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Biomedical subjects

M Vanderschueren-Lodeweyckx

Publications and source records attributed to M Vanderschueren-Lodeweyckx.

At least 19 recordsLinked to original sources
PubMed1996

Follow-up of three years of treatment with growth hormone and of one post-treatment year, in children with severe growth retardation of intrauterine onset.

Seventy-eight prepubertal, non-GH-deficient children aged 8.1 +/- 0.2 y, with very short stature (mean, -3.2 SD) of intrauterine onset, were treated for 3 y with GH [0.4 (dose D1) or 1.2 (dose D2) IU/kg/wk] and 66 were followed during a 4th y without GH therapy. A 2-y intermediary report had demonstrated a GH dose-dependent acceleration of growth. During the 3rd y on GH, patients D2 (1.2 IU/kg/wk) continued with the same dose, whereas patients D1 (0.4 IU/kg/wk) were randomized to either continue on D1 (group D1) or be increased to D2 (group D1D2). After 3 y on GH, patients' mean height (SD) reached -2.37 (D1), -2.17 (D1D2), and -1.58 (D2) with a total mean height gain of 0.77 (D1), 0.93 (D1D2) (difference NS), and 1.61 SD (D2 significantly higher than D1 and D1D2, p < or = 0.0001). During the off-treatment year, mean growth rate (cm/y) decreased to 3.4 in patients D1, 3.7 in D1D2, and 4.1 in D2 (NS). During the 4 y, bone age advanced of 4.6, 4.6, and 5.3 y in D1, D1D2, and D2, respectively, and puberty started in 34 patients (10 during the off-treatment year). Age at onset of puberty, apparently within normal range, did not relate either to the dose or the duration of treatment. Clinical and biologic tolerance of treatment was good. In conclusion this study demonstrates a GH dose-dependent effect on growth acceleration in persistent postnatal severe growth retardation of intrauterine onset. This effect was sustained for 3 y at 1.2 IU/kg/wk followed by a peculiar growth deceleration at treatment discontinuation. Additional studies are necessary to optimize long-term GH treatment regimen and to document its effects on final height.

Body Height↗
PubMed1994

Variations in pituitary-gonadal suppression during intranasal buserelin and intramuscular depot-triptorelin therapy for central precocious puberty. Belgian Study Group for Pediatric Endocrinology.

This study evaluated pubertal development, growth and pituitary-gonadal suppression in 21 patients with central precocious puberty treated with buserelin intranasally and switched after a mean of 2.1 yr to depot-triptorelin given im for 1 year. Arrest or regression of puberty was observed in 12 patients while progression of puberty during therapy was seen in 9 patients (6 on buserelin, 2 on triptorelin and 1 on both therapies). The increment in serum LH and FSH concentrations after sc injection of short-acting triptorelin was greater on buserelin than on triptorelin therapy, particularly in patients with evidence of progression of puberty. Height velocity during therapy showed a reduction which paralleled the decelerating phase of the normal pubertal growth spurt. The rate of bone maturation during therapy was inversely related to pretreatment bone age. Predicted final height showed marked individual variations which were inversely related to predicted adult height before therapy. These data indicate that differences in the nature and route of administration of Gn-RH agonist therapy for central precocious puberty can be of importance for inhibition of pituitary gonadotropin secretion and development of secondary sex characteristics. Height velocity and bone maturation are age-related and the change in predicted adult height depends on pretreatment level.

Administration, Intranasal↗
PubMed1994

Dose-dependent catch-up growth after 2 years of growth hormone treatment in intrauterine growth-retarded children. Belgian and French Pediatric Clinics and Sanofi-Choay (France).

This study reports the results of a 2-yr clinical trial with GH in 95 short prepubertal children with non-GH-deficient intrauterine growth retardation. This randomized, double blind, controlled study compared the effects of placebo (restricted to the first 6 months) and two doses of GH (0.4 and 1.2 IU/kg.week) given sc 6 days/week for 2 yr. A significant GH dose-dependent growth acceleration was observed. Mean height gain (SDS/CA) was 0.66 +/- 0.07 in group I (low dose, 0.4 IU/kg.week) compared to 1.25 +/- 0.07 in group II (high dose, 1.2 IU/kg.week). Mean bone maturation progression (expressed in months) was 26.2 +/- 1.7 and 30.2 +/- 1.5 over 24 months in groups I and II, respectively. Onset of puberty was observed in some patients of both groups. Whether chronic use of a high GH dose will advance the onset of puberty remains to be established. A great variability of growth acceleration was seen among GH dose groups, suggesting that factors in addition to GH dose might modulate individual responses to treatment. In conclusion, it is suggested that in these patients, dose-dependent catch-up growth could be induced by GH treatment.

Analysis of Variance↗
PubMed1993

Serum levels of growth hormone-binding protein and insulin-like growth factor I in children and adolescents with type 1 (insulin-dependent) diabetes mellitus.

Serum levels of insulin-like growth factor I are reduced in patients with Type 1 (insulin-dependent) diabetes mellitus. To evaluate the role of the hepatic growth hormone receptor in the decreased serum concentrations of insulin-like growth factor I, serum levels of the high affinity growth hormone-binding protein, which is qualitatively and quantitatively related to the hepatic growth hormone receptor, and of insulin-like growth factor I were measured in 70 children and adolescents with Type 1 diabetes and 105 healthy control children. Analysis of variance revealed a significant negative effect of Type 1 diabetes on serum levels of the growth hormone-binding protein and of insulin-like growth factor I. In the diabetic patients, serum levels of the growth hormone-binding protein were positively related to body mass index and to insulin dose per kg body weight, and were not influenced by pubertal stage, gender, or plasma levels of haemoglobin A1c. Serum levels of insulin-like growth factor I increased during early puberty reaching peak levels at mid-puberty and decreasing thereafter. No relationship was found between serum levels of growth hormone-binding protein and of insulin-like growth factor I. Our data suggest that decreased liver somatogenic receptor levels, as reflected by the concentrations of circulating growth hormone-binding protein, play a minor role in the suppressed concentrations of circulating insulin-like growth factor I. Post-growth hormone receptor defects or changes in the insulin-like growth factor binding proteins probably contribute more to the lower serum levels of insulin-like growth factor I.

Adolescent↗
PubMed1993

Five-year follow-up of growth hormone antibodies in growth hormone deficient children treated with recombinant human growth hormone.

OBJECTIVE: The aim was to investigate the long-term evolution of circulating growth hormone antibodies (GH-AB) during and after treatment with methionyl-recombinant human growth hormone (met-rhGH). DESIGN AND PATIENTS: The investigation was performed on serum samples of 46 growth hormone deficient children, treated for at least 12 months with met-rhGH. Twenty patients had never been treated with hGH (previously untreated patients, Group I). Twenty-six subjects were previously treated with pituitary extracted hGH (treated patients, Group II). MEASUREMENTS: Serum levels of GH-AB were measured by radioimmunoassay using charcoal precipitation of free ligand. RESULTS: Fifteen patients (75%) of Group I and three patients (12%) of Group II developed GH-AB. In 15 GH-AB positive patients the antibodies became detectable during the first year of treatment with met-rhGH. In three patients, however, the GH-AB appeared during the second year. Once present, the GH-AB remained detectable throughout the period of treatment with met-rhGH. In six patients in whom treatment with met-rhGH was stopped, GH-AB levels decreased rapidly. In nine patients in whom treatment with met-rhGH was changed to rhGH, the levels of GH-AB decreased and ultimately became undetectable. In two patients GH-AB remained present during administration of rhGH. No effect of GH-AB on the growth-promoting effect of met-rhGH could be documented, either during the first or during the second year of treatment. CONCLUSIONS: This study confirms the high immunogenicity of met-rhGH, especially in patients not treated earlier with hGH. Once present, the GH-AB remain detectable throughout the period of treatment with met-rhGH. After stopping met-rhGH treatment or changing to rhGH the GH-AB disappear rapidly in most patients. No effect of GH-AB on the growth-promoting effect of rhGH could be documented.

Adolescent↗
PubMed1993

Influence of spontaneous or induced puberty on the growth promoting effect of treatment with growth hormone in girls with Turner's syndrome.

OBJECTIVE: The aim was to evaluate the effect of 3 years treatment with recombinant human growth hormone (rhGH) on height velocity and height in girls with Turner's syndrome (TS) and to study to influence of spontaneous or induced puberty on the growth promoting effect of rhGH. PATIENTS AND DESIGN: The investigation was performed in 36 girls with Turner's syndrome treated for 3 years with rhGH in a dose of 1 IU/kg week, administered as daily subcutaneous injections. Fifteen patients remained prepubertal throughout the observation period (Group 1). During the first 2 years of rhGH therapy, four girls developed puberty spontaneously (Group 2). During the 3rd year of rhGH treatment puberty was induced with 100 ng/kg day ethinyl oestradiol orally in 17 girls requesting pubertal development and with a bone age of at least 11 'years' (Group 3). RESULTS: During the first year of rhGH therapy height velocity increased significantly in all patients. Mean +/- SD height velocity was higher in the four patients with Turner's syndrome who developed spontaneous puberty than in 17 age-matched girls with Turner's syndrome without puberty (8.9 +/- 1.2 vs 7.4 +/- 1.2 cm/year; P < 0.05). During the second and third year of rhGH treatment height velocity decreased in all patients but remained above baseline levels. The induction of puberty with 100 ng/kg day ethinyl oestradiol in the patients of Group 3 did not lead to an acceleration of height velocity, but seemed in contrast to decelerate height velocity. After 3 years of rhGH treatment, 21 out of 36 patients have obtained a height at or above the initially calculated projected adult height and five girls are already taller than 150 cm. CONCLUSIONS: The onset of spontaneous puberty during the first years of rhGH treatment seems to have an additive effect to rhGH on height velocity. Induction of puberty with oral administration of 100 ng/kg day ethinyl oestradiol did not have any beneficial effect on height velocity and seems therefore not to be the optimal way to induce puberty with an adequate pubertal growth spurt in girls with Turner's syndrome under rhGH therapy. Different doses and routes of oestrogen administration have to be evaluated in order to mimic the growth promoting effect of spontaneous puberty as well as possible.

Adolescent↗
PubMed1993

Effect of oestrogen status on serum levels of growth hormone-binding protein and insulin-like growth factor-I in non-pregnant and pregnant women.

OBJECTIVE: Since there appears to be a relationship between circulating oestrogens and growth hormone, we have investigated the effect of the oestrogen status of adult women on serum levels of GHBP and IGF-I. DESIGN AND PATIENTS: The investigation was performed on serum samples of 14 spontaneously menstruating women, 10 women taking oral contraceptives containing 20-50 micrograms ethinyloestradiol, and 30 pregnant women at different stages of pregnancy. MEASUREMENTS: Serum levels of GHBP were measured by HPLC gel filtration and IGF-I levels were measured by RIA after acid-ethanol extraction. RESULTS: In the spontaneously menstruating women the mean +/- SD serum level of GHBP was 34.6 +/- 6.7% and of IGF-I 30 +/- 7 nmol/l. Serum GHBP levels were negatively (r = -0.67; P < 0.01) and IGF-I levels were positively related (r = 0.69; P < 0.01) to serum oestradiol concentrations. In the women taking oral contraceptives serum levels of GHBP were 47.0 +/- 7.4%. This was significantly (P < 0.001) higher than in spontaneously menstruating women. In contrast, IGF-I levels were not different from those obtained in spontaneously menstruating women. In the pregnant women, the mean +/- SD serum level of GHBP was not different from that observed in non-pregnant spontaneously menstruating women. Polynomial regression analysis, however, showed a significant (P = 0.01) second-order relationship between the duration of pregnancy and serum GHBP levels, with increasing levels during the first half of pregnancy and decreasing levels thereafter. Serum concentrations of IGF-I increased during the second half of pregnancy and were significantly (P < 0.005) elevated in the third trimester. CONCLUSIONS: In non-pregnant women the endogenous oestrogen status seems to modulate negatively GHBP levels and positively IGF-I levels, whereas oral oestrogen administration, in contrast, increases serum levels of GHBP without modification of IGF-I levels. During pregnancy serum GHBP levels increase slightly during the first half of pregnancy and decrease thereafter, whereas IGF-I concentrations increase during the second part of pregnancy. The oestrogen status of women has a complex effect on serum concentrations of GHBP and IGF-I and has therefore to be taken into account when evaluating serum levels of GHBP and IGF-I.

Administration, Oral↗
PubMed1993

The effect of simple obesity on growth and growth hormone.

Simple obesity is characterized by a normal or increased growth rate with an acceleration of bone age maturation. When longitudinal growth slows down in the presence of obesity, a hormonal disturbance should be sought. Despite normal growth, simple obesity is characterized by a reduced GH secretion evaluated by standard provocative tests, the administration of GH-releasing hormone or spontaneous 24-hour secretion. In obese children GH secretion may be as low as in poorly growing children with classical GH deficiency. The endocrine abnormalities along the GH axis seem to involve complex mechanisms at the hypothalamic, pituitary and peripheral level. Recent data suggest that simple obesity is associated with an increase in GH clearance and a decrease in GH synthesis and secretion. It is also associated with high insulin and insulin-like growth factor I levels which may interfere in the complex endocrine interactions. In conclusion, simple obesity is characterized by normal growth in the presence of 'hyposomatotropism'.

Adipose Tissue↗
PubMed1993

Opposite effects of growth hormone and estrogens on the pregnancy zone protein serum levels in children and adolescents.

Serum levels of pregnancy zone protein were measured in children with growth hormone deficiency and in girls with Turner syndrome, before and during treatment with recombinant human growth hormone and in healthy controls. The pregnancy zone protein serum levels in growth hormone deficiency patients before treatment were significantly higher than in controls (median value 2420 micrograms/l vs 434 micrograms/l; p < or = 0.001). In Turner syndrome patients they were within the normal range. The administration of rhGH to both growth hormone deficiency and Turner syndrome patients resulted in a significant decrease in the serum pregnancy zone protein levels by approximately 50%. The addition of 50 ng.kg-1.d-1 ethinylestradiol to the growth hormone treatment in Turner syndrome patients led to an increase in pregnancy zone protein concentrations in four out of five patients. Elevated pregnancy zone protein levels were also found in two children with growth hormone resistance (Laron type dwarfism). In one patient with placental growth hormone deficiency, pregnancy zone protein serum levels during pregnancy were within the normal range. These results suggest that the serum pregnancy zone protein levels are down-regulated by growth hormone.

Adolescent↗
PubMed1993

Comparison between the human serum growth hormone-binding protein and the water-soluble growth hormone-binding site released from IM-9 lymphocytes.

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.

Binding Sites↗
PubMed1993

Non-endemic Burkitt's lymphoma in a patient with Bloom's syndrome.

Bloom's syndrome is an autosomal recessive disorder characterized by intrauterine growth retardation, typical physical signs, immunodeficiency and an increased risk of developing neoplasms at a young age, compared to the general population. Factors possibly involved in the pathogenesis of non-endemic Burkitt's lymphoma in a five year old girl with Bloom's syndrome are discussed. These include immunodeficiency, upregulated c-myc expression and an Epstein-Barr viral infection.

Bloom Syndrome↗
PubMed1993

Intelligence, behaviour and psychosocial development in Turner syndrome. A cross-sectional study of 50 pre-adolescent and adolescent girls (4-20 years).

In this paper we report the findings and data on a cross-sectional study of 50 pre-adolescent and adolescent girls with Turner syndrome. We confirm the presence of a typical cognitive profile in the different age groups with normal verbal intelligence contrasting with lower results on performal IQ subtests, related to relative weaknesses on visuospatial subtests i.e. "Block Design" and "Object Assembly". 5% of the girls with a "classical" Turner syndrome karyotype (i.e. 2/40) were mentally retarded versus 30% (i.e. 3/10) in the group with "rare" karyotypic anomalies. We noted a positive influence of hormonal therapy on the visuospatial functioning. No evidence was found for a high risk for behavioural problems. Hyperactive behaviour was seen in the youngest patients contrasting with a tendency to hypoactivity around the age of normal puberty. Problems in social development were noted from the age of primary school on resulting in social immaturity and even isolation. A proposal for guidance of Turner girls during the different developmental periods is given.

Adolescent↗
PubMed1992

Serum levels of growth hormone-binding protein and insulin-like growth factor-I during puberty.

OBJECTIVE: The aim was to investigate the effect of pubertal development on serum levels of growth hormone binding protein (GHBP) and IGF-I, and to study the relationship between GHBP levels and height standard deviation score (SDS), nutritional state and IGF-I levels. DESIGN AND PATIENTS: The investigation was performed on serum samples from 72 healthy adolescents of different pubertal stage. Results were compared to those obtained in 46 prepubertal children. MEASUREMENTS: Serum levels of GHBP were measured by HPLC gel filtration and IGF-I levels were measured by RIA after acid-ethanol extraction. RESULTS: No effect of pubertal stage on serum levels of GHBP was found. A positive relationship was found between serum levels of GHBP and height SDS (r = 0.38; P < 0.005) and weight expressed as percentage of median weight for height age (r = 0.46; P < 0.0005). Serum levels of IGF-I increased during puberty and were not correlated with height SDS or weight for height age. In pubertal subjects, no relationship existed between serum levels of GHBP and IGF-I. In prepubertal subjects, however, a significantly positive relationship between GHBP and IGF-I levels (r = 0.66; P < 0.0005) was found. CONCLUSIONS: Pubertal development does not seem to influence serum levels of GHBP. Height SDS and nutritional state are related to the concentration of GHBP. Before puberty, the level of GHBP is positively related to IGF-I levels; during puberty, however, the increase in serum IGF-I levels is not accompanied by changes in the amount of circulating GHBP.

Adolescent↗