Background: Obstructive sleep apnea (OSA) is a significant cardiovascular risk factor, frequently co-existing with systemic hypertension. While the association between OSA and blood pressure elevation is well documented, its specific prevalence and impact among patients with resistant hypertension remain a critical area of clinical investigation. Objective: The primary aim of this study was to evaluate the prevalence and severity of obstructive sleep apnea (OSA) specifically within a cohort of patients with resistant hypertension (RHT). Additionally, we sought to identify the clinical and anthropometric factors that distinguish RHT patients with OSA from non-resistant hypertensive and normotensive controls, thereby clarifying the increased hypoxic burden and polysomnographic differences unique to this high-risk population. Methods: A total of 300 patients presenting with OSA symptoms were included. Participants were classified into three groups: Group 0 (n = 100), normotensive individuals; Group 1 (n = 100), non-resistant hypertension; and Group 2 (n = 100), confirmed resistant hypertension. Standard overnight polysomnography (PSG) was performed on all participants. Demographic data, comorbidities, anthropometric measurements, and PSG parameters were recorded and compared across groups. Results: Of the subjects, 50.3% were female (sex), and the mean age was 49.5 ± 12.3 years. Patients with RHT (Group 2) were significantly older and had a higher prevalence of diabetes mellitus. OSA prevalence was 94% in Group 2 (37% severe), 89% in Group 1 (22% severe), and 74% in Group 0 (only 2% severe). In PSG analysis, AHI and ODI values were significantly higher in hypertensive groups (Groups 1 and 2) compared to normotensive individuals (Group 0), while minimum and mean oxygen saturations were significantly lower. Conclusions: OSA is both more prevalent and more severe in patients with resistant hypertension. Furthermore, hypertensive OSA patients are characterized by an increased hypoxic load compared to normotensives. Systematic investigation and detailed polysomnographic evaluation of OSA are of paramount importance in hypertensive individuals, particularly those with resistant hypertension.

Background and Objective: Non-alcoholic fatty liver disease (NAFLD) induces systemic low-grade inflammation and lipotoxicity. While its microvascular effects on the inner ear are recognized, its impact on the middle ear remains unexplored. This study aimed to investigate subclinical biomechanical alterations in the middle ear of normal-hearing NAFLD patients using Wideband Tympanometry (WBT). Materials and Methods: This prospective observational study included 28 patients with ultrasonographically confirmed NAFLD and 30 healthy, sex-matched controls. All included participants had normal pure-tone hearing thresholds and Type A tympanograms. WBT was performed to measure Resonance Frequency (RF) and frequency-specific absorbance (226–8000 Hz). A subgroup analysis compared early-stage (Grade 1) and advanced-stage (Grades 2–3) hepatosteatosis. Results: The mean RF was significantly lower in the NAFLD group compared to the controls for both the right (781.6 ± 218.7 vs. 1010.6 ± 529.0 Hz; p = 0.035) and left ears (740.3 ± 212.7 vs. 1221.6 ± 754.2 Hz; p = 0.002). Furthermore, wideband absorbance was significantly elevated at lower frequencies (250 Hz and 500 Hz) in the study group (p < 0.001 for both ears). Middle ear resting pressures were similar between the groups. Subgroup analysis revealed no significant differences in WBT parameters between Grade 1 and advanced stages (p > 0.05). Conclusions: Normal-hearing NAFLD patients exhibit a mass-dominated biomechanical shift in the middle ear, characterized by a decreased RF and increased low-frequency absorbance. These subclinical alterations, observable even in early-stage hepatosteatosis, likely reflect mucosal micro-edema driven by systemic inflammation. WBT serves as a sensitive, non-invasive tool for detecting early metabolic-related otologic changes.

Aim: Obstructive sleep apnea (OSA) causes intermittent hypoxemia and sleep fragmentation, both of which may affect bone metabolism, yet studies of OSA and bone mineral density (BMD) have produced inconsistent results. We examined whether OSA status and conventional polysomnographic indices of OSA severity and nocturnal oxygenation were associated with lumbar spine and total hip T-scores in postmenopausal women. Methods: We conducted a retrospective cross-sectional study of 101 postmenopausal women with polysomnography (PSG) and dual-energy X-ray absorptiometry (DXA) records; 40 had PSG-confirmed OSA and 61 were controls. Lumbar spine and total hip T-scores were the primary outcomes. The OSA and control groups were compared with linear regression adjusted for age and body mass index (BMI). Four conventional indices (apnea–hypopnea index [AHI], oxygen desaturation index [ODI], mean SpO₂, and minimum SpO₂) were each examined in a separate model adjusted for age and BMI. Extended models, which added calcium, phosphate, alkaline phosphatase [ALP], vitamin D, and parathyroid hormone [PTH] and entered all four indices together, were treated as sensitivity analyses and were calculated. Results: Women with OSA were older than controls (63.9 ± 7.8 vs. 60.1 ± 7.2 years) and had a higher BMI (36.0 ± 7.0 vs. 30.6 ± 4.9 kg/m²). The unadjusted T-score differences were 0.28 (95% CI −0.30 to 0.86) at the lumbar spine and 0.11 (95% CI −0.34 to 0.56) at the total hip; neither was statistically significant. None of the indices were statistically significant in the extended models. The lumbar extended model was significant overall (p = 0.023), whereas the total hip model was not (p = 0.117). Conclusions: We found no statistically significant associations between the conventional indices and lumbar spine or total hip T-scores. The findings should be interpreted cautiously because of the modest sample size, possible overfitting and collinearity in the extended models, and the lack of data on cumulative hypoxic burden. They do not show that OSA has no effect on bone health. Because fractures were not assessed, these data cannot inform screening or fracture-risk decisions.