[Atherogenic dyslipidemia, metabolic syndrome and cardiovascular risk]. / Dislipidemia aterogena, sindrome metabolica e rischio cardiovascolare.

The combination of high serum triglyceride levels and small low density lipoprotein particles, with a reduction in high density lipoprotein cholesterol levels has been named atherogenic lipoprotein phenotype or, simply, lipid triad. These lipid factors are commonly associated with peripheral resistance to the action of insulin, hyperinsulinism, central and visceral obesity, hypertension, hyperuricemia, hypercoagulability. The clustering of these nonlipid factors along with the lipid factors has been called metabolic syndrome. Insulin resistance plays a central role in the development of the lipid triad increasing the production of triglyceride-rich lipoproteins and decreasing their catabolism. There is currently great interest about the origins of the metabolic syndrome. One question under considerable research is whether genetic or acquired factors predominate in causing this syndrome. There seems to be little doubt that the metabolic syndrome taken as a whole constitutes a major risk factor for coronary heart disease. What is less certain is that each component of the syndrome is an independent risk factor. People with lipid triad are at very high risk of developing coronary heart disease, and careful management is warranted. Nonetheless, appropriate therapeutic strategies that will modify the metabolic syndrome as a whole are needed. More investigations about key metabolic steps that simultaneously affect multiple pathways will be required to yield a satisfactory therapy for high risk patients exhibiting the metabolic syndrome.

Diabetologic in-service education for health professionals from non-diabetological departments.

In order to test whether or not an in-service requalification course on diabetes care for health professionals (HP) of nondiabetological departments can enhance their level of knowledge about diabetes and the quality of care for diabetic inpatients admitted for reasons other than diabetes, we carried out a requalification course involving 171 HP (161 nurses and 10 midwives) from nondiabetological departments of our hospital. Areas of intervention were: general knowledge of diabetes (GKD), bedside monitoring of blood glucose (BMG), insulin preparation and administration (IPA), diagnosis and treatment of hypoglycemic crises (DTH), and hospitalization-related problems (HRP). HP, divided into groups of about 20 each, completed a basal evaluation by means of a 25-item multiple choice questionnaire, and then attended six separate educative sessions, each of focusing on one topic, consisting of a theory lesson and an interactive exercise of equivalent length. At the end of the course, HP were re-evaluated with the same questionnaire, and their skills in BMG, IPA and DTH were tested by means of specific operational checklists, which divided each complex operation into a sequence of single operations, and then compared them with those of a control group of untrained colleagues (CG). The global knowledge of diabetes after the courses significantly improved, as gathered from the percentages of correct answers in each questionnaire (61.82% +/- 23.64% vs 31.18% +/- 20.00%; P < 0.001); separate analysis of different areas evidenced improvements in GKD (72.28% +/- 12.47% vs 31.46% +/- 20.56%; P < 0.01), BMG (68.77% +/- 15.75% vs 37.50% +/- 27.75%; P < 0.01), IPA (72.02% +/- 11.72% vs 33.45% +/- 21.22%; P < 0.05), and DTH (90.76% +/- 6.86% vs 49.82% +/- 26.68%; P < 0.05), but not in HRP. Professional skills profiles of HP, evaluated by measuring the number of errors done performing each task, were significantly (P < 0.001) better than those of CG, for BMG (1.09 +/- 0.73 vs 4.91 +/- 2.01), IPA (2.36 +/- 1.64 vs 5.64 +/- 2.25), and DHT (1.27 +/- 0.94 vs 3.82 +/- 1.12). Linear regression showed a significant (P < 0.001) correlation of skills and knowledge after the course for BMG (r2 = .49), IPA (r2 = .53), and DTH (r2 = .61). Positive although nonspecific indicators of outcomes of the course were the increase (of about 100%) of requests to our metabolic unit for diabetological consultations from other departments as well as the mentioning of diabetes in the diagnosis of discharge, and the 20% increase in the consumption of sticks for BMG. The course produced a significant improvement of knowledge and skills on specific diabetological items among participants.

[Cardiovascular effects of autonomic neuropathy in insulin-dependent diabetes mellitus]. / Effetti cardiovascolari della neuropatia autonomica nel diabete mellito insulino-dipendente.

The present study was designed to evaluate whether autonomic diabetic neuropathy is a marker of severe cardiovascular disease. We recruited three groups of 12 patients each with the same age, sex and body weight distribution: Group DAN + (diabetics with neuropathy), Group DAN- (diabetics without neuropathy) and Group C (healthy control group). The patients underwent two-dimensional color Doppler echocardiography and maximal electrocardiographic exercise test by cycloergometer (multistage program with 25 W increments 3 min steps). Cardiovascular autonomic function was evaluated by Ewing's tests (heart rate and blood pressure measurement during lying to standing, deep breathing, handgrip isometric stress test and Valsalva manoeuvre). Heart rate and blood pressure proved to be significantly higher in the Group DAN+, than in the other groups, either at baseline or during stress test. Only 33% of DAN+ patients proved to reach 100 W during stress test, compared to 82% of DAN- and 87% of control subjects. No DAN+ patients reached 125 W, compared with 45% of DAN- and 58% of Group C patients. Echocardiographic examination showed normal left ventricular systolic function in all groups, without any significant difference in ventricular dimensions, and impaired left ventricular diastolic function in DAN+ patients, compared to Group C subjects (peak E 66.75 +/- 8.36 vs 73.49 +/- 12.53 cm/s; peak A 72.1 +/- 13.42 vs 59.75 +/- 13.26 cm/s; E/A 0.84 +/- 0.21 vs 1.38 +/- 0.15 and isovolumetric relaxation time 101 +/- 21 vs 70 +/- 17 ms). Our data suggest that diabetic autonomic neuropathy is a marker of reduced exercise tolerance and of diastolic left ventricular dysfunction.