References of "Leroy, Patricia"
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See detailÉPIDÉMIOLOGIE ET CARACTÉRISTIQUES DES CONVULSIONS FEBRILES DE L'ENFANT
KAPUTU, Kalala Malu CELESTIN; MAFUTA, Musalu ERIC; DUBRU, Jean-Marie ULg et al

in Revue Médicale de Liège (2013), 68(4), 180-185

Summary : Febrile Seizures (FS), despite their usual benign clinical course, are still subject of controversies regarding the need for further investigation and treatment with anti-epileptic drugs (AEDs ... [more ▼]

Summary : Febrile Seizures (FS), despite their usual benign clinical course, are still subject of controversies regarding the need for further investigation and treatment with anti-epileptic drugs (AEDs). Our study aimed to inventory the clinical findings, laboratory and imaging data associated with FS and eventually influencing their management. 275 episodes admitted with FS at the emergency ward of the Liège CHR over a 5 year period were retrospectively analyzed regarding precipitating factors; clinical features; laboratory, electroencephalographic, and imaging studies; as well as treatment response. FS represented 1.4% of admissions to the pediatric service. 31.3% of patients had a family history of seizure disorder. 9% percent of seizures were focal, 11.7% recurrent, and 12.3% prolonged (greater than 10 minutes). Upper respiratory tract and otorhinolaryngologic viral infections were the most often implicated provoking factors, occurring in 69.5% of patients. Laboratory, electroencephalographic and radiographic studies were normal in more than 90% of cases. 73.8% of seizures resolved without intervention. An AED was required to manage the remaining 26.2%. This study confirms the favorable outcomes of FS as demonstrated in previous studies. This happens without requiring AEDs for resolution, and without recurrence. Laboratory, electroencephalographic and imaging studies, as well as initiation of AEDs should be based primarily on clinical severity. [less ▲]

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See detailHYPERINSULINISM-HYPERAMMONEMIA: AN UNUSUAL CAUSE OF HYPOKETOTIC HYPOGLYCEMIA
HARVENGT, Julie ULg; LEBRETHON, Marie-Christine ULg; leroy, patricia et al

Poster (2010, March)

BACKGROUND Etiological diagnosis of hypoglycaemia in infancy is a complex process, requiring careful integration of detailed history, clinical and laboratory data. The causes of recurrent infant ... [more ▼]

BACKGROUND Etiological diagnosis of hypoglycaemia in infancy is a complex process, requiring careful integration of detailed history, clinical and laboratory data. The causes of recurrent infant hypoglycaemia include excessive insulin secretion, surreptitious insulin administration, deficiency of counter-regulatory hormones and inborn errors of metabolism. CLINICAL CASE A 10 month old girl was admitted at our emergency unit for generalized seizures without fever. Routine laboratory investigations were normal but blood glucose level was at 31 mg/dl. No ketone bodies were found in the urine. Past medical history revealed failure to thrive. A first seizure episode at 8 months of age during family’s holiday is reported. Tests performed in a foreign hospital revealed glycaemia at 36mg/dl. During her stay in our paediatric unit, several hypoglycaemias (31-45 mg/dl) were documented related to irritability as initial symptom of neuroglucopaenia. Detailed medical history revealed that fast tolerance was shorten with hypoglycaemia documented between one to three hours after eating. Clinical examination showed absence of hepatomegaly and failure to thrive: weight, -3SD; height, -2SD, and cranial circumference -2SD. At the time of hypoglycaemia, urinary tests revealed absence of ketonuria, that basically evokes hyperinsulinism or fatty acid oxidation deficiencies but these deficiencies were rapidly excluded by the very short fast state. Blood acylcarnitine profile was normal. Hyperinsulinism is defined by a ratio glycaemia/insulin below 4 with insulin values not necessary high. Since hyperinsulinism can not be excluded with only one blood measure, series of taking were performed during 24 hours. One of these tests was clearly positive with ratio equal to 2.3 (glycaemia at 41 mg/dl, insulin at 18µU/ml). For this patient, ammonemia was also tested with values ranged from 242 to 275 µg/dl (normal < 125) and the diagnosis of hyperinsulinism/hyperammoniemia (hi/ha) was made and confirmed by molecular analysis (mutation c.965G>A (p.R269H) in the GLUD1 gene). The treatment consists in this case by diazoxide and reduction of leucine intakes (< 200 mg of leucine/meal). DISCUSSION Differential diagnosis of hypoglycaemia with absence of ketonuria and absence of hepatomegaly include fatty acids β-oxidation defects, ketogenesis defects and hyperinsulinisms. Short fasting and post-prandial induced hypoglycaemia pointed to hyperinsulinism in our patient. Congenital hyperinsulinism includes KATP, glucokinase or glutamate deshydrogenase mutations. Hi/ha syndrome is due to activating mutations in the GLUD1 gene, coding for the glutamate dehydrogenase (GDH). Such mutations reduce the sensitivity of the enzyme to allosteric inhibition by GTP and consequently increase its sensitivity to allosteric activation by L-leucine. Hyperactivity of the GDH is responsible for over-oxidation of glutamate in β-pancreatic cells, increase of the ATP/ADP ratio and insulin release. Hyperactivity of GDH in liver is also responsible for hyperammonemia, which is usually mild and considered harmless for the brain. Nevertheless, recent studies have shown an increased epilepsy risk in cohorts of patients with hi/ha. CONCLUSION This case points out the importance of necessity for first investigations of infant documented case of hypoglycaemia. Patient history must focus on symptoms such as shorten fast tolerance periods and neurological symptoms of glucose deprivation. Blood samples should be taken at the time of hypoglycaemia and urine samples as soon as possible after the episode of hypoglycaemia. Initial normal insulin values do not allow the exclusion of the diagnosis of hyperinsulinism. [less ▲]

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See detailActualites therapeutiques en neuropediatrie
Leroy, Patricia; Dubru, Jean-Marie ULg; Misson, Jean-Paul ULg

in Revue Médicale de Liège (2007), 62(5-6, May-Jun), 449-450

The most recent antiepileptic drugs used in children are lamotrigine, topiramate, oxcarbamaz6pine and levetiracetam. Their efficacy is proven, depending on the type of crisis, but in Belgium they are ... [more ▼]

The most recent antiepileptic drugs used in children are lamotrigine, topiramate, oxcarbamaz6pine and levetiracetam. Their efficacy is proven, depending on the type of crisis, but in Belgium they are reimbursed only in certain conditions. The treatment of children with attention deficit hyperactivity disorder (ADHD), which was only constituted of methylphenidate, can now benefit from atomoxetine whose mechanism of action is different. [less ▲]

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See detailA propos d'un cas d'hémiparésie aigue chez l'enfant
Daron, Aurore; Leroy, Patricia; Misson, Jean-Paul ULg

in Percentile (2005), 10

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See detailDéveloppement normal et anormal du cortex cérébral: un up-date
Misson, Jean-Paul ULg; Dubru, Jean-Marie ULg; Leroy, Patricia

in Percentile (2004), 9(1), 3-6

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See detailNeuronal migration disorders and epilepsies
Misson, Jean-Paul ULg; Dubru, Jean-Marie ULg; Leroy, Patricia et al

in Nehlig, Astrid; Motte, Jacques (Eds.) Childhood epilepsies and brain development (1999)

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See detailTumeurs Cérébrales chez l'Enfant : Expérience du Département Universitaire de Pédiatrie de Liège
Senterre, Thibault ULg; Leroy, Patricia; Misson, Jean-Paul ULg

in Percentile (1998), 3(1), 26-28

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See detailElectroencéphalographie du prématuré et du nouveau-né à terme
Dubru, Jean-Marie ULg; Leroy, Patricia; Misson, Jean-Paul ULg

in Percentile (1998), 3

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See detailTraumatismes crâniens et épilepsie
Leroy, Patricia; Dubru, Jean-Marie ULg; Misson, Jean-Paul ULg

in Percentile (1998), 3(1), 29-32

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See detailEpilepsies rebelles de l'enfant: définition et modalités de prise en charge hospitalière
Leroy, Patricia; Dubru, Jean-Marie ULg; Misson, Jean-Paul ULg

in Neurone (1997), 2(8), 285-288

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See detailLes convulsions fébriles: attitude actuelle
Misson, Jean-Paul ULg; Leroy, Patricia; Dubru, Jean-Marie ULg

in Tempo Médical (1996)

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See detailRetard neuromoteur et neuropsychologique: critères de recours à une prise en charge spécialisée
Misson, Jean-Paul ULg; Dubru, Jean-Marie ULg; Leroy, Patricia et al

in Percentile (1996), .(3), 103-107

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See detailReconnaissance des malformations et pathologies prénatales du système nerveux central
Misson, Jean-Paul ULg; Dubru, Jean-Marie ULg; Leroy, Patricia

in Acta Paediatrica Belgica (1996), 28(3), 204-215

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See detailCaractéristiques des lésions résultant d'une pathologie périnatale
Dubru, Jean-Marie ULg; Leroy, Patricia; Misson, Jean-Paul ULg

in Acta Paediatrica Belgica (1996), 28(3), 203-204

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See detailImages liées à la pathologie traumatique du système nerveux central
Leroy, Patricia; Dubru, Jean-Marie ULg; Misson, Jean-Paul ULg

in Acta Paediatrica Belgica (1996), 28(3), 216

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See detailLa Biologie clinique en pédiatrie: hypotonie et retard moteur
Misson, Jean-Paul ULg; Leroy, Patricia; Dubru, Jean-Marie ULg et al

in Acta Paediatrica Belgica (1996), 28(2), 95

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See detailLambdoid synostosis - pachycephaly: diagnosis and treatment
Misson, Jean-Paul ULg; Born, Jacques; Collignon, L. et al

in Developmental Medicine and Child Neurology. Supplement (1995), 37(3), 87

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