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Sudden onset sensorineural hearing loss has been associated with infection by severe acute respiratory syndrome coronavirus-2. However, little is known regarding how this differs from sudden onset sensorineural hearing loss of other aetiologies. This systematic review summarises existing literature on severe acute respiratory syndrome coronavirus-2 associated sudden onset sensorineural hearing loss treatment and outcomes.
Methods
A literature search using Ovid was performed for studies which evaluated treatments and outcomes of patients with sudden onset sensorineural hearing loss associated with severe acute respiratory syndrome coronavirus-2 infection.
Results
A total of 99 studies were identified, from which 14 studies were selected for inclusion - collectively including 154 patients. Nine of these studies were single participant case reports and five were larger case series. Corticosteroid treatment varied between studies in terms of administration route, dose, and duration. Only 63/154 patients in this review achieved complete resolution of their symptoms following steroid treatment.
Conclusion
Oral, intravenous, and intratympanic steroids demonstrate a good safety profile. However, the majority of patients are left with unresolved hearing loss.
Otitis media (OM) is a common reason for children to be prescribed antibiotics and undergo surgery but a thorough understanding of disease mechanisms is lacking. We evaluate the evidence of a dysregulated immune response in the pathogenesis of OM.
Methods
A comprehensive systematic review of the literature using search terms [otitis media OR glue ear OR AOM OR OME] OR [middle ear AND (infection OR inflammation)] which were run through Medline and Embase via Ovid, including both human and animal studies. In total, 82 955 studies underwent automated filtering followed by manual screening. One hundred studies were included in the review.
Results
Most studies were based on in vitro or animal work. Abnormalities in pathogen detection pathways, such as Toll-like receptors, have confirmed roles in OM. The aetiology of OM, its chronic subgroups (chronic OM, persistent OM with effusion) and recurrent acute OM is complex; however, inflammatory signalling mechanisms are frequently implicated. Host epithelium likely plays a crucial role, but the characterisation of human middle ear tissue lags behind that of other anatomical subsites.
Conclusions
Translational research for OM presently falls far behind its clinical importance. This has likely hindered the development of new diagnostic and treatment modalities. Further work is urgently required; particularly to disentangle the respective immune pathologies in the clinically observed phenotypes and thereby work towards more personalised treatments.
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