Background
Nasopharyngoscopy is a common method to evaluate velopharyngeal closure in patients with cleft palate. However, insertion of a fiberoptic nasopharyngoscope causes discomfort in patients. The aim of this study was to estimate the reliability of short-time exposure images obtained using 320-row area detector computed tomography (320-ADCT) as a novel evaluation method for the assessment of velopharyngeal function.
Methods
We evaluated five healthy adult volunteers and five postoperative adult patients with cleft palate. During a 3.3-s imaging exposure, the participants were asked to perform two tasks: nasal inspiration and subsequent oral expiration through a catheter into a water-filled cup. The movement of the velopharyngeal structures was recorded during each examination, and the presence of velopharyngeal insufficiency (VPI) and velopharyngeal closure (VPC) patterns were estimated. If VPI was detected, the cross-sectional area was also calculated. Cohen’s kappa and weighted kappa coefficients were used to evaluate the concordance of nasopharyngoscopy and 320-ADCT evaluation.
Results
Speech pathology evaluation did not reveal hypernasality in any study participant. Micro-VPI was detected by nasopharyngoscopy in one healthy volunteer and two patients. 320-ADCT detected micro-VPI in two more patients. The cross-sectional area of the VPI in these subjects ranged from 2.53 to 16.28 mm
2
. Nasopharyngoscopy and 320-ADCT were concordant in detecting VPI in eight participants (κ = 0.6) and in assessing VPC patterns in nine (κ = 0.82). Moreover, images obtained using 320-ADCT allowed for reduced dead angle and, thus, easy detection of micro-VPI and Passavant’s ridges.
Conclusion
Although the radiation exposure cannot be ignored, our novel evaluation method using 320-ADCT enables more detailed evaluation of VPC than nasopharyngoscopy. Future studies should investigate the relationship between 320-ADCT findings and speech pathology evaluations.
Electronic supplementary material
The online version of this article (10.1186/s12880-019-0350-4) contains supplementary material, which is available to authorized users.
This experiment was carried out to investigate the inhibitory effects of glycyrrhizin and its aglycon, glycyrrhetinic acid, on the metabolism of cortisol and prednisolone in vivo and in vitro. The effects of glycyrrhetinic acid on the metabolism of cortisol were examined in vitro using rat and bovine liver homogenate. Glycyrrhetinic acid inhibits both hepatic delta 4-5-reductase and 11 beta-hydroxysteroid dehydrogenase in a dose-dependent manner, resulting in the decrease of conversion of cortisol to cortisone, dihydrocortisol and tetrahydrocortisol in rats. The concentrations of glycyrrhetinic acid inducing 50% inhibition of rat liver delta 4-5-reductase and 11 beta-hydroxysteroid dehydrogenase were 2.5 x 10(-6) M and 8.5 x 10(-6) M, respectively. Glycyrrhetinic acid also inhibits bovine liver 11 beta-hydroxysteroid dehydrogenase and 20-hydroxysteroid dehydrogenase in a dose-dependent manner, resulting in the decrease of conversion of cortisol to dihydrocortisol and prednisolone to 20-dihydroprednisolone. The concentrations of this drug inducing 50% inhibition of 11 beta-hydroxysteroid dehydrogenase and 20-hydroxysteroid dehydrogenase were 8.2 x 10(-6) M and 6.5 x 10(-6) M, respectively. This is the first report which demonstrates the marked inhibitory effects of glycyrrhetinic acid on 11 beta-hydroxysteroid dehydrogenase and 20-hydroxysteroid dehydrogenase in vitro. The effects of glycyrrhizin on the rate of metabolism of cortisol as well as prednisolone were studied in 23 patients with or without adrenal insufficiency. Glycyrrhizin had no effect on diurnal rhythm of plasma cortisol in 7 control subjects with normal pituitary adrenal axis, whereas glycyrrhizin significantly increased the half-time (T 1/2) and area under the curve (AUC) for plasma cortisol in 4 patients with adrenocortical insufficiency taking oral cortisol. Glycyrrhizin also increased T 1/2 and AUC for plasma prednisolone in 12 patients taking an oral prednisolone for at least 3 months. These results indicate that the suppression of hepatic delta 4-5-reductase, 11 beta-hydroxysteroid dehydrogenase and 20-hydroxysteroid dehydrogenase by glycyrrhizin and glycyrrhetinic acid may delay the clearance of cortisol and prednisolone and prolong the biological half-life of cortisol or prednisolone.
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