High-dose growth hormone treatment of short children born small for gestational age

The effect of GH administration was evaluated over 2 yr in 50 short, prepubertal, non-GH deficient children born small for gestational age, who had been randomly allocated to a group receiving no treatment or daily sc GH treatment at a dose of 0.2 or 0.3 IU/kg. At the start of the study, mean age was 5.2 yr, bone age was 4.0 yr, height SDS was -3.5, height velocity SDS was -0.8, weight SDS was -2.7, and body mass index SDS was -1.9. Catch-up growth was observed in none of the untreated and all of the treated children. The response to GH treatment included a near doubling of growth velocity and of weight gain and a mean height increment of more than 2 SDS. GH treatment was associated with a distinct acceleration of bone maturation. The differences between the growth responses evoked by the two GH doses were minor. The prepubertal GH-induced catch-up growth was associated with elevated serum concentrations of insulin, insulin-like growth factor-I, insulin-like growth factor binding protein-3, and osteocalcin, whereas insulin-like growth factor-II levels remained unaltered. GH treatment was well tolerated. In conclusion, high-dose GH administration over 2 yr is emerging as a potential therapy to increase the short stature that results from insufficient catch-up growth in young children born small for gestational age. The long-term impact of this approach remains to be delineated.     

The treatment with biosynthetic growth hormone (GH) of familial short stature

The effect of growth hormone (GH) treatment in non-GH deficient subjects has been amply studied over the past few years. Although the results of these studies are encouraging, there are still no definitive data since the findings are not comparable due to the different characteristics of the populations examined. In the present study the authors examined the following parameters: stature, height SDS, growth rate, bone age and final height prediction according to Tanner, pubertal stage, before and after treatment with biosynthetic GH at a dose of 1.4 IU/kg of bodyweight for 12 months. The population treated consisted of 10 subjects (5 males and 5 females) aged between 7.3 and 9.5 years old, all prepubertal, with "familial short stature", selected according to the following criteria: stature below the 3rd centile, normal growth rate, normal GH response to stimuli using clonidine and insulin, correlation with parental stature between 25th and 75th centile, bone age correlated to chronological age, absence of other pathologies. After 12 months height SDS moved from -2.75 +/- 0.26 to -2.23 +/- 0.25 (p < 0.5); the growth rate changed from 5.75 +/- 0.63 to 6.66 +/- 0.56 (p < 0.05). No abnormal acceleration of bone age as observed: it moved from 8.2 +/- 0.62 to 9.5 +/- 0.72; all subjects continued to be prepubertal. The expected final stature changed from 154 +/- 2.38 to 159 +/- 0.7 (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Dietary protein restriction and selective preference for a protein-containing diet in the golden hamster (Mesocricetus auratus)

The corrected midparental height method was introduced by Tanner in 1970 (Tanner method) and is commonly used to estimate target height in children to evaluate the effectiveness of growth-promoting therapies. It has not been established if the equation used to compute target height should be the same for children with short, normal, or tall parents. In this study, we examined the predicted target height values by parental heights in a large population-based study (n = 2402). A simple linear function of midparental height (x) was proposed to estimate target height (y): y = 45.99 + 0.78x (boys), y = 37.85+0.75x (girls), with a 95% predicted interval of about +/-10 cm. The prediction model was similar for boys and girls in SD scores (SDS), and was not affected by assortative mating or difference in parental heights. The model may underestimate the potential stature by about 2 cm for children with midparental height below -2 SDS, or 163 cm. In comparison, the Tanner method may lead to a 6-cm error in underestimating target height for these children. The function would be a better choice than the Tanner method for estimating target height in the clinical evaluation of growth promotion treatments because it is common that short children also have short parents. Children with very short parents will usually be much taller than their parents in adult stature, and we believe that a different function should be developed. The results support the proposed nondominant, non-sex-linked, polygenic inheritance in stature. The estimated heritability values were 0.75-0.78 in cm or 0.55-0.60 in SDS.     

Selective incorporation of 111In-labeled PHOTOFRIN by glioma tissue in vivo

BACKGROUND: This study was to evaluate the efficacy, safety and immunogenicity of recombinant human growth hormone (rhGH) in treatment of children with growth hormone deficiency (GHD). METHODS: We selected 15 children with GHD for a 12-month clinical trial and separated them into three groups with each 5 patients receiving one of the 3 tested rhGH (Saizen by Serono, Aubonne, Switzerland; Genotropin by KabiVitrum, Stockholm, Sweden and Humatrope by Eli Lilly, Indianapolis, USA). RESULTS: In Saizen group, 3 boys and 2 girls with a mean chronological age (CA) of 10.6 +/- 1.7 yrs and bone age (BA) of 6.7 +/- 1.2 yrs, at dose of 0.2 IU/kg sc tiw, gained an average BA of 2.1 +/- 1.3 yrs. The mean height velocity (HV) increased from 3.7 +/- 1.2 to 11.1 +/- 3.3 cm/yr. The height standard deviation score (SDS) increased from -4.2 +/- 3.1 to -3.1 +/- 2.9. In Genotropin group, 2 boys and 3 girls with a mean CA of 9.2 +/- 2.3 yrs and BA of 5.6 +/- 2.1 yrs, at dose of 0.1 IU/kg sc qd, gained an average BA of 0.8 +/- 0.2 yr. The mean HV increased from 3.4 +/- 0.7 to 11.3 +/- 2.0 cm/yr. The height SDS increased from -4.0 +/- 0.5 to -2.7 +/- 0.7. In Humatrope group, 4 boys and 1 girl with a mean CA of 10.3 +/- 3.5 yrs and BA of 5.8 +/- 2.9 yrs, at dose of 0.1 IU/kg sc qd, gained at average BA of 0.8 +/- 0.7 yr. The mean HV increased from 4.0 +/- 1.3 to 9.4 +/- 1.9 cm2yr, and the height SDS increased from -2.9 +/- 0.7 to -2.2 +/- 1.0. Very low titers of anti-rhGH antibodies were noted only in two patients, one in Saizen group (titer = 1:10) and the other in Genotropin group (titer = 1:6). Their HV was not affected (Saizen: 13.3 cm/yr, Genotropin: 11.2 cm/yr). One patient evolved subclinical hypothyroidism whereas no side effect at all was noted in the rest of patients. CONCLUSIONS: Three tested GH (Saizen, Genotropin, Humatrope) produced by recombinant DNA technology appear to make no significant difference in this clinical trial, and rhGH therapy is an effective and safe treatment for prepubertal GHD children.     

Final height outcome of growth hormone-deficient patients treated since less than five years of age

Thirteen growth hormone deficient infants underwent substitutive treatment for a least 9 years, since less than 5 years of age until adulthood. They presented with average growth failure reaching 4.1 SDS and attained an adult mean height close to target height. In eight subjects final height exceeded the respective target height and only three patients failed to achieve an end height within the target range. The analysis of the factors conditioning ultimate stature pointed out that height outcome correlated negatively with chronological age at therapy initiation and positively with height at puberty onset. It is concluded that full catch-up growth to target percentile is possible in growth hormone-deficient children, provided that substitutive treatment is begun within the 5 years of life. This conclusion is substantiated for the first time by data on end stature.     

Short- and long-term (final height) data in children with normal variant short stature treated with growth hormone

Seventeen children with normal variant short stature and a predicted height below -2 SDS were treated with growth hormone (GH) six times a week for a period of 5 years. Patients were randomly selected to receive three different doses of GH, group 1 (n = 6) 3 IU/m2 per day, group 2 (n = 6) 4.5 IU/m2 per day and group 3 (n=5) 3 IU/m2 per day in the 1st year and 4.5 IU/m2 per day thereafter. There was a significant increase in height after 1 and 2 years for all patients and for all subgroups. However, this increase was not dependent on GH dose. The decrease in height velocity during the 2nd year was not prevented by the increase of GH dose in group 3. The change of predicted height after 2 years was +0.75 SDS (according to Tanner Whitehouse). Fourteen children have been treated for 4 years and 8 children for 5 years without a further change in height prediction. Nine patients have reached final height which was 2.4 cm (+0.41 SDS) above pretreatment height prediction. Final height was nearly identical to predicted height after 1 year of therapy. CONCLUSION: An increment in height prediction was observed during the first 2 years of GH treatment and maintained thereafter. However, there was only a minor increase in final height over predicted height which does not justify the general use of GH in children with normal variant short stature.     

GH and GnRH analog treatment in children who enter puberty at short stature

It is well known that height at the onset of puberty is closely related to final height. To improve final height of short children who enter puberty at short stature, twenty-one short boys and six short girls were treated with a combination of GH and GnRH analog. The boys started the combination treatment at a mean age of 12.0 years when their mean height was 128.5 cm (-2.74 SD) and the girls at a mean age of 10.68 years when their mean height was 126.4 cm (-2.23 SD). The boys discontinued GnRH at a mean age of 16.88 years after a mean treatment period of 4.89 years when their height was 153.7 cm (-2.75 SD), and the girls at a mean age of 13.89 years after a mean treatment period of 3.20 years when their height was 143.3 cm (-1.94 SD). Bone age maturation significantly decelerated during the combination treatment. Bone age rarely exceeded 14 years in boys and did not exceed 13 years in girls. Bone age maturation during combination treatment decelerated after bone age 12 years in boys and 10.5 years in girls. On average, bone age matured at a mean rate of 0.48 years a year in boys and 0.56 years a year in girls during the combination treatment. During the combination treatment, height velocity did not decelerate rapidly and remained at 3-5 cm/year for a longer duration because of the bone age deceleration, although a definite pubertal growth spurt was not observed. As a consequence, the mean projected height SDS for bone age increased 1.50 (+/- 0.76) SD in boys and 1.24 (+/- 0.49) SD during the combination treatment. Although most of the patients have not yet reached their final height, combined GnRH analog and GH treatment should increase the pubertal height gain and the adult height in short children who enter puberty early for height, when the post-GST growth is taken into account. The combination treatment seems more effective in boys than in girls. This improvement is attributed to the lengthening of the treatment period by slower bone maturation and maintained growth velocity.     

Natural killer cell receptors specific for MHC class I molecules

The aim of this study was to describe serum GH, IGF-I, and IGF binding protein (BP) 3 levels at birth and during the first 2 y of life in intrauterine growth-retarded (IUGR) children and to correlate these hormonal values with auxologic parameters noted during this period to investigate their predictive value on the postnatal growth pattern. Three hundred and seventeen children were included at birth and studied for auxologic and biologic parameters at birth, 3 and 30 d, and 3, 6, 12, 18, and 24 mo of age. At birth, when analyzed according to gestational age, serum GH levels were increased (p = 0.0001) and serum IGF-I and IGFBP3 levels were decreased (p = 0.0001) in IUGR as compared with normal neonates. When two cohorts were established at birth as a function of the ponderal index (PI) (< or = or > 3rd percentile), serum IGF-I and IGFBP3 levels were found to be significantly reduced in the case of low PI. All parameters were within normal limits at 1 mo of age and remained normal thereafter. During the first 3 mo of life, a positive correlation was found between IGF-I increment and weight gain (r = 0.28, p = 0.002). None of the biologic parameters at birth were predictive either of later growth or of short stature at 2 y of age. In conclusion, low serum IGF-I and IGFBP3 levels at birth were related to fetal malnutrition and were not predictive parameters for later growth.     

Final height in Turner syndrome patients treated with growth hormone

The first treatment trials on patients presenting with Turner syndrome were successful in accelerating growth velocity. It is therefore essential to know the final height of the patients who were treated in order to ascertain whether or not growth hormone treatment increases final height. We are reporting on a group of 117 patients with Turner syndrome whose growth hormone treatment was initiated in 1986. The mean growth hormone dose was 0.74 IU/kg/week for an average period of 4 years. At the start of treatment, the patients' chronological age was 129/12 years, height -3.8 +/- 1.0 standard deviation scores (SDS) and bone age 10.5 +/- 2.1 years. Mean final height was 147.7 +/- 5.6 cm, i.e. a gain of 1.5 SDS. We noted no significant difference due to the type of chromosomal abnormality, nor to oxandrolone or estrogen-associated treatment. A significant correlation was found between final height, mean parental height, the duration of the treatment, height SDS at the start of treatment and growth hormone peak during pharmacological stimulation tests. However, there was no correlation between growth hormone dosage, chronological age and bone age at the start of treatment. These results show that the growth hormone treatment improves the final heights of patients with Turner syndrome.     

Three paediatric cases of primary sclerosing cholangitis treated with ursodeoxycholic acid and sulphasalazine

The aim of this study was to reveal the relationship of the plasma levels of the carboxy terminal propeptide of type I procollagen (PICP) and the pyridinoline cross-linked carboxyterminal telopeptide domains of type I collagen (ICTP) to age and height velocity (HV), and to compare PICP and ICTP levels in those who have not reached their final height with those who have. PICP and ICTP levels were measured by RIA in 271 healthy children (161M, 110F) aged from 10 to 15 y. The HV was calculated from their health check-up cards. The subjects were divided into two groups in this study: the final height (FH) group whose HV was <1.0 cm/y, and the non-final height (NFH) group whose HV in the last year was > or =1.0 cm/y. PICP and ICTP levels almost paralleled the values of age-related changes of HV. Furthermore PICP and ICTP levels significantly correlated with HV. PICP and ICTP levels of the FH group were higher than those of adults previously reported. The values will be useful as reference for healthy children and growth disorder. Before reaching final height, PICP and ICTP can be useful makers of not only bone turnover but also of linear growth. Bone turnover rate is still increasingly active just after linear growth has been completed, and then it become similar to the levels of adults.     

Yearly stepwise increments of the growth hormone dose results in a better growth response after four years in girls with Turner syndrome. Dutch Working Group on Growth Hormone

To optimize the growth promoting effect of growth hormone (GH), 65 previously untreated girls with Turner syndrome (TS), chronological age (CA) 2-11 yr, were randomized into 3 dosage regimen groups: A, B, and C, with a daily recombinant-human GH dose during 4 study years of 4-4-4-4, 4-6-6-6, and 4-6-8-8 IU/m2 b.s. The first GH dosage increase in groups B and C resulted in a significantly higher mean height velocity (HV) compared with constant dose group A. During the third year, when the dose was raised again only in group C, mean HV was significantly higher in groups B and C than in group A, and in group C compared with group B. In year 4 only group C mean HV remained significantly higher than group A. The pattern of change in HSDSCA (Dutch-Swedish-Danish Turner references) was identical; however, in year 4 mean delta HSDSCA in group B also remained significantly higher than group A. After 4 yr GH treatment, the following was determined. 1) The mean delta HSDSCA was significantly higher for groups B and C compared with group A, but not significantly different between groups B and C. 2) Although significantly higher compared with estimated values for untreated Dutch girls with TS, bone maturation of the GH treated girls was not significantly different between groups. 3) It was positively related with the degree of bone age (BA) retardation at start of study and negatively with baseline CA. 4) Both the modified Index of Potential Height (mIPHRUS) and a recently developed Turner-specific final height (FH) prediction method (PTSRUS), based on regression coefficients for H, CA, and bone age, showed significant increases in mean FH prediction, without significant differences between groups. PTSRUS values were markedly higher than the mIPHRUS values. Dose dependency could be shown for the area under the curve (AUC) for GH, but delta HSDSCA was not linearly related with AUC. Baseline GH binding protein (BP) levels were in 84% of the cases within the normal age range; the decrease in mean levels after 6 months GH was not significant. Mean insulin-like growth factor I (IGF-I) and IGFBP-3 plasma levels increased significantly, without significant differences between groups. delta HSDSCA during GH was dependent on IGF-I plasma levels at baseline and during the study period, beta-0.002 and beta-0.0004. Thus, a stepwise GH-dosing approach reduced the "waning" effect of the growth response after 4 yr treatment without undue bone maturation. FH prediction was not significantly different between treatment groups. Irrespective of the GH dose used, initiation of GH treatment at a younger age was beneficial after 4 yr GH when expressed as actual cm gained or as gain in FH prediction, but was not statistically significant when expressed as delta HSDSCA over the study period.     

Exercise tolerance and blood pressure response to exercise testing in children and adolescents after renal transplantation

Intrauterine growth retardation (IUGR), defined as birth weight and/or length less than 3rd percentile (P) or less than-2 standard deviations (SD), concerns about 3% of newborns. About 85% born IUGR show spontaneous postnatal catch-up to a height > P3 or > -2 SD during the first two years of life. After the age of 4 year, the children without catch-up will remain short up to final height. Classical growth hormone (GH) deficiency usually does not seem responsible for the absence of catch-up in those children. A two-year GH therapy at supraphysiological doses increases growth velocity. The effect of this treatment on final height remains to be studied, as well as optimal treatment's modalities. Attention should be paid on the possible side-effects. Finally, the evaluation of the psychological impact of GH treatment will be critical.     

The effect of oestrogen treatment on body proportions in constitutionally tall girls

Body proportions were studied in 31 girls with constitutional tall stature during treatment with 200 micrograms ethinyl oestradiol per day continuously, combined with 5-10 mg medroxyprogesterone on the first 10 days of each month. Their mean (+/- SD) predicted adult height was 186.0 (+/- 4.0) cm. At the start of therapy, leg length (LL) standard deviation score (SDS) (3.8 +/- 0.7) was significantly greater than the sitting height (SH) SDS (2.3 +/- 1.1). During therapy, the mean sitting height increased by 2.9 cm, in contrast to an increment of only 0.8 cm for LL. The SDS of the ratio between SH and LL remained below zero. The expected gain without therapy, assuming a stable SDS position over time, was 5.4 cm for SH and 4.4 cm for LL, significantly more than the observed gains. In conclusion, tall girls have relatively long legs. Oestrogen therapy leads to an almost complete stop of leg growth, while the growth of the trunk is reduced to a lesser extent. This selective inhibition results in a trunk/leg ratio which is closer to, though still significantly different from that of normal girls.     

The effects of recombinant human growth hormone (r-hGH, SM-9500, genotropin) on growth failure in children with uremia. Japanese Multi-Center Study (Genotropin) Group on Children with Renal Disease

We treated 90 pediatric patients with chronic renal failure with recombinant growth hormone (r-hGH) for 12 months to improve their growth retardation due to uremia. They were divided into two groups, non-dialyzed and dialyzed children. The dose of r-hGH was 0.5 or 1.0 IU/kg/week in dialyzed children. After 12 months of the treatment using r-hGH, growth velocity was significantly increased in any group of children. Growth velocity was stimulated to about twice as much as before treatment (that were: in non-dialyzed group, 4.2 +/- 2.6cm/year vs. 6.2 +/- 2.0cm/year, P < 0.05, in dialyzed children treated with 0.51U of r-hGH: 2.7 +/- 1.8cm/year vs. 5.2 +/- 2.6cm/year, P < 0.001, and in dialyzed children treated with 1.01U of r-hGH: 3.0 +/- 1.5cm/year vs. 6.3 +/- 2.2cm/year, P < 0.001). No severe side effects was noted and no disturbance of renal function. Our results were consistent with those reported from Europe and USA. We conclude that r-hGH treatment is very effective in improving retarded growth in children with renal disease.     

Stature in Ecuadorians heterozygous for growth hormone receptor gene E180 splice mutation does not differ from that of homozygous normal relatives

Heterozygosity for certain mutations of the GH receptor (GHR) gene has been proposed as the cause of partial resistance to GH, and there has been a recent demonstration of a dominant-negative effect of such a mutation in a mother and child. To examine the effect of heterozygosity in a large genetically homogeneous population with GHR deficiency, in which a substantial number of heterozygous (carrier) subjects and homozygous normal individuals can be compared, we studied a population in Ecuador in which 70 individuals with GHR deficiency were homozygous for the E180 splice mutation. We found that 58 heterozygous relatives of probands were not significantly shorter than 37 homozygous normal relatives [SD score (SDS) for height -1.85 +/- 1.04 (SD) vs. -1.55 +/- 0.96, P > 0.10]. When only those families with both homozygous normals and carriers were compared, the 33 heterozygous and 29 normal relatives did not differ significantly in height SDS (-1.98 +/- 1.07 vs. -1.77 +/- 0.91, P > 0.3). If heterozygosity for the E180 splice mutation were to influence stature, heights of heterozygous parents of probands would be expected to correlate with those of probands and of carriers who are their offspring and not with heights of their homozygous normal children. Parental height SDS did not correlate with height SDS of affected offspring (r = 0.24). For unaffected siblings as a group or analyzed separately as normals or carriers, there was a strong correlation between parental and offspring SDS for height (P < 0.01 for all comparisons). Thus, the effect of homozygosity for the GHR mutation was so profound as to abolish parental influence on height, and there was no difference in the influence of parental stature between carrier and noncarrier offspring. These findings demonstrate no meaningful effect on stature of heterozygosity for the E180 splice mutation of the GHR, which is a functional null mutation and, in the homozygous state, results in profound short stature from severe insulin-like growth factor-I deficiency.     

The relationship of partner support to outcomes for teenage mothers and their children: a review

OBJECTIVE: To examine the growth response over 3 years of growth hormone deficient (GHD) and non-GHD children who have received growth hormone (GH) in Australia. METHODOLOGY: A retrospective study of a group of patients (1362 children) who commenced GH prior to 1 September 1990. Data were collected at 12 growth centres located in major cities throughout Australia. The data were transferred after informed consent to the national OZGROW database located at the Royal Alexandra Hospital for Children, Sydney, NSW. Of the 1362 children, 898 had received 3 years or more GH therapy and were eligible for this analysis. This cohort was then categorized by diagnosis. Growth response was assessed using height standard deviation score, estimated mature height, growth velocity (GV), GH dose and bone age (years). RESULTS: For children who completed 3 years therapy, the baseline characteristics among diagnostic groups were similar with mean height standard deviation score (SDS) less than -3 SDS (except for the malignancy group) and mean GV ranging from 3.5 to 4.4cm/year. The GV during the first year improved in all groups (7.7-9.4cm/year)followed by an attenuated response during the second and third years of therapy. After 3 years GH therapy the GHD group with peak levels <10 mU/L demonstrated the greatest change in estimated mature height and height SDS. The GHD group with peak levels between > or = 10 but <2OmU/L had a growth response similar to the non-GHD children for all outcome parameters. Change in bone age ranged from 3.1 to 3.8 years with no differences being noted between the diagnostic groups, nor consistently with pubertal status. CONCLUSIONS: Australian GH guidelines have targeted very short children when compared to other series. This large cohort of non-GHD children has demonstrated short-term benefits of GH therapy; however, the long-term benefit remains unclear until these children reach final adult height.     

Intradermal transgenic expression of granulocyte-macrophage colony-stimulating factor induces neutrophilia, epidermal hyperplasia, Langerhans'' cell/macrophage accumulation, and dermal fibrosis

Bone age maturation and growth velocity were analyzed longitudinally by the TW2 RUS method standardized for Japanese children in 45 GH-treated boys with idiopathic GH deficiency (GHD). The patients were divided into three groups: Group I consisted of four isolated GHD patients who underwent spontaneous puberty without gonadotropin suppression treatment (GST) and had a mean final height of 151.9 cm; Group II consisted of 24 GHD patients with associated gonadotropin deficiency who received sex hormone replacement treatment (GRT) and had a mean final height of 165.3 cm; Group III consisted of 17 isolated GHD patients who underwent spontaneous puberty and had a mean final height of 158.3 cm after being treated with combined GH and GST. Bone age matured along with chronological age in Group I, whereas bone age in Group II decelerated significantly after a bone age of 12 years and did not reach a bone age of 14 years. Bone age maturation in Group III showed an intermediate pattern between Groups I and II; bone age decelerated significantly after a bone age of 12 years but mean bone age advanced beyond a bone age of 14 years. Height velocity in Group I during GH treatment decelerated rapidly after the pubertal growth spurt, as usually seen in normal puberty. A definite pubertal growth spurt was not observed in the height velocity of Group II during GH treatment before receiving GRT; the mean height velocity gradually declined, remaining at 3.5-4.5 cm/year even after 18 years. Mean height velocity in Group III during GH treatment and GST showed a similar tendency as Group II, but it declined more rapidly. Since a growth velocity of around 3 cm/year was preserved with GH treatment despite the decline in growth velocity, the slower the advance of bone age, the longer the treatment period and, therefore, the taller the final height achieved by GST compared to Group I. It is recommended to start GST at a bone age between 11.5 years and 13 years. The timing, namely when to start GRT in GHD with gonadotropin deficiency or when to stop GST in isolated GHD, can be estimated according to the patient's desired final height and bone age-growth potential.     

Prospective study of lung volumes in young asthmatic children

In a 9-y prospective study, the occurrence and duration of lung volume abnormalities in 21 young asthmatic children (median age at recruitment 4 y, range 3-8 y) was determined. The median functional residual capacity (FRC) at recruitment was 135% of that predicted for height (range 79-187%) and 13 children were hyperinflated. The median FRC decreased significantly after 3 y of follow-up and by 9 y only one child remained hyperinflated. We conclude that persistent elevation of lung volume in young asthmatic children appears to be uncommon.     

Effect of beclomethasone dipropionate on bone mineral content assessed by X-ray densitometry in asthmatic children: a longitudinal evaluation

There is little information on bone turnover in asthmatic children taking long-term treatment with inhaled steroids (ICS). The aim of this longitudinal study was to determine the effects of inhaled beclomethasone dipropionate (BDP) on bone mineral density (BMD), in asthmatic children treated over a period of six months. BMD and growth were studied in two age- and sex-matched groups of asthmatic children. These comprised: 14 asthmatic children (Group 1) who had taken BDP in a dosage of 300-400 micrograms daily through a 145 ml spacer device for at least 6 months (mean age 9.1 yrs); and a control group of 16 age- and sex-matched asthmatic patients (Group 2) not treated with ICS (mean age 9.5 yrs). Mean duration of asthma was 5.7 yrs in Group 1 and 5.5 yrs in Group 2. Vertebral BMD (L2-L4) was measured by dual energy X-ray absorptiometry (DEXA) at the beginning (baseline) of the study and 6 months later. There were no significant differences in the baseline bone mass (mean +/- SEM) between the two groups (0.63 +/- 0.03 and 0.64 +/- 0.02 g.cm-2 in Group 1 and 2, respectively). During the observation period, bone density increased, by 4% (95% confidence interval (95% CI) 2-6) in the control group and by 2.3% (95% CI 0.4-4.2) in the group under BDP treatment, showing no significant influence of the treatment. No difference was found in height velocity evaluated before starting BDP and after 6 months of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Genetic profile of pNOB8 from Sulfolobus: the first conjugative plasmid from an archaeon

Recently, children born small for gestational age (SGA) with a catch-up growth failure, have been selected for high dose growth hormone (GH) treatment. In order to gain greater insight concerning dentofacial growth and maturation of these patients, and to evaluate the possible effects of high does GH administration on facial structures, craniofacial growth and dental maturation were evaluated in short SGA persons. Seventy-seven cephalograms and orthopantomograms were available from 48 subjects, aged between 2 and 32 years. Craniofacial growth was assessed by calculating age- and gender-specific standard deviation scores (SDS) for eight linear and five angular measurements. Tooth formation was evaluated by means of a dental delay score (i.e. dental age minus chronological age). The SDS for craniofacial growth measurements for the lateral aspect showed a short anterior cranial base (-1.8 SDS), a small retropositioned mandible (< or = -1.7 SDS) and a small maxilla (-1.5 SDS); a high mandibular plane angle (+1.9 SDS) and a wide cranial base angle (+1 SDS). These findings result in a small retrognathic face with a relatively increased lower anterior face height (+1.7 SDS). In contrast to skeletal maturation, dental age was not delayed. The general growth retardation is, apparently, reflected to a differential extent within the craniofacial complex, while dental maturation appears to be a distinct process tightly linked to chronological age, and independent of general growth and bone age.