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1.
Healthcare (Basel) ; 11(2)2023 Jan 12.
Article in English | MEDLINE | ID: mdl-36673608

ABSTRACT

Sugammadex has several pharmacological advantages over neostigmine, including faster reversal of neuromuscular blockade and fewer adverse effects. However, the economic impact of sugammadex remains controversial due to the considerable heterogeneity of study designs and clinical settings in previous studies. In a post-hoc analysis of a randomized controlled trial, we evaluated patients who underwent elective surgeries and general anesthesia with endotracheal intubation in a medical center in Taiwan between March 2020 and August 2020. Patients were divided into either the sugammadex or neostigmine group based on the neuromuscular blocking drug used. Propensity score matching was used to balance the baseline patient characteristics between the two groups. The patient's recovery from anesthesia and the putative cost-effectiveness of sugammadex versus neostigmine was assessed. Derived cost-effectiveness using personnel costs in the operating room and the post-anesthesia care unit was estimated using multiple linear regression models. A total of 2587 and 1784 patients were included before and after matching, respectively. Time to endotracheal extubation was significantly shorter in the sugammadex group (mean 6.0 ± standard deviation 5.3 min) compared with the neostigmine group (6.6 ± 6.3 min; p = 0.0032). In addition, the incidence of bradycardia was significantly lower in the sugammadex group (10.2%) compared with the neostigmine group (16.9%; p < 0.001). However, the total costs were significantly lower in the neostigmine group (50.6 ± 21.4 United States dollars) compared with the sugammadex group (212.0 ± 49.5 United States dollars). Despite improving postoperative recovery, the benefits of sugammadex did not outweigh its higher costs compared with neostigmine, possibly due to the low costs of labor in Taiwan's healthcare system.

2.
Atherosclerosis ; 265: 87-92, 2017 Oct.
Article in English | MEDLINE | ID: mdl-28865327

ABSTRACT

BACKGROUND & AIMS: The relationship between stroke and diabetes is not completely understood. This study evaluated diabetes risk and post-diabetes adverse events in patients with stroke. METHODS: We identified 10,255 adults, newly diagnosed with stroke from 2000 to 2005, using the Taiwan's National Health Insurance Research Database. A comparison cohort of 41,020 adults without stroke was randomly selected from the same dataset, frequency matched by age and sex. Diabetes events from 2000 to 2013 were ascertained from medical claims. Adjusted hazard ratios (HRs) and 95% CIs were calculated for diabetes associated with stroke. A nested cohort study of 33,437 patients with inpatient care for diabetes between 2008 and 2013 was conducted to calculate the adjusted odds ratios (ORs) and 95% CIs for adverse events after diabetes, in patients with and without stroke. RESULTS: During 489,561 person-years of follow-up, there were 10,742 newly diagnosed diabetes cases. The incidence of diabetes for people with and without stroke was 43.9 and 17.8 per 1000 person-years, respectively (p < 0.0001). Compared to that for people without stroke, the adjusted HR for diabetes was 2.69 (95% CI 2.56-2.82) for stroke patients. The ORs of post-diabetes pneumonia, urinary tract infection, and mortality associated with stroke were 1.35 (95% CI 1.17-1.55), 1.52 (95% CI 1.36-1.70), and 1.71 (95% CI 1.27-2.29), respectively. CONCLUSIONS: We provide evidence that the consequences of stroke are not limited to the neurological defect, but evoke diabetes and a plethora of associated medical, psychological and social impacts the physician must be strongly aware of if evaluating and treating stroke patients.


Subject(s)
Diabetes Mellitus/epidemiology , Socioeconomic Factors , Stroke/epidemiology , Administrative Claims, Healthcare , Adult , Aged , Aged, 80 and over , Case-Control Studies , Chi-Square Distribution , Comorbidity , Databases, Factual , Diabetes Mellitus/mortality , Diabetes Mellitus/psychology , Diabetes Mellitus/therapy , Female , Humans , Incidence , Income , Male , Middle Aged , Multivariate Analysis , Odds Ratio , Pneumonia/epidemiology , Prognosis , Proportional Hazards Models , Risk Factors , Stroke/mortality , Stroke/psychology , Stroke/therapy , Taiwan/epidemiology , Time Factors , Urbanization , Urinary Tract Infections/epidemiology , Young Adult
3.
Acta Anaesthesiol Taiwan ; 50(4): 159-66, 2012 Dec.
Article in English | MEDLINE | ID: mdl-23385038

ABSTRACT

OBJECTIVES: Both overproduction of nitric oxide and oxidative injury to the cardiovascular and pulmonary systems contribute to fatal pathophysiology during endotoxemia. We investigated the effect of propofol on oxidative stress-related enzymes in lung (L2), heart (H9C2) and macrophage (NR8383) cells during endotoxemia. METHODS: Experimental endotoxemia was induced by co-culture of Escherichia coli lipopolysaccharide (15 µg/mL) in the abovementioned three types of cells that were under the effect of propofol (15 or 30 µM for 1 or 4 hours). Cellular expression of induced nitric oxide synthase (iNOS), superoxide dismutase (SOD) 1 and 2, and p47phox (representing NADPH oxidase) were determined by immunoblotting. The cellular oxidative burst activity was determined using a dihydroethidium method via flow cytometry to represent the level of reactive oxygen species. The in vivo endotoxemia model was also employed for comparison using a systemic injection of lipopolysaccharide (15 mg/kg) under propofol maintenance (15 or 30 mg/kg/h). The Student t test (two groups) was used for statistical evaluation among the means, and the Newman-Keuls test was used for analysis of variance in the statistical analysis. RESULTS: In lung L2 cells, propofol significantly reduced the expression of iNOS, SOD1, SOD2, and p47phox under LPS-induced endotoxemia. However, in H9C2 cardiac cells and NR8383 macrophages, only the expression of iNOS was significantly suppressed, but not that of SOD1, SOD2, or p47phox. The level of reactive oxygen species was suppressed in all three kinds of cell. In in vivo animal tissue, except for the suppression of iNOS expression in lung and heart cells, propofol in lung cells produced only SOD1 suppression, but in rat heart the expression of both SOD1 and SOD2 was suppressed. CONCLUSION: These results suggest that propofol may have a protective role for lung cells. This effect is associated with its suppression of oxidative-related enzymes, including iNOS, SOD1, SOD2, and p47phox. In cardiac myocytes and macrophages, propofol also provides an antioxidative effect, probably via its inhibition of iNOS. The overall effect of propofol in the organs may be a combination of its effects on various cells. In addition, a reduction in reactive oxygen species plays a major role in the beneficial effect of propofol on experimental endotoxemia.


Subject(s)
Endotoxemia/drug therapy , Oxidative Stress/drug effects , Propofol/pharmacology , Animals , Endotoxemia/metabolism , Lung/cytology , Lung/drug effects , Lung/metabolism , Macrophages/drug effects , Macrophages/metabolism , Male , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/metabolism , NADPH Oxidases/analysis , Nitric Oxide Synthase Type II/analysis , Propofol/therapeutic use , Rats , Rats, Sprague-Dawley , Reactive Oxygen Species/metabolism , Superoxide Dismutase/metabolism
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