Introduction: Sudden sensorineural hearing loss (SSHL) has been proposed as a symptom of underlying vascular problems. The purpose of this work is to evaluate the genetic and acquired risk factors. Methods: Ninety-nine patients were tested for the presence of common polymorphisms related to thrombophilia (prothrombin and factor V Leiden) in order to assess genetic risk factors, and several parameters classically associated with vascular disorders (cardiovascular events, brain stroke and antiphospholipid syndrome) were evaluated. Additional assessments of personal and familial history risk factors for vascular disorders were performed in each patient. Results: Thrombophilia studies did not demonstrate statistically relevant differences between the patients and control group. However, lipidemia profile and directed personal and familial histories showed positive trends for SSHL. Conclusion: The lack of clear relationships between SSHL and other vascular risk factors suggests multicausality as a predominant disease profile. Although preliminary results point at a vascular involvement in SSHL, a long-term prospective study is necessary to demonstrate that SSHL represents an early vascular symptom.

These results suggest that BQs has a considerable impact on quality of life while nasal polyposis has no additional impact on the quality of life of patients with BQs.

One year after TLM patients present a very good QOL. Relevant voice impairment is detected especially in locally advanced tumors, reinforcing the necessity of preoperative counseling and postoperative rehabilitation. Adjuvant radiotherapy and neck dissection negatively influenced disease-specific QOL.

Background: The main causative process in idiopathic sudden sensorineural hearing loss (iSSNHL) has yet to be explained or demonstrated. The clinical picture supports vascular involvement, but obvious limitations of inner ear study make this difficult to corroborate. Objectives: To determine the role of thrombophilic genetic variants that may affect platelet function and to assess the cardiovascular risk profile in a cohort of patients with iSSNHL. Patients and Methods: 118 Caucasian patients with iSSNHL were recruited from the same geographical area and enrolled prospectively in this study. Clinical data were obtained for each patient. Polymorphisms of the platelet glycoprotein subunit IIIa gene, ITGB3 (PLA1/A2, rs5918), and of the platelet glycoprotein subunit Ia gene, ITGA2 (C807T, rs1126643) were analyzed. A control group of 161 age- and gender-matched healthy individuals from the same geographical area was recruited for genetic comparisons. In order to determine the cardiovascular risk profile of each patient and of our cohort, a cross-sectional assessment was performed by means of a calibrated Framingham coronary heart disease risk scale. Risk factor proportions were compared to those recommended in European guidelines for coronary prevention, which are also based on the Framingham function. Results: A significantly high prevalence of the 807T allele of platelet glycoprotein subunit Ia was found in patients compared to controls. There was a significant correlation between the 807TT homozygous genotype and a low probability of recovery. The PLA1/A2 polymorphism of platelet glycoprotein subunit IIIa was not associated with recovery, with a similar genotype prevalence being found in patients and controls. In terms of cardiovascular risk profile, patients did not present an excess of baseline coronary risk factors compared to the general population in the same geographical area. Conclusions: Patients with iSSNHL had a higher prevalence of the 807T thrombophilic polymorphism of platelet glycoprotein Ia/IIa. Patients homozygous for this polymorphism are less likely to recover from iSSNHL. Classical cardiovascular risk factors were not related to iSSNHL.

Ameloblastomas are the most frequent odontogenic tumours, accounting for 1% of all tumours of the maxilla and mandible. Sinonasal ameloblastomas are most common between the ages of 55 and 65, and mandibular ameloblastomas between 40 and 50. Incidence is higher in males than in females, and there are no differences between races. These locally aggressive tumours originate in the mandible in 80% of cases and in the maxilla in 15-20%. We report an unusual primary nasosinusal ameloblastoma presented in a 68-year-old male. The tumour was completely resected by (para)lateral rhinotomy and treated with postoperative radiotherapy. Histological analysis demonstrated a plexiform ameloblastoma. The patient remains well without disease after 50 months of postoperative follow-up.