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Many epidemiologic and clinical studies have shown significant links between the degree of sleep disturbance and severity of impairment of selective cognitive functions, including the risk of neurodegenerative diseases. However, the sleep parameters that affect cognitive function in old age are unclear. Therefore, we investigated the association between sleep parameters and cognitive function in older patients. Patients aged above 65 years who complained of sleep-disordered breathing were enrolled consecutively. The Mini-Mental-State Examination tool was used to evaluate cognitive function. Eighty patients (normal cognitive function, n = 32 and cognitive impairment, n = 42) were included in this study. Multiple linear regression and binary logistic regression analyses were performed to explain the relationship between sleep parameters and cognitive function. We found that the body mass index (BMI) was significantly lower in the cognitive impairment group than in the normal cognitive function group. Additionally, the cognitive impairment group showed significantly decreased sleep efficiency and an increased apnea index compared with normal subjects. Moreover, lower BMI, reduced sleep efficiency, and high frequency of apnea events during sleep were associated with an increased risk of cognitive impairment.
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OBJECTIVES: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a more severe inflammatory form of CRS that often coexists with obstructive sleep apnea (OSA). However, little is known about the relationship between OSA and the immune profile in patients with CRSwNP. We aimed to investigate the immune profile of patients with CRSwNP according to OSA severity. METHODS: This study included 63 patients with CRSwNP and nine control subjects. Protein levels of inflammatory mediators were determined using multiplex immunoassays. All patients underwent standard polysomnography. RESULTS: In patients with eosinophilic CRSwNP (ECRSwNP), interleukin (IL)-6 and chemokine [C-X-C motif] ligand (CXCL)-1 (type 1 immune-related markers) were upregulated in cases of moderate-to-severe OSA. Additionally, IL-4, IL-13, C-C motif chemokine (CCL)-11, CCL-24 (type 2 immune-related markers), and IL-17A (a type 3 immune-related marker) were present at elevated levels in patients with moderate-to-severe OSA. Although there were no significant differences in type 1, 2, or 3 immune-related markers among patients with non-eosinophilic CRSwNP (NECRSwNP) according to the severity of OSA, transforming growth factor-beta expression was higher in those with moderate-to-severe OSA. Furthermore, in ECRSwNP with moderate-to-severe OSA, associations were detected between serum markers and some upregulated inflammatory markers. CONCLUSION: OSA may increase the heterogeneity of the immune profile (types 1, 2, and 3) in patients with ECRSwNP, but not in those with NECRSwNP.
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BACKGROUND: Mild hypothermia may be frequently induced due to cool environments in the operating room. The study analyzed patient recovery time and response to sugammadex after a prolonged rocuronium-induced deep neuromuscular block (NMB) during mild hypothermia. METHODS: Sixty patients were randomly (1:1) allocated to the mild hypothermia and normothermia groups, defined as having core temperatures between 34.5-35°C and 36.5-37°C, respectively. Patients received 0.6 mg/kg of rocuronium, followed by 7-10 µg/kg/min to maintain a deep NMB [post-tetanic count (PTC) 1-2]. After surgery, the deep NMB was reversed with sugammadex 4.0 mg/kg. The primary end-point was the time until the train-of-four (TOF) ratio was 0.9. RESULTS: The appropriate neuromuscular function (TOF ratio ≥ 0.9) was restored after sugammadex was administered, even after hypothermia. The length of recovery in the hypothermia patients [mean (SD), 171.1 (62.1) seconds (s)] was significantly slower compared with the normothermia patients [124.9 (59.2) s] (p = 0.005). There were no adverse effects from sugammadex. CONCLUSIONS: Sugammadex safely and securely reversed deep rocuronium-induced NMB during mild hypothermia. An additional 46 s was required for recovery from a deep NMB in hypothermia patients. Based on the results, we think this prolonged recovery time is clinically acceptable. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT01965067.
