References of "DELWAIDE, Jean"
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See detailL'hépatite E
Delwaide, Jean ULg; Gerard, Christiane ULg

in Les Hépatites virales, Roche (1998)

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See detailAlcoholic liver disease: how to detect alcoholism?
Delwaide, Jean ULg

in Problem solving in hepatobiliary diseases (1998)

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See detailLe syndrome hépato-pulmonaire
Lamproye, Anne ULg; Weber, T.; Delwaide, Jean ULg et al

in Revue Médicale de Liège (1997), 52(10), 666-670

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See detailLes modes de transmission du virus de l'hépatite C
Delwaide, Jean ULg; Gerard, Christiane ULg; Sondag, Danièle ULg et al

in Revue Médicale de Liège (1997), 52(6), 388-391

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See detailPolymorphous light eruption-like lesions on sun-protected injection sites of recombinant IFN-alpha-2b
Nikkels, Arjen ULg; Delwaide, Jean ULg; Letawe, C. et al

in Journal of Dermatological Treatment (1997), 8(4), 285

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See detailLes modes de transmission du virus de l'hépatite C
Delwaide, Jean ULg; Gerard, Christiane ULg; Sondag, Danièle ULg et al

in Médecine & Chirurgie Digestives (1997), 26

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See detailLa vaccination contre les hépatites A et B
Delwaide, Jean ULg; Belaiche, Jacques ULg

in Revue Médicale de Liège (1997), 52(10), 639-643

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See detailAnswers to frequently asked questions concerning hepatitis C
Gerard, Christiane ULg; Delwaide, Jean ULg

in Decker, R.; Troonen, H. (Eds.) Hepatitis C 1997: Essays and Expert Opinions on its Natural History, Epidemiology, Diagnosis and Therapy (1997)

Supporting a referral center in a university hospital, our staff is regularly exposed to amultitude of questions concerning hepatitis C from a great variety of individuals including laboratorians, general ... [more ▼]

Supporting a referral center in a university hospital, our staff is regularly exposed to amultitude of questions concerning hepatitis C from a great variety of individuals including laboratorians, general practitioners and their patients, nurses, gastroenterologists, and affiliated health care professionals. The following reflects our collective experience in answering the most frequently posed questions. [less ▲]

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See detailAcromégalie et polypes coliques
Beckers, Albert ULg; Delhougne, B.; Deneux, C. et al

in Beckers, Albert (Ed.) Acromégalie : Les conséquences de l'hypersomatropisme (1996)

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See detailLe cas clinique du mois. Hemochromatose genetique
Collignon, Nathalie ULg; Delwaide, Jean ULg; Belaiche, Jacques ULg

in Revue Médicale de Liège (1996), 51(2), 150-153

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See detailThe prevalence of colonic polyps in acromegaly : a prospective colonoscopic and pathological study in 103 patients.
Delhougne, B.; Deneux, C.; Abs, R. et al

in Journal of Clinical Endocrinology and Metabolism (1995), 80(11), 3223-3226

Patients with acromegaly are reported to be at risk of developing adenomatous colonic polyps, which are considered to be preneoplastic lesions. This assumption is, however, usually drawn from results ... [more ▼]

Patients with acromegaly are reported to be at risk of developing adenomatous colonic polyps, which are considered to be preneoplastic lesions. This assumption is, however, usually drawn from results obtained in rather small series of patients or without a control group. We, therefore, undertook a prospective colonoscopic and pathological study comprising 103 acromegalic patients and 138 nonacromegalic control subjects referred for irritable bowel syndrome. The prevalence of adenomatous colonic polyps was significantly increased in acromegalic patients compared to that in control subjects (22.3% vs. 8.0%; P = 0.0024). The significance was similarly present in male acromegalic patients (28.6% vs. 5.5% in male control subjects; P = 0.0026), but was absent in female acromegalic patients. The prevalence of colonic polyps was also significantly increased in the group of acromegalic patients under 55 yr of age (20.0% vs. 3.0% in the control group of the same age; P = 0.0026). Other characteristics of adenomatous colonic polyps in acromegaly were the multiplicity and the presence proximal to the splenic flexure. No difference in the duration of acromegaly was found between patients with or without adenomatous polyps. The prevalence of hyperplastic colonic polyps was also significantly increased to 24.3% in acromegalic patients vs 4.4% in control subjects (P < 0.001). In conclusion, in view of the increased incidence of adenomatous colonic polyps, colonoscopy should be part of the follow-up examination in acromegaly. [less ▲]

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See detailIncreased prevalence of colonic adenomas in acromegalics patiens
Delhougne, B.; Deneux, C.; Abs, R. et al

in Belgian week of gastroenterology : Knokke, March 16th-18th 1995 - Abstract book (1995, March)

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See detailIncreased prevalence of colonic adenomas acromegalic patients
Delhougne, B.; Deneux, C.; Abs, R. et al

in Fourth Meeting of the Belgian Endocrine Society : 19 november 1994 - Abstract book (1994, November 19)

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See detailGastroentéropathies avec pertes de protéines
Belaiche, Jacques ULg; Delwaide, Jean ULg; Louis, Edouard ULg

in Encyclopédie médico-chirurgicale (1994)

Le tractus gastro-intestinal joue un rôle important dans l'homéostasie des protéines plasmatiques, aussi bien chez le sujet normal que dans les états pathologiques. A l'état physiologique, les protéines ... [more ▼]

Le tractus gastro-intestinal joue un rôle important dans l'homéostasie des protéines plasmatiques, aussi bien chez le sujet normal que dans les états pathologiques. A l'état physiologique, les protéines présentes dans la lumière intestinale ont une double origine: exogène, constituée des protéines alimentaires, et endogène, provenant des sécrétions digestives, de la desquamation cellulaire et des protéines plasmatiques sécrétées ou exsudées. L'exagération de ce dernier mécanisme définit l'entéropathie exsudative qu'il est plus logique de dénommer gastroentéropathie exsudative ou gastroentéropathie avec pertes de protéines dans la mesure où l'estomac peut participer à t'exsudation et que les pertes portent surtout sur les protéines normalement présentes dans le sang, la lymphe et le liquide interstitel. Citrin et coll. [26] ont été les premiers, en 1957, à mettre en évidence une déperdition d'albumine marquée a l'iode 131 chez un malade présentant une maladie de Ménétrier. Le terme d'entéropathie exsudative (<< protein-losing enteropathy ») a été utilisé pour la première fois en 1959 par Gordon aux Etats-Unis et Schwartz et Jarnum au Danemark. En France, c'est à Cattan et Vésin r2~] que l'on doit les premiers travaux consacrés à cette entité. Il s'agit en fait d'un syndrome relevant de causes multiples. Dans la majorité des cas, les manifestations cliniques et biologiques de l'exsudation sont au second plan, masquées par l'affection en cause. Le diagnostic est plus rarement évoqué devant une hypoprotidémie avec ou sans syndrome oedémateux non expliquée par une origine hépatique ou rénale. [less ▲]

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See detailH3-receptor regulation of vascular gastrin and somatostatin releases by the isolated rat stomach.
Bado, A.; Moizo, L.; Laigneau, J. P. et al

in Yale Journal of Biology and Medicine (The) (1994), 67(3-4), 113-121

We have studied the effects of the H3-receptor agonist (R) alpha-methylhistamine [(R) alpha-MeHA] and the H3-receptor antagonist thioperamide (Thiop) on basal- and carbachol-stimulated vascular gastrin ... [more ▼]

We have studied the effects of the H3-receptor agonist (R) alpha-methylhistamine [(R) alpha-MeHA] and the H3-receptor antagonist thioperamide (Thiop) on basal- and carbachol-stimulated vascular gastrin release (GR) and somatostatin release (SR) by the isolated rat stomach. Carbachol dose-dependently stimulated and inhibited GR and SR, respectively. Maximal stimulation of GR (500 +/- 112 percent of basal; p < .01), and maximal inhibition of SR (-62 +/- 9 percent under basal; p < .01) were obtained with 1 micron carbachol. Neither (R)alpha-MeHA nor Thiop, up to 10 microns, affected GR. However, SR was dose-dependently enhanced by Thiop (25 +/- 8 percent for 10 microns). Carbachol stimulation of GR was strongly inhibited by Thiop (30 +/- 7 percent for 100 nM and 73 +/- 14 percent for 1 microgram), whereas it was potentiated by (R)alpha-MeHA. Carbachol inhibition of SR was reversed by Thiop and (R)alpha-MeHA. However, the reversal effect of (R)alpha-MeHA was prevented by the CCKB/gastrin receptor antagonist PD134308. These results support H3-receptor regulation of basal and cholinergically-stimulated GR and SR. [less ▲]

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See detailEffects of Proglumide and Enprostil on Omeprazole-Induced Fundic Endocrine Cell Hyperplasia in Rats
Delwaide, Jean ULg; Latour, Pascale ULg; Gast, Pierrette ULg et al

in Gastroentérologie Clinique et Biologique (1993), 17(11), 792-6

Long-term treatment with omeprazole induces hyperplasia of enterochromaffin-like cells, closely related to hypergastrinemia. We studied whether proglumide, an antagonist of gastrin/CCK receptor, and ... [more ▼]

Long-term treatment with omeprazole induces hyperplasia of enterochromaffin-like cells, closely related to hypergastrinemia. We studied whether proglumide, an antagonist of gastrin/CCK receptor, and enprostil, a synthetic prostaglandin E2 derivative, might inhibit this hyperplasia. Six groups of 8 rats were treated for 10 weeks: a) untreated controls; b) omeprazole 10 mumol/kg; c) proglumide 500 mg/kg; d) enprostil 30 micrograms/kg; e) association of omeprazole and proglumide; f) association of omeprazole and enprostil. Serum gastrin levels were measured at different times during treatment. After sacrifice, fundic argyrophil cells were assessed by Grimelius' staining. Serum gastrin levels and argyrophil cell density were not modified in proglumide- and enprostil-treated groups, as compared with controls. Omeprazole increased significantly these two parameters. When given with omeprazole, proglumide decreased significantly serum gastrin levels and argyrophil cell density, as compared to omeprazole alone, while enprostil did not modify significantly these two parameters. These results indicate that proglumide, but not enprostil, can counteract the omeprazole-induced argyrophil cell hyperplasia in rats. [less ▲]

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