Background: Patients and physicians are increasingly utilizing online video sharing sites such as YouTube for obtaining and disseminating health-related information in multimedia format; however, due to its free, open-access platform, YouTube videos fall short in providing validated, up-to-date medical information, and may even convey unintended messages to patients who are seeking additional information on surgeries. We evaluated the relevance, reliability, and quality of YouTube videos on novel surgical techniques in thyroid surgery. Methods:The top 50 indexed YouTube videos for the queries, "robotic thyroid surgery" and "transoral thyroid surgery", were assessed by two independent reviewers for video quality and reliability for patient understanding. Videos were scored using Global Quality Score (GQS), a scale for video quality, and DISCERN Scoring, a questionnaire for reliability and quality measures of information presented.Results: The mean ± standard deviation (SD) duration of the videos (n=50) was 8.1±3.7 minutes. Total views were 261,440 and the mean ± SD time since upload was 3.6±2.6 years. The median and interquartile range of video power index (VPI) was 1.9 (0.5-3.7), GQS was 3.0 (2.0-4.0), and DISCERN score was 2.8(2.3-3.2). Most videos were uploaded by physicians (75.8%) and the highest number of videos (63.6%) uploaded were from the United States (US). Videos with higher quality and reliability scores were uploaded by academic professionals, and included videos of physicians who described procedural information, perioperative instructions, and possible postoperative complications (P<0.05). Adequate medical information on the procedure and discussion of complications in YouTube videos were independent predictors of advanced educational quality and reliability.Conclusions: Clinical information on new surgical techniques such as transoral and robotic thyroid surgeries in YouTube videos scored low on quality and reliability as a source of patient education. Physicians should provide supplemental educational material online and offline to aid patient understanding of novel procedures.

Disruption of calcium homeostasis is common to all forms of hyperparathyroidism (HPT), but the underlying biochemical mechanisms that distinguish the various forms of HPT pathology remain poorly characterized. We previously have observed that the kinetics and amplitude of CASR-mediated signaling vary significantly among parathyroid (PT) adenomas and found specific functional and gene expression profiles preferentially associated with increased risk of bone density loss. While these data established a clear connection between CASR activity and clinical phenotype, a direct comparison of the kinetics of PTH secretory behavior between normal and neoplastic intact human PT tissue has yet to be performed. Utilizing eucalcemic normal human organ donor tissues (n=3) as a reference standard, we examined a series of cryopreserved live PT tissue specimens obtained from patients with primary (n=9), secondary (n=12) and tertiary (n=5) HPT. PT tissue fragments matched for viability, mass, and cellular content were placed on permeable membranes and exposed to a series of extracellular calcium concentrations over equivalent time intervals of challenge and normocalcemic recovery to interrogate dynamic PTH secretory induction or suppression. As expected, normal tissue exhibited a sigmoid response curve indicative of allosteric calcium-mediated inhibition, with a mean EC50 of 0.95 mM (95% CI: 0.859–1.254). In contrast, the majority of primary HPT adenomas (n=6) displayed a concave response curve indicative of non-competitive inhibition, consistent with a primary sensing deficit, such as loss of CASR expression. Two distinct PTH secretory behaviors were observed in secondary HPT specimens. One subset (secondary type 1, n=4) retained a sigmoid response curve but with a modest EC50 increase (mean EC50=1.50 mM, 95% CI: 1.41–1.61) and maximal suppression similar to normal tissue, features reflective of competitive inhibition in response to elevated calcium. This pattern could indicate enhanced CASR antagonist activity relative to normal tissue. A second subset, (secondary type 2, n=8) demonstrated a large EC50 shift (mean EC50=2.46 mM; 95% CI: 1.844–2.621), a sigmoid response curve, and an elevated threshold of persistent PTH secretion at high calcium conditions. These parameters are suggestive of non-competitive inhibitory behavior, consistent with loss of a CASR-dependent downstream effector. Three of the primary HPT adenomas shared this response phenotype. Of the tertiary specimens, four matched the primary HPT adenoma pattern, while one exhibited secondary type 2 behavior. These results reveal a series of progressively attenuated dynamic response patterns, where PTH secretion becomes increasingly uncoupled from extracellular calcium sensing. These findings suggest that primary, secondary, and tertiary HPT arise through distinct mechanisms of calcium sensing failure.