Expression of a disintegrin and metalloproteinase-33 protein in vocal fold polyps.

BACKGROUND: This study aimed to evaluate the association of a disintegrin and metalloproteinase-33 protein ('ADAM-33') expression in vocal polyp formation and to determine its correlation with clinical characteristics. METHODS: Medical charts and histological sections of 32 patients diagnosed with vocal polyps who underwent surgery were analysed. Controls were histopathologically normal vocal fold tissues obtained from 36 patients who underwent surgery for laryngeal squamous cell carcinoma. Immunohistochemical staining was performed to detect ADAM-33 expression in epithelial cells, stroma and vessels. RESULTS: All epithelial, stromal and vascular staining scores were significantly greater in polyp tissue than in controls (p < 0.001). Stromal ADAM-33 staining scores were higher in vocal polyp patients with a symptom duration of less than six months (p < 0.05). Vocal overuse or the presence of reflux symptoms, sinonasal symptoms or allergy did not affect ADAM-33 immunostaining scores (p = 0.05). CONCLUSION: In this study, ADAM-33 immunostaining was significantly increased in vocal polyps. Therefore, over-expression of this protein may be associated with vocal polyp pathogenesis.

Expression of "a disintegrin and metalloproteinase-33" (ADAM-33) protein in laryngeal squamous cell carcinoma.

OBJECTIVE: A disintegrin and metalloproteinase domain containing protein 33 (also known as ADAM-33) is a member of a matrix metalloproteinase family which mediates extracellular matrix remodelling and changes in cellular adhesion. This study aimed to evaluate expression of this protein in laryngeal squamous cell carcinoma, and to determine its correlation with patients' clinicopathological characteristics. SUBJECTS AND METHODS: Forty paraffin blocks of laryngeal carcinoma underwent immunohistochemical staining to detect "a disintegrin and metalloproteinase-33" expression. Case records were reviewed to determine patient characteristics. RESULTS: All epithelial, vascular and stromal staining scores were significantly increased in tumour tissue compared with controls (p < 0.001). However, patients' clinical characteristics at the time of diagnosis, and their disease extent, did not correlate significantly with the immunohistochemical staining scores. CONCLUSION: This study suggests that increased expression of "a disintegrin and metalloproteinase-33" may play a role in the pathogenesis of laryngeal carcinoma.

Evaluation of vestibular evoked myogenic potentials during benign paroxysmal positional vertigo attacks; neuroepithelial degeneration?

OBJECTIVE: Recent studies show that benign paroxysmal positional vertigo (BPPV) may also affect the macula of the saccule. We investigated vestibular evoked myogenic potential (VEMP) results in patients with BPPV. MATERIALS AND METHODS: The study group included 31 patients (31 ears) diagnosed with posterior canal BPPV and the control group included 23 healthy volunteers (46 ears) with no neurotologic symptoms. After VEMP recordings were performed, mean latency values for p13 of the study and control groups were compared. RESULTS: VEMP responses were elicited in all controls (46 ears). In the study group, responses were normal in 19, delayed in 5, and absent in 7 ears. There was a significant difference between abnormal VEMP rates for patients versus controls (p < 0.001). Although VEMP responses were elicited in all non-affected ears of patients, there was a delayed response in 6 (19%) non-affected ears. This was statistically significant when compared with controls (p = 0.002). There was no correlation between abnormal VEMPs and the number of canalith reposition maneuvers required (p = 0.392). CONCLUSION: Our findings suggest the prolongation of mean latency values for p13 of VEMP in patients with BPPV might signify neuronal degeneration in the macula of the saccule, and the absence of VEMP waves might represent the extent of damage. Also, high latency values for p13 in non-affected ears of patients might indicate bilateral neural degeneration in BPPV.