Analysis of long-term anatomic results of radical mastoidectomy.

A long-term, retrospective, non-controlled study was performed on the drainage results of mastoidectomy (both radical and modified radical) and the relevant statistical factors that could influence the anatomic outcome were defined. The present study took into consideration the same cohort of 200 patients we have communicated with before in our previous studies concerning the long-term functional results of mastoidectomy and long-term results of ossicular replacement with biovitroceramic prosthesis. The patients were clinically followed for the same period of 8.12 years. The drainage (anatomic) results, similar to previously published functional results, were defined by analytical function of the severity and the period of evolution of disease. The main goal was to define the situations and factors (presence of complications, type of disease, type of tympanic perforation or status of ossicular chain) that influenced the drainage results that could provide us with some type of anatomical prognosis. The follow-up started at the moment of complete epithelization for each cavity as time represents the main study comparison criteria. Drainage failure was assessed by the number of otorrhea episodes. It was concluded that practically and ideally, a maximum of 84% of the mastoid and petrous cells can be cleaned out. The results of 78% drainage success are congruent to this theory. The remaining 16% of cells may contain irreversible lesions.

Analysis of long-term functional results of radical mastoidectomy.

We performed a long-term, retrospective, non-controlled study on the functional results of mastoidectomy (both radical and modified radical) and defined the relevant statistical factors that may influence the hearing outcome. In a cohort of 200 patients, we performed both radical and modified radical mastoidectomy (MRM) and followed them clinically for a period of 8.12 years. The functional results were defined by the analytical function of the severity and the period of evolution of the disease. These parameters were defined by assessing the pre-operative absolute hearing threshold (AHT), bone conduction threshold (BCT) and age of the patient at the moment of the operation. The two parameters evolved inversely proportional to the functional results and represented a complete and precise analytical tool. The global average hearing gain ratio was 32% and the ratio for unmodified pre-operative hearing (status quo ante) was 61%. With favorable prognostic factors, the average gain rate was 56% and the hearing-loss rate was 5% (1-dB SPL nominal value). The maximum ratio for gain was 81% and for hearing loss this was 0%.

Prevalence of GJB2 gene mutations correlated to presence of clinical and environmental risk factors in the etiology of congenital sensorineural hearing loss of the Romanian population.

Although etiologically heterogeneous at least 50% of all early on-set hearing losses have a genetic cause and of these, the large majority, 75-80% are most probably autosomal recessive and 70% are non-syndromic. The rest of the congenital hearing losses are determined by clinical and environmental factors such as ototoxic medication, prematurity, and complications at birth. During the last decade it became clear that 50-80% of all such afflictions result from mutations in a single gene, GJB2, which encodes the protein Connexin 26. In order to, at least partially clarify this problem, especially in an emerging country such as Romania, where the problem is not studied adequately, we developed a comprehensive study of genetic, clinical and environmental risk factors for congenital hearing loss. The two most common variations of this gene, 35delG and W24X in children with positive diagnosis of bilateral severe to profound sensorineural hearing loss were investigated. A cohort of 34 children (20 female and 14 male), ages between 2 and 10 (mean age 4.62 years), coming from 33 non-related families were evaluated. All cases were diagnosed with severe or profound bilateral congenital SNHL. A statistical comparison of genetic and environmental/clinical prevalence was also attempted since the presence of a genetic disorder cannot rule out the role of other documented risk factors in the etiology of SNHL. The results showed that, 29.4% of cases (10/34) were homozygotic for the 35delG mutation 35delG/35delG), also known as genotype Δ/Δ. 5.88% of cases (2/34) belong to the heterozygotic bi-genic group 35delG/W24X. The clinical factors with high statistical significance for SNHL in a non-genetic group have no significance for genetic SNHL patients. Thus, the present study confirms the relatively high prevalence of the 35delG and W24X mutations in cases of congenital non-syndromic severe of profound bilateral SNHL.