Normative Values and Interrelationship of MDVP Voice Analysis Parameters Before and After Endotracheal Intubation.

PURPOSE: The Multi-Dimensional Voice Program (MDVP) is used for assessment of voice quality. A simple procedure for MDVP recordings was used in a randomized clinical trial (RCT) on induced vocal fold trauma due to intubation. This secondary study compares the common MDVP parameters with other normative values for adults and investigates the correlation between these MDVP parameters in relation to the "standardized" trauma of endotracheal intubation. METHODS: Preoperative and postoperative assessments of vocal fold pathology with flexible videolaryngoscopy and voice analysis with MDVP using the best-of-three standardized recording were performed in 121 patients with normal voices included consecutively in the RCT. The procedures of anesthesia were standardized. RESULTS: The normative MDVP values of this study are consistently lower compared with most normative values presented in other studies. The preoperative to postoperative differences in jitter values (jitter and relative average perturbation) were closely correlated to the shimmer values for patients with postoperative vocal fold edemas. In the patients with edema, the preoperative to postoperative differences in jitter had a correlation coefficient of 0.95 (P < 0.0001) to the difference in shimmer, compared with a correlation coefficient of 0.39 (P < 0.0001) in the patients without edema. CONCLUSIONS: This study supports the use of the "Best-of-Three" procedures for precise and relevant MDVP parameter calculations. The MDVP parameters, with closely correlated changes in jitter and shimmer values, accurately reflect the induced vocal fold edema when using the preoperative to postoperative changes.

Endogenous incretin hormone augmentation of acute insulin secretion in normoglycemic relatives of type 2 diabetic subjects: a 10-year retrospective pathophysiological study.

AIMS/HYPOTHESIS: The pathophysiological role of gut incretin hormone argumentation on acute insulin release in the genesis of type 2 diabetes (TDM2) is uncertain. We examined retrospectively at 0 year and 10 years the endogenous incretin hormone action (IHA) on acute insulin release and glucose tolerance in normoglycemic relatives (REL) of TDM2 and control (CON) subjects. METHODS: At 0 year and 10 years, glucose tolerance, paired oral glucose tolerance test (OGTT)- and i.v. glucose tolerance test (IVGTT)-induced acute (0-30 min) insulin release (insulinogenic index IGIOGTT and IGIIVGTT), and IHA were calculated in 19 REL and 18 CON subjects by cross-correlation linear regression slope analyses of the OGTT (0-30 min) matched insulin/glucose profiles vs the early (0-5 min) and delayed (10-30 min) IVGTT profiles. RESULTS: At 0 year, REL and CON IGIOGTT and IGIIVGTT were similar, but the REL 2- to 5-min IVGTT-induced insulin responses were reduced (P < .03). By 10 years, glucose tolerance deteriorated in nine dysglycemic REL (RELDGT), with raised fasting glucose and 2-hour OGTT glucose. Retrospective analyses of RELDGT at 0 year demonstrated raised proinsulin/insulin molar ratios and fasting glucose and a reduced IVGTT insulin/glucose slope, but the RELDGT IHA was similar to normoglycemic REL (RELNGT) and CON. By 10 years, RELDGT OGTT insulin/glucose slopes were reduced (P = .03-.01), but more so for the early (P < .01-.003) and delayed (P < .005-.002) IVGTT slopes, compared to the normoglycaemic REL and CON subjects. CONCLUSIONS: IHA on acute insulin release is maintained in normoglycemic REL and CON subjects over 10 years. The apparent deterioration in IHA in RELDGT is consistent with a progressive failure of acute ß-cell function over 10 years.

The metabolic responses induced by acute dexamethasone predict glucose tolerance and insulin secretion over 10 years in relatives of type 2 diabetic subjects.

BACKGROUND: This study aimed to compare the metabolic and insulin secretory responses to dexamethasone with the metabolic responses observed at 10 years in normoglycaemic relatives of type 2 diabetic and healthy control subjects. METHODS: Twenty relatives and 20 matched control subjects were studied twice at 0 year (pre- and post-dexamethasone) and at 10 years, employing a 75-g oral glucose tolerance test (OGTT), with serial measurements of glucose and insulin, for determination of glucose tolerance and calculations of acute insulin release (ΔI30 /ΔG30 ; insulinogenic index) and insulin sensitivity (SIHOMA ). RESULTS: Following dexamethasone, the relatives group developed varying degrees of glucose intolerance, associated with reduced insulin sensitivity and insulinogenic index. By 10 years, fasting glucose and 2-h OGTT glucose were raised in the relatives group, especially in the relatives most metabolically affected by dexamethasone, including a reduced insulinogenic index. Multiple regression analysis of the data in relatives demonstrated that the 2-h OGTT glucose and fasting glucose values at 10 years depended on the 0-year post-dexamethasone 2-h OGTT glucose, post-dexamethasone fasting glucose and post-dexamethasone insulin sensitivity, r(2) adj = 56% (p < 0.001) and r(2) adj = 60% (p < 0.0001), respectively. No pre-dexamethasone metabolic or insulin secretory responses entered these models. CONCLUSIONS: In relatives, fasting and 2-h OGTT glucose concentrations and ß-cell responses to acute dexamethasone-induced insulin resistance are similar to those observed at 10 years, especially in relatives who develop the most disturbed dexamethasone-induced glucose intolerance and impaired acute insulin secretion. The combined 0-year, post-dexamethasone fasting and 2-h OGTT glucose concentrations and insulin resistance, measured as SIHOMA , are the best predictors in relatives of future dysglycaemia.