Objectives. To explore whether peripheral inflammatory, metabolic, and hemostatic parameters could predict the pathogenesis of successive bilateral sudden sensorineural hearing loss (SSNHL). Methods. This study reviewed 33 patients with successive bilateral SSNHL and 215 patients with unilateral SSNHL. Clinical characteristics and hematological parameters were compared, including the inflammatory markers (like neutrophil lymphocyte ratio (NLR), monocyte lymphocyte ratio (MLR), and platelet lymphocyte ratio (PLR)) and metabolic features (including hypertension, triglyceridemia, dyslipidemia, and hyperglycemia), as well as hemostatic indices (including prothrombin time (PT), activated partial thromboplastin time (APTT), and fibrinogen). Results. In the successive bilateral SSNHL group, older average onset age (48.67±15.36 vs. 42.71±13.58, p<0.05), higher male to female ratio (18 : 15 vs. 112 : 103, p>0.05), and poorer therapeutic efficacy (12% vs. 59%, p<0.01) were observed than those in the unilateral SSNHL group. Compared to the unilateral SSNHL group, NLR, MLR, and PLR in the successive bilateral SSNHL group were significantly higher (NLR: 5.72±2.23 vs. 4.45±2.82, p=0.01; MLR: 0.25±0.15 vs. 0.17±0.11, p<0.01; PLR: 190.70±69.79 vs. 148.18±65.67; p<0.01); the LDL level was significantly higher; yet, the HDL level was significantly lower (LDL: 3.79±0.53 vs. 3.49±0.74; HDL: 1.33±0.32 vs. 1.44±0.26; p<0.05 for both); fibrinogen was significantly higher (4.03±0.47 vs. 3.70±0.65; p<0.01). Logistic regression analysis demonstrated that the risk factors for successive bilateral SSNHL included age, NLR, MLR, PLR, LDL, HDL, diabetes, and fibrinogen. However, only NLR, MLR, PLR, diabetes, LDL, and HDL independently predicted successive bilateral SSNHL. Conclusion. Selected blood inflammatory markers combined with metabolic parameters were positively correlated with successive bilateral SSNHL.

Triggering receptor expressed on myeloid cells (TREM) has been broadly studied in inflammatory disease. However, the expression and function of TREM-2 remain undiscovered in acquired cholesteatoma. The expression of TREM-2 was significantly higher in human acquired cholesteatoma than in normal skin from the external auditory canal, and its expression level was positively correlated with the severity of bone destruction. Furthermore, TREM-2 was mainly expressed on dendritic cells (DCs). In human acquired cholesteatoma, the expression of proinflammatory cytokines (IL-1β, TNF-α and IL-6) and matrix metalloproteinases (MMP-2, MMP-8 and MMP-9) were up-regulated, and their expression levels were positively correlated with TREM-2 expression. Osteoclasts were activated in human acquired cholesteatoma. In an animal model, TREM-2 was up-regulated in mice with experimentally acquired cholesteatoma. TREM-2 deficiency impaired the maturation of experimentally acquired cholesteatoma and protected against bone destruction induced by experimentally acquired cholesteatoma. Additional data showed that TREM-2 up-regulated IL-1β and IL-6 expression via TLR4 instead of the TLR2 signaling pathway and promoted MMP-2 and MMP-8 secretion and osteoclast activation in experimentally acquired cholesteatoma. Therefore, TREM-2 might enhance acquired cholesteatoma-induced bone destruction by amplifying the inflammatory response via TLR4 signaling pathways and promoting MMP secretion and osteoclast activation.

In order to clarify the central reorganization in acute period of hearing loss, this study explored the aberrant dynamics of electroencephalogram (EEG) microstates and the correlations with the features of idiopathic sudden sensorineural hearing loss (ISSNHL) and tinnitus. We used high-density EEG with 128 channels to investigate alterations in microstate parameters between 25 ISSNHL patients with tinnitus and 27 healthy subjects. This study also explored the associations between microstate characteristics and tinnitus features. Microstates were clustered into four categories. There was a reduced presence of microstate A in amplitude, coverage, lifespan, frequency and an increased presence of microstate B in frequency in ISSNHL patients with tinnitus. According to the syntax analysis, a reduced transition from microstate C to microstate A and an increased transition from microstate C to microstate B were found in ISSNHL subjects. In addition, the significant negative correlations were found between Tinnitus Handicap Inventory (THI) scores and frequency of microstate A as well as between THI scores and the probability of transition from microstate D to microstate A. While THI was positively correlated with the transition probability from microstate D to microstate B. To sum up, the significant differences in the characteristics of resting-state EEG microstates were found between ISSNHL subjects with tinnitus and healthy controls. This study suggests that the alterations of central neural networks occur in acute stage of hearing loss and tinnitus. And EEG microstate may be considered as a useful tool to study the whole brain network in ISSNHL patients.