The role of Onodi cells in sphenoiditis: results of multiplanar reconstruction of computed tomography scanning / Papel das células de Onodi na esfenoidite: resultados da tomografia computadorizada com reconstrução multiplanar

Abstract Introduction Onodi cells are the most posterior ethmoid air cells and extend superolateral to the sphenoid sinus. These cells are also intimately related with the sphenoid sinus, optic nerve, and carotid artery. Radiologic evaluation is mandatory to assess for anatomic variations before any treatment modalities related to the sphenoid sinus. Objective To evaluate the effect of Onodi cells on the frequency of sphenoiditis. Methods A retrospective analysis was performed in 618 adult patients who underwent high-resolution computed tomography between January 2013 and January 2015. The prevalence of Onodi cells and sphenoiditis was evaluated. Whether the presence of Onodi cells leads to an increase in the prevalence of sphenoiditis was investigated. Results Onodi cell positivity was observed in 326 of 618 patients and its prevalence was found to be 52.7%. In the study group, 60.3% (n = 73) were ipsilaterally (n = 21) or bilaterally (n = 52) Onodi-positive, whereas 39.7% (n = 48) were Onodi-negative (n = 35) or only contralaterally Onodi-positive (n = 13). Of the control group, 48.3% (n = 240) were Onodi-positive and 51.7% (n = 257) were Onodi negative. The co-existence of Onodi cells ipsilaterally was observed to increase the identification of sphenoiditis 1.5-fold, and this finding was statistically significant (p < 0.05). Conclusion The prevalence of sphenoiditis appears to be higher in patients with Onodi cells. However, it is not possible to state that Onodi cells are the single factor that causes this disease. Further studies are needed to investigate contributing factors related to sphenoiditis.

Resumo Introdução As células de Onodi são as células etmoidais mais posteriores, que se prolongam superolateralmente ao seio esfenoidal. Essas células também se encontram em íntima relação com o seio esfenoidal, o nervo óptico e a artéria carótida. Para análise de variações anatômicas antes da implantação de qualquer modalidade terapêutica relacionada ao seio esfenoidal, a avaliação radiológica é obrigatória, Objetivo Nosso objetivo foi avaliar o papel das células de Onodi na frequência de esfenoidite. Método Em nosso estudo, foi feita uma análise retrospectiva em 618 pacientes adultos que se submeteram à tomografia computadorizada de alta resolução entre janeiro de 2013 e janeiro de 2015. Avaliamos a prevalência de células de Onodi e de esfenoidite. Investigamos se a presença de células de Onodi leva a um aumento na prevalência de esfenoidite. Resultados A positividade para células de Onodi foi observada em 326 de 618 pacientes e sua prevalência foi de 52,7%. No grupo de estudo, 60,3% (n = 73) eram CO-positivas: ipsilateral (n = 21) ou bilateralmente (n = 52); e 39,7% (n = 48) eram CO-negativas (n = 35) ou apenas contralateralmente CO-positivas (n = 13). No grupo de controle, 48,3% (n = 240) eram CO-positivas; e 51,7% (n = 257) eram CO-negativas. Observamos que a coexistência de CO ipsilateralmente aumentava em 1,5 vez a associação com esfenoidite e esse achado foi estatisticamente significante (p < 0,05). Conclusão A prevalência de esfenoidite parece ser maior em pacientes com células de Onodi, mas não é possível afirmar que elas são isoladamente o fator causador dessa doença. Novos estudos precisam ser feitos para uma investigação dos fatores contributivos relacionados à esfenoidite.

GJB2 and mitochondrial A1555G gene mutations in nonsyndromic profound hearing loss and carrier frequencies in healthy individuals.

This study aimed to assess mutations in GJB2 gene (connexin 26), as well as A1555G mitochondrial mutation in both the patients with profound genetic nonsyndromic hearing loss and healthy controls. Ninety-five patients with profound hearing loss (>90 dB) and 67 healthy controls were included. All patients had genetic nonsyndromic hearing loss. Molecular analyses were performed for connexin 26 (35delG, M34T, L90P, R184P, delE120, 167delT, 235delC and IVS1+1 A-->G) mutations, and for mitochondrial A1555G mutation. Twenty-two connexin 26 mutations were found in 14.7% of the patients, which were 35delG, R184P, del120E and IVS1+1 A-->G. Mitochondrial A1555G mutation was not encountered. The most common GJB2 gene mutation was 35delG, which was followed by del120E, IVS1+1 A-->G and R184P, and 14.3% of the patients segregated with DFNB1. In consanguineous marriages, the most common mutation was 35delG. The carrier frequency for 35delG mutation was 1.4% in the controls. 35delG and del120E populations, seems the most common connexin 26 mutations that cause genetic nonsyndromic hearing loss in this country. Nonsyndromic hearing loss mostly shows DFNB1 form of segregation.