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See detailHypofractionation in retinoblastoma: an increased risk of retinopathy.
Coucke, Philippe ULg; Mirimanoff, R-O; Schmid, C et al

in Radiotherapy & Oncology (1993), 28

Forty-four eyes in 38 children were treated between 1963 and 1991 by external radiotherapy for retinoblastoma. Treatment modalities varied widely during this period; in addition to radiotherapy there was ... [more ▼]

Forty-four eyes in 38 children were treated between 1963 and 1991 by external radiotherapy for retinoblastoma. Treatment modalities varied widely during this period; in addition to radiotherapy there was chemotherapy (16/44), photocoagulation (14/44), and laser therapy or cryotherapy (14/44). Treatment technique and dose fractionation also varied widely; lateral beam technique (39/44) versus anterior or anterior/lateral beam; doses per fraction ranged from 1 to 4.5 Gy, total doses from 30 to 61.5 Gy, and overall times from 22 to 49 days. Patients were followed at 3-month intervals, and actuarial survival at 10 years was 88%, with 62% local control. Ten eyes showed clinical evidence of retinopathy. A multivariate analysis of factors associated with increased risk of retinopathy was carried out using the Cox proportional hazards model and the mixture model of Farewell. The estimated latent time was 17 months (95% confidence interval, 14-20 months). The only factors found to be significantly associated with retinopathy were total dose multiplied by dose per fraction, or total dose normalized to the equivalent total dose in 2-Gy fractions as estimated from the LQ model, and these gave equivalent descriptions. There were trends (not significant) for increased risk of retinopathy when treatments included chemotherapy or photocoagulation, and for decreased risk (also not significant) when cryotherapy was used in conjunction with radiotherapy. No significance could be attached to any of the following: number of sites per eye, Reese-Ellsworth stage, and family history. We conclude that hypofractionation carries a significant risk for retinopathy in the treatment of retinoblastoma. [less ▲]

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See detailHypofractionation in retinoblastoma: an increased risk of retinopathy.
Coucke, Philippe ULg; Schmid; Balmer et al

in Radiotherapy & Oncology (1993), 28(2), 157-161

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See detailL'hypoglycemie du patient diabetique. Recommendations of ALFEDIAM (French Language Association for the Study of Diabetes and Metabolic Diseases.
Grimaldi, A.; Slama, G.; Tubiana-Rufi, N. et al

in Diabètes & Métabolism (1997), 23(1), 100-8

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See detailHypoglycémie et hypoxie cérébrales
Battisti, Oreste ULg; Bertrand, J. M.; Langhendries, J. P.

Conference (1988)

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See detailL'hypoglycemie reactive: un phenomene critique mysterieux, insidieux, mais non dangereux.
Scheen, André ULg; Lefebvre, Pierre ULg

in Revue Médicale de Liège (2004), 59(4), 237-42

Numerous individuals complain of malaise attributed to hypoglycaemia. However, the diagnosis of hypoglycaemia is rarely documented and most often overstated. Reactive hypoglycaemia in the postprandial ... [more ▼]

Numerous individuals complain of malaise attributed to hypoglycaemia. However, the diagnosis of hypoglycaemia is rarely documented and most often overstated. Reactive hypoglycaemia in the postprandial state is rather exceptional. The diagnosis relies upon the measurement of plasma glucose concentration (< 3 mmol/l or 55 mg/dl) at the time of the malaise. Reactive hypoglycaemia is generally associated with adrenergic symptoms and, less often, with cognitive disturbances. Importantly, a plasma glucose concentration below 3 mmol/l during an oral glucose tolerance test is not sufficient to decide that the patient suffers from reactive hypoglycaemia. Treatment is based on dietary advices including frequent small split meals and limitation of carbohydrates with high glycaemic index. Acarbose, a specific inhibitor of gut alpha-glucosidase enzymes, may be helpful in case of diet failure. As compared with true reactive hypoglycaemia, a postprandial hyperadrenergic reaction without real concomitant hypoglycaemia is much more prevalent. Careful anamnesis may suspect such a diagnosis, but other diagnoses such as panic attack or vasovagal reaction should be excluded. Treatment is purely symptomatic and essentially empiric. [less ▲]

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See detailHypogonadism in a patient with a mutation in the luteinizing hormone beta-subunit gene
VALDES SOCIN, Hernan Gonzalo ULg

Master of advanced studies dissertation (2008)

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See detailHypogonadism in a Patient with a Mutation in the Luteinizing Hormone Beta-Subunit Gene
Valdes Socin, Hernan Gonzalo ULg; Salvi, R.; Daly, Adrian ULg et al

in New England Journal of Medicine [=NEJM] (2004), 351(25), 2619-2625

A 30-year-old man who presented with delayed puberty and infertility was found to have hypogonadism associated with an absence of circulating luteinizing hormone. The patient had a homozygous missense ... [more ▼]

A 30-year-old man who presented with delayed puberty and infertility was found to have hypogonadism associated with an absence of circulating luteinizing hormone. The patient had a homozygous missense mutation in the gene that encodes the beta subunit of luteinizing hormone (Gly36Asp), a mutation that disrupted a vital cystine knot motif and abrogated the heterodimerization and secretion of luteinizing hormone. Treatment with human chorionic gonadotropin increased circulating testosterone, promoted virilization, and was associated with the appearance of normal spermatozoa in low concentrations. This case illustrates the important physiological role that luteinizing hormone plays in male sexual maturation and fertility. [less ▲]

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See detailHypogonadisme congénital chez un homme, associé à une LK immunoréactive normale, élévation de FSH et azoospermie
Valdes Socin, Hernan Gonzalo ULg; Chachati, Anne-Sophie ULg; De Roux, N. et al

in Annales d'Endocrinologie (2010, September), 71(5), 355

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See detailHypogonadisme par déficience de LH.
Beckers, Albert ULg

in Bulletin et Mémoires de l'Académie Royale de Médecine de Belgique (2007), 162(5-6), 291-7298

A 30-year-old man was investigated for delayed puberty and infertility. These investigations showed a complete absence of circulating luteinizing hormone (LH). Genetic studies revealed a missense mutation ... [more ▼]

A 30-year-old man was investigated for delayed puberty and infertility. These investigations showed a complete absence of circulating luteinizing hormone (LH). Genetic studies revealed a missense mutation in the LHbeta gene (G36D). This mutation disrupts a vital cystine knot motif and abrogates the heterodimerization and secretion of LH. Treatment with hCG was instituted, which led to arise in testosterone and improvement in spermatogenesis. After in vitro fertilization the patient had a son who was heterozygous for the G36D mutation. A second patient with similar clinical and biological presentation has been explored. A non-frame shift deletion of 3 base-pairs was discovered at position 20 which led to the deletion of a lysine residue. The proband and his prepubescent brother were homozygotic for this mutation. These cases illustrate the important physiological role of LH in male sexual maturation and fertility. [less ▲]

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See detailHypogonadismes hypogonadotropes par déficience en LH
Beckers, Albert ULg; Burlacu, M. C.

Scientific conference (2008, May)

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See detailHypomelanosis of Ito: pigmentary mosaicism with immature melanosome in keratinocytes.
Devillers, Céline; QUATRESOOZ, Pascale ULg; Hermanns-Le, Trinh ULg et al

in International Journal of Dermatology (2011), 50(10), 1234-9

BACKGROUND: Hypomelanosis of Ito is a rare genetic disorder characterized by whorled areas of hypomelanosis. The purpose of the present study was to revisit some aspects of Ito's hypomelanosis. METHODS ... [more ▼]

BACKGROUND: Hypomelanosis of Ito is a rare genetic disorder characterized by whorled areas of hypomelanosis. The purpose of the present study was to revisit some aspects of Ito's hypomelanosis. METHODS: Clinical observations included ultraviolet-light-enhanced visualization (ULEV) method. Histochemistry, immunohistochemistry, and electron microscopy were performed on biopsy samples from the hypopigmented areas and the surrounding skin. RESULTS: Both the ULEV and microscopic examinations revealed the heterogeneity of the pigmentation. Hypomelanosis was characterized by a reduction in melanosomes, both in melanocytes and keratinocytes. These organelles were immature and atypical, showing a weak tyrosinase immunoreactivity. Melanosome macroautophagy was prominent in keratinocytes. Some clusters of the same cells exhibited strong immunoreactivity for the Mac 387 antibody (Ca(2+) -dependent calprotectin). Ulex europaeus agglutinin-1 (UEA-1) decorated the superficial layers of the epidermis. Such features are typically found in functionally altered keratinocytes. A number of dermal cells exhibited intense phagocytic activity linked to lysozyme immunoreactivity. CONCLUSIONS: Both the melanosome depletion and macroautophagy of immature melanosomes in keratinocytes appeared to represent prominent aspects of hypomelanosis of Ito. In sum, Ito's hypomelanosis combines structural and functional changes affecting both the melanocytes and keratinocytes in the skin. [less ▲]

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See detailHyponatrémie induite par la carbamazépine et affection rénale : à propos d'un cas
PITCHOT, William ULg; ANSSEAU, Marc ULg; PAPART, Patrick ULg et al

in Psychiatrie et psychobiologie (1989)

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See detailHypophosphatémie et ostéomalacie oncogénique
Van der Rest, Catherine; CAVALIER, Etienne ULg; COLSON, Laurent ULg et al

in Revue Médicale Suisse (2011), 7

In this article, we will discuss about hypophosphatemia due to tumor-induced osteomalacia. This disease is characterized by severe muscular and articular tenderness inducing profound walking limitation ... [more ▼]

In this article, we will discuss about hypophosphatemia due to tumor-induced osteomalacia. This disease is characterized by severe muscular and articular tenderness inducing profound walking limitation. Clinical chemistry results show severe hypophosphatemia due to hyperphosphaturia. Fibroblast growth factor 23 (FGG-23) is abnormally high. Physiological role of FGF-23 is examined. We also consider the pathophysiology of tumor induced osteomalacia, the use of different investigations to localize the tumor and therapies available to treat this rare disease. [less ▲]

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See detailHypophyseal failure and amaurosis revealing an extensive inflammatory pseudotumor
Hansen, I.; Ronci, N.; Stevenaert, Achille ULg et al

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

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See detailHypophysite du Post-Partum
Beckers, Albert ULg

Scientific conference (2004, December 03)

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See detailHypopituitarism in pituitary gigantism (results of an international study)
Rostomyan, L; Daly, Adrian ULg; Shah, N 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 detailHypopituitarism in pituitary gigantism (results of an international study)
Rostomyan, Liliya ULg; Daly, Adrian ULg; Shah, NS et al

in The 3rd ENEA Workshop : Hypopituitarism - Abstract book (2013, December)

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See detailHypopituitarisme consécutif aux atteintes cérébrales: le traumatisme cranien et l'hémorragie sous-arachnoidienne mis en cause.
Valdes Socin, Hernan Gonzalo ULg; Vroonen, Laurent ULg; Robe, Pierre ULg et al

in Revue Médicale de Liège (2009), 64(9), 457-463

Brain injuries namely traumatic brain injuries (TBI) and subarachnoid haemorrhage (SAH) are relevant causes of acquired adult hypopituitarism, perhaps more prevalent than ever believed. TBI represent a ... [more ▼]

Brain injuries namely traumatic brain injuries (TBI) and subarachnoid haemorrhage (SAH) are relevant causes of acquired adult hypopituitarism, perhaps more prevalent than ever believed. TBI represent a major health problem with an annual incidence of 300 cases per 100.000. SAH affects six new cases per 1.000.000 habitants in USA. In Belgium we estimate nearly 30.000 new TBI cases and 600 SAH cases per year. In the English literature, TBI secondary hypopituitarism has been well documented in 14 retrospective and prospective series accounting for 1.077 cases. In all these series the main pituitary deficits were: GH (14%), ACTH (14%), gonadotrope (18%), TSH (7%) and diabetes insipidus (4%). SAH was documented as a cause of hypopituitarism in three retrospective series accounting for 110 cases and in one prospective series. In all these series main pituitary deficits were GH (25%), ACTH (15%), gonadotrope (8.5%), TSH (6%) and diabetes insipidus (4%). In this review, we analyze recent data and discuss diagnostic and treatment features of secondary hypopituitarism due TBI and SAH. [less ▲]

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See detailHypotension du grand prematuré
Rigo, Vincent ULg; Beauduin, Philippe; Rigo, Jacques ULg

in Revue Médicale de Liège (2007), 62(2), 86-93

One out of four very preterm infants will present with circulatory maladaptation during the first two days of life, with an increased risk of early complications and long term sequelae. Appreciation of ... [more ▼]

One out of four very preterm infants will present with circulatory maladaptation during the first two days of life, with an increased risk of early complications and long term sequelae. Appreciation of those transitional difficulties cannot be limited to blood pressure. Assesment of blood pressure itself must be done in relation with gestational age and birth weight adapted norms. The effects of therapies for low systemic blood flow on blood pressure, organs and cerebral circulations are better understood, but none of them has assessed for mortality or neurodevelopmental outcomes. [less ▲]

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