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See detailEpidemiologische bewaking van boviene spongiforme encefalopathie in Belgïe: Jaaroverzicht voor 1998
Saegerman, Claude ULg; Dechamps, P.; Vanopdenbosch, E. et al

in Vlaams Diergeneeskundig Tijdschrift (2000), 69

In 1998 werden 6 runderen tussen de 54 en 71 maanden ouderdom, afkomstig van de provincies West-Vlaanderen (3 gevallen), Oost-Vlaanderen (2 gevallen) en Luik (1 geval), gediagnostiseerd als gevallen van ... [more ▼]

In 1998 werden 6 runderen tussen de 54 en 71 maanden ouderdom, afkomstig van de provincies West-Vlaanderen (3 gevallen), Oost-Vlaanderen (2 gevallen) en Luik (1 geval), gediagnostiseerd als gevallen van boviene spongiforme encephalopathie (BSE). De hypotheses betreffende de oorsprong van de infectie op zijn de volgende : het optreden van sporadische gevallen zonder duidelijk definieerbare oorzaak; de mogelijke kruiscontaminatie tussen voeder voor monogastrische dieren met daarin dierlijk meel en voeder voor herkauwers waarin geen dierlijk meel is verwerkt en dit tijdens het fabricatieproces, de stockage, het transport of de distributie; het gebruik van dierlijk beendermeel in het voeder voor runderen geproduceerd voor de ban (van kracht vanaf 27/7/1994). Algemeen kan men dus stellen dat in België de aanwezigheid van gecontamineerd diermeel als risicofactor voor BSE niet kan worden uitgesloten. De oorsprong van deze diermelen kon nog niet gedetermineerd worden. [less ▲]

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See detailEpidemiology
Guillaume, Michèle ULg; Lissau, I

in Burniat, W; Cole, TJ; Lissau, I (Eds.) et al Child and Adolescent Obesity (2002)

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See detailEpidemiology and clinical reporting of candidaemia in Belgium : a national prospective study (TANSIR trial)
Trouvé, Charlotte; Blot, Stijn; Hayette, Marie-Pierre ULg et al

Poster (2015, April 26)

Objectives The aim of this multicenter study was to gather epidemiological data on candidemia in the Belgian population. Another goal was to determine the time in real life setting for reporting to the ... [more ▼]

Objectives The aim of this multicenter study was to gather epidemiological data on candidemia in the Belgian population. Another goal was to determine the time in real life setting for reporting to the treating physicians of the species involved and its antifungal susceptibility. Methods Prospective study in 29 Belgian hospitals. From March 1st, 2013 till February 28, 2014 the first Candida isolate from each episode of candidemia was included. Identification and susceptibility testing were performed according to local procedures and isolates were sent to the National Reference Lab with a completed case report form. Species identification was checked by MALDI-TOF mass spectrometry (MS) and ITS sequencing in case no reliable identification was obtained by MS. Antifungal susceptibility testing was performed according to EUCAST guidelines. The total number of patient admissions and hospitalization days during the study period was retrieved from each hospital. Results 341 isolates were retrieved from 325 patients (53.2% male, median age 66 years, range 1-94 years) admitted to the ICU (34.4%), medical wards (30.8%), surgical wards (15.2%), onco-haematology (10.6%), pediatrics (3.0%), neonatology (1.7%) and other wards (4.3%). The mean incidence rate of candidemia was 0.42 per 1,000 admissions (range 0.07 to 1.44) and 0.60 per 10,000 patient days (range from 0.11 to 2.03). Candida albicans was the main cause of candidemia (51.9%), followed by Candida glabrata (26.7%), Candida parapsilosis (9.9%), Candida tropicalis (4.4%), Candida guilliermondii (2.6%), Candida dubliniensis (1.5%), Candida lusitaniae (1.2%), Candida krusei (1.2%) and Candida metapsilosis (0.6%). Overall resistance to fluconazole was 6.7% and to anidulafungin 0.6% (2 C. glabrata isolates were echinocandin resistant). Resistance to amphotericin B was detected in 1 C. tropicalis isolate, all C. albicans, C. glabrata and C. parapsilosis isolates remained susceptible to this drug. Resistance to fluconazole ranged from 3.5% in C. albicans, 8.6% in C. glabrata, 5.6% in C. parapsilosis to 35.7% (5/14 isolates) in C. tropicalis. These five C. tropicalis isolates showed cross resistance to voriconazole and posaconazole. MIC values for caspofungin ranged from <0,016 to >8mg/L, with MIC50 of 0.06mg/L and MIC90 of 0.25mg/L. The median time between blood sampling and positivity of the blood culture bottle was 37h07min (Q1-Q3: 25h42min-54h28min). The median time between blood culture positivity and reporting of isolate identification and susceptibility to the treating physician was 29h58min (Q1-Q3: 23h21min-40h34min) and 59h34min (Q1-Q3: 48h28min-75h20min) respectively. Conclusions A large variation in the incidence of candidemia among Belgian hospitals was observed. Resistance to azole drugs remained low but emerging resistance to these drugs among C. tropicalis was noted. Resistance to echinocandins remains rare in Belgian Candida isolates. These data will be further analyzed in order to evaluate the influence of the identification and susceptibility testing method on the time to report results to the treating physicians. [less ▲]

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See detailEpidemiology and Diagnosis of Q Fever in Animals and Humans in the 21st Century
Mainil, Jacques ULg; Monseur, Christine ULg; Saegerman, Claude ULg et al

Scientific conference (2015, November 13)

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See detailEpidemiology and familiarity
Beckers, Albert ULg

Scientific conference (2009, November)

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See detailEpidemiology and genetics of FIPA
Beckers, Albert ULg

Scientific conference (2011, November 18)

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See detailEpidemiology and genetics of FIPA
Beckers, Albert ULg

in 15th annual Canadian Society of Endocrinology and metabolism - Abstract book (2012, October)

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See detailEpidemiology and genetics of FIPA
Beckers, Albert ULg

Scientific conference (2011, June 06)

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See detailEpidemiology and genetics of FIPA
Beckers, Albert ULg

in 12th ESE PostGraduate Course in Clinical Endocrinology - Abstract book (2012)

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See detailEpidemiology and Genetics of pituitary adenomas
Beckers, Albert ULg

Scientific conference (2009, May 01)

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See detailEpidemiology and genetics of pituitary adenomas
Beckers, Albert ULg

Scientific conference (2014, March 14)

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See detailEpidemiology and Genetics of pituitary adenomas
Beckers, Albert ULg

Scientific conference (2009, March 02)

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Peer Reviewed
See detailThe epidemiology and genetics of pituitary adenomas.
Daly, Adrian ULg; Tichomirowa, M. A.; Beckers, Albert ULg

in Best Practice & Research. Clinical Endocrinology & Metabolism (2009), 23(5), 543-554

According to data derived from autopsy and radiological imaging series, pituitary tumours occur very commonly in the general population; however, most of these tumours are incidental findings with no ... [more ▼]

According to data derived from autopsy and radiological imaging series, pituitary tumours occur very commonly in the general population; however, most of these tumours are incidental findings with no obvious clinical impact. The historical data on the prevalence of pituitary adenomas in the clinical setting are scant and point to such tumours being relatively rare. Recent studies have shown that the prevalence of clinically relevant pituitary adenomas is 3-5 times higher than previously reported, which adds impetus to research into the aetiology of these tumours. Although the majority of pituitary adenomas are sporadic, approximately 5% of all cases occur in a familial setting and over half of these are due to Multiple Endocrine Neoplasia Type 1 (MEN-1) and Carney's Complex (CNC) disorders. Since the late 1990 s, we have described non-MEN1/CNC familial pituitary tumours that include all tumour phenotypes as a condition termed Familial Isolated Pituitary Adenomas (FIPAs). The clinical characteristics of the FIPAs vary from those sporadic pituitary adenomas, as patients with FIPAs have a younger age at diagnosis and larger tumours. About 15% of the FIPA patients have mutations in the aryl hydrocarbon receptor-interacting protein gene (AIP), which indicates that the FIPA may have a diverse genetic pathophysiology. [less ▲]

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See detailEpidemiology and genetics of pituitary tumors
Beckers, Albert ULg

Scientific conference (2007)

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See detailEpidemiology and genetics of pituitary tumors
Beckers, Albert ULg

Scientific conference (2013, February)

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See detailEpidemiology and genetics of pituitary tumors
Beckers, Albert ULg

Scientific conference (2007, February 01)

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See detailEpidemiology and genetics of pituitary tumours
Beckers, Albert ULg

in Chanson, Philippe (Ed.) Best Practice Research - Clinical Endocrinology and Metabolism (2008)

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See detailEpidemiology and Genetics of Pituitary Tumours
Daly, Adrian ULg

Doctoral thesis (2008)

To have a full understanding of a disease, it is necessary to at least know how frequently it occurs, its clinical features and by what means it is caused. In the case of pituitary adenomas, data in the ... [more ▼]

To have a full understanding of a disease, it is necessary to at least know how frequently it occurs, its clinical features and by what means it is caused. In the case of pituitary adenomas, data in the literature on the epidemiology of these tumors is conflicting, with some studies suggesting a high frequency, others that they occur rarely in the clinical setting. In parallel, the understanding of the pathophysiology of endocrine tumors like pituitary adenomas has advanced greatly with the advent of molecular genetic techniques. However, much remains unclear regarding pathophysiology. A valuable avenue for studying the causes of endocrine tumors has been to focus on the familial setting. With respect to pituitary adenomas, apart from multiple endocrine neoplasia type 1 (MEN1) and Carney complex (CNC), the field of familial pituitary tumors is poorly understood. Indeed, apart from familial acromegaly, there have been virtually no studies on other pituitary adenomas occurring in the familial setting. The aims of the work described in this thesis were based on addressing aspects of the epidemiology and genetics of pituitary tumors. Firstly, the disconnect between the prevalence rates for pituitary adenomas from autopsy/radiology studies (incidentalomas being very common) and cancer registries/population data (rare) was studied. An intensive, comprehensive, case-finding study of the prevalence of pituitary adenomas was performed in three tightly-defined geographical areas in the Province of Liège. In this study, which involved a population of more than 70,000 people, diagnosed pituitary adenomas were sought in collaboration with the entire group of community medical practitioners in the study areas, and the demographics and clinical, hormonal, radiological and pathological features of all patients were confirmed independently. On a fixed date, it was found that clinically diagnosed pituitary adenomas occurred with a prevalence of 1 case per 1064 individuals residing within the geographic boundaries of the study. These results report a clinical prevalence of pituitary adenomas that is 3.5 to 5 times higher than previous population/registry estimates. It suggests that clinically relevant pituitary adenomas occur frequently in the everyday clinical setting, which may have important implications for health resource allocations. Also, it is possible to undertake detailed, comprehensive, crosssectional epidemiological studies in well-defined geographic areas, and this methodology can be applied internationally Studying the familial occurrence of pituitary adenomas outside of MEN1 and CNC was the next aim of the work described. Up to this time, only the familial occurrence of acromegaly had been reported with any frequency in the literature. An international study was undertaken to assess whether isolated pituitary adenomas of all types could occur in the familial setting, a suspicion raised in Liège over the past decade. This study demonstrated that familial isolated pituitary adenomas (FIPA) occur in about 2% of pituitary adenoma populations, and 64 FIPA families were characterized clinically. The study demonstrated for the first time that all phenotypes of pituitary adenomas can occur together in families; some families exhibit only one phenotype among affected members (homogeneous FIPA kindreds), others have multiple tumor types among affected family members (heterogeneous FIPA). In FIPA families, pituitary tumors were more aggressive and tended to occur at a younger age than sporadic pituitary adenomas. FIPA families display a high degree of familiality, suggesting a dominant mode of inheritance. Subsequent studies were performed on the genetic and pathological features of pituitary adenomas, particularly those occurring as FIPA. The discovery of a novel gene, aryl hydrocarbon receptor interacting protein ( AIP), mutations in which were associated with isolated pituitary adenomas, led us to undertake the first such genetic studies in FIPA. AIP mutations account for a minority (15%) of FIPA families and 50% of familial acromegaly kindreds in FIPA. This suggests that other genetic causes for FIPA also exist. In AIP mutation carrying FIPA families, tumors were larger and had a younger age at diagnosis than non- AIP mutated FIPA kindreds. A series of 9 novel AIP mutations were identified, the majority of which led to predicted loss of vital ligand and receptor interacting regions of the AIP protein. AIP mutations in FIPA were associated with multiple pituitary adenoma types, including acromegaly, prolactinomas, mixed growth hormone/prolactin secreting adenomas and non-secreting tumors. It was also found that the same AIP mutation was responsible for different pituitary adenoma types in two separate FIPA families. A detailed follow-up study of an individual FIPA kindred with an AIP mutation found for the first time that non-pituitary tumor-associated endocrine abnormalities (elevated circulating insulin-like growth factor-1) occur in AIP mutation carriers. A detailed analysis of germline and somatic DNA from a large international European cohort of sporadic (non-familial) pituitary adenoma cases showed that AIP mutations occur rarely in this setting. In conclusion, the work undertaken has provided new understanding of the true prevalence of clinically-relevant pituitary adenomas in the population, in addition to codifying and characterizing FIPA, a new clinical entity that represents a potentially valuable area for genetic and clinical studies involving the function of AIP and other as yet unidentified associated genetic causes. [less ▲]

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See detailThe epidemiology and management of pituitary incidentalomas
Daly, Adrian ULg; Burlacu, M. C.; Livadariu, E. et al

in Hormone Research (2007), 68(Suppl. 5), 195-198

Prevalence: The prevalence of pituitary tumors has been a topic of controversy for many years. Autopsy and radiological series show that pituitary incidentalomas may be present in one of six people ... [more ▼]

Prevalence: The prevalence of pituitary tumors has been a topic of controversy for many years. Autopsy and radiological series show that pituitary incidentalomas may be present in one of six people. Recent epidemiological data suggest that clinically apparent pituitary adenomas have a prevalence of approximately one in 1,000 people in the general population. The disconnect between these two prevalence rates underlines the common clinical quandary of how to manage pituitary incidentalomas, particularly those lacking clinical signs/symptoms or hormonal abnormalities. Management: The natural history of incidentalomas suggests that periodic hormonal, clinical and radiological follow-up is the optimal approach. In the absence of tumor growth or relevant symptoms, screening can be continued intermittently or curtailed based on the clinical judgment of the physician. In the presence of hormonal hypersecretion, the management of pituitary incidentalomas, whether they are micro- or macroadenomas, should follow accepted clinical guidelines. For incidental pituitary macroadenomas without hormonal hypersecretion, clinical management should also include assessments for visual field impairment or hypopituitarism. In such cases, regular radiological and hormonal follow-up is required to identify tumor growth or the appearance of new symptoms. In the presence of tumor growth or new hormonal abnormalities, surgical options should be considered and discussed with the patient. Copyright (C) 2007 S. Karger AG, Basel. [less ▲]

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