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Biomedical subjects

K Albertsson-Wikland

Publications and source records attributed to K Albertsson-Wikland.

At least 55 records · Page 3Linked to original sources
PubMed1998

Short-term changes in serum leptin levels provide a strong metabolic marker for the growth response to growth hormone treatment in children. Swedish Study Group for Growth Hormone Treatment.

The growth response to GH treatment varies between children. Besides regulating longitudinal growth, GH exerts important metabolic effects, including lipolysis. In this study we examined whether GH-induced changes in serum levels of the adipose tissue-derived hormone leptin can be used as a marker for the long term growth response to GH treatment in short prepubertal children. The study group consisted of 150 children (21 girls and 129 boys), who were 3-15 yr of age at the start of GH treatment and had a maximum GH secretory capacity ranging from very low to high. They were treated with GH (0.1 IU/kg x day) and followed for at least 1 yr. The first year mean increase in height SD score was 0.79 (SD, 0.34), with a broad range (0.08-2.27). Serum leptin concentrations were significantly reduced after 1, 3, and 12 months of GH treatment compared with levels at the start of treatment. The growth response correlated with the serum leptin concentration at the start of treatment (r = 0.49; P < 0.0001) and with the change in serum leptin concentration after both 1 month (r = -0.41; P < 0.01) and 3 months (r = -0.60; P < 0.0001) of treatment. When multiple stepwise regression analysis was applied to the auxological and biochemical variables that correlated (P < 0.10) with the first year growth response to GH treatment, the 3-month change in serum leptin concentration was the single most important variable for explaining the variance in individual growth responses. We conclude that leptin levels at the start of GH treatment as well as short term changes in leptin levels in response to GH treatment are valuable markers of the long term growth response.

Adolescent↗
PubMed1998

Variations in glucocorticoid levels within the physiological range affect plasma leptin levels.

OBJECTIVE: Leptin, the obese gene product, is thought to regulate body fat through its action on hypothalamic receptors that influence satiety. The hormonal regulation of leptin is important, since it might affect adiposity. Leptin regulation in man is poorly understood. We studied the relation between endogenous cortisol and leptin levels as well as the acute and chronic effects of a low dose of dexamethasone (DEX) on plasma leptin levels in healthy male volunteers. SUBJECTS AND EXPERIMENTAL PROTOCOL: The correlation between basal plasma levels of leptin and cortisol and the chronic effect of DEX treatment were studied in 12 subjects. Plasma leptin and cortisol levels were determined every other hour for 24 h, before and after 2 weeks of oral administration of 0.1 mg DEX twice daily. The acute effect was studied in 20 subjects, who received 1 mg DEX at 2300 h. Fasting blood samples were taken at 0800 h on the same day (i.e. before DEX) and on the day after. RESULTS: Under basal conditions, we found a correlation between mean plasma levels of leptin and cortisol (r = 0.7, P<0.02). Mean plasma leptin levels had increased by 50% after 2 weeks of DEX treatment (P<0.05). The circadian rhythm of leptin was preserved, but the night peak occurred 2.5 h earlier (P<0.05). Fasting plasma leptin levels were 20% higher 9 h after 1 mg DEX orally than at the same time on the day before (P<0.002). CONCLUSION: Physiological variations in cortisol are involved in the regulation of leptin.

Adult↗
PubMed1998

Length and body mass index at birth and target height influences on patterns of postnatal growth in children born small for gestational age.

OBJECTIVE: Previous growth studies on children born small for gestational age (SGA) indicate that birth length, weight, and target height are important predictors for postnatal catch-up growth in SGA. Their influences on different phases of catch-up growth are still not described. The aim of this study was to clarify the influences of target height, length, and nutritional status at birth on different phases of postnatal catch-up growth (infancy, childhood, puberty) in SGA and the long-term consequences. METHODS: Data were obtained from a longitudinal population-based growth study on Swedish children (N = 2815). Primary outcome measurements include heights, the changes in height standard deviation scores (SDS) during various phases of growth and relative risk for adult shortness. RESULTS: The difference in final height in children born SGA was attributable to their difference in target height and the magnitude of catch-up growth during the first 6 months of life, rather than the difference in length or body mass index (BMI) at birth. Length at birth showed negative influence on catch-up growth during infancy (0 to 2 years of age), but no significant influence thereafter. The BMI or weight for length SDS at birth showed no significant influence on catch-up growth during any growth phase. Target height showed positive influence on catch-up growth from the onset of childhood. Neither target height nor length and BMI at birth showed any significant influence on catch-up growth during puberty. The magnitude of catch-up growth during infancy, especially the first 6 months of life, is most critical in decreasing risk at adult shortness. We confirmed that the SGA group had a sevenfold greater risk for adult shortness than the non-SGA group (relative risk = 7.31; 95% confidence interval: 3.96-13.52). However, approximately 40% of children who were below -2 in height SDS at 2 years of age remained short at final height in both SGA and non-SGA groups. The mean height SDS of children born SGA increased by 1.65 from birth to final height, but the length deficit in centimeters at birth (-5.4 cm) persisted into adulthood (-5.9 cm). CONCLUSIONS: BMI at birth is not related to postnatal catch-up growth in infants born SGA, but birth length and target height are important. The genetic influence on catch-up growth appears to start from the onset of childhood. Being born short or becoming short during the first 2 years of life is similar in terms of risk for adult short stature.

Body Height↗
PubMed1998

Psychological aspects of Turner syndrome.

Turner syndrome (TS) is a sex-chromosome disorder, occurring in 1 in 2500 female births. The principal features of TS are short stature and dysfunctional gonads, resulting in a lack of sex hormones, incomplete pubertal development and impaired fertility. The aim of this paper is to review the literature on the psychological effects of TS. The main areas covered relate to well-being and psychopathology, self-esteem, social functioning, gender identity, partner relations and sexual functioning, coping, family aspects and clinical aspects of cognitive impairment. Research on the psychological effects of medical intervention is described, and the methods used for psychological and educational support are presented. Finally, methodological issues are discussed and areas for future research are proposed.

Adaptation, Psychological↗
PubMed1998

Midline brain lesions in children with hormone insufficiency indicate early prenatal damage.

The relationships between midline brain morphology, anterior visual pathway morphology and hormonal status in children with impaired growth were studied. Intracranial morphology was studied by magnetic resonance imaging in 47 children (14F, 33M), median age 9.7y (range 2.6-18.7y) undergoing growth hormone treatment (GH; 0.1 U/kg/d). They were chosen to represent various birth sizes and a spectrum of hormone insufficiencies. There was a relationship between GH secretion and the morphology of the neurohypophysis, the pituitary stalk and the anterior visual pathways, i.e. the greater the GH insufficiency, the more abnormal were these structures. The children with anterior visual pathway abnormalities had the lowest GH levels and the smallest adenohypophysis. The association between abnormalities of the anterior visual pathways and the hypothalamo-pituitary structures may reflect a common prenatal neural damage in embryologically and anatomically closely related structures.

Adolescent↗
PubMed1997

Growth and growth hormone secretion after treatment for childhood non-Hodgkin's lymphoma.

The aim of this study was to evaluate the growth and growth hormone (GH) secretion, as assessed by the rate and pattern of secretion, in patients in remission from non-Hodgkin's lymphoma (NHL) who had been treated with corticosteroids and intense chemotherapy. None of the patients had received cranial irradiation. Twelve children were investigated yearly by taking 24-hour GH profiles starting 1 year from the time of diagnosis. The mean age at onset of the disease was 7.5 years. Another 12 young adults were studied in a cross-sectional manner 4.1-21.3 years (mean, 9.0 years) after diagnosis of NHL. The mean age at onset of the disease was 10.7 years. The median height velocity was significantly decreased during the 1st year following diagnosis (standard deviation scores [SDS] -0.15, P < .001), especially during the first 3 months (SDS -0.75, P < .001) when the most intense treatment was given. During the 2nd year height velocity was still somewhat reduced (SDS -0.13, P < .001). However, there was no reduction in final attained height. Spontaneous GH secretion, in terms of both secretory rate and pulsatile pattern, was evaluated by measuring integrated GH concentrations in 20-minute blood samples collected over a 24-hour period. The plasma GH concentrations were transformed into GH secretion rates by means of a deconvolution technique. Fourier time series analysis was applied to determine possible disturbances of rhythmicity of the GH secretion. The GH secretion rate and the pulsatile pattern of secretion in the NHL patients were similar to those of the reference population of pubertal matched healthy controls. There was no influence of the age at diagnosis or of the time from diagnosis of NHL on the GH secretion rate. Growth impairment in children with a malignant disease treated only with steroids and chemotherapy is therefore probably not caused by disturbed GH secretion, but rather by direct interference with bone growth of the cytotoxic drugs used. There was no significant influence on weight gain during the treatment period so an indirect effect of chemotherapy on bone growth through interference with adequate nutrition seems unlikely. However, GH secretion was not evaluated during the period of growth retardation, and therefore a transient deficiency was not excluded.

Adolescent↗
PubMed1997

Increased LH and FSH secretion after cranial irradiation in boys.

The effect of high-dose cranial- and craniospinal irradiation and chemotherapy on the gonadotropin-sex steroid axis was studied during different stages of puberty by measuring pulsatile secretion of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone. The patients were thirteen boys who had been treated for malignant brain tumor residing well away from the hypothalamo-pituitary region. The median time to follow-up was 9 (1-16) years. The onset of puberty was early in the patients, median 10.5 years, compared to the average age for Swedish boys, which is at median 12.4 years. There was, before puberty, no significant difference in LH and FSH secretion between patients and a control group of normal boys. In early, mid- and late stages of puberty, however, LH and FSH secretion was increased in the patients overall, whereas testosterone secretion was maintained within the normal range in spite of signs of gonadotoxocity with small testicular volumes. These results indicate that the vulnerable parts of the gonadotropin releasing hormone (GnRH)-gonadotropin (LH, FSH)-gonadal axis are the regulatory system that determines the timing of pubertal induction and the gonads. The GnRH-LH, FSH-releasing neurons appear relatively resistant to cranial irradiation as they are able to respond with supranormal LH and FSH levels for long periods of time after treatment.

Adolescent↗
PubMed1997

Reference values for height, height velocity and weight in Turner's syndrome. Swedish Study Group for GH treatment.

As Northern Europeans are currently the tallest people in the world, specific growth charts for girls with Turner's Syndrome from this area are needed. Based on height and weight measurements from 598 girls with Turner's Syndrome (372 from the Netherlands, 108 from Denmark, 118 from Sweden) not treated with growth-promoting substances and without signs of spontaneous puberty, we constructed growth charts for height-for-age, height-velocity-for-age, weight-for-age, weight-for-height and Body Mass Index for age. Reference tables and regression equations for mean and standard deviation are provided allowing calculation of Standard Deviation Scores. The height and height velocity curves show a low birth length, gradual deviation from the normal percentile curves without pubertal growth spurt, and a prolonged growth until the early 20s. Mean adult height was 146.9 +/- 7.8 cm. Mean weight-for-age was lower than in normal reference children but height-adjusted weight was higher, except in infancy and early childhood. Further studies are required on the factors influencing the weight-height relationship in Turner's Syndrome.

Adolescent↗
PubMed1997

Hormonal status of short children born small for gestational age.

The present study was undertaken to evaluate the hormonal status in a subgroup of prepubertal children born small for gestational age (SGA) who lacked postnatal catch-up growth. In this subgroup, a reduced rate of growth hormone (GH) secretion was found, compared with reference groups of healthy children born appropriate for gestational age, of either normal or short stature at the time of investigation. In addition, an abnormal pattern of GH secretion was observed in short children born SGA, which was most pronounced in the younger children, and involved an increased frequency of GH peaks of low amplitude, combined with increased baseline secretion. Levels of insulin-like growth factor I (IGF-I) and IGF-binding protein-3 were also reduced in short children born SGA, compared with the reference groups. These findings may explain, in part, the lack of postnatal catch-up growth in short children born SGA.

Adolescent↗
PubMed1997

Postnatal growth of children born small for gestational age.

A large, population-based representative study (n = 3656) has shown that the vast majority of healthy, full-term, singleton infants born small for gestational age (SGA) achieve catch-up growth during the first 2 years of life. Indeed, most of the increase in height SDS occurs by 2 months of age. Children born SGA who do not show postnatal catch-up growth and so remain short at 2 years of age, have a higher risk of short stature (< -2 SDS) in later life, with a relative risk at 18 years of age of 5.2 if born light and of 7.1 if born short.

Adolescent↗
PubMed1997

Growth hormone treatment of short children born small for gestational age: reappraisal of the rate of bone maturation over 2 years and metanalysis of height gain over 4 years.

A minority of children born small for gestational age (SGA) fail to achieve sufficient catch-up growth during infancy and remain short throughout childhood, apparently without being growth hormone (GH) deficient. A previous metanalysis of four trials revealed that GH treatment over a period of 2 years induced a dose-dependent acceleration of linear growth and, to a lesser extent, of the rate of bone maturation in short, prepubertal children born SGA. The rate of bone maturation and the change in height SDS for bone age from the previous 2-year metanalysis have been re-analysed according to chronological age (two prepubertal age groups: group A, 3.0-5.9 years old; group B, 6.0-8.9 years old). The rate of bone maturation was slower in younger than in older prepubertal children; this difference was more marked in children receiving high-dose (0.2 or 0.3 IU/kg/day) GH treatment (p < or = 0.01). Accordingly, the change in height SDS for bone age was increased by high-dose GH treatment in both age groups (p < or = 0.01), and was more pronounced in younger than in older children (1.45 +/- 0.28 versus 0.63 +/- 0.20; p < or = 0.01). Height SDS data from 100 short, prepubertal children born SGA have been analysed over 4 years. The change in height SDS appeared to be related to the average dose of GH. A mean GH dose of 0.1 IU/kg/day over 4 years was administered either as 0.1 IU/kg/day for 4 years (continuous) or as 0.2 IU/kg/day for 2 years, followed by 2 years without GH treatment (discontinuous). After 4 years of treatment, the increase in height SDS for the continuous and discontinuous treatment schedules was similar, being 1.42 +/- 0.10 SDS and 1.58 +/- 0.17 SDS, respectively. In a second regimen, a mean GH dose of 0.2 IU/kg/day over 3 years was administered either as 0.2 IU/kg/day for 3 years (continuous) or as 0.3 IU/kg/day for 2 years, followed by 1 year without GH treatment (discontinuous). After 3 years, the increase in height SDS with the continuous and discontinuous treatment schedules was similar, being 2.01 +/- 0.18 SDS and 2.22 +/- 0.16 SDS, respectively. GH administration was well tolerated in all treatment groups. In conclusion, the rate of bone maturation in short, prepubertal children born SGA treated with GH appeared to depend not only on the dose of GH, but also on the age of the child. GH treatment resulted in a prolonged increase in height SDS, the magnitude of the rise being dependent on the average GH dose rather than on the continuous or discontinuous mode of GH administration.

Body Height↗
PubMed1997

Serum leptin concentrations in relation to pubertal development.

OBJECTIVES: The amount of adipose tissue influences pubertal development and fertility in girls. A candidate for mediating this is the hormone leptin, derived from adipocytes. This work was carried out to determine whether the leptin concentration in serum is regulated during pubertal development. SUBJECTS AND METHODS: Serum concentrations of leptin were determined by radioimmunoassay in a sample of 252 healthy children representing all pubertal stages. RESULTS: Serum leptin concentrations correlated directly with age (r = 0.53), body mass index (BMI) (r = 0.71), and weight for height SD score (r = 0.44) in girls and with BMI (r = 0.33) and weight for height SD score in boys (r = 0.36). Leptin concentrations increased with pubertal development in girls, resulting in significantly higher concentrations at pubertal stages 4 and 5 than at the prepubertal stage, whereas there was no change in the boys. CONCLUSIONS: Serum leptin concentrations increased during pubertal development in the girls, but remained constant in the boys. Whether the increase in serum leptin concentrations in girls is of importance for, or a consequence of, pubertal development is still to be determined.

Adolescent↗
PubMed1997

Factors determining pubertal growth and final height in growth hormone treatment of idiopathic growth hormone deficiency. Analysis of 195 Patients of the Kabi Pharmacia International Growth Study.

A total of 195 children (117 males and 78 females) with idiopathic growth hormone deficiency (IGHD) treated with growth hormone (GH) for at least 1 year before puberty onset and who had completed treatment to adult height, were selected from the KIGS database for study of growth during puberty. Spontaneous and induced puberty started at 13.8 and 14.9 years in boys and at 12.9 and 13.7 years in girls, respectively. Duration of GH treatment and height gained prepubertally were greater when puberty was induced; prepubertal catch up growth (expressed as a percentage of the difference between target height and height at start of GH) was greater when puberty was induced in boys (59% induced vs. 45% spontaneous, p < 0.001), and in girls (72% induced vs. 53.9% spontaneous, p < 0.01). Final height was attained at 17.8 and 19.2 years in boys and at 16.0 and 17.0 years in girls following spontaneous and induced puberty, respectively. Final heights were greater after induced puberty compared with spontaneous puberty in boys (171.3 vs. 166.0 cm, p < 0.001) and in girls (157.0 vs. 155.0 cm, n.s.). Target height was also significantly greater in boys with spontaneous puberty (172.2 cm vs. induced = 174.2 cm) as compared to girls (spontaneous = 158 cm vs. induced = 160 cm). Duration of pubertal growth was longer in boys compared to girls (3.6 vs. 3.0 years, p < 0.001) and was negatively correlated with age, height, and distance from target height at onset of puberty, but was not correlated with the dose of GH. Catch-up growth during puberty (expressed as a percentage of the difference between target height and height at puberty onset) after induced and spontaneous puberty was 87.9% and 80.5% (not significant) in boys and 66.4% and 75.5% (not significant in girls. Total pubertal growth (TPG) (cm) was inversely correlated with prepubertal growth by simple linear regression. Multiple linear regression analysis indicated 5 independent predictors of TPG accounting for 78% of the variability, namely sex (boys grew more), distance of target height from height at onset of puberty (+), dose of GH at onset of puberty (+), age at onset of puberty (-), and age at end of growth (+).

Adolescent↗
PubMed1997

Influence of gender on the correlation between plasma growth hormone profiles and urinary growth hormone excretion.

A lot of interest has been directed towards the measurement of urinary growth hormone (GH) excretion instead of plasma GH profiles or provocation tests. We investigated the factors influencing the relationship between 24- and 3-hour plasma GH profiles and urinary GH excretion in a cohort of 113 pediatric patients with growth disorders and healthy volunteers. Plasma and urinary GH were measured by polyclonal immunoassays differing in cross-reactivity with 20 kD GH (100 versus 46%), but not with 22-kD, dimer, deamidated and pituitary GH. In the 24-hour urine samples, only urinary GH excretion expressed as nanograms per 24 h correlated with plasma GH parameters, whereas the correlations for short-term samples were strongest if urinary GH excretion was expressed as nanograms per gram creatinine (r = 0.70-79, p < 0.00005-0.0001). In short-term samples urinary GH excretion depends on urinary volume and should thus be expressed in nanograms per gram creatinine, whereas 24-hour samples correlate best when urinary GH is expressed as nanograms per period. We found a significant sex difference (p < 0.02) in the correlation between 24-hour plasma GH profiles and urinary GH excretion with strong correlations in the female group (r = 0.63-0.78, p < 0.00005-0.0002) and a lack of correlation in the male group. The sex difference in the correlations between serum and urinary GH may reflect sex differences in GH profiles and metabolism, with urinary GH better reflecting the basal and slowly clearing portion of plasma GH than spontaneous GH peaks. The difference in cross-reactivities of molecular GH forms in polyclonal assays may have an impact on the correlation between plasma and urinary GH. Thus, the diagnostic value of urinary GH measurement as compared to serum GH profiles needs to be further evaluated.

Adolescent↗
PubMed1997

Growth hormone treatment induces a dose-dependent catch-up growth in short children born small for gestational age: a summary of four clinical trials.

In the present study, data from 230 short children born small for gestational age, who were participating in four clinical trials, were pooled and analysed. At the start of GH treatment, median age and height SDS were 5.3 years and -3.2 SDS, respectively. A dose-dependent increase in height SDS was observed following 2 years of GH treatment: 1.1, 1.7 and 2.5 SDS for the three GH treatment groups (0.1, 0.2 and 0.3 IU/kg/day, respectively), compared with an increase of 0.14 SDS in the control group. In a multiple regression analysis, four variables were found to correlate independently with the gain in height SDS following 2 years of GH treatment. These are given below in order of importance: gain in height SDS = 7.7 x dose of GH (IU/kg/day) -0.11 x age (years) -0.08 x parental-adjusted height SDS + 0.05 x birth length SDS (SD = 0.5; r2 = 0.64). At the end of the 2-year study period, a total of 48%, 66% and 90% of patients in the groups given GH at 0.1, 0.2 and 0.3 IU/kg/day, respectively, had a parental-adjusted height greater than -1.0 SDS.

Body Height↗
PubMed1997

The timing of early postnatal catch-up growth in normal, full-term infants born short for gestational age.

Postnatal catch-up growth in infants born small for gestational age has been reported to occur mainly during the initial 3-9 months of life. The study presented here characterized early postnatal growth in healthy, full-term infants born short for gestational age (GA) (< -2 standard deviation scores [SDS] in birth length) in two populations. Results from a longitudinal growth study from birth to final height of 139 infants born short for GA between 1973 and 1975 in Göteborg, Sweden, were compared with results from an ongoing detailed prospective 6-month follow-up of 41 Hong Kong Chinese infants born short for GA in 1995 and 1996. For both populations, height was expressed in SDS using the updated Swedish growth reference data at birth and postnatally. In the Swedish study, 92% of the children born short for GA reached a final height greater than -2 SDS; 76% had a height greater than -2 SDS by 2 months of age. In the Hong Kong study, 79% reached a height greater than -2 SDS by 5 months of age (the longest follow-up time to date). A third population of Hong Kong Chinese infants born short for GA in 1967 was studied; 65% had reached the normal height range by 5 months of age. In the later Hong Kong study (1995-1996), catch-up growth could be identified as early as 12 weeks of age, which has important implications for clinical practice. Thus, growth monitoring during the first weeks of postnatal life gives useful information on catch-up growth in infants born short for GA.

Body Height↗
PubMed1997

Circadian cortisol rhythms in healthy boys and girls: relationship with age, growth, body composition, and pubertal development.

To provide basic information on the normal functioning of the hypothalamus-pituitary-adrenal axis in relation to pubertal development, growth (weight and height), body composition, and gender and to obtain reference data for serum cortisol concentrations in children, we investigated the basal circadian rhythm of serum cortisol in a group of 235 healthy children (162 boys and 73 girls). The age range was between 2.2-18.5 yr. Serum cortisol was analyzed from venous blood samples taken at 1400, 1800, 2200, 0200, 0400, 0600, and 1000 h. No evidence was found for differences in temporal placement or level of the circadian cortisol rhythm in relation to age, growth, or body composition. However, we found a broad range of cortisol levels in a healthy population, with individual mean diurnal levels ranging from 100-510 nmol/L. Regardless of high or low mean diurnal cortisol levels, repeated measurements within and between pubertal stages indicated that an individual remains in his or her cortisol range throughout pubertal development. In conclusion, the present study shows that 1) serum cortisol levels do not correlate with either age or gender; 2) there is a large and significant interindividual variability in endogenous mean diurnal cortisol levels; and 3) despite this variability between individuals, there is no correlation between cortisol levels and either body composition or growth rate. This suggests that the variability in cortisol levels is an expression of normal homeostasis rather than pathology.

Adolescent↗