et al. Improved sinonasal symptom and endoscopy sinus scores with dose-escalated intranasal mometasone irrigation in patients with refractory chronic rhinosinusitis. Int
Objectives: Laryngopharyngeal reflux (LPR) is an extraesophageal variant of gastroesophageal reflux disease associated with intermittent dysphonia, throat-clearing, and chronic cough. This study aims to evaluate the impact of race and insurance status on symptoms often attributable to LPR. Methods: Retrospective review of all patients with suspected LPR from 2017 to 2019 was performed at a tertiary care center. The diagnostic criteria comprised evaluation by a fellowship trained laryngologist and Reflux Symptom Index (RSI) scores. Demographics, patient history, and insurance status were recorded. Descriptive statistics were calculated for each parameter using SPSS version 22. Results: A total of 170 patients (96 White, 44 Black, 26 Latinx, 4 Asian) were included in this study. About 57.1% had private insurance, 30.6% had Medicare, and 11.8% had Medicaid. Black and Latinx patients demonstrated higher RSI scores (26.67 ± 8.61, P = .017) when compared to their White and Asian counterparts. RSI scores between all 3 insurance types also varied significantly ( P = .035). Medicaid patients reported higher RSI scores (28.65 ± 10.09, P = .028), while private insurance patients reported significantly lower scores (23.75 ± 7.88, P = .03). Controlling for insurance type eliminates the statistically significant association between RSI scores and Black and Latinx patients. Particularly, within the Medicaid group, Black, Latinx, and White patients did not have statistically different RSI scores. Conclusions: Black and Latinx patients presented with higher RSI scores than White and Asian patients. Similarly, Medicaid patients reported higher RSI scores than the Non-Medicaid cohort. These findings suggest that access to appropriate healthcare, due to varied insurance coverage and socioeconomic, may potentially influence symptoms attributed to LPR.
Recently, we described a phenomenon whereby apoptotic cells generate and release CrkI-containing microvesicles, which stimulate proliferation in surrounding cells upon contact to compensate for their own demise. We termed these microvesicles “ACPSVs” for Apoptotic Compensatory Proliferation Signaling microvesicles. As immune cells and a majority of current cancer therapeutics destroy tumor cells primarily by apoptosis, we conducted a small pilot study to assess the possibility that ACPSVs may also be generated in squamous cell carcinomas. We first evaluated a primary and a metastatic squamous cell carcinoma cancer cell lines for their ability to produce ACPSVs under normal and apoptotic conditions. We next conducted a pilot study to assess the occurrence of ACPSVs in solid tumors extracted from 20 cancer patients with squamous cell carcinomas. Both cancer cell lines produced copious amounts of ACPSVs under apoptotic conditions. Interestingly, the metastatic squamous cell carcinoma cancer cell line also produced high levels of ACPSVs under healthy condition, suggesting that the ability to generate ACPSVs may be hijacked by these cells. Importantly, ACPSVs were also abundant in the solid tumors of all squamous cell carcinoma cancer patients. Detection of ACPSVs in cancer has potentially important ramifications in tumor biology and cancer therapeutics which warrants further investigation.
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