Does the addition of hyperbaric oxygen therapy to conventional treatment modalities influence the outcome of soldiers with idiopathic sudden sensorineural hearing loss?

BACKGROUND: Idiopathic sudden sensorineural hearing loss (ISSNHL) is defined as a 30-decibel (dB) loss in hearing over three contiguous frequencies within 3 days. The cause remains unknown, and there is currently no consensus in the literature as to how it is best treated. Conventional treatment in our unit comprises steroids, pentoxyphiline and dextran, with the potential addition of hyperbaric oxygen therapy (HBOT). METHODS: A prospective randomised trial was performed on all soldiers diagnosed with ISSNHL in our institution from 1 January 2007 to 31 December 2016. Participants were randomly allocated to one of two groups. Group A was treated with conventional treatment plus HBOT. Group B was treated with conventional treatment only. Data collection included age, gender, clinical symptoms, pure-tone audiometry results and treatment outcome. RESULTS: 60 participants were enrolled (53 male, 7 female) with ages ranging from 18 to 65 years (mean age of 30.3). No significant differences were observed in the baseline characteristics between the two groups, including gender, age, site, associated symptoms, duration of symptoms and severity of hearing loss. Hearing recovery using Siegel's criteria on days 8 and 13 showed no significant differences between treatment groups. However, the hearing recovery on day 180 was significantly better in those who received the conventional treatment plus HBOT (P<0.05). Additionally, no significant side effects were observed in either group. CONCLUSIONS: HBOT plus existing conventional treatment was associated with a better outcome than conventional treatment alone. We would recommend the addition of HBOT is recommended as a first-line treatment modality for all soldiers presenting with ISSNHL.

Intracellular zinc release-activated ERK-dependent GSK-3ß-p53 and Noxa-Mcl-1 signaling are both involved in cardiac ischemic-reperfusion injury.

Oxidative stress and nitrosative stress are both suggested to be involved in cardiac ischemia-reperfusion (I/R) injury. Using time-lapse confocal microscopy of cardiomyocytes and high-affinity O(2)(-•) and Zn(2+) probes, this study is the first to show that I/R, reactive oxygen species (ROS), and reactive nitrogen species (RNS) all cause a marked increase in the [O(2)(-•)](i), resulting in cytosolic and mitochondrial Zn(2+) release. Exposure to a cell-penetrating, high-affinity Zn(2+)(i) chelator, TPEN, largely abolished the Zn(2+)(i) release and markedly protected myocytes from I/R-, ROS-, RNS-, or Zn(2+)/K(+) (Zn(2+)(i) supplementation)-induced myocyte apoptosis for at least 24 h after TPEN removal. Flavonoids and U0126 (a MEK1/2 inhibitor) largely inhibited the myocyte apoptosis and the TPEN-sensitive I/R- or Zn(2+)(i) supplement-induced persistent extracellular signal-regulated kinase 1 and 2 (ERK1/2) phosphorylation, dephosphorylation of p-Ser9 on glycogen synthase kinase 3ß (GSK-3ß), and the translocation into and accumulation of p-Tyr216 GSK-3ß and p53 in, the nucleus. Silencing of GSK-3ß or p53 expression was cardioprotective, indicating that activation of the ERK-GSK-3ß-p53 signaling pathway is involved in Zn(2+)-sensitive myocyte death. Moreover, the ERK-dependent Noxa-myeloid cell leukemia-1 (Mcl-1) pathway is also involved, as silencing of Noxa expression was cardioprotective and U0126 abolished both the increase in Noxa expression and in Mcl-1 degradation. Thus, acute upstream Zn(2+)(i) chelation at the start of reperfusion and the use of natural products, that is, flavonoids, may be beneficial in the treatment of cardiac I/R injury.