Center Hospitalier Jolimont Lobbes

Nivelles, Belgium

Center Hospitalier Jolimont Lobbes

Nivelles, Belgium
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Wiegman A.,University of Amsterdam | Gidding S.S.,DuPont Company | Watts G.F.,University of Western Australia | Chapman M.J.,University Pierre and Marie Curie | And 35 more authors.
European Heart Journal | Year: 2015

Familial hypercholesterolæmia (FH) is a common genetic cause of premature coronary heart disease (CHD). Globally, one baby is born with FH every minute. If diagnosed and treated early in childhood, individuals with FH can have normal life expectancy. This consensus paper aims to improve awareness of the need for early detection and management of FH children. Familial hypercholesterolæmia is diagnosed either on phenotypic criteria, i.e. an elevated low-density lipoprotein cholesterol (LDL-C) level plus a family history of elevated LDL-C, premature coronary artery disease and/or genetic diagnosis, or positive genetic testing. Childhood is the optimal period for discrimination between FH and non-FH using LDL-C screening. An LDL-C ≥5 mmol/L (190 mg/dL), or an LDL-C ≥4 mmol/L (160 mg/dL) with family history of premature CHD and/or high baseline cholesterol in one parent, make the phenotypic diagnosis. If a parent has a genetic defect, the LDL-C cut-off for the child is ≥3.5 mmol/L (130 mg/dL). We recommend cascade screening of families using a combined phenotypic and genotypic strategy. In children, testing is recommended from age 5 years, or earlier if homozygous FH is suspected. A healthy lifestyle and statin treatment (from age 8 to 10 years) are the cornerstones of management of heterozygous FH. Target LDL-C is <3.5 mmol/L (130 mg/dL) if >10 years, or ideally 50% reduction from baseline if 8-10 years, especially with very high LDL-C, elevated lipoprotein(a), a family history of premature CHD or other cardiovascular risk factors, balanced against the long-term risk of treatment side effects. Identifying FH early and optimally lowering LDL-C over the lifespan reduces cumulative LDL-C burden and offers health and socioeconomic benefits. To drive policy change for timely detection and management, we call for further studies in the young. Increased awareness, early identification, and optimal treatment from childhood are critical to adding decades of healthy life for children and adolescents with FH. © 2015 The Author.


PubMed | University of Witwatersrand, Center Hospitalier Jolimont Lobbes, University of Helsinki, University of Western Australia and 24 more.
Type: Journal Article | Journal: European heart journal | Year: 2015

Familial hypercholesterolaemia (FH) is a common genetic cause of premature coronary heart disease (CHD). Globally, one baby is born with FH every minute. If diagnosed and treated early in childhood, individuals with FH can have normal life expectancy. This consensus paper aims to improve awareness of the need for early detection and management of FH children. Familial hypercholesterolaemia is diagnosed either on phenotypic criteria, i.e. an elevated low-density lipoprotein cholesterol (LDL-C) level plus a family history of elevated LDL-C, premature coronary artery disease and/or genetic diagnosis, or positive genetic testing. Childhood is the optimal period for discrimination between FH and non-FH using LDL-C screening. An LDL-C 5 mmol/L (190 mg/dL), or an LDL-C 4 mmol/L (160 mg/dL) with family history of premature CHD and/or high baseline cholesterol in one parent, make the phenotypic diagnosis. If a parent has a genetic defect, the LDL-C cut-off for the child is 3.5 mmol/L (130 mg/dL). We recommend cascade screening of families using a combined phenotypic and genotypic strategy. In children, testing is recommended from age 5 years, or earlier if homozygous FH is suspected. A healthy lifestyle and statin treatment (from age 8 to 10 years) are the cornerstones of management of heterozygous FH. Target LDL-C is <3.5 mmol/L (130 mg/dL) if >10 years, or ideally 50% reduction from baseline if 8-10 years, especially with very high LDL-C, elevated lipoprotein(a), a family history of premature CHD or other cardiovascular risk factors, balanced against the long-term risk of treatment side effects. Identifying FH early and optimally lowering LDL-C over the lifespan reduces cumulative LDL-C burden and offers health and socioeconomic benefits. To drive policy change for timely detection and management, we call for further studies in the young. Increased awareness, early identification, and optimal treatment from childhood are critical to adding decades of healthy life for children and adolescents with FH.


Heller F.,Center Hospitalier Jolimont Lobbes
Acta Clinica Belgica | Year: 2013

Differences in response to medications both in terms of clinical activity and side-effects have long been recognised by physicians. Genetics has been recently considered as a potential factor to explain part of this variability. Pharmacogenetics focuses on the variants within one or more candidate genes while pharmacogenomics evaluates the entire genome for associations with pharmacologic phenotypes. Genetic variants can effect drug metabolism, drug transport or drug targets. Drug metabolism is responsible 1. for the conversion of prodrugs into active compounds or conversion of drugs to toxic or inactive metabolites mostly through reactions mostly catalysed by cytochromes (CYP) P450 (phase I reactions) and 2. for transforming drugs to compounds that are more water soluble and more easily excreted (phase type II reactions). Genetic polymorphisms can modify the activity of several CYPs such as CYPs 2D6, 2C9, 2C19 with altered responses to codeine, tamoxifen, clopidogrel, warfarin, ̇ or of enzymes of the phase II reactions with abnormal responses to drugs like irinotecan, 5-fluorouracil, azathioprine, ̇ Proteins involved in the transport of drugs in or out the cells such as chemiotherapeutic agents, simvastatin, ̇ can also be affected by genetics. Genetics can also modify drug targets by mutations affecting tumour cells rending these latter more or less responsive to drugs. Genetic tests have been launched for screening polymorphisms before giving drugs such as warfarin and several biomarkers are available in oncology. However, many challenges exist. For example, we need more prospective studies to have a better knowledge of the clinical impact and the cost-effectiveness of these tests. It remains that in the future pharmacogenetics/ genomics will probably help to personalise medicine by conferring to the clinician the possibility of giving the right drug to the right patient and by this way improving efficacy and safety of medications.


de Vroey B.,Gastroenterology | Schapira M.,Gastroenterology | Peny M.O.,Center Hospitalier Jolimont Lobbes | Ghilain J.M.,Gastroenterology
Acta Gastro-Enterologica Belgica | Year: 2011

Collagenous colitis is a cause of chronic diarrhea of incompletely elucidated origin, defined by normal laboratory tests, a normal endoscopic appearance of colonic mucosa and specific microscopic inflammatory features on colonic biopsies. We report two cases of macroscopic endoscopic lesions observed in patients suffering from chronic diarrhea, whose biopsies confirmed a diagnosis of collagenous colitis and who were successfully treated in that setting, achieving clinical and endoscopic remissions. By means of a literature review, we summarize what is known about collagenous colitis. We particularly discuss macroscopic findings in that context, drawing attention on the so called "microscopic colitis" in the differential diagnosis of that type of lesions.


Descamps O.S.,Center for Medical Research at Jolimont | Descamps O.S.,Center Hospitalier Jolimont Lobbes | Tarantino E.,Center for Medical Research at Jolimont | Guilmot P.-F.,Center Hospitalier Jolimont Lobbes
BMC Genetics | Year: 2014

Background: Low weight at birth is associated with obesity in later life. One hypothesis to explain such an association is that genetic variants that increase the risk of obesity also reduce fetal weight. Recently, obesity in adults was found to be associated with common variants of the fat mass and obesity-associated (FTO) gene. We examined the association between FTO polymorphisms and birth weight in a singleton, full-term birth cohort of 494 newborn-mother pairs without any complications. Results: The risk alleles for obesity ("A" allele for the rs9939609 FTO variant and "G" allele for the rs9930506 FTO variant) were associated with low weight at birth. The mean differences per risk allele were -79g (95% CI: -129 to -30; p = 0.002) for rs9939609 and -84g (95% CI: -131 to -36; P < 0.001) for rs9930506. The level of association remained statistically significant after adjustment for the maternal risk allele and for variables usually associated with birth weight (-50g, 95% CI: -99 to 0; p = 0.05 for rs9939609 and -48g, 95% CI: -100 to 0; p = 0.05 for rs9930506). In the follow-up, the allelic difference in weight was attenuated over time. Conclusions: The FTO variants that confer a predisposition to obesity later in life appear to be associated with low weight at birth. This finding favors the hypothesis of a common genetic denominator that predisposes to a low weight at birth and obesity in adults. © Descamps et al.


De Greef J.,Center Hospitalier Jolimont Lobbes | Jaumotte C.,Center Hospitalier Jolimont Lobbes | Quivron B.,Center Hospitalier Jolimont Lobbes | Derue G.,Center Hospitalier Jolimont Lobbes
Acta Clinica Belgica | Year: 2014

Reversible lesions of the splenium of the corpus callosum constitute a clinicoradiological syndrome that has been associated to various medical conditions. We report the case of a 47-year-old man who presented with encephalopathy associated to auto-immune thyroid disease in which a reversible splenial lesion was isolated. Although encephalopathy associated to auto-immune thyroid disease is characterized by variable radiological findings, it has only been once associated with a reversible splenial lesion. © Acta Clinica Belgica 2014.


Lemaire J.,Cliniques Universitaires Saint Luc | Delaunoit T.,Center Hospitalier Jolimont Lobbes | Molle G.,Cliniques Universitaires Saint Luc
Acta Chirurgica Belgica | Year: 2014

A sixty years-old patient was admitted with a gastric tumor corresponding to an adenocarcinoma developed in ectopic pancreatic tissue. Hundred cases of gastric heterotopic pancreas are shown in literature. This entity may remain asymptomatic. Symptoms such abdominal pain are described as the result of tumour growth. Carcinogenesis of ectopic pancreas (EPa) is however rare. Diagnosis is rarely pre-operative because modern imaging depicts a gastric tumour with no more information. The only treatment is surgery, with a best interest in frozen sections to direct the procedure, in this case a total gastrectomy with D2 lymphadenectomy. Based on this case report, an analysis of the literature focusing on diagnosis and treatment is presented. © Acta Chirurgica Belgica.


PubMed | Center Hospitalier Jolimont Lobbes
Type: Case Reports | Journal: Acta gastro-enterologica Belgica | Year: 2011

Collagenous colitis is a cause of chronic diarrhea of incompletely elucidated origin, defined by normal laboratory tests, a normal endoscopic appearance of colonic mucosa and specific microscopic inflammatory features on colonic biopsies. We report two cases of macroscopic endoscopic lesions observed in patients suffering from chronic diarrhea, whose biopsies confirmed a diagnosis of collagenous colitis and who were successfully treated in that setting, achieving clinical and endoscopic remissions. By means of a literature review, we summarize what is known about collagenous colitis. We particularly discuss macroscopic findings in that context, drawing attention on the so called microscopic colitis in the differential diagnosis of that type of lesions.


PubMed | Center Hospitalier Jolimont Lobbes
Type: Journal Article | Journal: Nature reviews. Gastroenterology & hepatology | Year: 2011

The management of IBD remains a challenge, with the main issue being to combine therapeutic efficiency with minimal side effects and optimal quality of life. Efforts towards achieving this objective continued in 2010we discuss some of the most relevant publications and their potential impact on daily practice in the future.


Marchandise S.,Cliniques Universitaires St Luc | Scavee C.,Cliniques Universitaires St Luc | Badot D.,Center Hospitalier Jolimont Lobbes | Deceuninck O.,Catholic University of Leuven | And 4 more authors.
Journal of Cardiovascular Electrophysiology | Year: 2012

Adenosine and Ablation of Typical Atrial Flutter. Introduction: Early recovery of conduction (ER) after cavotricuspid isthmus (CTI) ablation for typical atrial flutter (AFl) occurs in approximately 10% of the patients. If not recognized, ER might lead to AFl recurrences. In this study, we hypothesized that intravenous adenosine (iADO) can be used to predict ER in the CTI immediately after RF ablation and distinguish functional block from the complete destruction of the CTI myocardium. Methods: We prospectively included 68 consecutive patients (age: 65 ± 14 years; male: 78%) referred in our centers for AFl ablation. Immediately after bidirectional isthmus block validation, a bolus of iADO was given during continuous pacing from the proximal coronary sinus. Patients with functional block revealed under iADO (iADO+) and those without (iADO-) were subsequently observed for a 30-minute waiting period (ER-) or until sustained recovery of the conduction through the CTI (ER+). Results: Seven patients presented a persistent recovery (ER+, 10.3%, mean time to recovery: 14 ± 9 minutes). None of them presented even a transient resumption of conduction under iADO (iADO+: 0). With univariate analysis, we identified a heavy patient weight (>95 kg) as a predictor of ER (sensitivity: 71%). Conclusions: Adenosine does not predict early recovery in the CTI after linear ablation for atrial flutter. We found that a patient weight over 95 kg predicted early recovery of conduction through the CTI with a sensitivity of 71%. (J Cardiovasc Electrophysiol, Vol. 23, pp. 1201-1206, November 2012) © 2012 Wiley Periodicals, Inc.

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