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See detailThe effects of growth hormone replacement therapy on bone metabolism in adult-onset growth hormone deficiency: A 2-year open randomized controlled multicenter trial
Bex, M.; Abs, R.; Maiter, D. et al

in Journal of Bone and Mineral Research (2002), 17(6), 1081-1094

Adult hypopituitary patients with growth hormone deficiency (GHD) show a significant decrease in bone mass and an increased fracture rate. Replacement therapy with GH increases bone turnover. Most of the ... [more ▼]

Adult hypopituitary patients with growth hormone deficiency (GHD) show a significant decrease in bone mass and an increased fracture rate. Replacement therapy with GH increases bone turnover. Most of the long-term data on bone mineral content (BMC) and bone mineral density (BMD) have been acquired in open, noncontrolled trials involving limited numbers of patients. To determine whether long-term GH therapy is beneficial for bone despite the increased bone turnover, 100 patients (59 men and 41 women), aged 25-65 years (mean, 49.7 years) with adult-onset GHD were randomized to treatment with GH (40 men and 28 women; mean dose, 0.18 IU/kg per week) or to a nontreated control group (19 men and 13 women) for 24 months. Despite a similar increase in parameters of bone turnover (osteocalcin [OC], procollagen type I carboxy-terminal propeptide [PICP], and pyridinolines ([PYD]) in male and female GH-treated patients compared with controls, the effects on BMC and BMD as evaluated by dual-energy X-ray absorptiometry were gender specific. A significant increase in spine BMC and BMD and total hip BMD and a decrease in BMD at the ultradistal radius over time was observed in male GH-treated patients compared with the evolution in controls (mean +/- SEM change at 24 months: + 6.8 +/- 1.1% and p = 0.009, +5.1 +/- 0.8% and p = 0.005, +3.5 +/- 0.7% and p = 0.02, and -2.6 +/- 0.8% and p = 0.008, respectively). No significant treatment effects were observed in female patients. Despite the increase in the total remodeling space induced by GH treatment, prolonged GH therapy in adult-onset GHD has a positive effect on bone balance, maintaining bone mass in women, and even increasing it in men over a 2 year-period. [less ▲]

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See detailCabergoline in the treatment of Hyoerprolactinemia : A study in 455 patients
Verhelst, J.; Abs, R.; Maiter, D. et al

in 9th Meeting and workshop of the European Neuroendocrine Association - Abstract book (1999)

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See detailCharacterization of menin from leucocytes of normal and men 1-affected individuals
Poncin, J.; Closset, J.; Legros, J.-J. et al

in 7th International workshop on Multiple Endocrine Neoplasia - Abstract book (1999)

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See detailEffects of growth hormone therapy on bone metabolism in patients with adult-onset : a 2-year open randomized controlled multicentre trial
Bex, M.; Abs, R.; Maiter, D. et al

in The 6th International Pituitary Congress - Abstract book (1999)

See detailCharacterization of menin from normal individuals and MEN1 patients
Poncin, Jacques ULg; Closset, J.; Legros, J. J. et al

in 6th International Pituitary Congress - Abstract book (1999)

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See detailCharacterization of menin from leucocytes of normal and men-1 affected individuals
Poncin, Jacques ULg; Closset, Jean ULg; Legros, Jean-Jacques ULg et al

in 81st Annual Meeting of the Endocrine society - Abstract book (1999)

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See detailMutation analysis of the MEN1 gene in Belgian patients with multiple endocrine neoplasia type 1 and related diseases.
Poncin, Jacques ULg; Abs, R.; Velkeniers, B. et al

in Human Mutation (1999), 13(1), 54-60

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by tumors in parathyroids, enteropancreatic endocrine tissues, anterior pituitary, and other tissues. The gene ... [more ▼]

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by tumors in parathyroids, enteropancreatic endocrine tissues, anterior pituitary, and other tissues. The gene for MEN1 has recently been cloned and shown to code for a 610-amino acid protein of enigmatic function which probably acts as a tumor suppressor. Several mutations causing the MEN1 phenotype have been recently identified. In order to determine the spectrum of MEN1 gene mutations in a sample of 25 Belgian patients, we have systematically screened the 10 exons and adjacent sequences of the MEN1 gene by means of an automatic sequencing protocol. Twelve different mutations were identified including nonsense, frameshift, splicing, and missense mutations. Two of these mutations (D172Y and 357del4) occurred more than once. A missense mutation was also found in a kindred with familial hyperparathyroidism. We observed no significant correlation between the nature or position of mutation and the clinical status. We have also detected 6 intragenic polymorphisms and DNA sequence variants and have analyzed their frequencies in our population. [less ▲]

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See detailMutation analysis of the MEN1 gene in Belgian patients with multiple endocrine neoplasia type I and related diseases
Poncin, Jacques ULg; Abs, R.; Velkeniers, B. et al

in IV european Congress of Endocrinology - Abstract book (1998)

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See detailMutation analysis of the MEN1 gene in Belgian patients with multiple endocrine neoplasia type I and related diseases
Poncin, Jacques ULg; Abs, R.; Velkeniers, B. et al

in 5th Euroregional Oncology meeting - abstract book (1998)

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See detailThe spectrum of MEN1 gene mutations in Belgian patients with MEN1 and related diseases
Poncin, Jacques ULg; Abs, R.; Velkeniers, B. et al

in The 5th International Pituitary congress - Abstract book (1998)

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See detailThe spectrum of MEN1 gene mutations in Belgian patients with MEN1 and related diseases
Poncin, Jacques ULg; Abs, R.; Velkeniers, B. et al

in 80th Annual Meeting of the Endocrine society - Abstract book (1998)

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See detailTwo years of replacement therapy in adults with growth hormone deficiency.
Verhelst, J.; Abs, R.; Vandeweghe, M. et al

in Clinical Endocrinology (1997), 47(4), 485-494

OBJECTIVES: Although several studies have shown beneficial short-term effects of recombinant human growth hormone (rhGH) therapy in adult GH deficient (GHD) patients, few data are available on large ... [more ▼]

OBJECTIVES: Although several studies have shown beneficial short-term effects of recombinant human growth hormone (rhGH) therapy in adult GH deficient (GHD) patients, few data are available on large groups of patients treated for more than one year. In addition, the optimal dose of rhGH for each patient and the baseline parameters that predict which patients will benefit most from therapy or will have adverse events are not entirely elucidated. DESIGN: 148 adult GHD patients were enrolled in a multicentre 2-year rhGH replacement study which was placebo controlled for the first six months. rhGH (Genotropin/Genotonorm Pharmacia & Upjohn) was given in a dose of 0.25 IU/kg/week sc (1.5 IU/m2/day). MEASUREMENTS: Every 3-6 months body composition was measured using body impedance analysis and general well being was assessed using the Nottingham Health Profile (NHP) and social self-reporting questionnaire. At the same time patients had a full clinical examination and blood was sampled for glucose, HbA1c, IGF-1, creatinine, full blood count, thyroid hormones and liver function tests. RESULTS: With rhGH therapy IGF-1 levels increased from -2.00 +/- 2.60 SDS to 1.47 +/- 2.6 SDS after six months (P < 0.001), continued to rise despite no change in dose to 1.84 +/- 2.8 SDS after one year and remained constant thereafter (1.98 +/- 2.4 after 2 years). 56% of patients ultimately attained supranormal IGF-1 levels (+2 SD), 22% had levels below the mean, of which 9% were below -2 SD. Within 3 months lean body mass (LBM) increased by +5.09% (P < 0.001), total body water (TBW) by +5.40% (P < 0.001), while body fat (BF) dropped by -10.89% (P < 0.001) and waist circumference by -1.42% (P < 0.004). These effects were maintained during the first year of therapy, but the effect was attenuated after 24 months: LBM, +3.91% (P < 0.001); TBW, +3.28%, P < 0.001, BF, -6.42% (P < 0.001) and waist -2.22% (P < 0.009). Individual differences in response were large and could not be predicted by any of the baseline parameters, except for a better response in males. Treatment resulted in a large and progressive improvement on the NHP scale, especially energy, emotions and sleep, but a similar change was also found in patients during placebo treatment. With rhGH the number of full days of sick leave/6 months decreased from 12.17 +/- 3.90 days (SEM) to 7.15 +/- 3.50 days after six months (P = 0.009), 2.93 +/- 1.55 days after 12 months (P = 0.01), 0.39 +/- 0.17 days after 18 months (P < 0.001) and 3.3 +/- 2.51 days after 24 months (P = 0.026). Similarly, the hospitalization rate went down from 14.9 to 7% after 6 months and remained at this level thereafter (P = 0.12). About one third of patients on rhGH experienced fluid-related adverse events, most often within the first 3 months. They usually disappeared spontaneously or responded well to dose reduction. Cumulative dropout rates were 29% after 1 year and 38% after two years. Two thirds of these patients stopped treatment because of insufficient subjective improvement. Neither drop-outs nor fluid retention could not be predicted by any of the baseline parameters. CONCLUSIONS: We confirmed in a large group of patients the beneficial effects of rhGH therapy on body composition, metabolic parameters and general well-being and found a consistent drop in number of sick days and hospitalization rate. These effects were maintained during two years of therapy, except for an attenuation in body composition changes after 24 months. The high incidence of fluid-related adverse events suggests that it may be better to start with lower doses of rhGH and to increase the dose more slowly over a number of weeks. The finding of suboptimal high or low IGF-1 levels in many patients reinforces guidelines not to give rhGH in a weight-dependent dose but to titrate it individually for each patient. [less ▲]

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See detail125I-Tyr0-hCRH labelling characteristics of corticotropin-releasing hormone receptors: differences between normal and adenomatous corticotrophs.
Abs, R.; Smets, G.; Vauquelin, G. et al

in Neurochemistry International (1997), 30(3), 291-297

The presence of corticotropin-releasing hormone (CRH) receptors has been previously demonstrated in corticotrophs from normal pituitaries using a method combining immunocytochemistry and liquid emulsion ... [more ▼]

The presence of corticotropin-releasing hormone (CRH) receptors has been previously demonstrated in corticotrophs from normal pituitaries using a method combining immunocytochemistry and liquid emulsion autoradiography. The aim of this study was to compare the characteristics of the 125I-Tyr0-hCRH binding in corticotrophs from normal pituitaries (three obtained at autopsy and one obtained at surgery) with corticotrophs from pituitary adenomas (six corticotroph adenomas responsible for Cushing's disease and two silent corticotroph adenomas secreting a biologically inactive ACTH molecule). In normal corticotrophs, the larger part of the 125I-Tyr0-hCRH binding was localised in patchy conglomerates at the centre of the cell and, to a much lesser degree, in a diffuse pattern at the cell periphery. In adenomatous corticotrophs, CRH receptor expression is disturbed both quantitatively and qualitatively. Except for a minority of cells in one adenoma, all adenomatous corticotrophs showed only peripherally bound 125I-Tyr0-hCRH and no centrally localised binding. Furthermore, adenomatous corticotrophs revealed a statistically significant lower signal intensity when compared to normal corticotrophs and a strongly negative correlation was found between the labelling area in adenomatous corticotrophs and both the basal and CRH-stimulated plasma ACTH levels. These findings suggest defective processing of CRH receptors and could be relevant to the sustained ACTH secretion by adenomatous corticotrophs in Cushing's disease and, more generally, provide an explanation to its pathology. The silent corticotrophs secreting a biologically inactive ACTH molecule were characterised by a very faint signal intensity, although present on almost every cell. [less ▲]

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See detailCabergoline, a new long-acting dopamine agonist, in the treatment of acromegaly
Abs, R.; Verhelst, J.; Verbessem, G. et al

in 10th international Congress of Endocrinology - Abstract book (1996)

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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 detailTwo years or replacement therapy in 148 adults with growth hormone déficiency in Belgium
Verhelst, J.; Abs, R.; Mockel, J. et al

in 10th international Congress of Endocrinology - Abstract book (1996)

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See detailThe treatment of prolactinomas with cabergoline
Beckers, Albert ULg; Louis, O.; Verhelst, J. et al

in 10th international Congress of Endocrinology - Abstract book (1996)

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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 detailEffect of naloxone and metoclopropamide on LH secretion in a hyperprolactinemic, hypogonadotropic, postmenopausal woman, fertility and sterility.
Verhelst, J.; Beckers, Albert ULg; Abs, R.

in Fertility and Sterility (1995), 64(5), 969-971

OBJECTIVE: To determine the role of opioidergic and dopaminergic activity in the suppression of GnRH0LH in a hyperprolactinemic state. DESIGN: Case report. SETTING: University hospital. PATIENT: A 68-year ... [more ▼]

OBJECTIVE: To determine the role of opioidergic and dopaminergic activity in the suppression of GnRH0LH in a hyperprolactinemic state. DESIGN: Case report. SETTING: University hospital. PATIENT: A 68-year-old woman with a macroprolactinoma. INTERVENTIONS: Serial 10-hour IV infusions of naloxone and metoclopramide. MAIN OUTCOME MEASURE: Serum LH concentration. RESULTS: Naloxone induced a small but significant rise of serum LH levels, which displayed a pulsatile pattern. By contrast, metoclopramide elicited no significant response in LH secretion. CONCLUSION: Opioidergic but not dopaminergic neurotransmission plays a direct role in the suppression of LH secondary to hyperprolactinemia. [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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