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See detailLe Syndrome auto-immun thyrogastrique
VALDES SOCIN, Hernan Gonzalo ULg

Conference given outside the academic context (2014)

The thyrogastric autoimmune syndrome (TAS) was described in patients in whom the serum cross-reacted both with gastric parietal cells antigens and thyroid antigens. We describe several cases illustrating ... [more ▼]

The thyrogastric autoimmune syndrome (TAS) was described in patients in whom the serum cross-reacted both with gastric parietal cells antigens and thyroid antigens. We describe several cases illustrating the spectrum of pathogical features of TAS. Autoimmune thyroiditis include Hahimoto’s Thyroiditis and Graves Disease. Autoimmune gastritis may present at first only micronutrients deficiency (B12, iron) whereas Biermer anemia with gastric atrophy and gastrin cell hyperplasia is the consequence of long standing disease. One possible presentation of gastric autoimmunity is the association with Helicobacter pylori infection. Gastric autoimmunity is potentially reversible if Helicobacter is erradicated. When gastric autoimmunity is irreversible, this condition leads to gastric severe atrophy, hypochlorhydria and hypergastrinemia. Hypergastrinemia stimulates enterochromaffin cell hyperplasia, progressing eventually to neuroendocrine tumors. The thyrogastric syndrome should be considered a risk factor to develop a neuuroendocrine tumor. We propose a diagnostic approach to improve the characterization of TAS. We review the literature on the subject and discuss some interesting animal models of infectious gastric autoimmunity [less ▲]

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See detailBASES NEUROENDOCRINES DU STRESS: du combat ou la fuite, au Syndrome de Cushing.
VALDES SOCIN, Hernan Gonzalo ULg

Scientific conference (2014, March 12)

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See detailNovel fibroblast growth factor receptor 1 mutation causing normosmic idiopathic hypogonadotropic hypogonadism
Chachati, AS; Potorac, I; DEBRAY, François-Guillaume ULg et al

in Abstract book - Symposium "Perspectives in Endocrinology" Congresses Highlights 2013:ECE Copenhagen, ENDO SF, SFE Paris (2014, February)

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See detailEl sindrome tirogastrico autoinmune : sus efectos sobre los micronutrientes y la tumorigenesis gastrica
VALDES SOCIN, Hernan Gonzalo ULg; LUTTERI, Laurence ULg; Cavalier, Etienne ULg et al

in Revista Argentina de Endocrinologia y Metabolismo (2014), 51

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See detailPersistent low levels of serum hCG: please do not miss phantom hCG! (pseudohypergonadotropinemia syndrome)
VALDES SOCIN, Hernan Gonzalo ULg; SYRIOS, Petros ULg; GADISSEUR, Romy ULg et al

in Acta Clinica Belgica (2013), 68(6), 465

Introduction: Beyond pregnancy, persistent low levels of hCG may be associated with various benign and malignant conditions, i.e. quiescent gestational trophoblastic disease (QTD), raised pituitary hCG or ... [more ▼]

Introduction: Beyond pregnancy, persistent low levels of hCG may be associated with various benign and malignant conditions, i.e. quiescent gestational trophoblastic disease (QTD), raised pituitary hCG or false positive elevation caused by circulating heterophilic antibodies. This situation requires a clinico-biological approach in order to avoid misunderstandings that could lead to inappropriate diagnostic or therapeutic attitudes. Observation: A 23 years old woman (GOPO status) consulted his gynaecologist because of persistent abdominal pain. She was diagnosed of having trophoblastic disease on the basis of persistently positive human chorionic gonadotropin (hCG) test (Roche Modular) results, in the absence of pregnancy. Persistent low levels of hCG (around 10 U/L) were detected in her plasma. The patient underwent a trial with methotrexate chemotherapy. Abdominal pain was unrelieved whereas plasma hCG was 8.9 U/L. A serology test for Chlamydia indicated persistent infection and a course of antibiotic treatment was underwent without any relief. A laparoscopic exploration ruled out any trophoblastic residue or pelvic adherences. The patient was referred to the Endocrine Unit for further pituitary and hormonal investigations. Plasma and urine samples were sent to Biology Service to exclude a false hCG positive value. While low levels of hCG were detected in serum by assay, no significant hCG was detected in the urine (0,1 U/L). When serum was treated with HBT tube for the detection of heterophilic antibodies, hCG levels were 0.98 U/L. After mouse serum treatment, hCG was not further detected in our patient, indicating the presence of phantom hCG due to the presence of human anti mouse heterophilic antibodies. Conclusions: Textbooks on obstetrics and gynecology emphasize the importance of plasma hCG testing in patients with trophoblastic diseases. The ability of laboratory measurements to guide the clinician appropriately in every circumstance is limited. Caution should be exercised when clinical findings and laboratory results are discordant. Current protocols for the diagnosis and treatment of trophoblastic disease should include a compulsory test for hCG in urine and a test for heterophilic antibodies when appropriate. In this case report, we demonstrated that phantom hCG, was caused by heterogenous human anti mouse antibodies. [less ▲]

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See detailRefractory hypercalcemia and ectopic calcitonin secretion in a malignant pancreatic neuroendocrine tumor: hypocalcemic effects on cinacalcet
VALDES SOCIN, Hernan Gonzalo ULg; rubio almanza, Matilde; LOLY, Jean-Philippe ULg et al

in Acta Clinica Belgica (2013), 68(6), 42

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 detailFemoral-facial syndrome: long term follow-up and associated array CGH abnormalities.
JACQUINET, Adeline ULg; VALDES SOCIN, Hernan Gonzalo ULg; LIBIOULLE, Cécile ULg et al

Poster (2013, October 22)

The femoral-facial syndrome is usually sporadic and its aetiology remains unknown. Non-genetic factors as maternal diabetes mellitus have been associated. Reports of familial cases have otherwise ... [more ▼]

The femoral-facial syndrome is usually sporadic and its aetiology remains unknown. Non-genetic factors as maternal diabetes mellitus have been associated. Reports of familial cases have otherwise suggested autosomal dominant inheritance. We report the 20 years clinical follow-up of a girl with femoral-facial syndrome diagnosed at birth. Recently, array CGH investigation identified a 1400 kb duplication at 9q31.1, including the gene SMC2, and a 343 kb deletion at 12q24.33 including the genes CHFR, ZNF26, ZNF140, ZNF10 and ZNF268. Moreover, the patient presents a Mayer-Rokitansky-Kuster-Hauser syndrome diagnosed at puberty. Femoral-facial syndrome and Mullerian agenesis may reflect different defects in the primary axial mesodermal development, being the consequences of same environmental or/and genetic factors during blastogenesis. Among these genetic factors, we suggest the possible involvement of the two copy number variants reported here [less ▲]

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See detailNovel fibroblast growth factor receptor 1 mutation causing normosmic idiopathic hypogonadotropic hypogonadism
Chachati, Anne-Sophie ULg; Potorac, Iulia ULg; DEBRAY, François-Guillaume ULg et al

in 23rd meeting of the Belgian Endocrine Society - Abstract book (2013, October 19)

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See detailHypercalcemia treated by sunitinib
LOLY, Jean-Philippe ULg; VALDES SOCIN, Hernan Gonzalo ULg; Daly, Adrian ULg et al

in 23rd meeting of the Belgian Endocrine Society - Abstract book (2013, October 19)

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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 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 detailLa Vitamine B12 et la Santé
VALDES SOCIN, Hernan Gonzalo ULg

Scientific conference (2013, May 13)

Objectifs: Révision sur le rôle de la vitamine B12 et sur les évidences qui suggèrent que la vitamine B12 peut réduire le risque de certaines maladies chroniques. Evidences: recherche dans Medline depuis ... [more ▼]

Objectifs: Révision sur le rôle de la vitamine B12 et sur les évidences qui suggèrent que la vitamine B12 peut réduire le risque de certaines maladies chroniques. Evidences: recherche dans Medline depuis 1999 jusqu'en 2013 en utilisant le mot clé vitamin B12. Les articles les plus conséquents (150) étaient associés avec le cancer, la maladie cardiovasculaire, la santé mentale et les altérations du tube neural. Résultats: Le déficit avéré de la vitamine B12 est classiquement associé à l'anémie pernicieuse, à une poly neuropathie avec atteinte de la moelle épinière, à une glossite atrophique et à une hyperhomocystéinémie. Le traitement lorsqu’il y a malabsorption est l’administration IM de cyanocobalamine (Cyanocobalamine 1000µg/J x 7jours puis 1amp/mois IM), mais certaines évidences suggèrent que 1% de la vit B12 est quand mémé absorbée par transport passif (Cyanocobalamine 1000 µg/J PO pendant 1 mois puis 1000µg/semaine (par ex stérop B12© ). Les doses élevées de vitamine B12 (1 à 5mg PO/J) peuvent normaliser le déficit dans certains cas. Les compléments en vitamine B12, quant à eux, pourraient, s'associer avec certains bénéfices de la santé. Un bénéfice particulier est constaté dans la protection des anomalies du tube neural (évidences de type II). Son rôle dans la protection de maladies cardiovasculaires et le cancer n’est pas confirmé après 8 études randomisées contrôlées versus placebo (évidence de type I). Le rôle protecteur de la vitamine B12 dans la santé mentale reste aussi controversé. Les éventuels rôles bénéfiques de la supplémentation en vitamine B12 sur les maladies chroniques nécessitent d'être confirmés encore par des larges études interventionnelles randomisées en double aveugle (évidence de type I) [less ▲]

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See detailHipogonadismo masculino
VALDES SOCIN, Hernan Gonzalo ULg

Scientific conference (2013, March)

Conferencia: Hipogonadismo masculino Aula Prof Niepominitzce. Hospital de Clinicas . Universidad de Buenos Aires. Argentina Marzo 2013 El hipogonadismo congénito es un síndrome clínico que se caracteriza ... [more ▼]

Conferencia: Hipogonadismo masculino Aula Prof Niepominitzce. Hospital de Clinicas . Universidad de Buenos Aires. Argentina Marzo 2013 El hipogonadismo congénito es un síndrome clínico que se caracteriza por un impuberismo parcial o completo. El hipogonadismo congénito puede resultar de una estimulación insuficiente del eje hipotalámico y de la liberación del GnRH, o bien de una secreción insuficiente de las gonadotropinas hipofisarias LH y FSH o bien manifestarse primariamente a nivel testicular. En el hombre, varios genes participan en la vía de la olfacción y de la migración de las neuronas de GnRH, pudiendo interactuar durante la vida embrionaria y postnatal. Se empieza a describir un creciente número de mutaciones en genes diferentes, responsables del hipogonadismo masculino congénito (1). Esta presentación incluye el reconocimiento de diferentes patologías que cursan con un hipogonadismo genético (síndromes de Klinefelter, Kallman, Noonan, Prader Willy, testículo feminizante). En la segunda parte de la presentación resumimos los datos clínicos, biológicos y estudios genéticos de un paciente que es visto en el hospital universitario de Lieja por hipogonadismo, presentando un eunucoidismo y un cierto grado de espermatogénesis. Casi 50 años después de la descripción los médicos argentinos Pasqualini y Bur pudimos reconocer, en colaboración con un equipo suizo, la causa genética de este síndrome, a saber un déficit de la LH debido a una mutación invalidante homocigota de la subunidad beta de dicha hormona(2). Un tratamiento en base a hCG permitió por primera vez restituir la fertilidad al paciente. Su esposa quedo embarazada gracias a un tratamiento de fertilidad asistida , y ambos tuvieron un niño, heterocigoto para la mutación de beta LH (3,4). La tercera parte de la conferencia está dedicada a los avances en la fisiología y endocrinología de las kispeptinas. Las mutationes del gen de kisspeptina y de su receptor son una nueva causa de hipogonadismo congénitos. Describimos nuestra experiencia en la determinación plasmática de kisspeptina en pacientes obesos e hipo gonádicos (5). Demostramos asimismo la diferente expresión espacio-temporal de kisspeptina en las placentas normales y patológicas (6). En la última parte de la conferencia incluimos todas estas nuevas causas de hipogonadismo en un modelo para mejorar la comprensión del funcionamiento del eje reproductor en el hombre. Referencias 1-H. Valdes-Socin , F.G. Debray, A.S. Parent, M.C. Lebrethon, J.P. Bourguignon, V. Bours A. Beckers. Comment je diagnostique un hypogonadisme hypogonadotrope congénital isolé? Rev Med Liège 2010 Nov;65(11):634-41. 2-H Valdes-Socin, R Salvi, A Daly, F Pralong, R Gaillard R and A Beckers. Hypogonadism in a patient with a mutation in the luteinizing hormone beta-subunit gene.N Engl J Med. 2004 Dec 16;351(25):2619-25 3-H Valdes-Socin, R Salvi , A Thiry, AF. Daly, F P. Pralong, R Gaillard, A Beckers. Testicular effects of isolated luteinizing hormone deficiency and reversal by long-term human chorionic gonadotropin treatment. J Clin Endocrinol Metab. 2009 Jan;94(1):3-4. 4-Daly, A., Valdes-Socin, H., Beckers, A. “A tall man with hypogonadism”. In: Wartofsky L. editor. Diagnostic Dilemmas: Images in Endocrinology. The Endocrine Society Press. (2011). p.204-207. 5-Valdes Socin, H. G, Cavalier, E, Beckaert, A. C, Carlisi, A, Chavez, M, & Beckers, A. (2011). Elévation des kisspeptines plasmatiques chez les hommes obèses avec hypogonadisme acquis et chez les hommes avec hypogonadisme congénital : Etude pilote des modifications plasmatiques des kisspeptines avant et après administration de hCG et testostérone. Annales d'Endocrinologie - 28ème congrès de la société Française d'Endocrinologie. 6-H Valdes-Socin , C Munaut , M Chavez, F Chantrain, K Delbecque , P Delvenne, JM Foidart , A Beckers: expression et localisation spatio-temporelle de kiss1 et de son récepteur KissR dans le placenta humain normal et pathologique. Annales d'Endocrinologie 2012. Société Française d'Endocrinologie [less ▲]

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See detailThe clinical characteristics of pituitary adenomas (PA) in patients with primary hyperparathyroidism (PHPT) with and without MEN1 mutation
Filipponi, S; Rostomyan, Liliya ULg; VALDES SOCIN, Hernan Gonzalo ULg et al

in Symposium "Perspectives in Endocrinology" - Congresses Highlights 2012: ECE Firenze, ENDO Houston, ESPE Leipzig, SFE Toulouse, IWMEN Liège (2013)

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See detaille syndrome auto-immun thyrogastrique: ses effets sur les micronutriments et la tumorigénèse gastrique.
VALDES SOCIN, Hernan Gonzalo ULg; LUTTERI, Laurence ULg; CAVALIER, Etienne ULg et al

in Revue Médicale de Liège (2013)

Summary : The thyrogastric autoimmune syndrome (TAS) was described in patients in whom the serum cross-reacted both with gastric parietal cells antigens and thyroid antigens. We report two cases ... [more ▼]

Summary : The thyrogastric autoimmune syndrome (TAS) was described in patients in whom the serum cross-reacted both with gastric parietal cells antigens and thyroid antigens. We report two cases illustrating the spectrum of pathogical features of TAS. The first case associates Hashimoto’s thyroiditis and anemia perniciosa,and develops a gastric neuroendocrine tumor during follow up. The second case presents with a Graves’ disease and an autoimmune reversible gastritis, secondary to Helicobacter Pylori. Whereas type III autoimmune polyendocrinopathy is rare, TAS is frequent in our experience. Some 13% (32/240) of patients that we have prospectively followed affected with thyroiditis have also autoimmune gastritis. Helicobacter pylori is clearly implicated in 16% of autoimmune gastritis cases. Infection, malabsorption and gastritis are potentially reversible after bacterial eradication treatment. In the other 84% of gastritis patients, no histological or serological proof of Helicobacter pylori is found. Gastric autoimmunity is then irreversible, leading to gastric severe atrophy, hypochlorhydria and hypergastrinemia. Hypergastrinemia stimulates enterochromaffin cell hyperplasia, possibly progressing c to neuroendocrine tumors. We propose a diagnostic approach to improve the characterization of TAS. We review the literature on the subject and discuss some interesting animal models of infectious gastric autoimmunity [less ▲]

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