryngeal Cyst as a Rare Cause of Stridor in Infants: Two Case Reports.

Congenital laryngeal cysts are a rare cause of stridor in infants. These cysts may have serious clinical implications if not promptly recognized. A small laryngeal cyst may remain asymptomatic. However, if large, it can block the laryngeal inlet leading to acute airway obstruction, which is potentially life-threatening. In pediatric patients presenting with respiratory distress, prompt diagnosis and surgical management are crucial to avoid infant morbidity and mortality. We describe two cases of laryngeal vallecular cysts in infants and their management in our clinical practice.

Intracranial Complication as a Manifestation of Clinical Onset in a Child With Insidious Ear Infection.

Acute mastoiditis is a common consequence of acute otitis media and may lead to intracranial complications. Common clinical presentations include otological complaints (i.e., otorrhea, otalgia, fever). Intracranial complication remains a rare manifestation of middle ear infection. We present the case of a child who presented with non-specific symptoms without any otological complaints. Prompt clinical assessment and imaging revealed an otogenic brain abscess with concurrent mastoiditis. Management of this child required both medical and surgical treatment by a multidisciplinary team.

SLC26A4 expression among autoimmune thyroid tissues.

CONTEXT: The PDS gene (SLC26A4) is responsible for Pendred syndrome (PS). Genetic analysis of PDS using Tunisian samples showed evidence for linkage and association with autoimmune thyroid diseases (AITD) emergence. In addition, the PDS gene product, pendrin, was recently identified as a novel autoantigen in Graves' disease (GD) or Hashimoto thyroiditis (HT) patients' sera. OBJECTIVE: The aim of this study was to quantify the PDS gene expression and to evaluate the pendrin in vivo and in vitro immunolocalisation. PATIENTS: A total of 52 thyroid gland tissue samples (22 GD, 11 HT, 5 multinodular goiter (MNG), 3 normal thyroid tissues, 8 papillary thyroid carcinoma (PTC), 1 follicular thyroid carcinoma (FTC) and 2 medullar thyroid carcinoma (MTC)) were explored. METHOD: PDS and pendrin expression levels were determined using quantitative RT-PCR and immuno-detection methods. TSH and thyroglobulin (Tg) effects on pendrin expression were investigated by immunofluorescence on primary cell culture from GD thyroid tissues. RESULTS: The relative quantification using PDS transcript level among GD thyroid tissues was increased compared to normal thyroid tissues used as calibrator (mean: 27.17-fold higher than normal thyroid tissues). However, thyroids with HT, carcinoma and MNG showed a decrease expression level (means: 92.05-, 77.68-, 14.3-fold lower than normal thyroid tissues, respectively). These results were confirmed by immunoanalysis. Immunofluorescence results showed an apical and a cytoplasmic pendrin localisation on GD thyroid tissues and a marked pendrin expression reduction on HT thyroid tissues. GD primary cell cultures under TSH and Tg stimulation showed a trafficking improvement of pendrin apical localisation. CONCLUSIONS: Our data point to the presence of a relation between SLC26A4 expression in AITD and thyroid function.