Comparison of the incidence of smell and taste disorders between influenza and COVID-19.

OBJECTIVE: Smell and taste disorders among patients with COVID-19 has become increasingly reported in the literature, however the prevalence varies. Post-infectious respiratory dysfunction has also been linked to influenza. In this study, we aimed to compare the rates of smell and taste disorders between COVID-19 and Influenza in unvaccinated patients. STUDY DESIGN: Retrospective cohort study. SETTING: TriNetX research network. METHODS: Two queries were made on 7/1/2023 to include Influenza without a diagnosis of COVID-19 and a COVID-19 without a diagnosis of Influenza. The queries included patients from January 1 to December 31, 2022 from 102 Healthcare Organizations. The resultant population of patients with ICD-10 codes for COVID-19 and Influenza were matched using demographic characteristics to evaluate the risk of smell disorders. RESULTS: The overall 3-month incidence of smell and taste disorders was 0.73 % in the COVID-19 population and 0.1 % in the influenza population. The 3-month matched risk ratios were 11.1 [95 % CI (8.8,13.8)]; p < 0.001) times higher for disorders of the smell and taste secondary to COVID-19 compared to influenza. CONCLUSIONS: Disorders of the smell and taste are more common among patients with COVID-19 compared to patients with Influenza. Beyond smell loss, patients experience additional nasal and sinus-related rhinological symptoms, pointing to COVID-19's and influenza's wider impact on overall rhinological health. We believe that due to the transient nature of these disorders, they might go underreported.

Noddy, a mouse harboring a missense mutation in protocadherin-15, reveals the impact of disrupting a critical interaction site between tip-link cadherins in inner ear hair cells.

In hair cells of the inner ear, sound or head movement increases tension in fine filaments termed tip links, which in turn convey force to mechanosensitive ion channels to open them. Tip links are formed by a tetramer of two cadherin proteins: protocadherin 15 (PCDH15) and cadherin 23 (CDH23), which have 11 and 27 extracellular cadherin (EC) repeats, respectively. Mutations in either protein cause inner ear disorders in mice and humans. We showed recently that these two cadherins bind tip-to-tip in a "handshake" mode that involves the EC1 and EC2 repeats of both proteins. However, a paucity of appropriate animal models has slowed our understanding both of the interaction and of how mutations of residues within the predicted interface compromise tip link integrity. Here, we present noddy, a new mouse model for hereditary deafness. Identified in a forward genetic screen, noddy homozygotes lack inner ear function. Mapping and sequencing showed that noddy mutant mice harbor an isoleucine-to-asparagine (I108N) mutation in the EC1 repeat of PCDH15. Residue I108 interacts with CDH23 EC2 in the handshake and its mutation impairs the interaction in vitro. The noddy mutation allowed us to determine the consequences of blocking the handshake in vivo: tip link formation and bundle morphology are disrupted, and mechanotransduction channels fail to remain open at rest. These results offer new insights into the interaction between PCDH15 and CDH23 and help explain the etiology of human deafness linked to mutations in the tip-link interface.

A Case of an Immature PIT1-Lineage Pituitary Neuroendocrine Tumor of the Nasopharynx.

Pituitary neuroendocrine tumors (PitNETs) located in the nasopharynx are a rare occurrence. This case report highlights a case of a 64-year-old female diagnosed with a PitNET incidentally found in her nasopharynx. The tumor was initially seen on MRI, excised, and analyzed with immunohistochemistry, ultimately confirming an immature pituitary-specific positive transcription factor 1 (PIT1)-positive-lineage pituitary neuroendocrine tumor. The tumor contained thyrotropes, somatotrophs, and lactotrophs expressing thyroid stimulating hormone, growth hormone, and prolactin, respectively. These tumors have the potential to exhibit aggressive behavior and can disrupt the surrounding tissue. Furthermore, they can be clinically silent or, conversely, secrete multiple hormones, causing hyperthyroidism, hyperprolactinemia, and acromegaly. For these reasons, they are deemed high risk. Treatment includes surgical excision with or without anti-hormone medications prior to surgery. Medications such as somatostatin analogs are used to decrease tumor size and reduce excessive hormone excretion.

Evaluation of In-Office Cryoablation of Posterior Nasal Nerves for the Treatment of Rhinitis.

BACKGROUND: Chronic rhinitis is a common condition generally treated with medical therapies. However, 10-22% of patients are refractory to medical therapies. A cryotherapy handheld device targeting the postganglionic nerve fibers of the posterior nasal nerve (PNN) now serves as an additional option for therapy. This study evaluates the efficacy of the cryosurgical ablation device of the PNN in the clinic setting. METHODS: This was a prospective single-arm trial of 24 adult patients at seven locations within a large health maintenance organization. Patients with chronic rhinitis that failed medical therapy were offered an in-office cryoablation of PNN. Patients completed the Total Nasal Symptom Score (TNSS) questionnaire consisting of 5 items reported based on the previous 12 hours and 2 weeks at the following time points: pre-treatment, 30 days, 90 days and 1 year post-treatment. RESULTS: Following cryoablation of the PNN, the TNSS 12-hour symptom score improved from 6.92 (±2.9) to 3.17 (±2.4, P < 0.001) at 30 days, 2.92 (±1.4, P < 0.001) at 90 days and 3.08 (±2.6, P < 0.001) at 1 year post treatment. Similar results were noted for the 2 weeks scores improving from 7.75 (±3.1) to 3.79 (±2.1, P < 0.001) at 30 days, 3.88 (±1.9, P < 0.001) at 90 days and 3.76 (±2.1, P < 0.001) at 1 year post-treatment. 64.7% of respondents stated the procedure decreased or eliminated nasal sprays. CONCLUSIONS: Our independent evaluation of cryoablation of the PNN shows improvement in nasal symptoms over a 1 year period and is consistent with other published data.

Transient receptor potential melastatin 1: a hair cell transduction channel candidate.

Sound and head movements are perceived through sensory hair cells in the inner ear. Mounting evidence indicates that this process is initiated by the opening of mechanically sensitive calcium-permeable channels, also referred to as the mechanoelectrical transducer (MET) channels, reported to be around the tips of all but the tallest stereocilia. However, the identity of MET channel remains elusive. Literature suggests that the MET channel is a non-selective cation channel with a high Ca(2+) permeability and ~100 picosiemens conductance. These characteristics make members of the transient receptor potential (TRP) superfamily likely candidates for this role. One of these candidates is the transient receptor potential melastatin 1 protein (TRPM1), which is expressed in various cells types within the cochlea of the mouse including the hair cells. Recent studies demonstrate that mutations in the TRPM1 gene underlie the inherited retinal disease complete congenital stationary night blindness in humans and depolarizing bipolar cell dysfunction in the mouse retina, but auditory function was not assessed. Here we investigate the role of Trpm1 in hearing and as a possible hair cell MET channel using mice homozygous for the null allele of Trpm1 (Trpm1(-/-)) or a missense mutation in the pore domain of TRPM1 (Trpm1(tvrm27/tvrm27)). Hearing thresholds were evaluated in adult (4-5 months old) mice with auditory-evoked brain stem responses. Our data shows no statistically significant difference in hearing thresholds in Trpm1(-/-) or Trpm1(tvrm27/tvrm27) mutants compared to littermate controls. Further, none of the mutant mice showed any sign of balance disorder, such as head bobbing or circling. These data suggest that TRPM1 is not essential for development of hearing or balance and it is unlikely that TRPM1 is a component of the hair cell MET channel.