Publications by authors named "Iavicoli M"

The aim of this study was to evaluate the effect of sc insulin (INS) compared with sulfonylurea (SUL) therapy, at the same level of blood glucose control, on the low density lipoprotein (LDL) subfraction profile in normolipidemic type 2 diabetic patients. Nine normolipidemic type 2 diabetic men (age, 56+/-3 yr; body mass index, 26.5+/-0.

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This study evaluates the effects of insulin versus glibenclamide on lipoprotein metabolism at comparable levels of blood glucose control, in particular on the concentration and distribution of VLDL subfractions and lipolytic enzyme activities in nine NIDDM men (aged 56 +/- 3 years, BMI 26.5 +/- 0.9 kg/m2) (means +/- SE) participating in a crossover study.

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We studied the effects of GH administration on myocardial structure and function in 20 patients with hypopituitarism (14 males and 6 females; mean +/- SE age, 47.2 +/- 2.6 yr; range, 31-59 yr) developed in adulthood because of pituitary or parapituitary tumors.

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Metabolic control, insulin secretion and insulin action were evaluated in seven Type 2 (non-insulin-dependent) diabetic patients with secondary failure to oral antidiabetic agents before and after two months of combined therapy with supper-time insulin (Ultratard: 0.4 U/kg body weight/day) plus premeal glibenclamide (15 mg/day). Metabolic control was assessed by 24 h plasma glucose, NEFA, and substrate (lactate, alanine, glycerol, ketone bodies) profile.

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Circulating insulin antibodies at birth and the degree of maternal metabolic control were measured in 68 infants of insulin-treated diabetic mothers. Their correlation with neonatal B cell function and with the clinical features of the infants was evaluated in order to better understand their influence on fetal outcome. Maternal metabolic control was assessed on the basis of blood glucose levels, glycosuria and the occurrence of hypoglycemia and/or ketonuria.

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The influence of combined therapy using insulin and oral hypoglycaemic agents on blood glucose control and on insulin secretion in Type 2 diabetic patients with secondary failure to oral hypoglycaemic agents was evaluated. Type 2 diabetic patients (n = 180) (98 normal-weight, 82 over-weight), at least 3 years from diagnosis, and having poor blood glucose control on oral hypoglycaemic agents for at least 3 months (fasting plasma glucose greater than 10.0 mmol l-1) despite intensive efforts at improvement, were included in the study.

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The present study was planned to evaluate if a longterm follow-up would show any modification of insulin antibodies in IDDs transferred from porcine to human monocomponent insulins. Nineteen IDDs, treated for more than one year with porcine monocomponent insulins, were transferred to the equivalent formulations of human insulin (Actrapid HM, Monotard HM); insulin antibodies, metabolic control, insulin dose, adverse drug reactions were evaluated during a 42-month follow-up. A reduction of IgG insulin antibodies was observed after 22 months of the follow-up and became significant (2p less than 0.

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The presence of islet cell antibodies (ICA), complement fixing islet cell antibodies (CF-ICA), other organ-specific autoantibodies, insulin antibodies and two different types of immune complexes (AgAb) in diabetic pregnant women treated with insulin during pregnancy was investigated and compared with maternal metabolic control and with the course and outcome of pregnancy. One hundred and eighteen pregnant diabetic women were grouped according to type of diabetes: 56 were insulin-dependent diabetic patients who had been previously treated with insulin (Group 1); 23 were non-insulin-dependent diabetic patients who had previously received diet or oral treatment (Group 2); 39 had gestational diabetes (Group 3). 94 patients were subjected to regular check-ups during pregnancy and blood samples were taken during the last month of pregnancy (phase A); some were treated with standard preparations of insulin, the remainder with purified insulins.

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Biologic and immunogenic activities of semisynthetic human monocomponent insulins were examined in insulin-dependent diabetic patients (group 1). Patients treated with porcine monocomponent (group 2) and conventional (group 3) insulins were studied for control purposes. The patients were examined before the beginning of insulin treatment and for a 6-mo follow-up period.

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Subsets of peripheral T lymphocytes by monoclonal antibodies and circulating immune complexes by two different methods were evaluated in 36 long-standing diabetic patients, 19 Type 1 (insulin dependent) and 17 Type 2 (non-insulin dependent). In all patients the presence of microangiopathy was assessed by retinal fluoroangiography, albuminuria and creatinine clearance. In patients with Type 1 diabetes a significant decrease of total T and of T cells with helper phenotype (T4), together with an increase of T cells with suppressor/cytotoxic phenotype (T8), were observed.

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The relationship between immune complexes and insulin antibodies was evaluated in 237 insulin treated subjects with a duration of diabetes of more than 1 year. Ninety-seven diabetics were selected at random (group 1) whereas 140 according to the presence of diabetic microangiopathy (group 2). Immune complexes were evaluated by the solid phase C1q binding test in all patients and by conglutinin radioimmune assay in most of them.

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The influence of sex, age, duration of diabetes and type of antidiabetic treatment on soluble immune complexes levels was investigated in the sera of 276 randomly selected diabetics. Immune complexes were detected by the solid phase C1q binding test. The prevalence of immune complexes was significantly higher in insulin treated than in non-insulin treated diabetics.

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Peripheral T-lymphocytes subsets have been investigated in 36 patients with type I (insulin-dependent) diabetes of varying duration, 18 patients with type II (non-insulin-dependent) diabetes, and in 23 healthy subjects, using six different monoclonal antibodies. At the time of diagnosis of type I diabetes, there was evidence of an increase in cytotoxic T-lymphocytes, a decrease in suppressor T-lymphocytes, but a normal proportion of helper/inducer T-lymphocytes. In six of seven newly diagnosed cases studied, there was evidence of an increased number of activated T cells.

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In 41 Type 1 (insulin-dependent) diabetic patients, islet cell antibodies, anti-insulin antibodies, and immune complexes measured by two different methods (the C1q solid phase assay and the conglutinin binding test) were studied at diagnosis, and the influence of treatment with insulins of different purity was investigated during the first year of treatment. Twenty subjects were treated with conventional insulins (group 1) while 21 were treated with monocomponent porcine insulins (group 2). The prevalence of islet cell antibodies significantly decreased during the 12-month study period in the 41 patients.

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An investigation on circulating immune complexes (AgAb) was carried out in 80 diabetics with severe microangiopathy and in 71 diabetics without microvascular lesions. The duration of the disease, the type of diabetes, the type of treatment and the main localization of microangiopathy (retinopathy and nephropathy) were taken into account. AgAb were detected by two different methods: the solid phase Clq binding test (ClqSP) and the conglutinin binding test (KgBt).

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An increase in circulating immune complexes (AgAb) of medium size has been observed in diabetics with late complications. This increase may be related either to an increased formation or reduced clearance. Alternatively, both mechanisms may be involved.

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Circulating immune complexes (AgAb) were studied in 183 serum samples from 119 patients with Crohn's Disease. AgAb were studied by the solid phase C1q binding test in all sera and also by the conglutinin binding assay in 161 sera. A significantly higher prevalence of circulating AgAb was observed in Crohn's disease patients in comparison with the control population.

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To study the effect of carbohydrate metabolism on lymphocyte reactivity, we performed phytohaemoagglutinin and pokeweed mitogen induced lymphocyte transformation after insulin induced hypoglycaemia in normal subjects. A statistically significant increase of PHA-LT and a slight increase of PKW-LT were detected 30 minutes following insulin administration. These data suggest a stimulating effect of insulin induced hypoglycaemia on T lymphocyte reactivity and this finding has clinical importance in regard to the management of diabetic patients.

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Soluble immune complexes (AgAb) as detected and quantitated by the solid phase Clq assay (Clq-SP) were found to be increased in (a) long-duration diabetics with proliferative retinopathy and (b) short duration diabetics with early onset of retinopathy irrespective of whether they were treated with insulin or oral hypoglycaemic agents (OHA), in comparison to a normal population. No such increases were observed in diabetics of comparable duration without retinopathy. The trend for long-term diabetics to show an increased prevalence of AgAb according to the severity of retinopathy was statistically significant.

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Eleven insulin-dependent ketosis-prone diabetics were given glibenclamide (5 mg/day) in addition to their usual insulin treatment for a period of 1 or 6 mo. There was significant reduction in arginine-induced IRG and hGH secretion and no change in blood glucose levels after either 1 or 6 mo of treatment. During that time no change in weight or insulin requirement was observed.

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The sera of ten patients with unexplained hypoglycaemia were examined for antibodies to pancreatic islets. Antibodies to pancreatic A, B and D cells (ICAb) were detected in one patient with an associated gastrointestinal tumour.

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