Subischial Leg Length Research Articles

Predictive factors in the determination of final height in boys with constitutional delay of growth and puberty

Seventy-eight patients who had constitutional delay of growth and puberty were included in a retrospective study to determine whether, at the time of first evaluation, any predictive features could suggest final height outcome. Mean chronologic age was 14.3 years (range, 12 to 18 years), and all were either prepubertal or in an early stage of pubertal maturation (4 ml testicular volume). Initial mean (±SD) height standard deviation score was −:2.74 (±0.71); 85% had a relatively short spine compared with subischial leg length. Mean (±SD) growth rate was 4.8 (±1.6) cm/year, and epiphyseal maturation was delayed by 2.4 (±1) years. Sixteen boys were treated with a sustained-action preparation of testosterone (50 mg monthly for 3 to 4 months), six with oxandrolone (1.25 mg daily for a mean of 4 months), and one with both drugs in sequence. At final height attainment, 58% of the boys failed to achieve their full genetic potential; among the remaining 42%, only 0.7% attained a final height above corrected mid-parental height. The relative disproportion between the segments had no significant change at final height attainment. Regression analysis showed that final height impairment (the difference between mid-parental height and final height) was negatively influenced by standing height and growth velocity when initially evaluated and positively by the degree of segmental body proportion; that is, patients who were taller, were growing at a faster rate, and who had a major degree of segmental body disproportion with a short spine and long leg length attained a final height closer to their mid-parental height, irrespective of the degree of delayed epiphyseal maturation. Neither testosterone nor oxandrolone administered during early puberty modified final height attainment or segmental proportion. We conclude that a late onset in the timing of puberty seems to be deleterious to spinal growth and consequently to final height attainment. An alternative diagnosis should be sought among patients with features of constitutional delay of growth and puberty who do not have a significant degree of body disproportion. In these patients, as well as in those who are extremely short, who have a poor growth rate, or who have an unfavorable genetic potential, an alternative therapeutic approach may be required. ( J PEDIATR 1995;126:545-50)

Growth of sitting height, subischial leg length and weight in well-off northwestern Indian children.

This paper reports attained means and tempo unconditional 1-year velocities of sitting height, subischial leg length and weight of well-off northwestern Indians based on two time measurements taken by the same measurer. A 3-year difference is observed in reaching the peak sitting height velocity between girls (11 years) and boys (14 years) as in their peak height velocity. While in girls the peak subischial leg length velocity is reached a year earlier, at 10 years, than that of their peak sitting height velocity, in boys it is reached at the same time as in sitting height (14 years). Comparisons of the attained means with the British standards show that while sitting height is shorter throughout in the Indians, the subischial leg length is longer until 12 years in girls and 14 years in boys, after which it becomes equal to that of the British. This differential growth of the two segments comprising stature produces shorter adult height. Though the weight velocities are not dissimilar, the Indian children are lighter throughout. This body shape and size, with relatively longer legs, is a useful adaptation to the northwestern Indian climate.

Treatment of growth delay in boys with isolated growth hormone deficiency

We report our experience in treating growth delay in boys with isolated growth hormone deficiency (IGHD) receiving biosynthetic human growth hormone. The study was performed in 15 boys with IGHD receiving GH. At the chronological age of 13.1 (1.1) years (SD), 13 were prepubertal, two were in early puberty and there was a mean bone age delay of 2.5 (1.4) years. A growth spurt was induced by either depot testosterone or oxandrolone. There was an increase in growth rate from 5.7 (1.6) cm/year, occurring the year before anabolic or sex steroid therapy, to 8.1 (1.2) cm/year during treatment (p < 0.05), followed by 7.3 (1.9) cm/year the year after the cessation of treatment (p < 0.05). There was no significant change in height SD score for bone age, which was -0.69 (0.97) at the commencement of anabolic or sex steroid therapy and -0.53 (0.84) at the end of treatment. Before the induced growth spurt, there was equal body proportion between sitting height and subischial leg length, which had no significant change following androgen treatment. Spontaneous progress in pubertal development was achieved by all patients with an increase in testicular volume from a mean of 2.9 (2-8) to 6.1 (4-10) ml. The pattern of growth presented by patients treated with oxandrolone or those with testosterone was similar. Our data suggest that growth delay and delayed puberty, in patients with IGHD during concomitant growth hormone therapy, can be treated without deterioration in height prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Pubertal growth in response to testosterone replacement therapy for radiation-induced Leydig cell failure.

The adolescent growth pattern of eight boys, who had puberty induced with androgen replacement therapy following radiation-induced Leydig cell failure, was studied from induction of puberty at a mean age of 13.1 years (range 11.6-14.5) to final height at mean age of 18.8 years (range 17.7-20.3). The mean gains during puberty (SD) for standing height, sitting height, and sub-ischial leg length were 18.56 cm (3.98), 10.46 cm (2.39), and 8.1 cm (2.01) respectively, which were significantly reduced compared with normal Tanner standards (P < .001). The peak velocity for each parameter occurred in the 1st year of induced puberty in contrast to the pattern in normal adolescence, although the mean peak velocity for each auxological parameter was not significantly different from the normal Tanner standards. The mean adult standing height (SD), 167.5 cm (9.88), and mean adult leg length (SD), 80.8 cm (6.19), were not significantly different from the normal Tanner standards, whereas the mean adult sitting height (SD), 86.7 cm (4.78), was shorter (P < .001). Three of the eight patients had a leg length standard deviation score less sitting height standard deviation score in excess of +2.96 suggesting the presence of significant skeletal disproportion. Seven of the eight boys reached target genetic height, though in six, the final height was below mid-parental height (P < .05). The modest loss in height potential was mainly due to radiation-induced skeletal dysplasia attenuating the growth of the spine. The families of boys with radiation-induced Leydig cell failure requiring androgen replacement therapy can be reasonably optimistic about height prognosis as seven of the eight boys reached target genetic height.

Body Proportions of the Infant

Growth is usually evaluated by single measurements which reflect only that direction of growth. At birth the relationship between measurements is often considered as Rohrer's Ponderal index which describes weight in relation to length but can be misleading especially when considering premature infants. We propose that it is more appropriate to study the relationship of different anthropometric measurements to define normality and thereby create limits from which abnormalities in growth may be diagnosed. Weight, crown heel length, crown rump length and head circumference were measured in 305 healthy infants, at 26 42 gestational weeks to obtain reference values. Subischial leg length was calculated. A multivariate model was made which could be useful to distinguish the form and shape of an infant and to identify abnormalities in growth.

Growth following single fraction and fractionated total body irradiation for bone marrow transplantation.

Total body irradiation (TBI) is used as preparative regimen prior to bone marrow transplantation (BMT). Since there are more long-term survivors, follow up studies are important. We have performed a retrospective analysis of growth for 49 children, who had undergone treatment with cyclophosphamide and TBI before BMT. Of these patients 26 received single fraction (SF) TBI as a dose of 900-1000 cGy, whereas 23 received fractionated (FF) TBI as a total dose of either 1200 cGy divided in six fractions or 1440 cGy divided in eight fractions over 3 days. Half of the patients in the SF-TBI group, and 9 in the FF-TBI group had received low-dose cranial irradiation prior to TBI. In all groups a decrease in height SDS was observed. By evaluating the major factors leading to growth impairment the influence of cranial irradiation, which was demonstrable in the 1st year after TBI, could not be shown after 3 years. At this time growth was significantly more impaired in the SF group with a mean height SDS of -0.9 (+/- SD 0.9) compared to a mean height SDS -0.22 (1.02) in the FF group (P < 0.05). Measurement of segmental proportions showed a significant difference in SDS for sitting height in comparison to SDS for subischial leg length, irrespective of the TBI regimen. This was already evident 1 year after TBI and decreased during the following years. Twenty four of the patients (17 in the single fraction and 7 in the fractionated TBI group) were treated with growth hormone, but demonstrated an inappropriate response with absent catch-up growth in their legs.(ABSTRACT TRUNCATED AT 250 WORDS)

SHORT STATURE IN HOMOZYGOUS β-THALASSEMIA IS DUE TO DISPROPORTIONATE TRUNCAL SHORTENING

OBJECTIVE: To determine by measuring sitting and standing height, whether growth failure in homozygous β-thalassemia is disproportionate. METHODS: Management of all patients with homozygous β-thalassemia in the State of Victoria (Australia) is centralised to one major teaching hospital; therefore treatment protocols are relatively standardised, and this group represents a population based cohort. Patients are transfused every 3-4 weeks to maintain hemoglobin values >10 g%, and desferrioxamine 60mg/kg/d, to a maximum of 3g/day, is given S.C. for iron chelation. Measurements were made using Holtain sitting and Harpendon standing stadiometers, in a random sample of 52 of 122 (43%) patients to date. Subischial leg length was determined by subtraction of sitting height from standing height. Standard deviation scores (sds) were used to enable comparisons irrespective of chronological age, and the patient group was analysed according to age: group 1 - 18y.o., n=10). Sitting height was significantly different from subischial leg length in both sexes and both age groups (p<0.0001) - subischial leg length was −0.1±1.5 sds (males <18 y.o., n=19), −0.5±1.1 sds (females<18y.o., n=13); 0.9±1.3 sds (males ≥18 y.o., n=10), 0.2±1.1 sds (females ≥18y.o., n=10). CONCLUSION: Short stature is mainly due to truncal shortening in this patient group. Hypogonadism and chelation therapy are possible etiological factors.

INTRAUTERINE GROWTH RETARDATION: HOW TO DEFINK IT

Intrauterine growth retardation (IUGR) is generally defined by birthweight below the P3. However, weight can be affected in the last weeks of pregnancy without necessarily reflecting prolonged impairment in intrauterine growth. Early in pregnancy growth is affected proportionatly and the term “intrauterine growth retardation” seems more appropritate. In an attempt to clarify this we assumed that by taking into account the proportions of the infant independent of weight, we could be able to define intrauterine growth better. Crown-rump length, subischial leg length and head circumference were measured and the proportion in a three dimensional way was studied in 49 infants with a birthweight below the third percentile.There was no correlation between the Ponderal Index and the P-score of the body proportions, nor for birthweight and P-score.These preliminary results indicate that the body proportion could be a more appropriate indication of IUGR than weight or than the relation weight to height (Ponderal index).

GROWTH OF CHILDREN AFTER LIVER TRANSPLANTATION (LT): LONGITUDINAL AND CROSS-SECTIONAL STUDY

Aims: to study the growth of children with liver disease before and after LT.Methods: longitudinal study (LS): 16 infants (9 M. 7 F); age 0.73 to 2.38 years (X 1.39) at LT; mean height (Ht) SDS at LT: −2.02 (SD 1.25). Post-LT medication: cyclosporine in tapering doses; prednisone, by daily regimen (DP) for the first 6-12 months, with tapering doses depending on clinical course, then on alternate day regimen (ADP). Cross-sectional study (CSS): 95 children (55 M. 40 F) aged 0.17 to 14.88 (X 3.83), observed before LT, after LT on DP, and on ADP (same medication).Results: LS: pre-LT height velocity (HV) SDS (x±SD −0.60±1.31) significantly lower (p<0.01) than ADP-HVSDS (2.84±1.59) but not significantly different from DP-HVSDS (−1.37±1.66). CSS: DP-HtSDS (X±SD −1.9±1.32) significantly lower (p<0.01) than pre-LT-HtSDS (−1.07±1.06) and ADP-HtSDS (−0.98±1.23). Similar results for sitting height (SH) SDS and subischial leg length (SLL) SDS: pre-LT and ADP-SLLSDS significantly greater than pre-LT and ADP-SHSDS (p=0.01); DP-SLLSDS not significantly different from DP-SHSDS. Significant improvement of head circumpherencc SDS and skinfold SDS on ADP.Conclusions: growth in children with liver disease does not improve after LT on DP while shows catch-up growth on ADP; therefore, it mainly depends on clinical course and cortieosteroid regimen.

Does constitutional delayed puberty cause segmental disproportion and short stature?

We have reviewed the growth of 98 boys and 34 girls with constitutional delay of growth and puberty followed until final height. At presentation chronological age was 14.1 (1.3) years (SD) in the boys and 13.0 (1.3) years in the girls. At presentation all patients were either prepubertal or in early pubertal maturation (4 ml testicular volume in the boys and breast stage II in the girls). Twenty-nine boys (30%) and 2 girls (6%) were treated with either sex or anabolic steroids. Mean height SDS in the boys at presentation was -2.7 (0.7) which rose to -1.9 (0.9) at final height attainment. This was significantly lower than the predicted final height SDS of -1.4 (0.8) and mid-parental height SDS of -0.5 (0.7). Similar results were obtained for the girls with a height SDS at presentation of -3.2 (0.8) which increased to -2.3 (0.7) at final height which was significantly lower than predicted final height SDS of -1.7 (0.6) and mid-parental height SDS of -0.8 (0.8). Both sexes had a relatively short sitting height at presentation; sitting height SDS -3.4 (1.0) and subischial leg length SDS -2.2 (1.0) in the boys and sitting height SDS -3.6 (1.1) and subischial leg length SDS -2.5 (0.7) in the girls. The relative disproportion between the segments had no significant change at final height. We are unable to explain the failure to achieve final height potential and the relatively disproportionate stature. Our data suggest that the late timing of the onset of puberty may be deleterious to spinal growth and consequently final height.(ABSTRACT TRUNCATED AT 250 WORDS)

The evolution of spinal growth after irradiation

Spinal growth has been monitored in 13 children treated with craniospinal irradiation for brain tumours. Six were irradiated prepubertally and seven peripubertally, all with 30 Gy to the whole spine over four weeks. The change in (subis-chial leg length (SILL) — sitting height (SH)) standard deviation score (SDS) was used as an index of disproportionate segmental growth, which allowed the influence of growth hormone deficiency on growth to be discounted. Spinal growth over the prepubertal years was relatively normal: annual change in (SILL-SH) SDS was +0.07 SD 0.2. However, over puberty, annual change in (SILL-SH) SDS had increased significantly to +0.41 SD 0.14 ( P = 0.03). If irradiated peripubertally, annual change in (SILL-SH) SDS to final height was +0.22 SD 0.23, not significantly different from the change over puberty in the prepubertal group. Relatively normal spinal growth after irradiation in the prepubertal child should be interpreted with caution, as it is during puberty that skeletal disproportion manifests itself.

Growth hormone treatment of growth failure secondary to total body irradiation and bone marrow transplantation.

Growth hormone was given to 13 children (nine boys, four girls) with acute leukaemia who had undergone treatment with cyclophosphamide and total body irradiation before bone marrow transplantation. Mean age at total body irradiation and bone marrow transplantation was 9.0 years (range 3.7-15.8). Endocrinological investigation was carried out at a mean of 2.0 years (range 0.4-4.0) after bone marrow transplantation. Peak serum growth hormone responses to hypoglycaemia were less than 10.0 micrograms/l (less than 20.0 mU/l) in 10, 10.5 micrograms/l (21.0 mU/l) in one, greater than 16.0 micrograms/l (greater than 32.0 mU/l) in two patients. Mean age of the patients at the start of growth hormone treatment was 12.2 years (range 5.8-18.2). The mean time between total body irradiation and bone marrow transplantation and the start of growth hormone treatment was 3.2 years (range, 1.1-5.0). Height velocity SD score (SD) increased from a mean pretreatment value of -1.27 (0.65) to + 0.22 (0.81) in the first year, +0.16 (1.11) in the second year, and +0.42 (0.71) in the third year of treatment. Height SD score (SD) changed only slightly from -1.52 (0.42) to -1.50 (0.47) in the first year, to -1.50 (0.46) in the second year, and -1.74 (0.92) in the third year. Measurement of segmental proportions showed no significant increase in subischial leg length from -0.87 (0.67) to -0.63 (0.65) in the first year, to -0.58 (0.70) in the second year, and -0.80 (1.14) in the third year of treatment. Our data indicate that children who have undergone total body irradiation and bone marrow transplantation respond to treatment with growth hormone in either of two dose regimens, with an increase in height velocity that is adequate to restore a normal growth rate but not to 'catch up', and that total body irradiation impairs not only spinal but also leg growth, possibly by a direct effect of irradiation on the epiphyses and soft tissues.

Growth characteristics and response to growth hormone therapy in patients with hypochondroplasia: genetic linkage of the insulin‐like growth factor I gene at chromosome 12q23 to the disease in a subgroup of these patients

Hypochondroplasia, a heterogeneous and usually mild form of chondrodystrophy, is a common cause of short stature. It often goes unrecognized in childhood and is diagnosed in adult life when disproportionate short stature becomes obvious. We performed restriction enzyme analysis of the insulin-like growth factor I (IGF-I) gene on the families of 20 white British Caucasian children with short stature attributed to hypochondroplasia by radiological and clinical criteria, who were undergoing human growth hormone (r-hGH) treatment, in 60 children with isolated growth hormone deficiency and in 50 normal individuals. The frequency of the heterozygous pattern (Hind III: 8.2, 5.2, 4.8, 3.2 kb fragments, Pvu: 8.4, 5.1, 4.7, 2.5 kb fragments) in children with hypochondroplasia was significantly higher (chi2: P less than 0.05) than in the control groups. The hypochondroplastic children whose response to r-hGH treatment was characterized by a proportionate increase in both spinal and subischial leg length were all heterozygous for two co-inherited IGF-I gene restriction fragment length polymorphism (RFLP) alleles (Hind III: 5.2, 4.8 kb; Pvu II: 5.1, 4.7 kb). Children whose response was characterized by accentuation of the body disproportion by r-hGH treatment were all homozygous for these alleles (Hind III: 4.8, 4.8 kb; Pvu II: 4.7, 4.7 kb). Their response to r-hGH treatment is significantly different (P less than 0.01). Studies of the families of the heterozygous affected children demonstrated strong linkage (lod score 3.311 at zero recombination) of the IGF-I gene locus at chromosome 12q23 to this subgroup of hypochondroplasia. The 5.2 kb Hind III and 5.1 kb Pvu II alleles are in strong linkage disequilibrium with this trait. These data indicate that IGF-I gene may be a candidate gene for involvement in the aetiology of short stature presenting with hypochondroplastic features and a proportionate response to r-hGH treatment; they also provide support for the concept of genetic heterogeneity in chondrodystrophy.

Growth and Growth Hormone Therapy in Hypochondroplasia

The growth of 84 patients with hypochondroplasia (56 male, 28 female) was studied. A wide spectrum of severity was found from quite severe short limbed dwarfism to short apparently normal prepubertal children who manifested disproportion only at puberty when growth failed. The onset of puberty was at the normal time but the pubertal growth spurt appeared not to materialize and it is this lack which resulted in severely compromised adult heights of 145-165 cm in boys and 133-151 cm in girls. Twenty (12 M, 8 F) hypochondroplastic children aged between 4.3 and 12.8 years were recruited to a study of the effects of biosynthetic growth hormone. All had normal growth hormone responses (greater than 15 mU/l) to a pharmacological test of growth hormone secretion. Biosynthetic growth hormone in doses between 12-32 mu/m2/week produced a significant acceleration in height velocity standard deviation score (SDS) for chronological age (CA) from a pretreatment mean of -1.66 (SD 1.36) to +1.62 (SD 1.52) (p less than 0.001). Significant increases were also observed in the height SDS for bone age (BA), sitting height (SH) SDS and subischial leg length (SILL) SDS. A longer period will be required to assess the effect of treatment on adult height prognosis.

Effect of abdominal irradiation on growth in boys treated for a wilms′ tumor

To study the effect of abdominal irradiation on spinal growth in childhood we have measured final height, sitting height, and leg length in 30 male survivors of a Wilms' tumor. Twenty-one patients received whole abdominal irradiation by either megavoltage therapy (MV: n = 11) or orthovoltage therapy (OV: n = 10); the remainder received flank irradiation. To examine the effect of the adolescent growth spurt on the irradiated spine we have followed prospectively seven patients who received whole abdominal irradiation and nine patients who received flank irradiation through puberty. Compared to a normal population there is a modest reduction in median final standing height SDS (H.SDS: -1.15) accompanied by a marked reduction in median final sitting height SDS (S.HT SDS: -2.41) with no apparent effect on median subischial leg length SDS (SILL.SDS: 0.04). This reduction in spinal growth is reflected by a strongly positive disproportion score (DPS; [SILL SDS-S.HT SDS] + 2.81). The incidence of scoliosis after abdominal irradiation has been low (10%). During puberty there is a significant fall in median sitting height SDS after both whole abdominal (median fall: -0.9, P = 0.02) and flank irradiation (median fall: -1.85, P = 0.01), and this is reflected in a significant increase in disproportion (DPS: whole abdominal; median rise +1.4, P = 0.02: flank, median rise +1.34, P = 0.01). After MV irradiation there is a significant correlation between the degree of disproportion and the age at treatment (P less than 0.0005). The younger the patient is at treatment the more severe is the restriction on spinal growth and the shorter and more disproportionate they become as an adult. The estimated eventual loss in potential height from abdominal irradiation at the age of one is 10 cm and at five years is 7 cm.

Growth and body proportions in congenital adrenal hyperplasia.

Total height, sitting height, and subischial leg length were measured in 27 patients (19 girls and eight boys aged 4.3-21.1 years) with congenital adrenal hyperplasia to determine the influence of chronic hyperandrogenaemia on body proportions. Proportions were normal in 24 patients with classical congenital adrenal hyperplasia who had received steroid treatment since birth, but one of three patients with non-classical (late onset) congenital adrenal hyperplasia had a disproportionately large trunk. Eleven patients with classical congenital adrenal hyperplasia had completed growth, of whom seven had height standard deviation (SD) scores for chronological age less than zero, and one had extremely short stature (SD score -3.25). In 13 patients who were still growing, nine had height SD scores for chronological age of less than zero despite having mean (SD) advances in bone age over chronological age of 1.64 (1.68) years. Height SD scores for bone age were less than 0 in all 13 patients, indicating a loss of height despite advanced skeletal maturation. Doses of glucocorticoid that permit mild chronic or intermittent hyperandrogenaemia also seem to be associated with mild growth retardation. An adult height below average may be an inevitable consequence for many patients with congenital adrenal hyperplasia receiving conventional glucocorticoid treatment.

155 BODY PROPORTIONS IN CONGENITAL ADRENAL HYPERPLASIA (CAH)

It has been proposed that testosterone-induced growth produces a disproportionate increase in trunk length. Since there is increased adrenal androgens in CAH from early fetal life which may continue intermittently postnatally, disproportionate growth might be expected. Body proportions were measured in 27 CAH patients (19F, 8M; 3 late-onset) aged 4-21 yr (CA) who had been treated with hydrocortisone 15-20 mg/m2/day in infancy and childhood, and dexamethasone 0.25 - 0.75 mg/day in later life. Bone age (BA) determined by the TW2 method was in advance of CA in all but one patient. Statural growth was complete in 9. Standard deviation scores (SDS) were calculated for sitting height (SH) and sub-ischial leg length (SLL). SH (SDS) and SLL (SDS) for CA were −0.47 ± 1.44 (mean ± SD) and −0.49 ± 1.10, respectively; when related to BA the scores were more negative (-1.32 ± 1.28 and −1.1 ± 1.19, respectively). The difference between the scores (SH (SDS) - SLL (SDS), equivalent to 0 in perfect proportion) was 0.01 ± 0.95 indicating normal body proportions. The exception was an untreated, late-onset girl whose SDS difference was +2.1, indicating disproportionate trunk growth. When stature is below normal in CAH, it is generally proportionate. Androgen-induced disproportionate growth only arises postnatally and after chronic androgen excess.

66 DEVELOPMENT OF A SOFTWARE PROGRAM PROVIDING A DATA BASE AND ENABLING MATHEMATICAL HANDLING AND GRAPHICAL PRESENTATION OF GROWTH DATA

A computer software program was developed aimed at three goals; to enable a retrospective or prospective analysis over one or more centers of the data proceeding from the diagnostic work-up and clinical follow-up of children with growth disturbances; 2: to transform the most common growth parameters as a function of the references for age and bone age; 3: to enable graphical representation of raw and transformed growth data. The database enables the storage and retrieval of administrative, clinical and laboratory data. Patients can be grouped into various study groups which all have their own specific data entry screens. In case of growth hormone therapy the weekly dosage per kg body weight and m2 body surface are calculated. The mathematical part expresses height, sitting height and subischial leg length as SDS for age and bone age. Weight is expressed as a percentage of the median for height. From bone age readings height predictions are calculated with the TW-2 and Greulich-Pyle method. Height velocities are calculated between chosen dates of observation and expressed as cm/year, SDS for age or bone age and as the change of height SDS per year. The transformed growth data can be further used in reference to various periods of growth hormone treatment. All raw and transformed growth data can be shown graphically. The software program works on a microcomputer with multicolor screen and a mathematical coprocessor, using dbase III+/Clipper.

Growth, growth hormone and sex steroid secretion in girls with central precocious puberty treated with a gonadotrophin releasing hormone (GnRH) analogue.

We have treated 14 girls with central precocious puberty for a mean period of 2.3 years (range, 0.5-3.9) with intranasal (D-Ser6) GnRH analogue administered in a mean dose of 28 micrograms/kg/day (range, 15-56). With the onset of treatment there was an initial increase in sitting height compared to subischial leg length, but overall there was no significant change in height standard deviation score for bone age. In this respect our results were indistinguishable from untreated children with central precocious puberty. There was a decrease in physiological GH secretion, associated with decreased sex steroid secretion, which probably accounts for the growth deceleration which has been described during GnRH analogue therapy. The effect of this growth deceleration combined with slowing of the rate of epiphyseal maturation may explain the absence of alteration in height prognosis.

Body segments and growth hormone.

The effects of human growth hormone treatment for five years on sitting height and subischial leg length of 35 prepubertal children with isolated growth hormone deficiency were investigated. Body segments reacted equally to treatment with human growth hormone; this is important when comparing the effect of growth hormone on the growth of children with skeletal dysplasias or after spinal irradiation.