JAMA otolaryngology-- head & neck surgery最新文献

Importance: Noise exposure is a major modifiable risk factor for hearing loss, yet it is not known whether it affects the rate of hearing decline in aging.

Objective: To determine the association of noise exposure history with the rate of pure-tone threshold change per year.

Design, setting, and participants: This longitudinal cohort study was conducted in the ongoing community-based Medical University of South Carolina Longitudinal Cohort Study of Age-Related Hearing Loss (1988 to present with the sample based in Charleston, South Carolina, and surrounding area). Following a comprehensive baseline examination, participants attended annual examinations, during which audiometric data were collected. Participants with audiometric data from at least 2 examinations and noise exposure history data were included in the study. Data were analyzed between September 2023 and July 2024.

Exposure: Noise exposure history, determined by a self-reported questionnaire and history of military service, was categorized as no/little, some, or high exposure.

Main outcomes and measures: Outcome measures were individual audiometric thresholds (0.25 kHz to 8.0 kHz) and pure-tone average (PTA) of thresholds at frequencies 0.5 kHz, 1.0 kHz, 2.0 kHz, and 4.0 kHz, averaged bilaterally. Linear mixed regression models were used to estimate the association of age (per every 1 additional year) with the rate of threshold change at each frequency and PTA, for each noise exposure category. The association of noise exposure with the rate of annual threshold change was determined by an interaction term of age (longitudinal time variable) and noise exposure in regression models.

Results: Of 1347 participants, the mean (SD) baseline age was 63 (14) years, and 772 (57%) were female. The mean (SD) follow-up time was 5.1 (5.7) years. Compared to the no/little noise exposure group, groups with some and high noise exposure had significantly higher baseline thresholds from 2.0 kHz to 8.0 kHz and PTA, and 1.0 kHz to 8.0 kHz and PTA, respectively. Those with high noise exposure (vs no/little) showed higher rates of threshold change per year at 1.0 kHz and 2.0 kHz. Participants with some and high noise exposure showed lower rates of change per year at 3.0 kHz to 8.0 kHz and 4.0 kHz to 8.0 kHz, respectively, where hearing loss had already occurred. The rate of PTA change per year did not differ across noise exposure groups.

Conclusions and relevance: In this cohort study, noise exposure was associated with poorer baseline hearing and higher rates of annual decline at some midfrequencies. Noise exposure can have immediate and potentially long-term negative impacts on hearing.

Importance: The increasing use of glucagon-like peptide-1 receptor agonists (GLP-1RA) demands a better understanding of their association with thyroid cancer.

Objective: To estimate the risk of incident thyroid cancer among adults with type 2 diabetes being treated with GLP-1RA vs other common glucose-lowering medications.

Design, setting, and participants: This was a prespecified secondary analysis of a target trial emulation of a comparative effectiveness study using claims data for enrollees in commercial, Medicare Advantage, and Medicare fee-for-service plans across the US. Eligible participants were adults with type 2 diabetes at moderate risk for cardiovascular disease and without history of thyroid cancer who had newly filled prescriptions for GLP-1RA, sodium-glucose cotransporter 2 inhibitor (SGLT2i), dipeptidyl peptidase-4 inhibitor (DPP4i), or sulfonylurea from January 1, 2014, to December 31, 2021. Data were analyzed February 1 to October 31, 2024.

Main outcomes and measures: Overall and piecewise (<1, 1-2, and ≥2 years since treatment initiation) hazard ratios (HRs) for thyroid cancer with use of GLP-1RA vs the other 3 drug classes were estimated using inverse propensity score weighted Cox proportional hazards models. Modified intention-to-treat (mITT) (primary) and as-treated (sensitivity) analyses were performed.

Results: Of 351 913 patients (mean [SD] age, 65.3 [8.5] years; 173 391 [49.3%] females and 178 522 [50.7%] males), 41 112 started treatment with GLP-1RA; 76 093, with DPP4i; 43 499, with SGLT2i; and 191 209, with sulfonylurea therapy. The numbers of patients diagnosed with thyroid cancer were 69 (0.17%) in the GLP-1RA group, 172 (0.23%) in the DPP4i group, 72 (0.17%) in the SGLT2i group, and 381 (0.20%) in the sulfonylurea group. In the mITT analysis, GLP-1RA initiation was not significantly associated with increased overall risk for thyroid cancer compared to the other 3 diabetes drugs (HR, 1.24; 95% CI, 0.88-1.76). However, the risk for thyroid cancer was significantly higher within the first year after GLP-1RA initiation (HR, 1.85; 95% CI, 1.11-3.08) and was amplified in the overall as-treated analysis that censored patients when therapy was discontinued or another medication was added (HR, 2.07; 95% CI, 1.10-3.95).

Conclusions and relevance: This secondary analysis of a target trial emulation of a comparative effectiveness study found that despite the low absolute risk of thyroid cancer among patients receiving GLP-1RA therapy, there was an increased risk of new thyroid cancer diagnoses within the first year of GLP-1RA initiation compared to 3 other diabetes drugs. This finding may have been due to enhanced early detection; therefore, further research is necessary to understand the underlying causes of this association.

Importance: Facial synkinesis refers to pathologic cocontraction and baseline hypertonicity of muscles innervated by the facial nerve, commonly attributed to the aberrant regeneration of nerve fibers following injury. The pathomechanism and optimal treatment of facial synkinesis remain unclear. The goal of this review is to highlight current understanding of the epidemiology, pathophysiology, clinical presentation, assessment, and treatment of facial synkinesis.

Observations: Research into the epidemiology and risk factors of facial synkinesis is limited due to a lack of large databases tracking patients with facial palsy, inherent selection bias, and the wide range of symptom severity. Misguided nerve regeneration, polyneuronal innervation, and cortical changes are implicated in the development of synkinesis, and a better understanding of these mechanisms is required to develop new treatments. The clinical presentation of facial synkinesis varies considerably among patients, and important prognostic questions regarding timing of onset and progression of symptoms remain incompletely answered. Current management options for facial synkinesis include noninvasive modalities, chemodenervation, myectomy, and selective neurectomy. Potential new treatments for facial synkinesis are being investigated in animal models, but few have been tested in humans.

Conclusions and relevance: The treatment of facial synkinesis is currently hindered by limitations in clinical research and understanding of pathomechanism. Current studies predominantly yield level 4 evidence or lower. The development of large datasets of patients with facial palsy and the translation of basic science evidence to humans will facilitate the advancement of new treatments.