Accuracy of self-reported height measurements in parents and its effect on mid-parental target height calculation

BACKGROUND: Clinical determination of mid-parental height is an important part of the assessment of a child's growth, however our clinical impression has been that parents cannot be relied upon to accurately report their own heights. Therefore, we conducted this study to assess the accuracy of parental height self-reporting and its effect on calculated mid-parental target height for children presenting to a pediatric endocrinology office. METHODS: All parents bringing their children for an initial evaluation to a pediatric endocrinology clinic over a period of nine months were questioned and then measured by a pediatric endocrinologist. Parents were blinded to the study. Mid-parental target heights, based on reported and actual height were compared. RESULTS: There were 241 families: 98 fathers and 217 mothers in our study. Mean measured paternal height was 173.2 cm, self reported 174.9 cm (p < 0.0001), partner reported 177 cm (p = 0.0004). Only 50% of fathers and 58% of mothers reported their height within ± 2 cm of their measured height, while 15% of fathers and 12% of mothers were inaccurate by more than 4 cm. Mean measured maternal height was 160.6 cm, self-reported 161.1 cm (NS), partner reported 161.7 cm (NS). Inaccuracy of height self-report had a small but significant effect on the mean MPTH (0.4 cm, p = 0.045). Analysis showed that only 70% of MPTH calculated by reported heights fell within ± 2 cm of MPTH calculated using measured heights, 24% being in ± 2–4 cm range, and 6% were inaccurate by more than 4 cm. CONCLUSION: There is a significant difference in paternal measured versus reported heights with an overall trend for fathers to overestimate their own height. A large subset of parents makes a substantial error in their height self-report, which leads to erroneous MPTH. Inaccuracy is even greater when one parent reports the other parent's height. When a child's growth is in question, measured rather than reported parental heights should be obtained

Prevention of Vitamin D deficiency in infancy: daily 400 IU vitamin D is sufficient

<p>Summary</p> <p>Aim-objective</p> <p>Vitamin D deficiency and rickets in developing countries continues to be a major health problem. Additionally, the increase of cases of rickets in children of some ethnic groups in the United States and European countries has provided this issue to be updated. Obviously, powerful strategies are necessary to prevent vitamin D deficiency nation-wide. In 2005, a nationwide prevention program for vitamin D deficiency was initiated, recommending 400 IU vitamin D per a day.</p> <p>This study was designed to evaluate the efficacy of the prevention program.</p> <p>Methods</p> <p>Eighty-five infants who were recalled as part of the national screening program for congenital hypothyroidism between February 2010 and August 2010 at Kocaeli University Children's Hospital were evaluated in terms of their vitamin D status as well. All babies had been provided with free vitamin D (Cholecalciferol) solution and recommended to receive 400 IU (3 drops) daily. Information regarding the age at start of supplementation, the dosage and compliance were obtained from the mothers with face-to-face interview. Serum 25-hydroxy vitamin D (25-OH-D), alkaline phosphatase (AP), parathormone (PTH) levels were measured.</p> <p>Results</p> <p>The mean age at which Vitamin D3 supplementation began was 16.5 ± 20.7 (3-120) days. Ninety percent of cases (n:76) were receiving 3 drops (400 IU) vitamin D3 per day as recommended; 70% of cases (n:59) were given vitamin D3 regularly, the remainder had imperfect compliance. Among those children who are older than 12 months, only 20% continued vitamin D supplementation. No subject had clinical signs of rickets. The mean 25-OH-D level was 42,5 ± 25,8 (median: 38.3) ng/ml. Ten subjects (12%) had their serum 25-OH-D levels lower than 20 ng/ml (6 between 15-20 ng/ml, 3 between 5-15 ng/ml and only one < 5 ng/ml).</p> <p>Conclusions</p> <p>400 U/day vitamin D seems adequate to prevent vitamin D deficiency. However, we believe that the program for preventing vitamin D deficiency in Turkey, needs to be reinforced to start immediately after birth, and to continue beyond 1 year of age at 400U regular daily dosage.</p

Systematic genetic testing for recessively inherited monogenic diabetes: a cross-sectional study in paediatric diabetes clinics

Data availability: The datasets supporting the current study have not been deposited in a public repository due to institutional ethics restrictions but are available from the corresponding author on request.This is the final version. Available from Springer via the DOI in this record. AIMS/HYPOTHESIS: Current clinical guidelines for childhood-onset monogenic diabetes outside infancy are mainly focused on identifying and testing for dominantly inherited, predominantly MODY genes. There are no systematic studies of the recessively inherited causes of monogenic diabetes that are likely to be more common in populations with high rates of consanguinity. We aimed to determine the contribution of recessive causes of monogenic diabetes in paediatric diabetes clinics and to identify clinical criteria by which to select individuals for recessive monogenic diabetes testing. METHODS: We conducted a cross-sectional study of 1093 children from seven paediatric diabetes clinics across Turkey (a population with high rates of consanguinity). We undertook genetic testing of 50 known dominant and recessive causes of monogenic diabetes for 236 children at low risk of type 1 diabetes. As a comparison, we used monogenic diabetes cases from UK paediatric diabetes clinics (a population with low rates of consanguinity). RESULTS: Thirty-four children in the Turkish cohort had monogenic diabetes, equating to a minimal prevalence of 3.1%, similar to that in the UK cohort (p = 0.40). Forty-one per cent (14/34) had autosomal recessive causes in contrast to 1.6% (2/122) in the UK monogenic diabetes cohort (p 10%) assisted the identification of the dominant (all p ≤ 0.0003) but not recessive cases (all p ≥ 0.2) in Turkey. The presence of certain non-autoimmune extra-pancreatic features greatly assisted the identification of recessive (p < 0.0001, OR 66.9) but not dominant cases. CONCLUSIONS/INTERPRETATION: Recessively inherited mutations are a common cause of monogenic diabetes in populations with high rates of consanguinity. Present MODY-focused genetic testing strategies do not identify affected individuals. To detect all cases of monogenic paediatric diabetes, it is crucial that recessive genes are included in genetic panels and that children are selected for testing if they have certain non-autoimmune extra-pancreatic features in addition to current criteria.Wellcome TrustRoyal SocietyNational Institute for Health Researc

Measured versus reported parental height

Parental height data are essential in the assessment of linear growth in children. A number of studies have documented inaccuracy in self-reported adult height. Two hundred parents (100 males; 100 females), mean (range) age 37.8 (20.8-69.3) years, were measured. Males overestimated height, with mean (SD) RHt-MHt 1.09 (1.96) cm, while females reported height relatively accurately, with RHt-MHt -0.09 (2.37) cm. The hypothesis that males overestimate height is confirmed. While the hypothesis that women underestimate is not supported, we recommend accurate measurement of both parents, given the considerable degree of individual variation in RHt-MHt for both sexes

Association of Adiponectin, Resistin and High Sensitive CRP Level with the Metabolic Syndrome in Childhood and Adolescence

Early markers are required in pathophysiological process of obesity, MS and type 2 diabetes. We aimed to clarify the usefulness of serum adipokines (adiponectin, AD and resistin) and inflammatory markers to identify obese and overweight children with MS. Three hundred and seven of 2491 subjects aged 11-19 with BMI >= 85 centile selected with a multistage, stratified sampling were included. Their height, weight and waist circumference were measured, all subjects underwent physical examination and standard OGTT. AD, resistin and hs-CRP were measured from baseline blood sample. The mean age of subjects was 14.2 +/- 1.8, 57.7% was girl (n=177) and 42.3% (n=130) boy. Of the 307 subjects 40 (13%) were classified as having MS. Serum AD levels were significantly lower in boys (p = 0.02), and decreased while BMI increased, but this trend was not significant (p>0.05). Although median resistin values were higher in obese than others (20, 18.5, 17ng/ml, respectively) it was not significant (p>0.05). In obese subjects, hs-CRP levels were significantly high (0.21 mg/L)(p=0.000). All three markers in obese and overweight children with and without MS were not significant (p>0.05). Girls with MS had lower adiponectin levels than those without MS. Waist circumference had the highest sensitivity and specificity for predicting MS in ROC analysis. The area under the curve (AUC) was 0.831 for WC standard error (SE) 0.033; 95% CI 0.767-0.896; p<0.0001. But the AUCs for the adiponectin, resistin, hs-CRP were not significant. In this study, we observed that adipokines or inflammatory markers have no predictive value in the diagnosis of MS. We concluded that the best marker for MS diagnosis is the measurement of waist circumference

Evaluation and Treatment Results of Ovarian Cysts in Childhood and Adolescence: A Multicenter, Retrospective Study of 100 Patients

PMID = 2816713