Background: Traditionally, measurement of plasma IGF-I and more recently of IGFBP-3 are used to distinguish GHD from idiopathic short stature in slowly growing children, using a single blood sample. In earlier studies it was claimed that IGFBP-3 was superior to IGF-I, but more recently doubts around this claim have arisen. The role of serum IGF-II has never been studied extensively. On theoretical grounds, it can also be hypothesized that molar ratios of these peptides might be of additional value. Design: Retrospective, multicentre, cohort study. Patients: 96 children evaluated for short stature. Methods: Serum IGF-I, IGF-II, IGFBP-3 and various molar ratios were, after correction for age and sex using SD scores, compared to the maximum serum GH peak after two standard provocation tests using four different methods (t-test, χ², likelihood ratios and ROC curves). In addition, the correlations between these parameters and the short-term (1 year) and long-term (3 years) response to GH therapy were calculated. Results: IGF-I performed better than IGFBP-3, but the best results were achieved by the molar ratio IGF-I:IGF-II. However, IGFBP-3 correlated better with the short-term response to GH therapy than IGF-I or the ratios, and none of the parameters investigated was found to be related to the response of long-term GH therapy.

Objective-To study the resumption of puberty and the final height achieved in children with central precocious puberty (CPP) treated with the GnRH agonist triptorelin. Patients-31 girls and five boys with CPP who were treated with triptorelin 3.75 mg intramuscularly every four weeks. Girls were treated for a mean (SD) of 3.4 (1.0) years and were foliowed up for 4.0 (1.2) years after the treatment was stopped. Results-The rate of bone maturation decreased during treatment and the predicted adult height increased from 158.2 (7.4) cm to 163.9 (7.5) cm at the end of treatment (p<0.001). When treatment was stopped bone maturation accelerated, resulting in a final height of 161.6 (7.0) cm, which was higher than the predicted adult height at the start of treatment (p<0.001). Height at the start of treatment was the most important factor positively influencing final height (r = 0.75, p<0.001). Bone age at cessation of treatment negatively influenced final height (r = -0.52, p = 0.03). A negative correlation between bone age and height increment after discontinuation of treatment was observed (r = -0.85, p = 0.001). Residual growth capacity was optimal when bone age on cessation of treatment was 12 to 12.5 years. Body mass index increased during treatment and remained high on cessation. At final height, the ratio of sitting height to subischial leg length was normal. Menarche occurred at 12.3 (1.1) years, and at a median (range) of 1.1 (0.4 to 2.6) years after treatment was stopped. The ovaries were normal on pelvic ultrasonography. Conclusions-Treatment of CPP with triptorelin increases final height, with normal body proportions, and seems to increase body mass index. The best results were achieved in girls who were taller at the start of treatment. Puberty was resumed after treatment, without the occurrence of polycystic ovaries.(Arch Dis Child 1996;75:292-297)

A poor preoperative MUCP seems to be an important prognostic factor for persistent incontinence after RRP. Non-nerve sparing approach seems to be an important prognostic factor for impairment of the urethral sphincter function as measured by UPP. More intensive physiotherapy seems to have no additional effect on the postoperative urethral sphincter function as measured by UPP.

Study Type – Therapy (RCT)
Level of Evidence 1b OBJECTIVE To compare the effect on the recovery of incontinence after retropubic radical prostatectomy (RRP) of intensive physiotherapist‐guided pelvic floor muscle exercises (PG‐PFME) in addition to an information folder, with PFME explained to patients by an information folder only (F‐PFME), and to determine independent predictors of failure to regain continence after RRP. PATIENTS AND METHODS We postulated that a 10% increase in the proportion of men who regained continence at 6 months with PG‐PFME compared with men treated with F‐PFME only would constitute a clinically relevant effect. To show statistical significance of this difference with a power of 80%, 96 men should be randomized to each of the two arms. One day before operation, all patients received verbal instruction and an information folder on PFME. Patients randomized to the F‐PFME arm received no further physiotherapist guidance, whereas those in the PG‐PFME arm received a maximum of nine sessions with the physiotherapist. The men underwent a 1‐h pad‐test at 1, 12 and 26 weeks, and a 24‐h pad‐test at 1, 4, 8, 12 and 26 weeks after catheter removal. We defined ‘continence’ as urine loss of <1 g at the 1‐h and <4 g at the 24‐h pad‐test. RESULTS During the 2‐year recruitment period, the number of patients randomized fell short of the target determined by the sample size calculation, because of limitations of resources and unexpected changes in treatment preferences. Despite this, we analysed the data. Of the 82 randomized patients, 70 completed the study. Of these, 34 and 36 men had been assigned to the PG‐PFME and the F‐PFME group, respectively. At 6 months after RRP, 10 (30%) and nine (27%) men were completely dry on both the 1‐h and 24‐h pad‐test in the PG‐PFME and the F‐PFME group, respectively (difference not significant). In a multivariate analysis the amount of urine loss at 1 week after catheter removal seemed to be an independent prognostic factor for failure to regain continence. CONCLUSION PG‐PFME seems to have no beneficial effect on the recovery of continence within the first 6 months after RRP, over an instruction folder‐guided approach. However, due to under‐powering there is a high risk of type II error. Nevertheless, these findings add to the knowledge base for availability in meta‐analyses and can serve as a starting point for the design of new randomized studies.

Isolated idiopathic growth hormone deficiency (GHD) and idiopathic short stature (ISS) can be difficult to distinguish, but the therapeutical consequences are different. In this report the data on final height of untreated and treated children with GHD and ISS are reviewed. Untreated GH-deficient individuals who underwent spontaneous puberty (22 male, 14 female patients) reached a mean final height of 4.7 SD (range 3.9 to 6.0) below the population's mean. If puberty was induced (19 male patients), mean final height SD score (SDS) was -3.1. Traditional regimens of GH administration (2-4 injections/wk) in 236 children (184 boys, 52 girls) with GHD and spontaneous puberty resulted in a final height SDS of -2.8 (range -1.5 to -4.7). In 190 children in whom puberty was induced (139 boys, 51 girls) mean final height was -1.6 (range - -1.1 to -2.4). The mean gain in final height SDS is therefore estimated at 1.5-2.0 in average cases, and 3.5 in extreme cases. Preliminary data suggest that on present regimens mean final height may approach target height. In untreated boys with ISS the mean final height was 2-5 cm lower than that predicted before puberty, whereas in girls it was almost equal to the prediction. After GH treatment the mean final height was 0.4-3.0 cm higher than the predicted adult height, which results in an average net gain in final height SDS of approximately 0.5-0.8 (3-5 cm).

The use of (costly) growth hormone (GH) treatment in short children is often justified by the assumption that short stature considerably reduces quality of life in adults. We tested this assumption in 5 groups of short adults: 25 patients with isolated GH deficiency; 17 male patients with childhood onset renal failure; 25 women with Turner syndrome and 26 patients who were presented as a child to a paediatrician for idiopathic short stature. A group of 44 short individuals with presumably idiopathic short stature, who had not been presented to a paediatrician for short stature, was sampled from the general population (‘normal shorts’). We measured quality of life in terms of socio-economic variables, the Nottingham Health Profile and time trade-off. The mean height of most groups was close to the 3rd percentile. The chance of having a partner was low for all groups, except for the normal shorts. Problems with job application were only reported in Turner syndrome. The scores on the Nottingham Health Profile were all within the normal range, but GH-deficient adults had a higher score on the domain energy than normal shorts. Women with Turner syndrome, individuals with renal failure, and those with idiopathic short stature had a wish to be taller, with an estimated reduction in quality of life of 2–4% (time trade-off). As the normal shorts did not show any sign of a reduced quality of life, we falsify the assumption of a direct relation between short stature and quality of life. The complaints of patients with idiopathic short stature around the 3rd percentile seem to be the result of unsuccessful coping strategies.

In univariate analysis, preoperative DOA is associated with a higher risk of remaining incontinent after surgery. However, in multivariate analysis, urodynamic parameters predictive of PRPI could not be identified. Therefore, standard preoperative filling cystometry and pressure-flow studies seem to have no role as preoperative predictors of PRPI in patients with localized prostate cancer. More intensive PFME might have a lowering effect on bladder outflow resistance after RRP.

In order to correct height velocities for the confounders age and sex, SD scores can be calculated using the mean and the SD of the height velocity in the normal population. However, current methods are inappropriate for prepubertal children in the age range in which puberty occurs, because reference groups then consist of a mixed prepubertal/ pubertal population. In the evaluation of growth disorders, height velocity is one of the main parameters by which we recognise abnormal growth and judge the impact oftherapeutic intervention. When groups of patients are studied, height velocity is usually expressed as SD score to remove the influences of age and sex. However, there is a serious methodological problem in using height velocity SD score for prepubertal children after the age at which children can start puberty. The reference population then consists of a changing mixture of prepubertal and pubertal children so that the mean height velocity of the whole cohort does not represent the mean of the prepubertal children. This also leads to a nonGaussian distribution. Therefore, mean and SD values for prepubertal children have been reported only up to the age of 8-75 years (boys) and 6-75 years (girls). ' To extend the age range, the best solution would be to measure height velocities in a large group of prepubertal, healthy, but relatively late maturing adolescents. However, no such data are available. To overcome this problem, in British studies the 50th centile from the whole cohort is used as mean and a hypothetical fixed SD (identical to the SD in late prepubertal years) is taken until the end of growth (CGD Brook and PC Hindmarsh, personal communication).2 However, the mixed prepubertal/ pubertal reference population gives an overestimation of the mean height velocity for prepubertal children. Others, including ourselves, have used height velocity SD scores for bone age by substituting bone age for chronological age, assuming that the mean height velocity for bone age in the population equals the height velocity for chronological age.3 This assumption is theoretically plausible for healthy children with an average bone maturation, but becomes unlikely for children with an extreme delay or advance of bone age. For example, in children with a delayed bone age the height velocity SD score for bone age is lower than the height velocity SD score for chronological age, due to the downward slope of the mean height velocity curve. Furthermore, no data are available about the SD values for height velocity for bone age.In this paper we present a new method of obtaining age references for height velocity during the whole period in which healthy children can remain prepubertal. MethodsAs basis for our model we adapted the infancychildhood-puberty (ICP) model.4 The reason for using this model is that it explicitly divides the total growth curve in a prepubertal and pubertal section. However, there are two disadvantages to using the ICP model in its present form as a reference model for height velocity.