The Effectiveness of Salvage Hyperbaric Oxygen Therapy Following Combined Steroid Therapy for Refractory Sudden Sensorineural Hearing Loss.

OBJECTIVE: Hyperbaric oxygen therapy (HBOT) is an accepted treatment option for sudden sensorineural hearing loss (SSNHL), but it is still recommended in combination with corticosteroids. We investigated the efficacy of salvage HBOT in refractory SSNHL that does not respond to corticosteroid combination therapy. METHODS: Eighty-four patients were included, who had unilateral SSNHL with an improvement of pure-tone average (PTA) less than 10 dB after using intratympanic plus systemic corticosteroids (combined therapy) as the initial therapy. The control group (n = 66) received no further treatment, and the HBOT group (n = 18) received additional treatment with HBOT (10 sessions in total with 2.5 atmospheres absolute for 1 hour). RESULTS: No differences in PTA or WDS were found between the 2 groups. However, the mean hearing gain in the HBOT group (16.8 ± 4.49 dB) was significantly higher than that in the control group (4.45 ± 1.03 dB) (P = .015). The proportion of patients with hearing recovery (hearing gain of 10 dB or more) after treatment was significantly higher in HBOT group (38.9%) than in the control group (10.6%). CONCLUSIONS: In patients with refractory SSNHL after steroid combined therapy, salvage HBOT showed a significant effect on hearing gain and recovery rate.

The Optimized Protocol of Hyperbaric Oxygen Therapy For Sudden Sensorineural Hearing Loss.

OBJECTIVE: This study aimed to determine the optimal protocol of hyperbaric oxygen therapy (HBOT) according to various treatment settings for sudden sensorineural hearing loss (SSNHL). METHODS: A 112 patients with SSNHL were enrolled in this prospective study. All patients were treated with systemic steroid therapy, intratympanic steroid therapy, and HBOT. According to the pressure and duration of HBOT (10 sessions in total), the patients were divided into three groups: group 1, 2.5 atmospheres absolute (ATA) for 1 h; group 2, 2.5 ATA for 2 h; and group 3, 1.5 ATA for 1 h. The pure-tone average (PTA), word discrimination score (WDS), and mean gain were compared. RESULTS: A total of 105 patients completed the 3-month follow-up, and 6 patients were excluded. Differences among groups were found in PTA, WDS, and mean gain. In the post-hoc analysis, group 3 had significantly lower WDS and mean gain than groups 1 and 2; however, group 2 showed no significant differences from group 1. The proportion of patients with hearing recovery after treatment was significantly higher in group 1 (57.6%) and group 2 (58.8%) than in group 3 (31.3%). CONCLUSIONS: When HBOT (10 sessions) was combined with corticosteroids as the initial therapy for SSNHL, a higher pressure (1.5 ATA vs. 2.5 ATA) provided better treatment results; however, increasing the duration (1 h vs. 2 h) under 2.5 ATA did not result in a significant difference. Therefore, HBOT for SSNHL may be performed at 2.5 ATA for 1 h in 10 sessions. Laryngoscope, 133:383-388, 2023.

A dietary anthocyanin cyanidin-3-O-glucoside binds to PPARs to regulate glucose metabolism and insulin sensitivity in mice.

We demonstrate the mechanism by which C3G, a major dietary anthocyanin, regulates energy metabolism and insulin sensitivity. Oral administration of C3G reduced hepatic and plasma triglyceride levels, adiposity, and improved glucose tolerance in mice fed high-fat diet. Hepatic metabolomic analysis revealed that C3G shifted metabolite profiles towards fatty acid oxidation and ketogenesis. C3G increased glucose uptake in HepG2 cells and C2C12 myotubes and induced the rate of hepatic fatty acid oxidation. C3G directly interacted with and activated PPARs, with the highest affinity for PPARα. The ability of C3G to reduce plasma and hepatic triglycerides, glucose tolerance, and adiposity and to induce oxygen consumption and energy expenditure was abrogated in PPARα-deficient mice, suggesting that PPARα is the major target for C3G. These findings demonstrate that the dietary anthocyanin C3G activates PPARs, a master regulators of energy metabolism. C3G is an agonistic ligand of PPARs and stimulates fuel preference to fat.