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The aim of this study was to identify predictors of the growth response to growth hormone (GH) during the first 2 years of GH treatment, using auxological data and the maximum GH response (GHmax) to provocation tests. The patients were 169 prepubertal short children (27F, 142M), with Gmax values ranging from 0 to 65 mU/l. Their mean age (+/- SD) was 8.3 +/- 2.4 years (range 3-13 years), mean height SDS -3.0 +/- 0.7 (range -1.5 to -6.0 SDS) and mean pretreatment height velocity was normal (+/- 0.0 SDS) (range -1.6 to +0.9 SDS). The increase in height SDS during the first 2 years of GH treatment (0.1 U/kg/day) varied from 0.10 to 3.75 SDS, with younger children having a better growth response. Individual growth responses correlated (p < 0.001) with GHmax (r = -0.37), age (r = -0.35), 1-year pretreatment delta SDS (r = -0.25), mid-parental height SDS (r = 0.34), height SDS at start of treatment (r = -0.22) and difference between height SDS of an individual child at the onset of GH treatment and mid-parental height expressed in SDS (diff SDS) (r = -0.43). In a multiple stepwise linear regression model, diff SDS and log GHmax were found to be the strongest predictors of the magnitude of the growth response. In the short children in this study who exhibited a broad range of GHmax values, 33% of the growth response during the first 2 years of treatment could be predicted.

To evaluate the developmental and sex-specific changes in spontaneous GH secretion in terms of both secretory rate and pulsatile pattern, we investigated 24-h GH profiles (integrated 20-min samples) in 208 healthy children (91 girls and 117 boys) of normal heights at all stages of puberty. The plasma GH concentrations were transformed to GH secretion rates by means of a deconvolution technique. In prepubertal boys and girls, the mean secretion rates were comparable (0.66 and 0.68 U/24 h), but increased during puberty differently: earlier in girls, already at stage 2, with the highest rates at stages 3 and 4 (1.70 and 1.96 U/24 h); later in boys, at stage 4 (1.66 U/24 h). In both sexes the GH secretion rate decreased to prepubertal values at stage 5. The GH secretion rate correlated negatively with weight for height expressed in SD scores only in puberty (boys, r = -0.44, P0.001; girls, r = -0.22; P0.05). The number of peaks with high amplitudes increased with the progress of puberty in both boys (stage 2) and girls (stages 3 and 4). In both prepubertal girls and boys, a marked day-night rhythm was observed, which disappeared in midpuberty in boys owing to a greater increase in peak amplitudes during the day than at night. The mean number of peaks per 24 h was unchanged in girls, but decreased in late pubertal boys. In summary, we found a sex-specific increase in the GH secretion rate during pubertal development that occurs at an earlier pubertal stage and is more pronounced in girls than in boys. There are underlying changes in the mean GH amplitudes in both boys and girls as well as an increased baseline secretion in girls. In puberty, body composition modulates the GH secretion rate in both sexes.

The aim of this study was to investigate the number of emerged primary teeth at various ages from 6 to 24 months in 1347 longitudinally followed Pakistan infants sampled from four socio-economically different areas in Lahore, Pakistan; from a very poor periurban slum to a privileged upper middle class group. The emergence of the primary teeth was found to be little, or not all related to sex or to the area of living. However, in comparison with studies conducted in other continents, the Indo-Pak subcontinent population lags behind in primary teeth emergence, especially in early life. This genetic difference makes it necessary to create specific standards of primary teeth emergence for this population.

Pubertal linear growth in 66 adopted Indian girls was studied. The infancy-childhood-puberty standard was used, since it is applicable to Indian girls, and enables determination of the onset and height gain of the pubertal growth phase in an individual. At arrival in Sweden, mean height was -2.8 SDS. Despite rapid catch-up growth, the girls were still below the reference mean (-0.8 SDS) at the onset of the pubertal growth spurt, which occurred approximately 1.5 years earlier than in Swedish girls and also earlier than in Indian girls. The pubertal height gain, however, was equivalent to that in Swedish girls with similar timing of puberty. The short final height found in some of these girls appears to be related to shortness prior to puberty and to very early onset of an otherwise normal pubertal growth component.

Serum samples were obtained from 44 infants vaccinated against diphtheria at the ages of 3, 5 and 12 months with an aluminium-adsorbed diphtheria-tetanus toxoid vaccine containing 15 Lf units of diphtheria toxoid. Toxin-neutralizing antibodies (antitoxin) were measured by the Vero cell assay and IgG, IgM and IgA antibodies against diphtheria toxoid by enzyme-linked immunosorbent assay. A neutralizing antibody titer of 10 corresponded to 0.01 IU/ml, the level considered necessary for short-term protection. Geometric mean neutralizing antibody titers at 3, 5, 6, 12, 13 and 30 months were 28, 21, 173, 61, 1076 and 61. All children had titers of greater than or equal to 10 (greater than or equal to 0.01 IU/ml) between 6 and 30 months of age. At 30 months only 48% had titers of greater than or equal to 100 (greater than or equal to 0.01 IU/ml), the level considered necessary for long-term protection. Geometric mean IgG antibody levels were 13, 36, 216, 64, 649 and 57. IgG antibodies significantly correlated with neutralizing titers and predicted neutralizing antibodies above or below 10 and 100 with an accuracy of 96 and 82%, respectively. IgG antibodies could not, however, be used to predict individual neutralizing antibody titers with great accuracy. IgM antibodies were only detected after the third vaccination. IgA antibodies were not detected in any serum sample from ten infants tested. In conclusion, the Swedish vaccination schedule results in protective antibody levels in infants until at least 30 months of age. The decline of the antibody titers indicates a need for further studies to establish the duration of protection.

The linear growth of Swedish children with cystic fibrosis (CF), is described using the infancy–childhood–puberty (ICP) growth model. Length/height was studied in 51 patients during their first 8 years of life. The median age at diagnosis was 0.4 years (range 0.0–6.1 years). At birth, their mean length was close to normal, but the gain in length over the first 0.25 years of life was significantly below normal, resulting in a mean length SDS of -1.3. Length remained subnormal up to 1.0 year of age. Thereafter, catch-up growth occurred, resulting in almost normal height (mean SDS -0.3) at 5.0 years of age. Between 5.0 and 8.0 years of age growth was normal. The mean age at onset of the childhood component was not significantly different from the controls. Hence, the catch-up growth did not occur until after the onset of the childhood component. This study shows that the postnatal linear growth rate is retarded in children with CF during the first months of life. This is almost completely compensated for by a supranormal growth rate that starts at the end of the first year of life.

Early normal human linear growth is unstable and oscillates owing to an increase in growth rate between 6 and 12 months of age. This defines the onset of the infancy-childhood growth spurt (IC spurt). The onset is identical with the onset of the childhood component of the infancy-childhood-puberty growth model. The IC spurt is completed when the infancy component of this model has virtually ceased, at around 3 years of age. Additional observations suggest that its onset represents the age at which growth hormone (GH) begins to regulate growth significantly. The negative impact of late onset of the IC spurt on attained height is illustrated and discussed. A delayed spurt is observed in 30-50% of children with growth-related disorders and of infants living in a poor area of a developing country. The IC spurt is absent in children with GH deficiency who receive no hormonal therapy.

The infancy-childhood-puberty (ICP) growth model divides human growth into three additive and partly superimposed phases: infancy, childhood, and puberty reflecting the endocrinology of the growth process. The childhood phase of the ICP model has been assumed to start during the second half-year of life and slowly decelerates, although it continues into puberty until growth ceases. This phase has been taken to mirror the effect of growth hormone (GH). The age at onset of the phase of growth, normally occurring between 6 and 12 months of age is recognized to be an important time event at postnatal human growth. The aims of this study were to study the age at childhood onset in Shanghai children and its effect on child growth, and to compare these results with the results obtained from Swedish longitudinal studies.The study population consisted of 1 720 children born between January 1, 1980, and December 31, 1990 in Fenglin Community, Shanghai, who got a continual monitoring at the clinic from birth to six years of age. The age at onset of the 'childhood phase' of growth was determined individually, in units of one month, by visual inspection of the data contained within the individual, computer-generated, ICP-based growth chart for both length and length velocity. T tests, chi(2) tests and multiple linear regression analyses were used in data analysis.There was a significant (P0.05) difference in the distribution of the age at onset of the childhood phase of growth between Shanghai and Swedish populations. The mean age of the infants at onset of the 'childhood phase' of growth was 11.2 months in boys and 10.7 months in girls. Compared to their Swedish counterparts, these means occurred 1.3 months later in boys and 1.4 months later in girls. Both age at onset of the 'childhood phase' of growth and length at six months of age significantly (P0.05) contributed to the attained height from 12 months of age onward; one month delay in the onset of the 'childhood phase' of growth reduced height, at 5 years of age, by 0.4 cm in boys and 0.56 cm in girls. The mean values of length/height among the four groups of the age of the childhood onset, i.e. 6 m-, 9 m-, 12 m-,/= 15 m, were found to be significantly (P0.05) different from 12 month of age onward. However, a significant (P0.05) difference in the mean length/height velocities among the four groups was in principle only found during the following intervals: 3 - 6, 6 - 9, 9 - 12, and 12 - 18 months of age. The mean values of BMI among the four groups of the age of the childhood onset showed significantly (P0.05) different only in 9 and 12 months of age. The mean values of BMI velocity among the four groups of the age of the childhood onset were found to be significantly (P0.05) different in four age intervals: 3 - 6, 6 - 9, 9 - 12, and 12 - 18 months of age. The age at onset of the 'childhood phase' of growth was negatively associated (P0.05) with mid-parental height, though positively related (P0.05) to height at six months of age. A simple linear regression was applied to the age at onset of the 'childhood phase' of growth and mid-parental height. It was found that the age at onset of the childhood phase' of growth was 1.5 months later in boys and 1.3 months later in girls, for children with a mid-parent height being -2SD below the mean in comparison to the children of tall parents, i.e. a mid-parental height equals to mean +2SD.The age at childhood onset is equally important when studying children from Shanghai, as it is with their Swedish counterparts.

To evaluate the Apgar score predictive power for mortality during different periods in the first year of life in a population with a very low mortality rate.The records of all singleton live births without severe congenital malformations and length of gestation25 wk (n = 976635) were collected from the Swedish Medical Birth Registry, 1990 to 1998. Receiver operating characteristic (ROC) analysis was utilized.Both the 1-min and the 5-min Apgar scores were shown to be good discriminators for early mortality, with the area under the ROC curve0.85. For babies at risk of early death, the selected cut-off values for the 1-min Apgar score was8 for preterm (true-positive (TP) rate: 83.9%; false-positive (FP) rate: 17.7%) and term babies (TP rate: 69.4%; FP rate: 6.7%). At 5 min, the analysis revealed that newborns with an Apgar score9 were at risk for early death (preterm babies: TP rate: 79.8%; FP rate: 13.3%; term babies: TP rate: 73.8%; FP rate: 3.4%).Our analysis did not support the common practice in the clinic or in research of grouping infants at risk in Apgar score groups, i.e. a score below 4 or a score below 7. However, the data presented here allow the clinicians and researchers to identify and define a suitable cut-off point in relation to the quality of neonatal care and resources available, rather than adhering to a historical cut-off value that has not been studied in depth.

Western infants with congenital heart disease have frequently been reported to have a low birthweight for gestational age. Studies in Asian infants seem to be lacking in this area. This is the first extensive study presenting the birthweight distribution of Chinese newborns with symptomatic congenital heart disease.The birth data of 454, mainly southern-Chinese infants with symptomatic cardiovascular defects, born between 1990 and 1995 and admitted to Grantham Hospital, Hong Kong in 1994 and 1995, were analysed retrospectively. Infants with (non)-genetic syndromes or other major extracardiac malformations were excluded.Fifteen per cent of all newborns had a birthweight below the reference mean of - 2 Z-score. After correction for length of gestation, no significant difference could be detected in birthweight between the cyanotic and acyanotic groups, nor between the different haemodynamic disturbances. Infants with atrial or ventricular septal defects, tetralogy of Fallot, pulmonary atresia with ventricular septal defect, heart with univentricular atrio-ventricular connection or double outlet right ventricle showed significant birthweight deficits. Transposition of the great arteries was not related to being small for gestational age.Similar to Western infants, prenatal growth impairment was a common feature in Chinese infants with symptomatic congenital heart disease. The birthweight distribution in Chinese might be comparable to that in Western populations. Exceptions are possibly the high frequency of low birthweight in Chinese newborns with atrial septal defect or a single-ventricle abnormality. Further studies on fetal anthropometry and haemodynamics are necessary to provide insight into the relation between cardiovascular malformations and being small for gestational age.

Objectives: To test the hypothesis that birth weight for gestational age and weight gain in early childhood have a long term association with psychological distress in adults. Design: Longitudinal study of 1958 birth cohort followed to age 42 years. Setting: Population based birth cohort study. Participants: 9731 cohort members with valid perinatal, postnatal, and adult data. Main outcome measures: Malaise inventory scores measured at ages 23, 33, and 42 years. Generalised estimating equations approach used to analyse repeated measures. Results: Psychological distress score was inversely related to birthweight z score and weight gain from birth to the age of 7 years. A unit increase in birthweight z score or childhood weight gain was associated with a mean reduction in psychological distress score of 0.10 (95% confidence interval 0.05 to 0.14) and 0.06 (0.02 to 0.10), respectively. Birth weight and weight gain were also inversely related to the odds of having a high level of psychological distress, with odds ratios being 0.90 (0.85 to 0.95) and 0.93 (0.89 to 0.98), respectively. Conclusions Psychological health in adults is related to fetal growth and growth in early childhood., published_or_final_version

This study aimed to update growth reference values for height, weight and head circumference in order to reflect the changes in body size in the Swedish population during the past two decades. The data came from a large longitudinal growth study on 3650 full-term healthy Swedish children who were born between 1973 and 1975. All of these 1801 girls and 1849 boys had longitudinal data for height and weight from birth to final height. Comparison with previous Swedish growth reference values based on children born between 1955 and 1958 revealed that there have been secular changes in body size. For instance, at 18 y of age, the updated height and weight reference values are 180.4 cm for males and 167.7 cm for females, i.e. 1.9 cm taller and 5.7 kg heavier for males and 2.3 cm taller and 3.4 kg heavier for females compared with the previous reference values.These new growth reference values provide current national standards for growth monitoring and evaluation since the year 2000.

Body mass index (BMI) is an important indicator of nutritional status. Many studies have been done to present BMI reference values in centile values rather than mean and SD values since its statistical distribution is positively skewed. Both height and weight growth charts are usually available in terms of mean and 1, 2 and 3 SD around the means; it would be of clinical value to produce BMI reference charts in a similar way. The aim of this work was to derive the mean and +/- 1, 2 and 3 SD BMI reference ranges as a supplement to the BMI centile reference values published previously for the same group of Swedish children. The method was based on an age-dependent Box transformation, and the beta-value was given as a third-degree polynomial function over the paediatric age. The BMI reference values can be given from mathematical functions in addition to values for specific ages.The BMI reference values and charts derived as described effectively reflect the nature of the variant age-dependent positive skewed statistical distribution of BMI values in the population, and can serve as a valid supplementary tool in the evaluation of growth and nutrition during paediatric years.

Evidence-based medicine shifts the basis for clinical decision making from intuition and unsystematic clinical experience to the examination of evidence resulting from clinical research. Evidence-based medicine is the same as good clinical research. The selection of a proper study design for a specific study objective is the most important cornerstone of good clinical research. Evidence-based medicine places great importance on the design of a study, with optimum evidence being obtained from the randomised, controlled clinical trial. However, various study designs are equally important-if properly used-in the process of searching for solid and important evidence for use in clinical practice. There should be an emphasis on a quality improvement shift in research design from retrospective to prospective, cross-sectional to longitudinal, uncontrolled to controlled, and non-randomised to randomised. The reasons for using suboptimal study designs in clinical research are the lack of formal research training and the pressure to obtain academic output without being motivated. Research design is one of the most important aspects to study and practice, and there are four simple rules: (1) avoid retrospective studies; (2) focus on prospective studies; (3) use controls, randomisation, and blinding; and (4) always discuss the research design with an experienced researcher or statistician before commencing the study.

Training courses in the concepts of clinical trials research methodology that include rules in good clinical practice have not yet been extensively implemented in Hong Kong. This study aims to define the current knowledge of rules in good clinical practice and identify any need for such training programmes. Between May and August 1996, 161 clinical research staff were asked non-randomly to fill in a questionnaire about their knowledge of research methodology and their interest in specific courses. The median number of correctly answered questions (maximum score, 20) was 5 and the mode was 4, which was the expected score if questions had been answered randomly. Only minor differences in score were detected between doctors, research staff, and industry employees. Many researchers were keen, however, to further their knowledge by attending future courses; on average, each person showed an interest in three of the eight proposed courses. The study shows that the knowledge of rules in good clinical practice among clinical research staff in Hong Kong is poor, but there is nevertheless a demand for training programmes.

The aims of this study were to determine the number of randomised clinical trials where the correspondence address included the words 'Hong Kong' for the years of publication between January 1987 and December 1996, and to study their characteristics: year of publication, disease area, sample size, and correspondence address of the department and institute; MEDLINE EXPRESS was used for the search. A total of 5605 publications were identified, of which only 170 (3.0%) were found to be randomised clinical trials. No significant increase in the proportion of randomised clinical trials could be seen during the decade of publication (P0.05). Approximatley 50% of the trials had a small sample size (fewer than 75 subjects) and most randomised clinical trials were performed in the field of internal medicine, followed by surgery, and obstetrics and gynaecology (total, 69%). The predominant research area was gastrointestinal disease (34%). Despite a relatively high academic output from Hong Kong, the number of randomised clinical trials has not increased much during the decade.

While previous research has suggested that body thinness is related to subsequent linear growth in children, it is unclear whether thinness at birth is related to linear growth in newborns and catch-up growth in small-forgestational age newborns. Drawing on data from a longitudinal growth study of 3,650 full-term Swedish babies, this study examines linear growth from birth to 6 months of age in three groups of newborns with short (-2 SDS), appropriate (-2 to 2 SDS) and long (2 SDS) body length for gestational age. Among infants short at birth, the Benn Index (kg/m2.69) at birth was not related to the odds of short stature (-2 SDS) at age 6 months (odds ratio = 1.03; p0.10). Nonetheless, the Benn Index was positively related to growth velocity in the first 6 months of life in the short (p = 0.060), appropriate (p0.05), and tall (p0.05) for gestational age newborns. Use of the Ponderal Index (kg/m3) would give similar results. The findings suggest that nutritional status at birth is related to linear growth velocity in newborns.

To study the effect of the body proportion and pubertal growth spurt on the stature of children with beta-thalassaemia major.The height, sitting height, upper to lower segment (U:L) ratio and pubertal development were determined in 71 Chinese children (38 girls and 33 boys) with beta-thalassaemia. The growth patterns of 20 patients with complete growth data between 3 years and final height, were analyzed according to whether they underwent a pubertal growth spurt or not.27% of the boys and 32% of the girls had a height below the 3rd percentile. About 60% of all the children had a U:L ratio below the 10th percentile for age. Abnormal body proportion was found in patients with or without growth retardation. 34% of the 41 children over the age of 14 years underwent spontaneous puberty. In 28 patients over the age of 16 years, a growth spurt was observed in 46% of the children during spontaneous or induced puberty. The retrospective analysis showed that the height deviation from the mean in adulthood was significantly higher in patients without pubertal growth acceleration than in those with a growth spurt (x = -11.8 cm, s = 7.6 cm vs x = -4.4 cm, s = 4.4 cm; P = 0.02).An abnormal U:L ratio was commonly observed in patients with beta-thalassaemia major and may be one factor contributing to the short stature of these patients. Abnormal puberty was present in a significant proportion of children and the lack of a pubertal growth spurt was found to be detrimental to adult height.

It is well known that some adult diseases, such as cardiovascular diseases, may be programmed during foetal life. It is not clear, however, whether final height may be predicted from foetal growth. A longitudinal cohort of full-term healthy Swedish babies (n = 3,650) was followed up from birth to maturity in a population-based growth study. Length or height and its changes were analysed from birth to 18 y of age; 2,807 children, with data available on birth length, final height and parental height, were included in this analysis. The result clearly shows that length at birth relates to final height. In terms of standard deviation scores (SDS), the mean difference in length at birth from the mean was greatly decreased in final height, but retained the same order as was seen at birth. In terms of centimeter difference from the reference mean values, the difference in length at birth remained roughly stable into final height. For instance, babies 5 cm above or below the mean birth length will end up approximately 5 cm above or below the mean in final height. Parental height-a surrogate value of the genetic final height potential of an individual-is shown to influence postnatal growth in height strongly. However, the difference from the mean in length at birth remained into adulthood within the same midparental height group.This study reveals that trends in foetal linear growth continue into maturity. Foetal growth is a significant predictor of postnatal growth. Final height is dependent on both the magnitude of foetal growth and the genetic potential in stature, and appears to some extent to be programmed from foetal growth.

The objectives of the present work were to present a new reference for the age at childhood onset of growth and to investigate the secular trend in the timing of puberty in a community-based normal population in Sweden. A total of 2,432 children with longitudinal length/height data from birth to adulthood were used to determine the two measures by visual inspection of the measured attained length/height and the change in growth velocity displayed on a computer-generated infancy-childhood-puberty (ICP) based growth chart. The series represents a sample of normal full-term children born around 1974 in Göteborg, Sweden. We found about 10% of children were delayed (12 mo of age) in the childhood onset of growth based on the previous reported normal range, i.e. 14% in boys and 8% in girls. Distribution of the age at childhood onset of growth was skewed. The medians were 10 and 9 mo for boys and girls, respectively. After natural logarithmic transformation, the mean and standard deviation (SD) were 2.29 (anti-log 9.9 mo) and 0.226 for boys, 2.23 (anti-log 9.3 mo) and 0.220 for girls, respectively. The 95% normal ranges were 6.3-15.4 and 6.0-14.3 for boys and girls, respectively. The distribution of the timing of PHV was close to the normal distribution. The mean values were 13.5 y for boys and 11.6 y for girls with 1 y SD for both sexes.A downward secular trend in the onset of puberty was clearly shown in the population. The age at childhood onset of growth did not correlate with the timing of puberty (r = -0.01 and 0.05, p0.7 and 0.1 in boys and girls, respectively). Normal ranges of the age at childhood onset of growth are in need of revise, as this study indicates. The new reference presented here could be a reliable indicator in further studies.

Previous growth studies have not explored how different growth phases-the fetal, infancy, childhood, and puberty phases-interact with each other in the development of adult shortness. In this paper, the authors attempt to describe the importance of each growth phase for adult shortness and the effect of growth in one phase on other, subsequent phases. The authors analyzed data from a longitudinal population-based growth study of 2,850 healthy, full term Swedish children born between 1973 and 1975. The height values were transformed into a centimeter score (CMS) by subtracting the raw values from the reference mean values for a particular age and sex. Subnormal growth in any growth phase, as defined by a decrease of 3 CMS or more during a growth phase, was associated with significant increased risk for final heights below 0, -6, and -12 CMS. For children with subnormal growth during one, two, and three phases, the percentages for final height below -12 CMS (a standard deviation score of approximately -2) were 0.5%, 9.4%, and 75%, respectively. Most children (57/62) with a final height below -12 CMS had subnormal growth in two or three phases. Height gains during the four growth phases were interdependent. The infancy phase was negatively associated with fetal growth (r = -0.33, p < 0.01); the childhood phase was positively associated with infancy growth (r = 0.21, p < 0.01); and the puberty phase was negatively associated with childhood growth (r = -0.10, p < 0.01).

The body mass index or BMI (weight/height2) is a somewhat crude estimate of nutritional status. However, due to its simplicity and high correlation with total body fat, it has been the method of choice in both paediatric clinics and research over the years. Since BMI is not an equivalent measure of the percentage of body fat in different ethnic groups and in the two sexes, population-specific BMI reference data is needed. Several BMI reference values have been published for French, American, British and Hong Kong children in recent years. In Sweden, weight-for-age and height-for-age reference values, which were published in 1976, are still used as the current national growth reference values. Updated growth reference values are needed for assessing nutritional status due to the secular trend toward and increasing prevalence of childhood obesity. The aim of this study was to produce BMI reference values for Swedish children of paediatric age. The series came from a large Swedish population-based longitudinal growth study of 3650 full-term babies followed from birth to 18 y of age. The children in this data set were born in the early 1970s. The pattern and level of 50th centile BMI values presented here are quite similar to those of the Swedish cohort study in the 1950s. In comparison with the US BMI reference values, the Swedish values are much lower, especially for the higher centile values.The new Swedish BMI chart from our study may provide a useful tool for paediatricians to assess body fat, and consequently nutritional status, in Swedish children.

Objective: To assess the prevalence of asthma and other allergies in children in Urumqi and Beijing, compared with that in Hong Kong. Methods: A total of 7754 primary school students were randomly selected to participate in the study. Data were collected in 1995–96 using the International Study of Asthma and Allergies in Childhood (ISAAC) protocol for 6- and 7-year-olds. The study design and data quality assurance in all aspects followed the protocol, including the double entry of data. Results: The questionnaire response rate was high (98.9%). Beijing children reported significantly more asthma than those living in Urumqi in three categories: wheezing or whistling in the chest in the past year (6.0%, 95% confidence interval (CI): 5.1–6.9%vs 2.9%, 2.3–3.5%, P < 0.001), sleeping disturbed due to wheezing (1.3%, 0.9–1.7%vs 0.6%, 0.3–0.9%, P < 0.03) and having experienced asthma ever (10.7%, 9.6–11.8%vs 7.6%, 6.6–8.6%, P < 0.001). The prevalence of allergic rhinitis (30.0%vs 31.1% estimated as 12-month nasal symptoms in Beijing and Urumqi, respectively) and eczema (2.8%vs 2.0% recorded as 12-month itchy rash) in the two cities were not significantly different. A similar study was also performed in Hong Kong in 1995 using the same ISAAC protocol. The children in Urumqi and Beijing had fewer (P < 0.05) allergic symptoms compared to those living in Hong Kong (n = 3618). The 12-month prevalence of wheezing, nasal symptoms and itchy rash found in Hong Kong were 9.2% (95% CI: 8.2–10.2%), 35.1% (33.5–36.7%) and 4.2% (3.5–4.9%), respectively. Conclusion: Urumqi, Beijing and Hong Kong represent communities at different stages of westernization and the results from these three cities reflect a worldwide trend for an increasing prevalence of allergies along with westernization. These three cities could assist in identifying risk factors involved in the increase in asthma, allergic rhinitis and eczema.

Racial group studies have identified differences in the occurrence of congenital heart disease (CHD) among ethnic populations. The aim of this study was to characterize the proportionate frequency and clinical profile of children with symptomatic cardiac abnormalities in Hong Kong. The hospital records of 666, mainly Southern Chinese children with symptomatic CHD, who were 4 years of age or younger and who were admitted to Grantham Hospital, Hong Kong, in 1994 and 1995 were analyzed retrospectively. Left-to-right shunting (45.0%) and pulmonary outflow obstruction (34.4%) were the most frequently diagnosed categories, followed by left ventricular outflow obstruction (8.3%), transposition of the great arteries (4.2%), conditions with intracardiac mixing (3.9%), and other cardiac lesions (4.2%). Compared with Western studies, pulmonary outflow obstruction (p < 0.0001), particularly tetralogy of Fallot and critical pulmonary stenosis, were more frequent in Chinese children. In contrast with previous reports, coarctation of the aorta (5%) does not seem to be uncommon in Chinese patients. Conversely, aortic stenosis and hypoplastic left ventricle may be rare in these children (1% vs 3% and 3–7%). Other cardiac lesions showed no consistent racial difference in the frequency of occurrence. Chinese patients with Down's syndrome had ventricular septal defect (38%) as the predominant lesion followed by atrioventricular septal defect (25%). Western studies usually report a reverse pattern for these two lesions. The mortality rate for the total cohort was 7.5%. However, of those with conditions with intracardiac mixing and left ventricular outflow tract obstruction many did not survive childhood (20% and 21%, respectively).

Target height, the genetic potential in stature, is commonly estimated by the corrected midparental height (CMH) method. A new model for estimating target height has recently been introduced based on a large, Swedish, population-based study. The aim of this study was to compare the validity of the two methods for estimating target height in Hong Kong Chinese children. The Hong Kong Chinese were more than 10 cm shorter than the Swedes in stature. The secular increase in height over the two generations, however, was 4.2-4.8 cm for the Hong Kong Chinese, much larger than that of the Swedes (0.7-1.0 cm). The two populations are thus at different stages in the secular trend. The new model derived from Swedish population for estimating target height was shown to be applicable to Hong Kong Chinese children; the mean of residual final height values was close to zero (-0.15 cm, p = 0.74). However, the mean of residual final height was significantly above the expected value of zero (4.5 cm, p0.0001) when the CMH method was applied to the data, which implies an underestimation bias of 4.5 cm. Consequently, if the CMH method is used to estimate target height and evaluate growth hormone treatment responses in short children, it may inflate the treatment response by 4.5 cm. In conclusion, the recently proposed model for target height estimation offers a better alternative for estimating target height in Hong Kong Chinese children and for assessing growth-promoting treatments.

The prevalence of asthma among schoolchildren in Costa Rica is very high -- at the level of 20-30% -- and the reason is still unknown. A group of children from our previous epidemiologic study was randomly selected in order to establish the relation between asthma symptoms and allergy sensitization to common allergens. Serum samples from children with and without asthma were analyzed for the presence of IgE antibodies to 36 different allergens, for the presence of IgE antibodies to a pool of 10 common allergens, and for total serum IgE. The most prevalent IgE antibodies were those to mite, cockroach, dog, and house-dust allergens with MAST pipettes for the serologic measurements. Positive reactions to house dust, mite, cat, and the two molds (Alternaria and Cladosporium), and food allergens such as egg white, peanut, and shellfish were significantly more prevalent among the asthmatics than the nonasthmatics. Sensitization was equally prevalent at different ages, but the house-dust, mite, cat, dog, cockroach, Alternaria, and egg-white allergens had sensitized boys more often than girls (P < 0.01). The result of the analysis of IgE antibodies to a pool of 10 common allergens by Phadiatop supported the MAST pipette results, showing allergen sensitization in 57.7% of the asthmatic children and 42.3% in the nonasthmatic group. The concentration of IgE was significantly higher among the asthmatic children (372.2 kU/l) than among the nonasthmatic children (249.1 kU/l) (P < 0.00001). Parasitic infestations were not examined in this study, but in most of Costa Rica these have largely been eliminated and could not explain the high total IgE levels. Our data indicate that the very high prevalence of bronchial asthma in Costa Rican schoolchildren can be related to sensitization, especially to airborne indoor allergens such as those of mites, cockroaches, and dogs.

Aims Growth stunting is prevalent in developing countries. The prevalence of stunting ranges from 10-80% or more. The critical period for growth faltering in length is between six and 18 months. The aims of this study were 1) to investigate the association between the age at onset of the childhood component and growth stunting in early life; 2) to develop a screening method for identifying any individual infant subject to stunting in early life. Materials & methods This community-based longitudinal study was carried out in Lahore, Pakistan. Three studied areas and one local control group were included in the study. There were 425 subjects for whom data were available for determining the age at onset of the childhood component. The onset was defined as an abrupt increase in length velocity. It was determined individually using the infancy-childhood-puberty growth model. Results The medians of the age at onset of childhood component were 15, 13, 10 and 9 months in the periurban, village, urban and control groups, respectively. The onset was significantly related to both length and length velocity during the critical period of stunting. Based on the distribution of individual length increment from 12 to 15 months, 2.0 and 3.0 cm were chosen as the cut-off points to identify a stunting infant. In the normal onset group, 84% of the children were identified as growing normally; in the delayed onset group, 61% were identified as stunting. Using this screening method, 97% of children have a delayed onset if their length increase is below 2 cm from 12 to 15 months; 99% of them have a normal onset if the increase is above 3 cm over the same period. Conclusions The age at onset of the childhood component can significantly explain the variations in both length and length velocity in early life. The stunting screening method reported here is simple. It can be used in almost any situation, such as a pediatric clinic or community-based survey.

A difference in length or height growth is observed between populations in developing and developed countries and, within a country, between well-off and poor subpopulations. The aim of this community-based study was to identify possible risk factors for growth stunting in early life using the infancy-childhood-puberty (ICP) growth model. A periurban slum, a village and an urban slum, plus a local control group in Lahore, Pakistan, were investigated. In total, there were 425 infants born from September 1984 to March 1987 in the study. Children were followed from birth to 24 months and anthropometric data were recorded at each examination. A well-designed questionnaire was used to collect background information to identify risk factors for growth faltering over this period. The age at onset of the childhood component was determined individually using the ICP growth model. A late onset was defined as onset after 12 months. Univariate odds ratio analysis identified 20 significant risk factors for a delayed childhood onset in the total sample. Backward logistical analysis showed that only six variables were significant, i.e. small number of rooms in a household, episode(s) of diarrhoeal diseases, poor house structure, low body mass index, early end of breastfeeding and birth in warm season. Stratified analysis showed that episode(s) of diarrhoeal diseases and birth in warm season were the only significant risk factors in the two poor areas. This study also found that the impact of diarrhoeal diseases on length growth persisted after allowing for birth season. Seasonal variation in length growth was seen in the age at onset of the childhood component. General socioeconomic status was found to be a risk factor for growth faltering in early life. Diarrhoeal diseases and being born in a warm season are particular risk factors for growth faltering in early life.

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.

We report early linear growth in 73 children (51 boys, 22 girls) with early onset of chronic renal failure (CRF). The inclusion criteria was onset of CRF before 6 months of age, two or more height measurements during the 1st year of life, follow-up for at least 3 years and continuously impaired renal function with a glomerular filtration rate below 50 ml/min per 1.73 m2 at 1 year or later. Only height measurements taken during conservative treatment or dialysis were included. The data were analysed in terms of the infancy-childhood-puberty growth model. There was an age-dependent growth failure in early life leading to an attained height of -3 standard deviation score (SDS) at 3 years of age. Approximately one-third of the reduction in height occurred during fetal life and one-third during the first postnatal months. Between 0.75 and 1.5 years of age height also decreased by 1 SD as a consequence of a delayed onset of the second, the 'childhood', phase of growth in 36% of the patients and by an 'offset childhood' growth pattern--i.e. a return to the infancy phase pattern after onset of the childhood phase--in 60% of the patients. Growth between 0.25-0.75 and 1.5-5 years of age was generally percentile parallel and thus less likely to be affected in CRF with early disease onset. The glomerular filtration rate was not related to the height gain in early life. We speculate that the growth failure during fetal life and the first postnatal months reflects metabolic and/or nutritional influences and the impaired growth at 0.75-1.5 years of age is related to a partial insensitivity to growth hormone.

The spontaneous growth process in Turner's syndrome is characterized by a progressive decline in height velocity during childhood and no pubertal growth spurt. Therefore, therapy aimed at improving height during childhood as well as increasing final height is desirable for most girls with Turner's syndrome. Forty-five girls with Turner's syndrome, 9-16 yr of age (mean age, 12.2 yr), were allocated to three study groups. Group 1 (n = 13) was initially treated with oxandrolone alone; after 1 yr of treatment, GH without (group 1a; n = 6) or with (group 1b; n = 7) ethinyl estradiol was added. Group 2 (n = 17) was treated with GH plus oxandrolone. Group 3 (n = 15) was treated with GH, oxandrolone, and ethinyl estradiol. The dosage were: GH, 0.1 IU/kg.day; oxandrolone, 0.05 mg/kg.day; and ethinyl estradiol, 100 ng/kg.day. A height of 150 cm or more was achieved in 61%, 75%, and 60% of the girls in groups 1, 2, and 3, respectively. The most impressive increase in height was seen in group 2. In this group the mean final height was 154.2 cm (SD = 6.6), which is equivalent to a mean net gain of 8.5 cm (SD = 4.6) over the projected final height. In group 3, in which ethinyl estradiol was included from the start of therapy, the initially good height velocity decelerated after 1-2 yr of treatment. Their mean final height was 151.1 (SD = 4.6) cm, equivalent to a mean net gain of 3.0 cm (SD = 3.8). A similar growth-decelerating effect of ethinyl estradiol was seen in group 1b. We conclude that in girls with Turner's syndrome who are older than 9 yr of age, treatment with GH in combination with oxandrolone results in significant growth acceleration, imitating that in normal puberty, leading to a more favorable height during childhood. This mode of treatment also results in a significantly increased final height, permitting a great number of the girls to attain a final height of more than 150 cm. However, early addition of estrogen decelerates the height velocity and reduces the gain in height.

Between October 1979 and January 1993, 85 Chinese neonates in Hong Kong underwent surgical repair for coarctation of the aorta. Their mean(s.e.) age and body weight at operation was 15.6(8.5) days and 3.06(0.56) kg, respectively. Simple coarctation was present in 17 babies, while 36 had additional ventricular septal defect and 31 had associated major complex intracardiac lesions. Subclavian flap aortoplasty was performed in 56 babies, resection with end-to-end anastomosis in 18 and aortoplasty with the use of a GORETEX patch in 11. The overall early mortality rate was 16.5%. To identify risk factors for early operative mortality, various clinical variables, surgical options, associated heart lesions and dimensions of the aortic arch at different sites for each patient were reviewed. Univariate analysis identified statistically significant differences between the survivors and non-survivors for the following factors: preoperative body-weight, arterial pH and base excess, serum urea and creatinine levels. Stepwise logistic regression further distinguished serum creatinine levels and the period of operation as two significant risk factors. Contrary to previous reports, the dimensions of the aortic arch and type of surgery did not affect early operative mortality. Among the 71 hospital survivors followed for 38.2(38) months, residual or recurrent coarctation of the aorta was detected in 12(17%). The different surgical operations were not related to the incidence of late complication. The size of the distal transverse arch, however, was different (P = 0.05) in those who did and did not develop aortic sequela. Successful balloon angioplasty was subsequently performed in 11 patients. In an era of echocardiography with prenatal diagnosis and therapeutic catheterization, early recognition of the disease with prompt prostaglandin infusion should prevent collapse of the baby, thus avoiding renal impairment and severe metabolic acidosis. Balloon angioplasty would offer a simple effective treatment for patients who developed aortic re-coarctation.

The aim of this study was to identify predictors of the growth response to growth hormone (GH) during the first 2 years of GH treatment, using auxological data and the maximum GH response (GHmax) to provocation tests. The patients were 169 prepubertal short children (27F, 142M), with Gmax values ranging from 0 to 65 mU/l. Their mean age (+/- SD) was 8.3 +/- 2.4 years (range 3-13 years), mean height SDS -3.0 +/- 0.7 (range -1.5 to -6.0 SDS) and mean pretreatment height velocity was normal (+/- 0.0 SDS) (range -1.6 to +0.9 SDS). The increase in height SDS during the first 2 years of GH treatment (0.1 U/kg/day) varied from 0.10 to 3.75 SDS, with younger children having a better growth response. Individual growth responses correlated (p0.001) with GHmax (r = -0.37), age (r = -0.35), 1-year pretreatment delta SDS (r = -0.25), mid-parental height SDS (r = 0.34), height SDS at start of treatment (r = -0.22) and difference between height SDS of an individual child at the onset of GH treatment and mid-parental height expressed in SDS (diff SDS) (r = -0.43). In a multiple stepwise linear regression model, diff SDS and log GHmax were found to be the strongest predictors of the magnitude of the growth response. In the short children in this study who exhibited a broad range of GHmax values, 33% of the growth response during the first 2 years of treatment could be predicted.

Summary The prevalence of asthma in children between the ages of 5 and 17 years in Costa Rica was determined using a large sample (n = 2682). The definition of asthma was based on a combination of a physician's diagnosis and a symptom score, using information from a questionnaire given to the parents. An overall asthma prevalence as high as 23·4% was found. Sex, age, urban/rural location, or rain precipitation did not show any association with the diagnosis of asthma. The presence of smokers in the home was found to be an important risk factor (odds ratio = 1·6). Another identified risk factor was a high yearly average outside temperature, i.e. above 25°C (odds ratio = 1·8). Furthermore, the proportion of children with more than four upper respiratory infections during the preceding year was found to be significantly increased in children with asthma (odds ratio = 4·3). The non-asthma group seemed to use equal amounts of drugs for the treatment of asthma as the asthma group. For a country like Costa Rica with limited economic resources the current work indicates two important issues for consideration in the future; firstly, to try to define the cause(s) of asthma and secondly, to continuously inform the physicians about the best way of diagnosing and treating asthmatic patients to ensure optimal handling of this large patient group.

We describe spontaneous longitudinal growth in girls with Turner's syndrome (TS), using the infancy-childhood-puberty (ICP) growth model. Length/height during the first 12 years of life was studied in 58 Swedish girls with TS. Their mean length at birth was 47.8 cm (SDS -1.4) and mean height at 12.0 years of age 127.3 cm (SDS -3.0). A clear age-dependent subnormality was observed in the change in length-height SDS (delta SDS). Mean delta SDS values at ages 0.0 to 0.5 and 3.0 to 6.0 years were normal. In contrast, the mean delta SDS at ages 0.5 to 3.0 and 6.0 to 12.0 years were subnormal. The onset of the childhood growth component (normally located between 0.5 and 1.0 year of age) was, on the average, delayed by 0.28 year. This accounts for the subnormality of delta SDS at 0.5 to 3.0 years of age. About 50% of the variation in height at 12.0 years of age, as determined by a multiple linear regression analysis, was significantly explained by length at 0.5 year of age, age at the onset of the childhood component, and delta SDS at 6.0 to 12.0 years of age.

An update of the Swedish reference standards for weight, length, and head circumference at birth, for each week of gestational age, is presented. It is based on the total Swedish cohorts of infants born 1977-1981 (n = 475,588). A "healthy population" (79%) was extracted, using prospectively collected data. Weekly (28-42 weeks) grouped data for length and head circumference were well approximated by the normal distribution, but the distributions for birthweight were positively skewed. The original skewed distributions for birthweight were transformed, using the square root, resulting in distributions close to the Gaussian. For smoothing purposes, the weakly values for the mean and the standard deviation were both fitted by a third degree polynomial function. These functions also make possible the calculation of the continuous variable, standard deviation score, for individual newborn infants as well as a comparison of distributions between groups of infants. The reference values and charts presented here have two major advantages over the current Swedish ones: the sample size used is now sufficiently large at the lower gestational ages, so that empirically found variations can be used, and the skewness of the birth weight distribution has been taken into account. The use of the reference standards presented here improves and facilitates evaluation of size deviation at birth.

The strategy for evaluating quality of life in clinical trials is an important and complex issue. By comparing the performance of different quality-of-life measures before and after estrogen replacement therapy, it was shown that disease-specific measures had obvious advantages. Although narrow in applicability to the particular patient group, they were the most responsive measures in detecting small, clinically important changes. In clinical trials more attention should be given to how side effects, which often have important implications with regard to quality-of-life, are recorded.

Although there are some Swedish studies giving reference values for height and weight in adulthood, no values of weight for height (W/H) are available. W/H is an essential measurement, as it permits comparison of weight independent of the height of an individual. We here present a method of constructing W/H standards, illustrated by a material sample of 4438 healthy individuals, 20–80 years of age, living in the Uppsala County during the period 1964–1971. In setting standards of W/H, the ‘normal’ increase in weight during adulthood and the distribution skewness of weight are both shown to be important. This weight gain starts at about 40 years of age, and is completed at approximately 55 years of age. It can be regarded as a ‘normal’ pattern, but not necessarily the optimum healthy one. Using ordinary growth charts for weight and height, a simple means of expressing W/H in standard deviation scores is outlined. It is difficult to find a representative Swedish sample, owing to geographical and psychosocial differences, and also to the secular trend phenomenon. However, the mean values for weight and height obtained in the present study fall between the mean values of two other recently conducted Swedish studies.