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Biomedical subjects

G Morgese

Publications and source records attributed to G Morgese.

At least 73 records · Page 4Linked to original sources
PubMed2000

Increased bone turnover in epileptic patients treated with carbamazepine.

Bone turnover has been investigated in 12 epileptic patients before and after treatment with carbamazepine and in 15 sex- and age-matched control subjects. We found higher values of markers of bone formation (serum bone alkaline phosphatase, osteocalcin, and propeptides of types I and III procollagen) and of bone resorption (serum telopeptide of type I collagen and urine N-telopeptides of type I collagen) in patients than in controls. Our study demonstrates that carbamazepine induces an increase of bone turnover.

Adolescent↗
PubMed1999

Serum leptin changes in epileptic patients who gain weight after therapy with valproic acid.

Weight gain has been recognized as an adverse effect of valproic acid therapy, but there are are no data about serum leptin levels in patients receiving this drug. To evaluate if valproic acid treatment in epileptic patients in whom obesity develops modifies serum levels of insulin and leptin, 40 female patients with epilepsy were evaluated before therapy and after 1 year of therapy. At the end of follow-up, 15 patients were obese and showed higher serum leptin and insulin levels than patients who did not gain weight. As in other types of obesity, elevation of serum leptin concentrations is related to the increase in body mass index.

Adolescent↗
PubMed1999

Calcium metabolism in adolescents and young adults with type 1 diabetes mellitus without and with persistent microalbuminuria.

Alterations in calcium metabolism can be demonstrated in the course of insulin-dependent diabetes mellitus. In order to clarify if the presence of persistent microalbuminuria (MA) can affect the main parameters of calcium metabolism, we studied 22 diabetic adolescents and young adults with persistent MA and compared them with 24 patients without MA and 24 healthy controls. Mean values of serum calcium, phosphorus and magnesium were similar in diabetic children and young adults without persistent MA and in controls. In addition, the mean values of PTH and 25-OHD, 1,25 (OH)2D3 and OC did not differ between these diabetics and controls. Diabetics with persistent MA showed no significant difference from the values of either controls or the group of diabetics without persistent MA for the mean values of serum calcium, phosphorus and magnesium and PTH. In contrast, diabetics with persistent MA had significantly (p<0.01) lower 25-OHD (26.5+/-5.2 ng/ml) and 1,25 (OH)2D3 (24.7+/-5.6 pg/ml) as well as OC levels (9.8+/-2.5 ng/ml; p<0.001) than controls (38.1+/-4.9 ng/ml, 40.7+/-6.4 pg/ml and 16.5+/-5.8 ng/ml, respectively) and subjects with normoalbuminuria (36.0+/-4.5 ng/ml, 38.8+/-8.9 pg/ml and 14.5+/-3.2 ng/ml). In conclusion, our study suggests that abnormalities in 25-OHD, 1,25(OH)2D3 and OC can be present in diabetic adolescents and young adults with incipient nephropathy.

Adolescent↗
PubMed1999

Eating disorders in adolescents with type 1 diabetes mellitus.

Although the causes of eating disorders remain unclear, epidemiological evidence suggests that peripubertal changes in body shape and weight predispose young women to develop unhealthy eating attitudes. A psychiatric diagnosis of an eating disorder can be made in up to 10% of young women with insulin-dependent diabetes mellitus (type 1 diabetes). Eating disorders, anorexia nervosa and bulimia nervosa, pose a particularly serious risk to health in young diabetic people. Several features associated with type 1 diabetes and its treatment, such as weight gain, dietary restraint and food preoccupation, may predispose young diabetic women to develop a clinical or subclinical eating disorder. The coexistence of these conditions could lead to poor metabolic control and an increased risk of microvascular complications.

Adolescent↗
PubMed1999

Carnitine deficiency and hyperammonemia in children receiving valproic acid with and without other anticonvulsant drugs.

Plasma ammonia and total and free carnitine were measured in 84 children requiring anticonvulsant drugs: 32 patients (group A) on valproic acid alone, 28 children (group B) on polytherapy including valproic acid, and 24 patients (group C) on polytherapy without valproic acid. The other anticonvulsant drugs used in groups B and C were carbamazepine and phenobarbital. Plasma ammonia concentrations were elevated in both group A and B compared with controls. Group B patients showed significantly higher hyperammonemia than group A (59.9 +/- 16.3 micrograms/dl vs. 36.7 +/- 12.4 micrograms/dl; P < 0.05). Group C patients had plasma ammonia levels similar to those of controls (31.1 +/- 14.7 micrograms/dl vs. 29.7 +/- 12.1 micrograms/dl; NS). In both group A and group B patients, plasma ammonia levels were correlated with the valproic acid dosage (r = 0.32, P < 0.01) and with serum concentrations of valproic acid (r = 0.41, P < 0.001). Moreover, a significant correlation between plasma ammonia and duration of valproic acid therapy was found in the patients as a whole (r = 0.31, P < 0.01). Plasma total and free carnitine concentrations were significantly reduced in groups A and B (total carnitine 36.9 +/- 6.9 mumol/l vs. 32.9 +/- 9.7 mumol/l; free carnitine 28.9 +/- 5.1 mumol/l vs. 25.7 +/- 4.3 mumol/l, respectively) compared with group C patients who did not receive valproic acid and in whom values were similar to controls (total carnitine 46.1 +/- 9.0 mumol/l vs. 47.7 +/- 10.1 mumol/l; free carnitine 40.1 +/- 7.1 mumol/l vs. 42.9 +/- 8.0 mumol/l, respectively). Twenty-eight patients (18 of group A and 10 of group B) were re-evaluated and showed a complete normalization of plasma ammonia, and total and free carnitine levels which were similar to controls. Our data suggest that hyperammonemia is an important problem in patients receiving valproic acid, particularly in association with other anticonvulsant drugs. This increase of plasma ammonia and the concomitant reduction of carnitine seem to be transient and completely reversible.

Adolescent↗
PubMed1999

Advanced glycation end products in children and adolescents with diabetes: relation to glycemic control and early microvascular complications.

OBJECTIVE: The measurement of serum advanced glycation end products (S-AGEs) in children, adolescents, and young adults with diabetes to determine whether increased S-AGE levels may be associated with long-term glycemic control and early microvascular complications. STUDY DESIGN: The study was performed in (1) 178 children and adolescents with type 1 diabetes mellitus (age range, 2 to 21 years, onset before the age of 12 years; duration longer than 2 years) without clinical and laboratory signs of microvascular complications, (2) 39 adolescents and young adults (age range, 16.1 to 28.8 years) with background or preproliferative retinopathy or persistent microalbuminuria, and (3) 98 healthy age- and sex-matched control subjects. RESULTS: S-AGEs were significantly increased in preschool and prepubertal children with diabetes and were particularly elevated in pubertal subjects with diabetes compared with control subjects. S-AGEs were markedly increased in adolescents with early microvascular complications compared with both control subjects and diabetic patients without retinopathy or nephropathy. No correlation was found between S-AGEs and albumin excretion rate or blood pressure values. Glycated hemoglobulin values and S-AGEs were significantly correlated (r = 0.32; P <.01). In children with poorly controlled diabetes (HbA1 c >10%), long-term (2 years) improvement of glycemic control resulted in a significant reduction of S-AGE levels in preschool and prepubertal children, as well as in pubertal individuals. CONCLUSIONS: S-AGE concentrations may be elevated even in preschool and prepubertal children with diabetes; this means that the risk of microvascular complications may be present at an early age. Improvement in glycemic control may be associated with a significant decrease in S-AGEs.

Adolescent↗
PubMed1999

Platelet count and function in children receiving sodium valproate.

To evaluate whether valproic acid (VPA) can cause thrombocytopenia and impaired platelet function, the authors prospectively studied 20 children (12 female and eight male; age range 4.9-9.2 years) before and after 6 months of VPA monotherapy. Fifteen healthy sex- and age-matched children served as control subjects. VPA was prescribed at normal dosages (19.7 +/- 9.9 mg/kg), and plasma levels were within the therapeutic range (60.1 +/- 16.5 microg/mL). At the first evaluation, no significant difference between patients and control subjects was observed for platelet count and function. At the second evaluation the platelet counts were significantly lower in the patients (194,200 +/- 37,800/microL; range 157,700-222,400) than in the control subjects (291,100 +/- 41,300/microL; range 261,000-332,500; P < 0.01). Significant differences occurred between patients and control subjects in the release of adenosine triphosphate (ATP) after collagen and adenosine diphosphate (ADP) stimuli and in aggregation after stimulation with collagen, ADP, and arachidonic acid. Significant correlations between platelet count, aggregation, and ATP release and VPA dosage and plasma concentration were also observed. VPA can cause a decreased platelet count and aggregation and ATP release impairment. These side effects can appear after a few months of therapy and with plasma valproate levels within the normal range. They do not seem to be associated with clinical symptoms, and drug discontinuation is not necessary.

Adenosine Triphosphate↗
PubMed1999

Centro-temporal spikes in non-epileptic children: a long-term follow up.

OBJECTIVE: This study was undertaken in order to determine the natural evolution of centro-temporal spikes (CTS) in a healthy paediatric population. METHODOLOGY: Forty children and adolescents (mean age +/- SD: 9.9 +/- 4.1 years) with non-epileptic disturbances (tics, headache, pavor nocturnus, vertigo, etc), who showed CTS during routine EEG recordings were studied. No patient suffered from seizures. A clinical and electroencephalographic follow-up of at least 5.5 years was carried out in all subjects. RESULTS: At the follow-up examination, 33 of the 40 cases (82.5%) had no CTS or other epileptic discharges in awake and sleep EEGs, while six subjects continued to show CTS discharges in sleep EEG. Among those subjects who showed persistence of CTS in sleep EEG, rolandic epilepsy developed in two cases, while all other subjects continued to be seizure free. CONCLUSIONS: This study demonstrates that CTS can be present in non-epileptic children and adolescents; in the majority of subjects this EEG abnormality disappears spontaneously and only a small percentage of subjects who have persistence of this pattern develops rolandic epilepsy.

Action Potentials↗
PubMed1999

Epilepsy with myoclonic absences with early onset: a follow-up study.

We studied six children (four girls and two boys) suffering from cryptogenic myoclonic absence seizures with early onset. The age at onset of the seizures ranged between 6 and 27.8 months (mean age +/- SD: 18.5+/-12.4 months). The neurologic evaluation was normal in all patients at the first hospital admission. After the diagnosis, we followed up all children for at least 5 years. At the end of follow-up, two of these patients (a girl and a boy) showed severe mental retardation, a high number (from one to three per day) of seizures, and persistent pathologic electroencephalograms. The other patients showed normal electroencephalograms: all of them were seizure free and without mental retardation. The two patients with mental retardation have been treated with polytherapy. In all other children we used valproate alone successfully. Our data suggest that myoclonic absence seizures with early onset can have a good long-term prognosis. Valproate is a useful anticonvulsant drug in these patients. Mental retardation is present only in patients with poor seizure control.

Anticonvulsants↗
PubMed1999

Growth hormone and IGF-I in diabetic children with and without microalbuminuria.

In order to evaluate the relationship between urinary GH, urinary IGF-I and plasma IGF-I levels and presence of incipient diabetic nephropathy in paediatric age, we studied fifty (25 male and 25 female) prepubertal patients with insulin-dependent diabetes mellitus (T1DM). The patients were subdivided into two groups according to the presence of persistent microalbuminuria defined as albumin excretion rate (AER) >20 microg/min in at least 5 urine collections in the 6 months prior to the beginning of the study: Group A: 18 patients with microalbuminuria; Group B: 32 patients without microalbuminuria. A group of 20 healthy subjects, sex-, age- and pubertal stage-matched, served as control. No difference was observed between the urinary output of IGF-I and GH and plasma IGF-I values between normoalbuminuric and control subjects (normoalbuminuric vs controls: urinary GH: mean+/-SD 7.9+/-0.7 ng/day vs 8.1+/-0.6; urinary IGF-I: 178.3+/-19.7 ng/day vs 175.5+/-20.3; plasma IGF-I: 203.9+/-31.2 ng/ml vs 199.4+/-43.2), but a significant difference was observed between the urinary output of IGF-I and GH and plasma IGF-I levels between microalbuminuric patients and normoalbuminuric and controls (microalbuminuric subjects: urinary GH: 13.1+/-1.4 p<0.01; urinary IGF-I: 451.3+/-45.9 p<0.001; plasma IGF-I: 326.5+/-63.2 p<0.01). Moreover, plasma IGF-I, urinary GH and urinary IGF-I were not significantly associated with microalbuminuria, while plasma IGF-I levels were positively related to glomerular filtration rate (GFR) (p<0.05). In conclusion, our study demonstrates that microalbuminuric patients have higher levels of urinary IGF-I, urinary GH, plasma IGF-I than normoalbuminuric diabetic subjects. These data support the hypothesis that IGF-I can have a role in the changes of renal function observed in patients with persistent microalbuminuria.

Adolescent↗
PubMed1998

Transient neonatal hypothyroidism after gestational exposure to amiodarone: a follow-up of two cases.

Amiodarone (AMD) is an antiarrhythmic drug which contains 37% of iodine. It can reach the fetus by transplacental passage and induce fetal hypothyroidism. Since in some pregnant women AMD represents a cardinal therapeutic opportunity, it is necessary to establish not only the risk of teratogenicity linked to fetal AMD exposure but also to evaluate the psychomotor development of children with neonatal thyroid dysfunction related to fetal AMD exposure. We report on two cases involving children with an AMD gestational exposure and transient neonatal hypothyroidism, who were followed-up until the age of 4 years 8 months and 5 years 6 months, respectively. Denver's developmental milestone test and Whechsler Preschool and Primary Scale of Intelligence (WPPSI) were administered to the patients in accordance to their age. A normal psychomotor development was observed in both patients with full scale IQ score, verbal and performance IQ scores within normal range. In conclusion, if these data were validated by larger studies, it might not be obligatory to discontinue AMD administration in cardiopathic pregnant women, since mental impairment may not necessarily occur in children with transient neonatal hypothyroidism caused by fetal AMD exposure. However, the evaluation of the thyroid function of these children is imperative.

Adult↗
PubMed1998

Hypoglycaemic symptoms described by diabetic children and their parents.

Hypoglycaemic events are frequent complications of insulin-dependent diabetes mellitus in children. The signs and symptoms referred to by young children can be difficult to understand and often seem to be different from those described by their parents. We analysed the hypoglycaemic symptoms described by a group of patients and their parents. We studied 40 pairs consisting of a parent and a diabetic child by using a structured questionnaire with 27 items concerning different symptoms of hypoglycaemia. The mean+/-SD age of the children was 10.4+/-2.4 years, with duration of disease 6.2+/-2.1 years and their HbA1c was 8.2 2.0%. For the statistical analysis we used the principal component analysis. All the children followed a multiple injection regimen. The frequency and intensity of the hypoglycaemic signs described by patients and parents were similar both for neuroglycopenic (uncoordination, confusion, odd behaviour, dizziness) and autonomic symptoms (trembling, sweating, pounding heart, hunger). Moreover, our questionnaire showed a high frequency of behavioural changes. In conclusion, from the analysis of the questionnaires collected, we found that both parents and children gave almost the same score to the symptoms observed. This means that there is a concordance between the symptoms reported by the children and those reported by their parents.

Adolescent↗
PubMed1998

Serum lipids and lipoproteins in patients treated with antiepileptic drugs.

The concentration levels of serum lipids and lipoproteins were measured in three groups of children and adolescents treated with antiepileptic drugs: carbamazepine (14 patients), phenobarbital (20 patients), and valproic acid (20 patients). Patients treated with these drugs revealed significant changes in lipids and lipoproteins, but when the authors reevaluated the three groups of children 1 year after the end of treatment, a complete return to normal of all parameters was observed. These data demonstrate that the changes induced by these drugs are transient and reversible.

Adolescent↗
PubMed1998

Diabetic nephropathy in children and adolescents: a critical review with particular reference to angiotensin-converting enzyme inhibitors.

Clinical diabetic nephropathy is a well-recognized cause of increased morbidity and mortality in patients with type 1 diabetes. The finding that microalbuminuria predicts progression to overt nephropathy has allowed early diagnosis and preventive interventions. Several studies have demonstrated that treatment with angiotensin-converting enzyme (ACE) inhibitors slows down the rate of decline of the glomerular filtration rate in type 1 diabetes patients with established proteinuria. The renoprotective properties of the ACE inhibitor captopril extend beyond its antihypertensive effects. ACE inhibitors represent the most appropriate class of antihypertensive drugs for treating type I diabetes patients because of their efficacy and safety. When microalbuminuria is detected and confirmed in a diabetic child or adolescent, and if it persists despite 6-12 months of improved metabolic control, treatment with ACE inhibitors should be started, even if the child is normotensive. Careful follow-up of renal function is essential.

Adolescent↗