G Massa

Jessa Hospital, Hasselt, Flanders, Belgium

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Publications (49)167.07 Total impact

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    ABSTRACT: Background: The transcription factor SIM1 (Single-minded 1) is involved in the control of food intake and in the pathogenesis of obesity. In mice, Sim1 is involved in the development of the paraventricular nucleus, and Sim1 deficiency leads to severe obesity and hyperphagia. In humans, chromosomal abnormalities in the SIM1 gene region have been reported in obese individuals. Furthermore, recent data also suggest that loss-of-function point mutations in SIM1 are responsible for SIM1 haplo-insufficiency that is involved in causing human obesity. In this study, we therefore wanted to expand the evidence regarding the involvement of SIM1 mutations in the pathogenesis of severe early-onset obesity. Methods: We screened 561 severely overweight and obese children and adolescents and 453 lean adults for mutations in the coding region of the SIM1 gene. Mutation screening in all patients and lean individuals was performed by high-resolution melting curve analysis combined with direct sequencing. To evaluate the effect of the mutations on SIM1 transcriptional activity, luciferase reporter assays were performed. Results: Mutation analysis identified four novel nonsynonymous coding variants in SIM1 in four unrelated obese individuals: p.L242V, p.T481K, p.A517V and p.D590E. Five synonymous variants, p.P57P, p.F93F, p.I183I, p.V208V and p.T653T, were also identified. Screening of the lean control population revealed the occurrence of four other rare SIM1 variants: p.G408R, p.R471P, p.S492P and p.S622F. For variants p.T481K and p.A517V, which were found in obese individuals, a decrease in SIM1 transcriptional activity was observed, whereas the transcriptional activity of all variants found in lean individuals resembled wild type. Conclusions: In this study, we have demonstrated the presence of rare SIM1 variants in both an obese pediatric population and a population of lean adult controls. Further, we have shown that functional in vitro analysis of SIM1 variants may help in distinguishing benign variants of no pathogenic significance from variants which contribute to the obesity phenotype.
    International journal of obesity (2005) 10/2013; 38(7). DOI:10.1038/ijo.2013.188 · 5.00 Impact Factor
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    ABSTRACT: What is already known about this subject BDNF is involved in the regulation of food intake and body weight. BDNF deficient animal models are obese. Chromosomal abnormalities cause obesity in humans. What this study adds Evaluation of point mutations in BDNF. Identification of BDNF mutations in obese children. Point mutations in BDNF are not a common cause of childhood obesity. INTRODUCTION: There is ample evidence that BDNF has a role in the regulation of food intake and body weight. Study of various mouse models gave a clear indication that BDNF deficiency leads to the development of obesity. Functional loss of one copy of the BDNF gene, due to chromosomal rearrangements or microdeletions, can cause an obesity phenotype in humans. Therefore, we wanted to investigate whether point mutations in the gene also result in a comparable phenotype. METHODS: We screened 554 severely overweight and obese children and adolescents and 565 lean adults for mutations in the coding region of BDNF. Mutation screening was performed by high-resolution melting curve analysis and direct sequencing. RESULTS: Screening of obese patients led to the identification of two synonymous variations (V37V and H65H) and two non-synonymous coding mutations (T2I and V46M) in the BDNF gene. When we subsequently screened our control population, we found T2I with comparable frequency and confirmed that this is a rare and non-pathogenic variant. In addition, we found another non-synonymous mutation (N187S) in the control population. CONCLUSIONS: In silico analysis of the V46M variant did not support a clear disease-causing effect and no family data were available in order to determine whether the mutation segregates with obesity. However, we cannot rule out a possible pathogenic effect for this variant. In general, we tend to conclude that mutations in the coding region of BDNF are uncommon in obese patients and are therefore not likely to play an essential role in the pathogenesis of childhood obesity.
    Pediatric Obesity 01/2013; 9(1). DOI:10.1111/j.2047-6310.2012.00131.x · 4.57 Impact Factor
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    ABSTRACT: Unlabelled: We aimed to investigate care processes and outcomes among children and adolescents with type 1 diabetes treated in hospital-based multidisciplinary paediatric diabetes centres. Our retrospective cross-sectional study among 12 Belgian centres included data from 974 patients with type 1 diabetes, aged 0-18 years. Questionnaires were used to collect data on demographic and clinical characteristics, as well as process of care completion and outcomes of care in 2008. Most patients lived with both biological or adoption parents (77 %) and had at least one parent of Belgian origin (78 %). Nearly all patients (≥95 %) underwent determination of HbA(1c) and BMI. Screening for retinopathy (55 %) and microalbuminuria (73 %) was less frequent, but rates increased with age and diabetes duration. Median HbA(1c) was 61 mmol/mol (7.7 %) [interquartile range 54-68 mmol/mol (7.1-8.4 %)] and increased with age and insulin dose. HbA(1c) was higher among patients on insulin pump therapy. Median HbA(1c) significantly differed between centres [from 56 mmol/mol (7.3 %) to 66 mmol/mol (8.2 %)]. Incidence of severe hypoglycaemia was 30 per 100 patient-years. Admissions for ketoacidosis had a rate of 3.2 per 100 patient-years. Patients not living with both biological or adoption parents had higher HbA(1c) and more admissions for ketoacidosis. Parents' country of origin was not associated with processes and outcomes of care. Conclusion: Outcomes of care ranked well compared to other European countries, while complication screening rates were intermediate. The observed centre variation in HbA(1c) remained unexplained. Outcomes were associated with family structure, highlighting the continuing need for strategies to cope with this emerging challenge.
    European Journal of Pediatrics 08/2012; 171(11). DOI:10.1007/s00431-012-1809-2 · 1.89 Impact Factor
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    ABSTRACT: Few data are available about parental concerns and psychosocial functioning of young children born small for gestational age (SGA) treated with growth hormone (GH). The present study focused on the perception of short stature and the concerns and expectations of the parents regarding GH treatment. Forty prepubertal short SGA children, randomized into a GH-treated and a GH-untreated group, and their parents were evaluated by a questionnaire and a semi-structured interview at start and after 2 years of follow-up. Before start, 85% of the parents were concerned about short stature, 76% expected an increase in adult height of > or =10 cm and 81% expected a positive impact on well-being. Half of the parents expressed fears regarding GH treatment. After 2 years, more parents of treated children reported obvious growth and physical changes, and fewer parents reported teasing because of short stature. An improvement of well-being was reported by half of the parents of treated and untreated children. Fears about GH treatment disappeared almost completely. The perspective of GH treatment induced major adult height expectations. In treated children, the physical effects of GH treatment became obvious, teasing because of short stature decreased and initial concerns about short stature and GH therapy decreased.
    Hormone Research 03/2008; 69(6):334-42. DOI:10.1159/000117389 · 2.48 Impact Factor
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    ABSTRACT: Children born small for gestational age (SGA) are not only at risk for short stature, but also for neurodevelopmental and behavioral problems. In this study, we analyzed the effects of high-dose GH therapy on cognitive development and psychosocial functioning in 34 prepubertal (3-8 years) short SGA children, equally randomized into a GH-treated group (TRG) and an untreated group (UTRG). At start and after 2 years, children underwent standardized tests measuring the intellectual abilities (Wechsler Preschool and Primary Scale of Intelligence-Revised, or Wechsler Intelligence Scale for Children-Revised); their parents completed a standardized questionnaire evaluating psychosocial functioning (Child Behavior Checklist; CBCL). At start, total IQ scores were significantly (P < 0.05) lower in the SGA group than in the general population: 32% of the SGA patients had scores below 85. After 2 years, IQ scores remained unchanged in the TRG, but increased significantly (P < 0.05) in the UTRG. After exclusion of children with developmental problems, however, no significant changes in IQ scores occurred in the UTRG as well as the TRG. At baseline, 24% (8/34) children had problematic CBCL total problems scores, equally distributed among the two groups; no significant changes in the different subscale scores occurred after 2 years. No beneficial effect of 2 years of GH therapy on cognitive and behavioral profile could be observed in a cohort of rather young short SGA children presenting a variable degree of developmental delay and behavioral problems. Subsequent follow-up could reveal potential long-term effects of GH therapy on development and behavior.
    European Journal of Endocrinology 03/2007; 156(2):195-201. DOI:10.1530/eje.1.02335 · 4.07 Impact Factor
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    Clinical Genetics 11/2006; 70(4):355-9. DOI:10.1111/j.1399-0004.2006.00686.x · 3.93 Impact Factor
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    ABSTRACT: The age at diagnosis of 242 girls with Turner syndrome (TS) treated in Belgium with growth hormone between 1991 and 2002 was evaluated. The median (range) age at diagnosis was 6.6 (0-18.3) years. Patients with 45,X karyotype were diagnosed earlier than patients with other karyotypes. Compared to a previous survey, performed on 100 patients 12 years earlier, more patients were diagnosed during infancy and childhood, and less during adolescence. However, in 22% of the girls the diagnosis was made after the age of 12 years; these girls showed the largest height deficit. As early diagnosis has several potential advantages we recommend that a cytogenetic analysis should be considered in all girls with unexplained short stature with height below -2 SD of the mean for age or below the parent specific lower limit of height.
    Archives of Disease in Childhood 04/2005; 90(3):267-8. DOI:10.1136/adc.2004.049817 · 2.90 Impact Factor
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    A Messaaoui · G Massa · S Tenoutasse · C Heinrichs ·
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    ABSTRACT: Central precocious puberty (CPP) is treated with GnRH analogues to stabilize secondary sexual characteristics and to prevent loss of final height (FH) due to accelerated bone maturation. However, some studies suggest that FH is not always improved and that treatment may induce excessive weight gain. We analysed data from 19 girls treated for CPP with monthly injections of 3.75 mg triptorelin. Pubertal development, bone age, height, weight and body mass index (BMI) were evaluated at start (chronological age: 7.8 +/- 1.8 yrs, mean +/- SD), at the end of treatment (10.6 +/- 1.1 yrs) and at FH (14.9 +/- 2.5 yrs). At start of treatment, breast (B) development was B3 (from 2 to 4), bone age 10.6 +/- 1.7 yrs, height 2.1 +/- 1.1 SDS and BMI 1.3 +/- 0.8 SDS. Treatment stabilized or reduced breast development and decreased bone maturation. Final height was 162.3 +/- 6.6 cm (0.0 +/- 1.1 SDS) and was comparable to predicted adult height at the start of treatment and to corrected mid-parental height. BMI SDS at the start, the end of treatment and at final evaluation were 1.3 +/- 0.8, 1.6 +/- 0.8 and 1.4 +/- 0.9 SDS. In conclusion, in our girls with central precocious puberty, treatment with GnRH agonist stabilized or decreased breast development and stabilized bone maturation, but did not increase neither final height nor weight. Aspects other than height should also be taken into account when considering treatment of children with precocious puberty.
    Revue medicale de Bruxelles 03/2005; 26(1):27-32.
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    ABSTRACT: Since the availability of recombinant human growth hormone (rhGH) all children with growth hormone deficiency (GHD) living in Belgium are offered rhGH treatment after approval by a peer-review board. In this study, we evaluated the prevalence and demographic features of childhood GHD in Belgium during the period 1986-2001 and we compared them with the data from other countries. Diagnostic, demographic and baseline auxological data of 714 children diagnosed as having GHD between 1986 and 2001 were retrieved from the database of the Belgian Study Group for Paediatric Endocrinology. The prevalence of GHD in Belgium was estimated to be 1/5600. The origin of GHD was idiopathic (idGHD) in 41% of the patients, congenital (congGHD) in 20% and acquired (acqGHD) in 35%. During the first 4 years (1986-1989) more patients were classified as idGHD; thereafter the distribution between the three aetiology groups did not change. In all groups, boys outnumbered girls but this preponderance was especially pronounced in congGHD patients (male:female=4:1) with a central malformation that associates an anterior pituitary hypoplasia, a missing, fine or normal pituitary stalk and an ectopic posterior pituitary. Thirteen percent of the patients with idGHD, 50% with congGHD and 52% with acqGHD had multiple pituitary deficiencies. Patients with congGHD were the youngest (mean+/-s.d. age: 6.5+/-4.7 years) and were the shortest (-3.0+/-1.3 standard deviation score (SDS)) at the start of rhGH treatment. There was no time trend over the studied period for age and height at onset of GH therapy. In Belgium, the prevalence of childhood GHD can be estimated as 1/5600 which is comparable to other recent surveys. The yearly number of new patients for the different aetiologies and the auxological parameters have remained relatively constant over the last 16 years.
    European Journal of Endocrinology 08/2004; 151(1):67-72. DOI:10.1530/eje.0.1510067 · 4.07 Impact Factor
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    ABSTRACT: Most girls with Turner syndrome (TS) are intensively followed by paediatricians, but are lost to follow-up when they reach adulthood. To gain insight into the adult medical and psychosocial situation, we performed a survey in young adult TS patients. A questionnaire concerning current health status, education, occupation and living situation was sent to 160 young adult TS women, all treated during childhood with GH and oestrogen if needed. We received 102 completed questionnaires. Mean +/- SD age at reception of the questionnaire was 23.4 +/- 3.3 years, height 153.3 +/- 5.2 cm, body mass index 23.7 +/- 4.9 kg/m(2). Age and auxological parameters were comparable between responders and non-responders. Thirteen (12.7%) responders were not under regular medical care; 15 (14.7%) were seen by a general practitioner, while 28 (27.4%) needed several specialists. Forty-one (40.2%) patients reported health problems. The most frequently reported problem was hypertension (10.7%), followed by hypothyroidism (5.8%) and back problems (4.9%). Twenty-four (23.5%) of the 41 patients were taking medication for the indicated health problems. Twenty-six (25.5%) women had undergone spontaneous puberty; 16 of them reported spontaneous menstruations while 10 received oestrogen replacement therapy. Of the 76 women with induced puberty, 11 (14.5%) were not taking any oestrogen anymore. Compared with the general population, more TS women attended university and more obtained higher education. Forty-six women (45.1%) were working full-time, 7 (6.9%) were unemployed, and 4 (3.9%) received an allocation. Seventy (68.6%) patients were still living with their parents, while 18 (17.6%) were living together or married, and 14 (13.7%) were living alone. The transition of adolescents with TS to adult medical care is not optimal in Belgium. Although 40.2% of these young women reported health problems, 12.7% did not consult any physician. Many TS women did not take oestrogen replacement therapy. A specialized multidisciplinary approach for adults with TS is needed in order to optimize health and psychosocial status in these women.
    Hormone Research 02/2004; 62(4):161-7. DOI:10.1159/000080099 · 2.48 Impact Factor
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    ABSTRACT: Although it has been well established that GH treatment increases final height (FH) in girls with Turner syndrome (TS), the optimal ages to start GH therapy and introduce estrogens for pubertal induction have not been defined. We evaluated retrospectively the influence of the age at onset of GH treatment and age at onset of puberty on FH of 186 adult TS women treated during childhood with GH. Puberty started spontaneously in 38 patients, and it was induced in 148 girls with ethinyl estradiol (mean +/- SD starting dose, 66 +/- 32 ng/kg.d). Patients with spontaneous or induced puberty were divided into quartiles on the basis of age at initiation of GH treatment (3-10, 10-12, 12-14, and 14-19 yr). FH was 151.7 +/- 6.0 cm; there were no FH differences between patients with induced or spontaneous puberty, nor were there differences between the age quartiles. Puberty started earlier in the girls with spontaneous puberty than in those with induced puberty (12.4 +/- 1.3 yr vs. 14.5 +/- 1.9 yr; P < 0.0001). The age at onset of puberty was not related to FH. Pubertal growth was 15.4 +/- 4.6 cm in the girls with spontaneous puberty and 8.6 +/- 4.3 cm in the girls with induced puberty (P < 0.0001). We conclude that GH treatment results in a significant increase in FH in most TS girls. Under the conditions of GH treatment and induction of puberty that we have used, the age at start of GH treatment was not related to FH; in addition, late or delayed induced or spontaneous puberty did not affect FH.
    Journal of Clinical Endocrinology &amp Metabolism 10/2003; 88(9):4168-74. DOI:10.1210/jc.2002-022040 · 6.21 Impact Factor
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    ABSTRACT: Background: Recent studies have shown that many patients treated with growth hormone (GH) during childhood because of idiopathic GH deficiency (GHD) are no longer GH deficient when retested after cessation of GH therapy when final height is achieved. These patients are labelled as transient GHD. We hypothesized that normalization of GH secretion in transient GHD could occur earlier during the course of GH treatment, which could allow earlier cessation of GH treatment. Methods: In a retrospective study, GH secretion was re-evaluated after cessation of GH treatment at final height in 43 patients diagnosed during childhood as idiopathic GHD (10 with multiple pituitary hormonal deficiencies (MPHD) and 33 with isolated GHD (IsGHD)). In a prospective study, GH secretion was re-assessed after interruption of GH treatment given for 1 year in 18 children with idiopathic GHD (2 MPHD, 16 IsGHD). GH secretion was evaluated by glucagon or insulin stimulation tests. Results: In the retrospective study, all the 10 patients with MPHD and 64% of the 33 patients with IsGHD were still deficient at re-evaluation using the paediatric criteria to define GHD (GH peak Conclusions: Although many patients diagnosed with IsGHD during childhood have a normalized GH secretory capacity when retested during adulthood, early retesting after interruption of GH treatment given for 1 year during childhood does not enable to determine if GH therapy has to be discontinued before cessation of growth.
    Hormone Research 02/2003; 59(1):7-15. DOI:10.1159/000067936 · 2.48 Impact Factor
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    ABSTRACT: The growth response to recombinant hGH (rhGH) treatment and final height of 61 Belgian children (32 boys) with idiopathic growth hormone deficiency (GHD) were studied. Two patient groups were compared: Group 1 with spontaneous puberty (n = 49), Group 2 with induced puberty (n = 12). The patients were treated with daily subcutaneous injections of rhGH in a dose of 0.5-0.7 IU/kg/week (0.17-0.23 mg/kg/week) from the mean +/- SD age of 11.9 +/- 3.1 years during 5.1 +/- 2.1 years. rhGH treatment induced a doubling of the height velocity during the first year and resulted in a normalisation of height in 53 (87%) patients. Final height was -0.7 +/- 1.1 SDS, being 170.4 +/- 7.2 cm in boys and 158.0 +/- 6.4 cm in girls. Corrected for mid-parental height, final height was 0.0 +/- 1.1 SDS. Ninety-two percent of the patients attained an adult height within the genetically determined target height range. Although height gain during puberty was smaller in the patients with induced puberty (boys: 17.1 +/- 7.0 cm vs. 27.5 +/- 6.6 cm (p < 0.005); girls: 9.6 +/- 7.4 cm vs. 22.2 +/- 6.1 cm (p < 0.005)), no differences in final height after adjustment for mid-parental height were found between patients with spontaneous or induced puberty. We conclude that patients with idiopathic GHD treated with rhGH administered as daily subcutaneous injections in a dose of 0.5-0.7 IU/kg/week reach their genetic growth potential, resulting in a normalisation of height in the majority of them, irrespective of spontaneous or induced puberty.
    Hormone Research 08/2001; 55(2):88-94. DOI:10.1159/000049976 · 2.48 Impact Factor
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    ABSTRACT: Divergent findings on the quality of life (QoL) and the psychosocial functioning of adults treated during childhood with growth hormone (GH) because of GH deficiency (GHD) have been reported. In the present study we evaluated the QoL and the perception of the effect of former GH treatment in Belgian young adults with childhood GHD. Thirty-six patients (22 males) were included in the study. They all were treated during childhood with GH for GHD. QoL was evaluated with a standardised questionnaire: the Quality of Life Assessment of Growth Hormone Deficiency in Adults (QoL-AGHDA). Psychosocial functioning, sexual experience and schooling were evaluated by semi-structured interviews and questionnaires. The influence of gender, type of hormone deficiency (isolated GHD vs multiple pituitary hormone deficiencies [MPHD]), age at the start of GH therapy (before 12 yr vs after 12 yr) and the height deficit at the start of GH therapy (< -3 SDS vs > -3 SDS) were studied. In addition, the patients' and parents' perception of height and of the effect of GH treatment was retrospectively evaluated by semi-structured interviews. Age (mean +/- SD) at the time of evaluation was 20.0 +/- 1.3 yr and final height was -0.5 +/- 0.9 SDS, comparable to mid-parental height (-0.6 +/- 0.8 SDS). The QoL-AGHDA score was 9 +/- 6. About half of the patients, especially those in whom GH treatment was started after the age of 12 years, complained of retrospective difficulties with self-confidence and social contact, and about one-quarter of the patients had current difficulties with self-confidence, social contact, contact with the opposite sex and with emotional life. Only 44% of the patients had had sexual intercourse--none of those with MPHD. According to the parents, the patients had and still have more difficulties with self-confidence and social contact than their siblings and/or peers, and they needed and still need more emotional support. In one out of four patients the parents expected difficulties in finding a job, in one out of three patients parents expected difficulties in leaving home or in having a stable relationship. The educational level of patients with a height deficit < -3 SDS at start of GH therapy was lower than in patients with a height deficit > -3 SDS. According to the parents, about half of the patients, especially those with MPHD, had more study problems compared to siblings. In all patients, satisfaction with final height and GH therapy was obvious. In conclusion, the psychosocial outcome of young adults with childhood GHD was more satisfying than in previous studies. This could be due to a more adequate GH treatment with better final height results. Nevertheless, more difficulties with respect to psychosocial functioning were observed in patients with MPHD, in patients in whom GH treatment was started after 12 years of age and in patients with a height deficit < -3 SDS at the start of GH therapy, underlining the need for early diagnosis and treatment of childhood GHD, and of continuing medical follow-up and psychosocial counselling, particularly in these subgroups of patients with GHD.
    Journal of pediatric endocrinology & metabolism: JPEM 01/2001; 14 Suppl 5:1249-60; discussion 1261-2. · 1.00 Impact Factor
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    ABSTRACT: Objectives: The potential benefit of growth hormone (GH) administration to increase adult height of normal children of short stature might be blurred by the accuracy and the precision of the prediction methods used to estimate final height before onset of therapy. The aim of the present study was to evaluate three prediction methods: Bayley-Pinneau (BP), Roche-Wainer-Thissen (RWT) and Tanner-Whitehouse Mark II (TW2) and to improve their accuracy and precision by exploring their correlation with various parameters obtained in peripubertal children with poor predicted adult height. Study Design: Accuracy and precision of the prediction methods were evaluated retrospectively by comparing predicted adult heights estimated in 62 boys at 13.7 ± 0.9 years and in 28 girls at 12.1 ± 0.9 years of age, with their adult heights measured respectively at 20.7 ± 2.6 years and 18.8 ± 2.8 years. Results: At the time of prediction, the height for chronological age was -2.07 ± 0.68 standard deviation scores for boys and -2.15 ± 0.6 years for girls. Measured adult heights were significantly lower than target heights (165.1 ± 5.1 vs. 169.4 ± 4.8 cm for boys; p Conclusions: The use of a factor correcting the accuracy of the BP method in boys and of the TW2 method in girls should be valuable in assessing the potential benefit of GH therapy to increase adult height in short normal children.
    Hormone Research 10/1997; 48(4):184-90. DOI:10.1159/000185511 · 2.48 Impact Factor
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    ABSTRACT: In 44 girls with Turner's syndrome, aged 4.0-15.3 yr, the effects of biosynthetic GH (25 U/m2.week) given as once daily or twice daily injections were compared. During 1 yr of treatment, the growth rate increased similarly by 3.5 +/- 1.3 cm/yr in the once daily group and 2.7 +/- 1.8 cm/yr in the twice daily group. Although pretreatment height velocity was negatively related to age, the increase in height velocity during therapy was not. The mean progression in bone age (TW2-RUS method), during therapy was 1.3 yr in both groups. No significant change in the median insulin secretory response to an oral glucose tolerance test was found. Serum cholesterol and triglyceride concentrations did not change significantly throughout the study in either treatment group. Thyroid hormone concentrations remained within normal limits. Normal increments in left ventricular wall thickness and left ventricular mass for age and body surface were observed after 1 yr of GH treatment. We conclude that division of the daily GH dose given to Turner's syndrome patients into two injections does not result in either a significantly different growth response or different side-effects from once daily treatment during the first year of therapy.
    Journal of Clinical Endocrinology &amp Metabolism 09/1994; 79(2):489-94. · 6.21 Impact Factor
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    ABSTRACT: The characteristics of the human serum growth hormone-binding protein (GHBP) were compared with those of a water-soluble GH-binding site prepared by incubating cultured IM-9 lymphocytes in assay buffer with 25 mmol/l iodoacetamide. High-performance liquid chromatography gel filtration of the water-soluble GH-binding site incubated with 125I-labeled human GH ([125I]hGH) revealed a large peak of bound [125I]hGH eluting at the same position as the peak of [125I]hGH bound to the GHBP in serum. The estimated M(r) of the peak was 120,000, presumably representing one [125I]hGH bound to two binding sites. The binding specificities of the serum GHBP, the water-soluble GH-binding site and the GH receptor on IM-9 lymphocytes were identical. The binding affinities for 22,000 hGH and for 20,000 hGH of the serum GHBP were similar to the binding affinity of the water-soluble GH-binding site but lower than those of the cellular GH receptor. These findings show that the characteristics of the serum GHBP are comparable to those of the water-soluble GH-binding site released from IM-9 cells and support the hypothesis that in man the serum GHBP is produced by proteolytic cleavage of the cellular GH receptor.
    Acta endocrinologica 01/1994; 129(6):559-64.

  • European Journal of Endocrinology 12/1993; 129(6):559-564. DOI:10.1530/acta.0.1290559 · 4.07 Impact Factor

  • Hormone and Metabolic Research 07/1993; 25(6):325-6. DOI:10.1055/s-2007-1002111 · 2.12 Impact Factor
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    ABSTRACT: The serum half-life of the glycosylated GH-BP in the human is currently unknown. Circulating levels of the high affinity GH-BP are low in the neonatal period compared to adult life (Massa et al, Pediatr Res 1992). During an exchange transfusion (ET) for neonatal hyperbilirubinemia, the blood of the newborn is nearly completely replaced by adult donor blood. To evaluate the elimination rate of GH-BP we measured serum levels of GH-BP by HPLC gel filtration before and at different time intervals after an ET in 4 term neonates. Before the ET the mean±SE serum binding of 125I-hGH (GH-BP) was 6.7±1.2%. At the end of the ET, serum GH-BP was increased to 25.3±2.6% (P<0.005). Thereafter serum GH-BP decreased slowly and was 84 to 96 hours later still higher than before the ET. Analysis of the elimination curve by exponential stripping suggested an elimination according to a bi-exponential model : GH-BP(%) = 40 × e(5.1 x-03 ×time) + 64 x e(−2.5x-04 × time). The seruin half-life of the GH-BP complex was estimated to be 1.9 days. These data demonstrate : 1) that the GH-BP can be transfused, and 2) that the serum half-life of the GH-BP complex in neonates is in the order of magnitude of days. (This work was supported by a grant from the Belgian study Group of Pediatric Endocrinology).
    Pediatric Research 05/1993; 33. DOI:10.1203/00006450-199305001-00317 · 2.31 Impact Factor

Publication Stats

728 Citations
167.07 Total Impact Points


  • 2013
    • Jessa Hospital
      Hasselt, Flanders, Belgium
  • 2004
    • Hôpital Universitaire des Enfants Reine Fabiola
      Bruxelles, Brussels Capital, Belgium
  • 2001
    • Catholic University of Louvain
      Лувен-ла-Нев, Wallonia, Belgium
  • 1984-1994
    • University of Leuven
      • Department of Human Genetics
      Louvain, Flemish, Belgium
  • 1987-1993
    • Universitair Ziekenhuis Leuven
      • • Department of Paedriatrics
      • • Department of Pedriatrics
      Louvain, Flanders, Belgium