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Biomedical subjects

A Verrotti

Publications and source records attributed to A Verrotti.

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

Thyroid function in children with perinatal human immunodeficiency virus type 1 infection.

OBJECTIVE: To study thyroid function in children with perinatal HIV-1 infection retrospectively and determine whether thyroid abnormalities are correlated with clinical condition, disease progression, immunological impairment, and viral load. STUDY DESIGN AND SETTING: Total (TT4) and free (FT4) thyroxine, total (TT3) and free (FT3) triiodothyronine, reverse triiodothyronine (rT3), thyrotropin (TSH), thyroglobulin (TG), and thyroid binding globulin (TBG) were measured twice in 56 children with perinatal human immunodeficiency virus type 1 (HIV-1) infection. Median age at first determination was 13.5 (range: 0.03-127.0) months; median age at second determination was 66.2 (range 3.42-147.4) months. Antithyroglobulin, antimicrosomal, thyroid peroxidase, and thyrotropin receptor antibodies were also evaluated. Fifty-three healthy children were selected as controls. RESULTS: TT3, TT4, FT4, and TG were significantly reduced and rT3, TBG, and TSH increased in children with HIV-1 infection when compared with controls. Thyroid dysfunction correlated with severe immunosuppression and high viral load early in life preceded the onset of the disease and worsened over time. Autoantibodies were negative in all children with HIV-1 infection in all determinations. CONCLUSION: Thyroid abnormalities are observed early in the course of perinatal HIV-1 infection; thyroid dysfunction is particularly pronounced in children with severe immunosuppression and high viral load. Modifications of thyroid function precede worsening of clinical course in HIV-1 infected children.

CD4 Lymphocyte Count↗
PubMed2000

Renal tubular function in patients receiving anticonvulsant therapy: a long-term study.

PURPOSE: The goal of the study was to evaluate the tubular renal function in children and adolescents who are undergoing monotherapy with sodium valproate (VPA), carbamazepine (CBZ), and phenobarbital (PB). METHODS: The urinary excretion of N-acetyl-beta-glucosaminidase (NAG), beta-galactosidase (beta-Gal), alanine-amino-peptidase (AAP), and alpha1-microglobulin (alpha1M) was measured in 58 epileptic patients (29 girls and 29 boys), aged 12.6 +/- 3.9 years, who were subdivided into three groups according to their therapy. Fifty healthy sex-and age-matched children served as controls. The measurements were taken before the beginning of therapy and after 6 months, 1 year, and 2 years of therapy. RESULTS: Before the beginning of therapy, there were no significant differences in NAG, beta-Gal, AAP, and alpha1M values between the control group and the three groups of epileptic children. After 6 months of therapy, patients treated with VPA and CBZ showed a significant increase in the urinary excretion of NAG and beta-Gal compared with baseline data and control values. After 1 and 2 years, these patients showed a persistence of the changes found after 6 months of therapy. In patients treated with PB, we did not find any significant variation in NAG, beta-Gal, AAP, and alpha1M urinary excretion. CONCLUSIONS: Our study demonstrates that in patients treated with VPA and CBZ, an impairment of tubular function can be present, whereas PB does not cause any significant change.

Adolescent↗
PubMed2000

Childhood epilepsy with occipital paroxysms and benign nocturnal childhood occipital epilepsy.

Two types of childhood epilepsy have recently been reported: childhood epilepsy with occipital paroxysms, and benign nocturnal childhood occipital epilepsy. This article reports the clinical evolution, electroencephalographic (EEG) changes, and response to therapy of eight children with childhood epilepsy with occipital paroxysms (five boys and three girls, aged from 1 1/12 to 8 years) and eight children with benign nocturnal childhood occipital epilepsy (six boys and two girls, aged from 1 4/12 to 8 3/12 years). A careful clinical and EEG follow-up of at least 7 years was carried out for all patients. At the end of follow-up, all but one of the patients with childhood epilepsy with occipital paroxysms were seizure-free, and only two were still receiving anticonvulsant drugs. All but three children had a normal EEG, and normal mental development was observed in all but two cases. Patients with benign nocturnal childhood occipital epilepsy had a good long-term prognosis; all but two children with benign nocturnal childhood occipital epilepsy had a normal EEG. These two patients showed learning disabilities and poor school performances, and required remedial education. Therefore, although childhood epilepsy with occipital paroxysms and benign nocturnal childhood occipital epilepsy are two different types of epilepsy, the long-term prognosis seems to be similar.

Anticonvulsants↗
PubMed2000

Febrile convulsions after 5 years of age: long-term follow-up.

In order to examine the natural history of febrile convulsions occurring after 5 years of age, we studied 44 children in whom febrile convulsions persisted after 5 years of age (group 1) and compared their development of unprovoked seizures with a group of 195 children in whom febrile convulsions occurred before 5 years of age (group 2). All subjects of group 1 were re-evaluated at the mean age of 13.4+/-1.7 years. The children in group 2 were followed up until they reached the same mean age as children in group 1 (13.1+/-2.3 years). In group 1, we found a higher percentage of unprovoked seizures than in children with febrile convulsions with onset before 5 years of age (18.1% vs 7.4%, P < .05). Our data suggest that children with febrile convulsions after 5 years of age probably must be considered as a group of patients at risk of developing unprovoked seizures.

Age of Onset↗
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

Neonatal suppurative parotitis: a study of five cases.

UNLABELLED: Suppurative parotitis is uncommon in newborns. During a 9-year study period, five cases of neonatal suppurative parotitis were detected in 3,624 hospital admissions. The relative risk of developing neonatal suppurative parotitis in admitted infants was 5.52 (0.62-49.35). Staphylococcus aureus was the causative organism most commonly detected in the hospital-acquired cases. Antimicrobial therapy was effective in all cases; surgery was not required. CONCLUSION: Although neonatal suppurative parotitis is now uncommon in the newborn, it cannot be considered a "vanishing disease".

Cross Infection↗
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

Headache in children with centrotemporal spikes.

The aim of the study was to evaluate the long-term evolution of headache associated with rolandic centrotemporal spikes (CTS). The patient group consisted of a group of 32 children who suffered from headache and presented CTS at electroencephalogram (EEG). As the control group, we selected 52 sex- and age-matched children with headache without any EEG abnormalities. During a follow-up of 5 years none of them showed epileptic seizures. The number of headache attacks decreased in the majority of patients, as in the controls. A good correlation could be identified between CTS and the number of headaches attacks both at baseline (r = 0.58, P < 0.001) and at follow-up (r = 0.64, P < 0.001). In four children (12.5%), the frequency of headache attacks increased and this increase was associated with a higher frequency of CTS. In two patients, a change in the EEG pattern was observed during follow-up, with a 'migration' of the epileptiform complex from central to parietooccipital leads. In conclusion, these findings confirm that CTS are not pathognomonic of centrotemporal epilepsy and that evolution of CTS and headache in children are statistically related.

Adolescent↗
PubMed1999

Elevated levels of circulating immunostimulatory 90K in Henoch-Schoenlein purpura.

In order to clarify the immunologic reaction present in Henoch-Schoenlein purpura (HSP), 20 children (11 boys and 9 girls; median age, 5.8 +/- 2.8 years) with HSP and 20 sex- and age-matched healthy children were studied. The 90K/Mac-2 BP serum concentrations were significantly higher in the patients than in the healthy controls (12.5 +/- 7.5 vs 4.5 +/- 2.7 micrograms/ml, respectively; P < 0.0001). 90K/Mac-2 BP values higher than the cutoff value were observed in 13 of 20 (65%) patient. The soluble intercellular adhesion molecule 1 concentrations were significantly higher in HSP patients than controls (P < 0.0001), with mean values of 1631 +/- 703 and 85 +/- 16 ng/ml, respectively. The 90K/Mac-2 BP serum levels were significantly correlated with soluble intercellular adhesion molecule 1 (r = 0.90, P < 0.0001). Although the underlying causes of these immunological abnormalities are unclear, these observations suggest that the 90K/Mac-2 BP protein may play a role in the immunological reactions involved in the development of HSP.

Age Distribution↗
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

Hypoglycaemia in children with type 1 diabetes mellitus.

Hypoglycaemia is a frequent acute complication of IDDM and is usually defined as a blood glucose level below 3.0 mmol/l. Hypoglycaemia stimulates several neuroendocrine responses, such as secretion of glucagon, adrenaline, growth hormone and cortisol, which are generally increased during this phenomenon. The true prevalence of hypoglycaemia is not known. Studies of the epidemiology of severe hypoglycaemia give prevalences ranging from 2.7 to 85.7 episodes per 100 patients per year. The major risk factor for severe hypoglycaemia is hypoglycaemia unawareness, which occurs particularly in patients with type 1 diabetes of long duration and in those with a history of frequent episodes of hypoglycaemia. The first step in the management of hypoglycaemia is to check blood glucose and to treat hypoglycaemia on the basis of symptoms. Hypoglycaemia requires urgent treatment with a fast-acting carbohydrate or, if severe, with parenteral glucagon or intravenous glucose. Prevention measures should be instituted to prevent subsequent episodes, particularly in younger children with hypoglycaemic seizures or when seizures are recurrent.

Adolescent↗