Clinical aspects and diagnostic relevance of neuroautonomic evaluation in patients with unexplained falls.

OBJECTIVE: To evaluate the diagnostic relevance of neuroautonomic evaluation in patients with unexplained falls compared to those with a syncope etiologically unexplained after initial evaluation. METHODS: It is an observational study, comparing 298 patients with unexplained fall with 989 patients with unexplained syncope. Each patient underwent supine and upright blood pressure measurement, tilt testing (TT) and carotid sinus massage (CSM). RESULTS: Patients with unexplained falls were older (75.3 ± 11.1 vs. 63.2 ± 19.2 years, p < 0.001), were more frequently hypertensive (66.1 vs. 47.2 %, p < 0.001) and more frequently prescribed antihypertensive drugs (62.4 vs. 48.7 %, p < 0.001) or benzodiazepines (15.7 vs. 10.6 %, p = 0.01), and in a greater proportion they experienced major traumatic injuries (77.5 vs. 29.6 %, p < 0.001) as a consequence of falls. The TT was less frequently positive in patients with unexplained falls (36 vs. 51.3 %, p < 0.001), whereas a Carotid Sinus Syndrome as suggested by CSM had a similar prevalence in the two groups (14.3 vs. 10.5 %, p = 0.074). Overall, either TT or CSM were positive in 61 % of patients with unexplained falls, and in 64 % of those with syncope (p = 0.346). After matching by age 298 patients with falls (75.3 ± 11.1 years) and 298 patients with unexplained syncope (75.4 ± 11.1 years), we found that the positivity prevalence of TT and CSM were similar in the two groups. CONCLUSIONS: The positivity prevalence of TT and CSM in patients with unexplained falls compared to patients with unexplained syncope is similar. Given its high diagnostic relevance, the neuroautonomic evaluation should be routinely performed in older patients with unexplained falls.

Group versus individual cognitive-behavioral treatment for obesity: results after 36 months.

OBJECTIVE: This study is aimed at the comparison between an individual and a group cognitive-behavioral program for the treatment of obesity. DESIGN: Parallel series, prospective, 3-year study. A group program of 10 weekly sessions focused on lifestyle modification was compared with a similar, individual 10-session program. Fifty-seven patients were assigned to individual treatment, and 84 patients to the group program. SUBJECTS: One hundred- forty-one obese female outpatients without binge eating disorder, aged 42.0+/-11.6 years (m+/-SD), with Body Mass Index (BMI) 37.3+/-5.2 kg/m(2). MEASUREMENTS: BMI and waist circumference were measured at 0, 6, 12 and 36 months. Analysis was performed on an intention-to-treat basis. RESULTS: Mean weight loss was superior with the group program at 6 months (2.0+/-3.9 vs 0.8+/-2.5 kg/m(2); p<0.05), while no difference between the two treatments was observed at 12 and 36 months. Mean waist circumference was significantly different at 6 months (group 97.4+/-2.5 vs individual 102.9+/-2.4, p<0.05), still remaining superior in the patients following individual treatment (100.2+/-5.0 vs 103.7+/-5.9) at 12 months, while no difference between the two treatments was observed at 36 months. The proportion of patients losing more than 5% of initial body weight with the group program (16.6, 15.5, and 38.1% at 6, 12, and 36 months, respectively) was not significantly different from that observed with individual treatment (5.3, 14.0, and 35.0%, respectively). CONCLUSION: A group cognitive-behavioral program for the treatment of obesity is not inferior to a similar program applied in individual setting, and it may enhance weight loss (especially fat mass, according to the waist measurement) in the short term.

Long term predictors of post-partum glucose metabolism in women with gestational diabetes mellitus.

AIMS: The question asked by this study was whether ß-cell function expressed by insulin secretion/sensitivity measured during pregnancy in women with gestational diabetes (GDM) predicts post-partum long-term derangement in glucose metabolism. METHODS: Seventy-four Caucasian women with previous GDM were retested through a 75 g-2-h-OGTT after 8 [6] years (median[interquartile range]) from index pregnancy, measuring at pregnancy and follow-up insulin sensitivity, insulin secretion (1-h-incremental-insulin-area/incremental-glucose-area: ΔAUC60 (I)/ΔAUC60 (G)) as well as the product of Stumvoll-first-phase - secretion x insulin sensitivity (insulin-secretion-sensitivity index (ISSI). RESULTS: At follow-up 47 women were normotelerant to glucose and 27 had altered glucose metabolism (AGM:10 with type 2 diabetes and 17 with IGT). Women progressed to AGM had at their index pregnancy higher mean 2-h-OGTT-glucose area (1.15±0.09 VS. 1.09±0.09 mol l 2-h (-1);p=0.014), and lower ΔAUC60 (I)/ΔAUC60 (median [interquantile range]) (54.4 [51.7] vs. 73.4 [60] pmol mmol (-1)) and ISSI (2 977 [766] vs. 3 708 [1 141]; p<0.05 for both), but similar insulin sensitivity index 2.9 [2.5] VS. 3.2 [2.2] ml min (-1) m (-2);p=NS). Two-h-OGTT-glucose area, or decrease in ΔAUC60 (I)/ΔAUC60 (G) and ISSI were significantly associated with glucose tolerance impairment and with raised adjusted risk for AGM while insulin sensitivity at pregnancy did no predict AGM development. CONCLUSIONS: In this group of women increased post-load plasma glucose and impaired ß-cell function assessed during GDM pregnancy predict long-term post-partum AGM, while insulin sensitivity measured at the same time does not.

Influence of gestational diabetes on the long-term control of glucose tolerance.

AIMS/HYPOTHESIS: Gestational diabetes (GDM) carries a high risk of subsequent diabetes. We asked what impact prior GDM has on beta cell function and insulin action in women who maintain normal glucose tolerance (NGT) for a long time. METHODS: Ninety-one women with NGT (aged 41 +/- 8 years, mean+/-SD) were studied (by mathematical modelling of the C-peptide response to an OGTT) 7 [6] years (median [interquartile range]) after the index pregnancy, during which 52 had GDM (pGDM) and 39 had NGT (pNGT). In all women an OGTT had also been performed at 29 +/- 3 weeks of the index pregnancy. RESULTS: Women with pGDM were matched with women with pNGT for age, familial diabetes, time and weight gain since index pregnancy, parity, BMI (25.4 +/- 3.9 vs 26.8 +/- 6.4 kg/m(2)), and fasting (4.64 +/- 0.56 vs 4.97 +/- 0.46 mmol/l) and 2 h plasma glucose levels (5.91 +/- 1.14 vs 5.91 +/- 1.21 mmol/l). Nonetheless, fasting (49 [29] vs 70 [45] pmol min(-1) m(-2), p < 0.001) and total insulin secretion (32 [17] vs 48 [21] nmol m(-2), p < 0.0001) and beta cell glucose sensitivity (slope of the insulin secretion/plasma glucose concentration-response function) (95 [71] vs 115 [79] pmol min(-1) m(-2) (mmol/l)(-1), p = 0.025) were reduced in the pGDM group compared with the pNGT group, while insulin sensitivity was preserved (424 [98] vs 398 [77] ml min(-1) m(-2)). At index pregnancy, women with pGDM and those with pNGT had similar age and BMI. However, both insulin sensitivity (359 [93] vs 417 [92] ml min(-1) m(-2), p = 0.0012) and the insulin/glucose incremental area ratio (an empirical index of beta cell function; 98 [74] vs 138 [122] pmol/mmol, p = 0.028) were reduced in women with pGDM. CONCLUSIONS: Even in women who maintain normal insulin sensitivity, impaired beta cell function is carried over into the NGT status several years after a GDM pregnancy.

Effects of metformin on glucagon-like peptide-1 levels in obese patients with and without Type 2 diabetes.

Metformin has been shown to increase glucagon-like peptide-1 (GLP-1) levels after an oral glucose load in obese non-diabetic subjects. In order to verify if this effect of the drug was also present in obese Type 2 diabetic patients who have never been treated with hypoglycemic drugs, 22 Type 2 diabetic and 12 matched non-diabetic obese patients were studied. GLP-1 was measured before and after a 100 g glucose load at baseline, after a single oral dose of 850 mg of metformin, and after 4 weeks of treatment with metformin 850 mg three times daily. Post-load GLP-1 levels were significantly lower in diabetic patients. A single dose of metformin did not modify GLP-1 levels. After 4 weeks of treatment, fasting GLP-1 increased in diabetic patients (3.8 vs 4.9 pmol/l; p<0.05), while the incremental area under the curve of GLP-1 significantly increased in both diabetic [93.6 (45.6-163.2) vs 151.2 (36.0-300.5) pmol x min/l; p<0.05] and non-diabetic [187.2 (149.4-571.8) vs 324.0 (238.2-744.0) pmol x min/l; p<0.05] subjects. In conclusion, GLP-1 levels after an oral glucose load in obese type 2 diabetic patients were increased by 4 weeks of metformin treatment in a similar fashion as in obese subjects with normal glucose tolerance.

Eating behavior in obese patients with and without type 2 diabetes mellitus.

OBJECTIVE: Aim of this study was the assessment of the prevalence of eating disorders, and of eating disorder symptoms, in obese patients with type 2 diabetes, compared to non-diabetic subjects. DESIGN: Three samples of individuals were studied: a series of 156 (76 male, 80 female) overweight and obese type 2 diabetic patients, aged 30-65 y, with a body mass index (BMI)>28 kg/m(2) (DM); a series of 192 (20 male, 172 female) obese (BMI>30 kg/m(2)) non-diabetic patients aged 30-65 y seeking treatment for weight loss (OC); and a non-clinical sample of 48 (22 male, 26 female) obese (BMI>30 kg/m(2)) subjects aged 30-65 y selected from the lists of two general practices (OP). Eating behavior was assessed using the Eating Disorder Examination (EDE 12.0D). RESULTS: The prevalence of Binge Eating Disorder was lower than 5% in all the three samples. Median EDE scores in females were significantly higher in OC (3.0) and OP (3.4) than in DM (1.7), while diabetic patients showed higher scores on Restraint than both non-diabetic samples. Among diabetic patients, a significant correlation of EDE scores with HbA(1)c was observed. CONCLUSIONS: Type 2 diabetes is unlikely to induce relevant eating disturbances in obese patients, apart from an increase in restraint. Abnormalities of eating attitudes and behavior are associated with an impairment of metabolic control.