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See detailX-LAG: How did they grow so tall?
BECKERS, Albert ULg; Rostomyan, Liliya ULg; Potorac, Iulia ULg et al

in Annales d'Endocrinologie (2017)

X-linked acrogigantism (XLAG) is a new, pediatric-onset genetic syndrome, due to Xq26.3 microduplications encompassing the GPR101 gene. XLAG has a remarkably distinct phenotype with disease onset ... [more ▼]

X-linked acrogigantism (XLAG) is a new, pediatric-onset genetic syndrome, due to Xq26.3 microduplications encompassing the GPR101 gene. XLAG has a remarkably distinct phenotype with disease onset occurring before the age of 5 in all cases described to date, which is significantly younger than in other forms of pituitary gigantism. These patients have mixed GH and prolactin positive adenomas and/or mixed-cell hyperplasia and highly elevated levels of GH/IGF-1 and prolactin. Given their particularly young age of onset, the significant GH hypersecretion can lead to a phenotype of severe gigantism with very advanced age-specific height Z-scores. If not adequately treated in childhood, this condition results in extreme final adult height. XLAG has a clinical course that is highly similar to some of the tallest people with gigantism in history. « X-linked acrogigantism » (XLAG) est un syndrome pédiatrique récemment décrit, lié à des microduplications du chromosome Xq26.3, englobant le gène GPR101, responsable de l’affection. Les patients XLAG présentent un phénotype remarquablement distinct des autres cas de gigantisme hypophysaire. Dans tous les cas décrits, la maladie s’exprime avant 5 ans soit beaucoup plus tôt que dans les autres formes. Les patients ont habituellement un gros adénome ou une hyperplasie mixte pour la GH et la prolactine et des taux très élevés de GH/IGF1 et prolactine. En raison de son début très précoce, l’hypersécrétion importante de GH peut conduire à un gigantisme extrêmement sévère avec un Z-score très important pour l’âge. Si cette condition n’est pas traitée pendant l’enfance, elle peut conduire à une taille finale extrême. XLAG montre une évolution clinique similaire à celle observée chez les géants les plus grands de l’histoire. [less ▲]

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See detailProblems with the PTH assays
CAVALIER, Etienne ULg; DELANAYE, Pierre ULg; Nyssen, Laurent ULg et al

in Annales d'Endocrinologie (2015), 76(2), 128-133

Even if the first assay for parathyroid hormone (PTH) was published in the early 1960s, its determination remains a challenge even today. Indeed, in the circulation, PTH is present in its active form (PTH ... [more ▼]

Even if the first assay for parathyroid hormone (PTH) was published in the early 1960s, its determination remains a challenge even today. Indeed, in the circulation, PTH is present in its active form (PTH 1-84), but many PTH fragments can also be present. These fragments accumulate when renal function declines and are recognized, at different extents, by the 2nd generation ("intact") PTH assays that are widely used in the clinical laboratories. Some assays, called "3rd generation PTH" do not recognize these fragments, but are not available everywhere. Hence, different problems are also linked with PTH determination. Among them, one can cite the lack of a reference method, the lack of standardization of the assays and, sometimes, the lack of consistent reference range. We can also point out stability problems and a large intra-individual variation. A workgroup is working on these problems under the auspices of the IFCC and we hope that some of these problems will be resolved in the next years. In this article, we will discuss all the possible issues of PTH determination. [less ▲]

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See detailParathyroid carcinoma : Challenges in diagnosis and treatment
BETEA, Daniela ULg; Potorac, Iulia ULg; Beckers, Albert ULg

in Annales d'Endocrinologie (2015), 76

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See detailHow to manage an isolated elevated PTH?
Souberbielle, Jean-Claude; CAVALIER, Etienne ULg; Cormier, Catherine

in Annales d'Endocrinologie (2015), 76(2), 134-141

The aim of this article is to discuss the diagnostic approach of an increased serum PTH concentration in a normocalcemic, normophosphatemicpatient. Detection of this biological presentation is frequent in ... [more ▼]

The aim of this article is to discuss the diagnostic approach of an increased serum PTH concentration in a normocalcemic, normophosphatemicpatient. Detection of this biological presentation is frequent in routine practice all the more that PTH reference values established in vitamin Dreplete subjects with a normal renal function are used by the clinical laboratories. The first step in this diagnostic approach will be to rule out acause of secondary hyperparathyroidism (SHPT). Among these, the most frequent are vitamin D deficiency, very low calcium intake, impairedrenal function, malabsorptions, drugs interfering with calcium/bone metabolism, such as lithium salts and antiresorptive osteoporosis therapies,hypercalciuria due to a renal calcium leak. If no cause of SHPT are evidenced, the diagnosis of normocalcemic primary hyperparathyroidism(PHPT) should be considered. A calcium load test is a very useful tool for this diagnosis if it shows that serum PTH is not sufficiently decreasedwhen calcemia rises frankly above the upper normal limit. In a normocalcemic patient with hypercalciuria and a high serum PTH concentration,a thiazide challenge test may help to differentiate SHPT due to a renal calcium leak from normocalcemic PHPT. Beyond the discussion of thisdiagnostic [less ▲]

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See detailPituitary gigantism : Causes and clinical characteristics
Rostomyan, Liliya ULg; Daly, Adrian ULg; Beckers, Albert ULg

in Annales d'Endocrinologie (2015), 76

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See detailEvaluation of circulating irisin levels in healthy young individuals after a single 100,000 IU vitamin D dose
CAVALIER, Etienne ULg; Mismetti, Valentine; Souberbielle, Jean-Claude

in Annales d'Endocrinologie (2014), 73(3), 162-164

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See detailHypothyroïdie infraclinique non auto-immune et statut iodé : étude prospective d'intervention
VALDES SOCIN, Hernan Gonzalo ULg; Tudorescu, A; Lutteri, L et al

in Annales d'Endocrinologie (2013, October), 74

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See detailLe carcinome parathyroïdien familial : une forme agressive d'hyperparathyroïdie primaire
Tudorescu, A; VROONEN, Laurent ULg; BETEA, Daniela ULg et al

in Annales d'Endocrinologie (2013, October), 74

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See detailUne néoplasie endocrinienne multiple particulière
Boccar, S; VROONEN, Laurent ULg; HAMOIR, Etienne ULg et al

in Annales d'Endocrinologie (2013, October), 74

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See detailLe PPNAD, une cause rare de syndrome de Cushing
PETIGNOT, Sandrine ULg; VROONEN, Laurent ULg; HAMOIR, Etienne ULg et al

in Annales d'Endocrinologie (2013, October), 74

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See detailReceptor expression in craniopharyngiomas causing tumor growth in pregnancy : case report and review of the literature
Tome, M; VROONEN, Laurent ULg; THIRY, Albert ULg et al

in Annales d'Endocrinologie (2013, October), 74

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See detailFIPA : étude clinique et génétique à l'Hôpital "King Edward Memorial", Bombay (Mumbai) Inde
Bothra, N; Daly, Adrian ULg; CASTERMANS, Emilie ULg et al

in Annales d'Endocrinologie (2013, October), 74

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See detailCoexistence entre adénom hypophysaire et phéochromocytome - présentation de cas
Rostomyan, Liliya ULg; Potorac, Iulia ULg; Filipponi, S et al

in Annales d'Endocrinologie (2013, October), 74

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See detailGerminome intracrânien bifocal : la biopsie est-elle toujours indispensable?
KREUTZ, Julie ULg; BONNEVILLE, Jean-François ULg; Potorac, Iulia ULg et al

in Annales d'Endocrinologie (2013, October), 74

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See detailCorrélations significatives de l'aspect en IRM haute résolution des adénomes hypophysairesà GH avant traitement
Potorac, Iulia ULg; PETROSSIANS, Patrick ULg; Schillo, F et al

in Annales d'Endocrinologie (2013, October), 74

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See detailLe gigantisme : Les résultats d'une étude clinique et génétique internationale
Rostomyan, Liliya ULg; Daly, Adrian ULg; Lila, A et al

in Annales d'Endocrinologie (2013, October), 74

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See detailHypercalcémie réfractaire et sécrétion ectopique de calcitonine dans un cancer neuroendocrine du pancréas : Effets hypocalcémiants du Cinacalcet
VALDES SOCIN, Hernan Gonzalo ULg; LOLY, Jean-Philippe ULg; BETEA, Daniela ULg et al

in Annales d'Endocrinologie (2013, September), 74(4), 235-462

Introduction: Paraneoplastic hypercalcemia is a sign of poor prognosis, as it is particularly resistant to the usual hypocalcemic treatments. Observation: In 2009, a well differentiated pancreatic ... [more ▼]

Introduction: Paraneoplastic hypercalcemia is a sign of poor prognosis, as it is particularly resistant to the usual hypocalcemic treatments. Observation: In 2009, a well differentiated pancreatic neuroendocrine tumor (Ki-67= 2%) is diagnosed in a 52-year-old diabetic man. The tumor is revealed with a splenic and hepatic carcinomatosis. Plasmatic calcium was: 3.54 mmol/L (2.15 - 2.6). Biology showed hypophosphatemia, PTH < 4 ng/ml, high 1-25 OH VitD, calcitonin: 1016 ng/ml (< 12 ng/ml). He had hypercalciuria and hypophosphaturia. He received for two years several cycles of Streptozotocin-ADRIAMYCIN and FOLFOX, with partial control of the tumor mass and calcium levels. In 2012, calcitonin levels are 29 ng/ml whereas calcemia is 3.17 mmol/L. Hypercalcemia is refractory to hyperhydration, diuretics, corticosteroids, and bisphosphonates therapy. Cinacalcet (Mimpara) is prescribed up to 120 mg/day (PO). Calcemia decreases gradually from 3 to 2.87 and then 2.76 mmol/L. PTH and calcitonin-the tumor mass remain unchanged. After two months of Cinacalcet treatment, Sunitinib (Sutent) 37.5 mg per day was added. During the third month, calcium levels dropped to 2.09 mmol/L and PTH raised to 78 pg/ml, requiring discontinuation of Mimpara. Calcitonin normalized, with a further improvement over pancreatic and metastatic lesions. Conclusion: Cinacalcet is a Calcium Sensing Receptor oral agonist. Cinacalcet hypocalcemic effects have not been previously documented in pancreatic paraneoplastic hypercalcemia. In our patient, Cinacalcet has significantly improved cancer prognosis: this drug could be a new alternative in paraneoplastic hypercalcemia. [less ▲]

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See detailGLP-1 receptor agonists or DPP-4 inhibitors: How to guide the clinician?
SCHEEN, André ULg

in Annales d'Endocrinologie (2013)

Pharmacological treatment of type 2 diabetes has been enriched during recent years, with the launch of incretin therapies targeting glucagon-like peptide-1 (GLP-1). Such medications comprise either GLP-1 ... [more ▼]

Pharmacological treatment of type 2 diabetes has been enriched during recent years, with the launch of incretin therapies targeting glucagon-like peptide-1 (GLP-1). Such medications comprise either GLP-1 receptor agonists, with short (one or two daily injections: exenatide, liraglutide, lixisenatide) or long duration (one injection once weekly: extended-released exenatide, albiglutide, dulaglutide, taspoglutide); or oral compounds inhibiting dipeptidyl peptidase-4 (DPP-4), the enzyme that inactives GLP-1, also called gliptins (sitagliptin, vildagliptin, saxagliptin, linagliptin, alogliptin). Although both pharmacological approaches target GLP-1, important differences exist concerning the mode of administration (subcutaneous injection versus oral ingestion), the efficacy (better with GLP-1 agonists), the effects on body weight and systolic blood pressure (diminution with agonists versus neutrality with gliptins), the tolerance profile (nausea and possibly vomiting with agonists) and the cost (higher with GLP-1 receptor agonists). Both agents may exert favourable cardiovascular effects. Gliptins may represent a valuable alternative to a sulfonylurea or a glitazone after failure of monotherapy with metformin while GLP-1 receptor agonists may be considered as a good alternative to insulin (especially in obese patients) after failure of a dual oral therapy. However, this scheme is probably too restrictive and modalities of using incretins are numerous, in almost all stages of type 2 diabetes. Physicians may guide the pharmacological choice based on clinical characteristics, therapeutic goals and patient's preference. [less ▲]

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