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Biomedical subjects

N Passariello

Publications and source records attributed to N Passariello.

At least 19 recordsLinked to original sources
PubMed1995

[Treatment of chronic hepatitis C with lymphoblastic interferon. Long-term follow-up].

OBJECTIVES: A randomized controlled trial was set up to assess the effect of two different therapy regimens with lymphoblastoid interferon on the treatment and follow-up of patients with chronic C hepatitis. METHODS: Eighty-five patients with chronic hepatitis C were randomized into two treatment groups (n = 30 respectively) and one control group (no treatment: n = 25). In one treatment group patients received three million units of alpha-lymphoblastoid interferon. The other received six million units. RESULTS: A rapid decline in both alanine aminotransferase and aspartataminotransferase levels was seen in most treated patients (a complete response in 51% from group A and 55% from group B; partial response 29% from group A, 25% from group B). In five partial responders and six complete responders from group A and in seven partial responders and six complete responders in group B serum aminotransferase levels returned to baseline values in the follow-up. No change in serum bilirubin, albumin, IgG and prothrombin time during interferon treatment were seen. The histologic staging remained unchanged throughout the entire study. CONCLUSION: alpha-interferon treatment improves the clinical picture, biochemical parameters and histologic pattern in a large percentage of patients with hepatitis C. Long-term remission was seen in only 37% of treated patients. Using six million units of alpha-interferon has not proven to be significantly better than three million units. Protracted treatment for nine months seems to increase the percentage of patients in biochemical and histologic remission.

Adult↗
PubMed1995

Low-dose iloprost infusion improves insulin action in aged healthy subjects and NIDDM patients.

OBJECTIVE: To investigate the effect of iloprost infusion on insulin action. RESEARCH DESIGN AND METHODS: Thirteen healthy subjects and 13 non-insulin-dependent diabetes mellitus (NIDDM) patients matched for age (68.2 +/- 0.5 vs. 67.9 +/- 0.5 years, NS), gender ratio (7 men:6 women vs. 6 men:7 women), body weight, body fat distribution, arterial blood pressure, and plasma triglyceride levels (1.89 +/- 0.09 vs. 1.87 +/- 0.08 mmol/l, NS) were studied. In eight healthy subjects and eight NIDDM patients, we studied insulin action by euglycemic glucose clamp (insulin infusion rate 2 mU.kg-1.min-1) along with saline and iloprost delivery (0.7 ng.kg-1.min-1). In the other five subjects of each group, forearm blood flow and insulin-mediated glucose uptake during saline and iloprost infusion (0.7 ng.kg-1.min-1) were investigated. RESULTS: Iloprost infusion improved insulin-stimulated whole-body glucose uptake and oxidative and nonoxidative glucose metabolism in both study groups. Forearm blood flow under basal conditions and with insulin infusion (2 mU.kg-1.min-1) did not show any significant difference from that during saline and iloprost infusion (0.7 ng.kg-1.min-1) in healthy subjects and diabetic patients. CONCLUSIONS: Iloprost infusion improves insulin action in healthy subjects and NIDDM patients.

Aged↗
PubMed1993

A clinical, genetic and echocardiographic study of hypertrophic cardiomyopathy in a large family.

OBJECTIVES: To confirm recent reports on the incidence of human lymphocyte antigens (HLA) in familial hypertrophic cardiomyopathy and to better define the genetic patterns found in these patients. METHODS: A large family (31 members, 18M, 13F, age range 6-80 years) with a high incidence of hypertrophic cardiomyopathy was screened for HLA, dermatoglyphic patterns and blood subtyping. RESULTS: Our finding show variable expression of the disease and reduced penetrance. No linkage between the disease-causing gene and HLA loci could be demonstrated in the family. There was no specific haplotype which present in all affected individuals and missing in all controls. Haplotype A2 B18 was the most commonly encountered in affected individuals but was absent in IV 3 and present in a few controls. No linkage was found between the disease-responsible gene and the blood groups. Finally, no typical pattern emerged from the dermatoglyphic studies. CONCLUSION: The genetic assessment of this family, in agreement with other European studies, showed no clear correlation between hypertrophic cardiomyopathy and blood groups ABO, Rh, Lewis, Duffy and was unable to show atypical or unusual dermatoglyphic patterns.

Adolescent↗
PubMed1992

[Hypertrophy of the masseter: a rare case associated with hypertrophic cardiomyopathy].

Masseteric hypertrophy is a rare, monolateral or bilateral lesion. The aetiology is often unknown and both congenital and acquired forms are reported in the literature. The authors report a case of masseteric hypertrophy associated with hypertrophic cardiomyopathy. Family history shows two brothers suffering from the same cardiac disease. Echography, computed tomography, EMG test and aspiration biopsy of masseteric muscle were performed. Echocardiography and HLA, B and C antigens of 16 relatives were also performed. In the report case the authors hypothesized a multifactorial background on a genetic basis.

Adult↗
PubMed1989

Dietary magnesium supplements improve B-cell response to glucose and arginine in elderly non-insulin dependent diabetic subjects.

Hypomagnesemia and low erythrocyte magnesium content are both common findings in non-insulin-dependent diabetic subjects. Moreover, intracellular magnesium may play a crucial role in modulating B-cell response to glucose by interfering with potassium permeability. Eight elderly, moderately obese, non-insulin-dependent diabetic subjects were treated with either magnesium supplementation (3 g/day) to the diet or placebo. Both treatment schemes lasted 4-weeks and were separated by a 'wash-out' of 3 weeks. At the end of each treatment period, in glucose test (0.33 g/kg for 3 min) and an iv arginine (5 g) test were performed to determine the B-and A-cell responses. Dietary magnesium supplementation vs placebo produced a slight but significant decrease in basal plasma glucose (8.6 +/- 0.3 vs 8.0 +/- 0.1 mmol/l, p less than 0.05) and an increase in acute insulin response after iv glucose (3.7 +/- 2.3 vs - 14.7 +/- 0.9 pmol.l 1. (10 min)-1, p less than 0.01) and after iv arginine (151 +/- vs 81 +/- 15 pmol.l-1. (10 min)-1, p less than 0.01), respectively. Plasma glucagon levels were unaffected by chronic dietary magnesium supplementation as well under basal conditions as in response to arginine. Net increase in acute insulin response after iv glucose and after iv arginine was significantly correlated to the net increase in erythrocyte magnesium content after dietary magnesium supplementation. We conclude that magnesium administration may be a useful adjuvant to the classic hypoglycemic agents in the treatment of non-insulin-dependent diabetic subjects.

Aged↗
PubMed1989

Improved insulin response and action by chronic magnesium administration in aged NIDDM subjects.

In eight aged non-insulin-dependent diabetes mellitus (NIDDM) subjects, insulin response and action were studied before and after chronic magnesium supplementation (2 g/day) to diet. Chronic magnesium supplementation to diet versus placebo produced 1) a significant increase in plasma (0.83 +/- 0.05 vs. 0.78 +/- 0.06 mM, P less than .05) and erythrocyte (2.03 +/- 0.06 vs. 1.88 +/- 0.09 mM, P less than .01) magnesium levels, 2) an increase in acute insulin response (AIR) (4.0 +/- 0.6 vs. -1.6 +/- 0.6 mU/L, P less than .05) to glucose pulse, and 3) an increase in glucose infusion rate (GIR) (3.6 +/- 0.6 vs. 2.9 +/- 0.5 mg.kg-1.min-1, P less than .025) calculated in the last 60 min of a euglycemic-hyperinsulinemic (100 mU.m2.min-1 during 180 min) glucose clamp. Net increase in AIR, glucose disappearance rate after glucose pulse, and GIR were significantly and positively correlated to the net increase in erythrocyte magnesium content calculated after chronic magnesium supplementation to diet. In conclusion, our data suggest that NIDDM subjects may benefit from therapeutic chronic administration of magnesium salts.

Aged↗
PubMed1988

Plasma glucose lowering effect of sparteine sulphate infusion in non-insulin dependent (type 2) diabetic subjects.

Sparteine sulphate, given i.v. as a bolus of 15 mg/ml plus 90 mg in 0.9% NaCl 100 ml over 60 min, increases plasma insulin and decreases plasma glucose and adrenaline in non-insulin dependent (Type II) diabetic subjects. The hypoglycaemic effect was also evident in the presence of a high plasma glucose level produced by Biostator changing glucose infusion from 20.2 +/- 2.8 to 26.4 +/- 4.2 mg.kg-1.min-1 (p less than 0.01), and it was potentiated by simultaneous infusion of arginine. No additional effect of sparteine on the peripheral sensitivity to insulin were detected by the euglycaemic, hyperinsulinaemic glucose clamp technique, as the glucose infusion rate (3.1 +/- 0.8 vs 2.6 +/- 1.2 mg.kg-1.min-1) was not statistically significant different in the last 60 min of the experiment. It is concluded that sparteine sulphate enhances beta-cell secretion, causing a fall in the plasma glucose concentration.

Adult↗
PubMed1988

Pharmacological doses of oxytocin affect plasma hormone levels modulating glucose homeostasis in normal man.

Pharmacological doses of oxytocin administered in basal conditions evoked a rapid surge in plasma glucose and glucagon levels followed by a later increase in plasma insulin and adrenaline levels. The effects of oxytocin on plasma glucagon and adrenaline levels were potentiated by hypoglycemia. When the endogenous pancreas secretion was suppressed by cyclic somatostatin (150 micrograms/h) and exogenous glucagon (3.5 micrograms/h) and insulin (0.2 mU/kg.min) were both replaced, oxytocin (0.2 U/min) evoked a transient but significant increase in plasma glucose levels suppressing the glucose infusion rate (GIR) in the first 60 min. On the contrary at higher insulin infusion rate (0.6 mU/kg.min) plasma glucose levels and GIR remained unaffected throughout the study. Oxytocin seems also to potentiate glucose-induced insulin secretion as evidenced by hyperglycemic glucose clamp. In conclusion, pharmacological doses of oxytocin seem to exert a prevalent hyperglycemic effect by a combined action at the liver site (as glycogenolytic agent) and at the endocrine pancreas (as a stimulatory agent of A cell secretion).

Adult↗
PubMed1987

Effect of sparteine sulphate upon basal and nutrient-induced insulin and glucagon secretion in normal man.

Infusion of a therapeutic dose of sparteine sulphate, increased the basal plasma insulin level and lowered plasma glucose. When an intravenous glucose tolerance test was performed with the infusion, the total insulin AUC was significantly larger than in absence of sparteine (2025 vs 1464 microU/ml X min), plasma glucose levels were lower and improved glucose utilization was observed (kg:1.55 vs 1.39%). In the presence of arginine, sparteine sulphate stimulated both beta and alpha cells, increasing both the total insulin (1907 vs 1516 microU/ml X min p less than 0.02) and total glucagon AUCs (7616 +/- 654 vs 6789 +/- 707 pg/ml X min p less than 0.01). Thus, sparteine sulphate increased both basal and nutrient-induced insulin and glucagon secretion in normal man.

Adult↗
PubMed1987

Impaired insulin-mediated erythrocyte magnesium accumulation in essential hypertension.

1. This study was designed to investigate variations in erythrocyte magnesium in the presence of insulin (0.1 unit/l) in hypertensive subjects. 2. Plasma and erythrocyte magnesium levels were found to be significantly lower in hypertensive than in normotensive subjects. 3. The impaired response to insulin (0.1 units/l) of erythrocytes from hypertensive patients was not reversed by elevated extracellular Mg2+ (3.6 mmol/l). 4. Erythrocytes of hypertensive subjects showed an increased membrane microviscosity compared with normotensive subjects. 5. Lidocaine decreased erythrocyte membrane microviscosity and increased erythrocyte magnesium levels in the presence of insulin.

Adult↗
PubMed1987

Impaired glucose metabolism in heroin and methadone users.

Plasma glucose and insulin responses to both oral and intravenous glucose stimulation were evaluated in heroin and methadone addicts, compared to healthy control subjects. Both groups of addicts had an altered response to oral and intravenous glucose load. These phenomena were linked to a reduced insulin response. Moreover, increased fasting insulin levels in both groups of addicts were observed. These data show that both heroin and methadone addiction may alter glucose metabolism, and, furthermore, stress the findings of similarities between opiate addicts and non-insulin dependent diabetics.

Adult↗
PubMed1987

Greater efficacy of pulsatile insulin in type I diabetics critically depends on plasma glucagon levels.

The aim of this study was to investigate the role of plasma glucagon levels on the blood glucose response to intravenous insulin administered continuously or in a pulsatile manner. Six type I diabetic patients proven to have no residual insulin secretion were investigated. Endogenous glucagon secretion was inhibited by a continuous intravenous infusion of somatostatin (100 micrograms/h) and replaced by exogenous infusions of the hormone at three different rates (7.5, 4.5, and 2.5 micrograms/h), resulting in three different plasma glucagon steady-state levels (i.e., approximately equal to 200, approximately equal to 130, and approximately equal to 75 pg/ml, respectively). Each subject, in random order and on different days, was infused intravenously with regular human insulin either continuously (0.17 mU X kg-1 X min-1) or with the same amount of insulin infused in a pulsatile manner (0.85 mU X kg-1 X min-1 during 2 min followed by 8 min during which no insulin was infused). At plasma glucagon levels approximately equal to 200 pg/ml, blood glucose rose from approximately 10 to approximately 13 mM without any difference between the two modalities of insulin infusion. For plasma glucagon levels approximately equal to 130 pg/ml, plasma glucose remained steady throughout the experiments, but during the last 40 min, plasma glucose levels were significantly lower when insulin was administered intermittently. This greater blood glucose-lowering effect of pulsatile insulin occurred earlier and was more pronounced for plasma glucagon levels averaging 75 pg/ml. We conclude that the greater hypoglycemic effect of insulin administered intravenously in a pulsatile manner in type I diabetics critically depends on plasma glucagon circulating levels.

Adult↗
PubMed1986

Insulin induces opposite changes in plasma and erythrocyte magnesium concentrations in normal man.

Plasma and erythrocyte magnesium levels were measured by atomic absorption spectrophotometry in 10 healthy volunteers during an oral glucose tolerance test and during an euglycaemic hyperinsulinaemic glucose clamp. At min 180 and 210 of the oral glucose tolerance test, a significant decline in plasma magnesium levels (p less than 0.01 and p less than 0.05 respectively) and a significant increase in erythrocyte magnesium levels (p less than 0.01 and p less than 0.05 respectively) were observed. Similar changes were seen during the second hour of the glucose clamp, during which euglycaemia (4.1 +/- 0.4 mmol/l) was maintained despite hyperinsulinaemia (110-130 mU/l). During in vitro incubations, glucose (5 mmol/l) did not modify erythrocyte magnesium levels. In contrast, erythrocyte magnesium levels were significantly increased (p less than 0.01) by insulin (100 mU/l), an effect entirely abolished by ouabain (5 X 10(-4) mol/l). These results suggest that insulin induces a shift of magnesium from the plasma to the erythrocytes both in vivo and in vitro. These data may help to interprete the abnormalities in magnesium circulating levels frequently reported in diabetic patients.

Adult↗
PubMed1986

Impaired insulin response to glucose but not to arginine in heroin addicts.

Plasma glucose, insulin, glucagon and growth hormone responses to both oral glucose and iv arginine were evaluated in 15 heroin addicts and 15 control subjects matched for age, sex and weight. The heroin users had an exaggerated rise in plasma glucose concentrations following oral sugar, which persisted until the end of the study (102 +/- 5 mg/dl in addicts vs 72 +/- 3 mg/dl in controls at 240 min, p less than 0.01) and significantly lower insulin responses (insulin peak 28 +/- 4 microU/ml in addicts vs 67 +/- 8 microU/ml in controls, p less than 0.01). The inhibitory effect of glucose on glucagon concentrations was less evident in addicts than in controls. The responses of plasma glucose, insulin and glucagon to arginine were not significantly different between addicts and controls, while the growth hormone rise was significantly greater in addicts. These results demonstrate that heroin users have impaired insulin secretion to oral glucose but not to arginine and suggest that: the impaired insulin secretion in heroin addicts is not dependent on beta-cell exhaustion, and a selective inhibition of glucose-induced insulin secretion is operative in these subjects, as it happens in patients with noninsulin-dependent diabetes mellitus.

Adult↗
PubMed1986

Effect of sparteine sulfate on insulin secretion in normal men.

This study aimed at evaluating the influence of sparteine sulfate either upon basal plasma glucose and insulin or glucose-induced insulin secretion in normal man. Thirteen overnight fasted volunteers took part in this study; five of them were submitted to sparteine sulfate bolus (15 mg in 10 ml of saline solution) followed by a slow infusion (90 mg/100 ml X 60 min) and eight subjects underwent two different glucose pulses (20 gr. i.v.) in absence or in presence of sparteine, infused as described above. In basal conditions, along with sparteine infusion, plasma glucose showed a progressive and significant decrease (P less than 0.0001) and plasma insulin was significantly higher from min 10 to 120' (P less than 0.0005-0.001). Even during the glucose-induced insulin secretion, in the presence of sparteine infusion, plasma glucose levels were significantly lower while plasma insulin levels were significantly higher when compared to those observed after glucose alone. The acute insulin response (AIR) was 42 +/- 10 microU/ml after glucose alone vs 67 +/- 9 microU/ml after glucose plus sparteine (P less than 0.05). Total insulinemic areas were significantly different being 1410 +/- 190 vs 2250 +/- 310 microU/ml/min (P less than 0.001) during glucose and glucose plus sparteine infusion, respectively. This study thereby, demonstrates that in normal man sparteine sulfate, administrated by intravenous infusion, is able to increase either basal or glucose-induced insulin secretion.

Adult↗
PubMed1986

Plasma calcitonin variations in normal women and in women with family history of diabetes during pregnancy.

In eight normal pregnant women and in eighteen women with a family history of diabetes, plasma calcitonin (CT), parathyroid hormone (PTH), insulin and glucagon variations and total plasma calcium levels were investigated. Calcitonin, parathyroid hormone and glucagon were all increased during the 2nd and 3rd trimester of pregnancy in normal women (N.W.) and in women with a family history of diabetes (W.F.H.D.). Plasma calcitonin levels were statistically significantly different between the two groups only in the 3rd trimester (118 +/- 4.9 vs 139 +/- 3.6 pg/ml p less than 0.01 in N.W. and W.F.H.D. respectively). Total plasma calcium levels were decreased significantly in the 3rd trimester in both groups: 3rd vs 1st trimester p less than 0.005 and p less than 0.001 in N.W. and W.F.H.D. respectively. Statistically significant difference between the two groups in total insulinemic area (p less than 0.001), in the rapid phase area (p less than 0.01) and insulinogenic index (p less than 0.05) were observed in the 3rd trimester.

Calcitonin↗