To Örebro University

Aim: Skinfold measurement is an inexpensive and widely used technique for assessing the percentage of body fat (%BF). This study assessed the accuracy of prediction equations for %BF based on skinfold measurements compared to dual-energy X-ray absorptiometry (DXA) in girls with type 1 diabetes and healthy age-matched controls.

Methods: We included 49 healthy girls and 44 girls with diabetes aged 12 to 19 years old, comparing the predicted %BF based on skinfold measurements and the %BF values obtained by a Lunar DPX-L scanner. The agreement between the methods was assessed by using an Bland-Altman plot.

Results: The skinfold measurements were significantly higher in girls with diabetes (p=0.003) despite a non-significant difference in total %BF (p=0.1). A significant association between bias and %BF was found for all tested equations in the Bland-Altman plots. Regression analysis showed that the association between skinfold measurements and %BF measured by DXA differed significantly (p=0.039) between the girls with diabetes and the healthy controls.

Conclusion: The accuracy of skinfold thickness equations for assessment of %BF in adolescent girls with diabetes is poor in comparison with DXA measurements as criteron. Our findings highlight the need for the development of new prediction equations for girls with type 1 diabetes.

Background: Long-term stress leading to burnout symptoms is prevalent in parents of chronically ill children. The aim of the study was to evaluate the effect of a group intervention by measuring changes in self-rated clinical burnout and performance-based self-esteem. In addition, the parental perceptions of the acceptability of the intervention were explored.

Methods: Previously, we have explored the prevalence of clinical burnout in parents of patients 1–18 years with type 1 diabetes mellitus (T1DM) and inflammatory bowel disease (IBD) in the county of Örebro. All parents who exhibited clinical burnout symptoms in accordance with the Shirom–Melamed Burnout Questionnaire (SMBQ) were then invited to participate in a group intervention, which was evaluated in the present small-scale study. The group intervention consisted of eight sessions over a 12-week period, including education about behaviour, cognition and symptoms associated with burnout, intending to help the parents to develop adequate strategies for coping with and reducing stress. We evaluated the effect of the intervention in terms of self-rated clinical burnout and performance-based self-esteem (PBSE). In addition, the acceptability of the intervention was evaluated by analyses of recruitment and retention and self-reports from parents.

Results: Sixteen parents (13 of children with TIDM and three of children with IBD) out of 104 reporting clinical burnout participated in the intervention. All participants completed the intervention, and the mean attendance rate at all sessions was 90%. Parents’ subjective evaluations were mainly positive, and SMBQ (p = 0.01) and PBSE scale (p = 0.04) measurements were significantly reduced, which effects remained 6 months after completion of the intervention.

Conclusions: Despite the small-scale study, we consider that this intervention for parents with clinical burnout was appreciated and well accepted. The significant reduction in clinical burnout symptoms requires further evaluation in randomised controlled studies based on larger groups of parents.

Background: The nutritional and hormonal state in utero may be a link between maternal obesity and obesity in the offspring. The gene expression in placentae in pregnancies complicated by diabetes is reduced for leptin, but increased for ghrelin. It is not known whether these genes’ expressions in placentae are altered in maternal obesity.

Objectives and hypotheses: To compare obese and normal-weight women and their children concerning gene expressions of leptin and ghrelin in placentae; leptin, ghrelin, adiponectin, and C-peptide levels in cord blood, birth size and postnatal growth. Changes in the expression of these adipocytokines may lead to an altered hypothalamic sensitivity to leptin and ghrelin resulting in an increased risk of obesity in the offspring.

Method: 32 women with pre-pregnancy obesity, but otherwise healthy, were compared to 32 matched, normal-weight controls. Full-term placenta biopsies were analysed with qPCR for leptin mRNA and ghrelin mRNA. Cord blood samples were examined with ELISA for leptin, ghrelin, adiponectin, and C-peptide concentrations. Birth size and postnatal growth of the children were collected from clinical registers at the Child Health Care Units.

Results: The leptin and ghrelin gene expressions in placentae did not differ between obese and normal-weight women. The leptin concentration in cord blood was higher in children of obese mothers (P=0.021). It correlated with birth weight Z-score (r=0.467, P<0.001) and C-peptide level in cord blood (r=0.446, P<0.001). Children of obese women were slightly heavier at birth, but postnatal growth did not differ between groups. Children with birth weight  ≤−0.67 Z-score had higher ghrelin levels in cord blood than heavier children (P=0.042). The leptin level in cord blood correlated negatively with weight gain at 6 months (r=−0.332, P=0.009). The ghrelin level in cord blood correlated with weight gain at 3 months in girls (r=0.611, P=0.001), but not in boys. The adiponectin level in cord blood correlated negatively with length gain at 3 years in the obese group (r=−0.571, P=0.033), but not in the normal-weight group.

Conclusion: Leptin and ghrelin placental gene expressions are not altered in obese women, but foetal adipocytokine production may influence early postnatal growth, possibly by influencing hunger signalling or insulin levels

Objective: To survey the placental gene expression of inflammatory markers and growth factors in non-smoking obese women with an uncomplicated pregnancy without associated morbidity and delivery at term compared with normal weight women.

Methods: Placental tissue samples from 32 obese women (body mass index, BMI >= 35.0 kg/m(2)) were compared with samples from 94 normal weight women (BMI 18.5-25.0 kg/m(2)) matched for age (+/- 1 year), gestational age (+/- 3 days), parity and mode of delivery. Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to analyse toll receptor-2 and -4, interleukin-6 and -8, tumour necrosis factor-alpha, leptin, adiponectin, insulin-like growth factor-1 and -2, hepatocyte growth factor, hepatocyte growth factor receptor and insulin receptor.

Results: There was no significant difference in gene expression in placental tissue samples from obese and normal weight women.

Conclusion: We found no difference in the occurrence of inflammatory marker and growth factor mRNA levels in placental tissue samples from a large group of obese women without associated morbidity and with healthy infants compared to a closely matched control group of healthy normal weight women. Compared with the previous studies, this anomalous finding may be explained by the absence of associated morbidity in the obese women in our study.

Introduction: A randomized multicenter study was conducted in the Stockholm-orebro areas in Sweden to evaluate how treatment aiming at normoglycemia affects fetal growth, pregnancy and neonatal outcome in pregnant women with severe hyperglycemia.

Material and methods: Pregnant women with hyperglycemia defined as fasting capillary plasma glucose <7.0 mmol/L and a two-hour plasma glucose value 10.0 and <12.2 mmol/L following a 75-g oral glucose tolerance test (OGTT) diagnosed before 34 weeks of gestation were randomized to treatment (n=33) or controls (n=36). Women assigned to the control group were blinded for the OGTT results and received routine care. The therapeutic goal was fasting plasma glucose 4-5 mmol/L, and <6.5 mmol/L after a meal. Primary outcomes were size at birth and number of large-for-gestational age (>90th percentile) neonates. Secondary outcomes were pregnancy complications, neonatal morbidity and glycemic control.

Results: The planned number of participating women was not reached. There was a significantly reduced rate of large-for-gestational age neonates, 21 vs. 47%, P<0.05. Group differences in pregnancy complications and neonatal morbidity were not detected because of limited statistical power. In total, 66.7% of the women in the intervention group received insulin. Of all measured plasma glucose values, 64.1% were in the target range, 7.2% in the hypoglycemic range and 28.7% above target values. There were no cases of severe hypoglycemia.

Conclusions: Aiming for normalized glycemia in a pregnancy complicated by severe hyperglycemia reduces fetal growth but is associated with an increased rate of mild hypoglycemia.

Background/Aims: Growth hormone (GH) treatment regimens do not account for the pubertal increase in endogenous GH secretion. This study assessed whether increasing the GH dose and/or frequency of administration improves pubertal height gain and adult height (AH) in children with low GH secretion during stimulation tests, i. e. idiopathic isolated GH deficiency.

Methods: A multicenter, randomized, clinical trial (No. 88-177) followed 111 children (96 boys) at study start from onset of puberty to AH who had received GH(33) mu g/kg/day for >= 1 year. They were randomized to receive 67 mu g/kg/day (GH(67)) given as one (GH(67x1); n = 35) or two daily injections (GH(33x2); n = 36), or to remain on a single 33 mu g/kg/day dose (GH(33x1); n = 40). Growth was assessed as height SDS gain for prepubertal, pubertal and total periods, as well as AH SDS versus the population and the midparental height.

Results: Pubertal height SDS gain was greater for patients receiving a high dose (GH(67), 0.73) than a low dose (GH(33x1), 0.41, p < 0.05). AH(SDS) was greater on GH(67) (GH(67x1), -0.84; GH(33x2), -0.83) than GH(33) (-1.25, p < 0.05), and height SDS gain was greater on GH(67) than GH(33) (2.04 and 1.56, respectively; p < 0.01). All groups reached their target height SDS.

Conclusion: Pubertal height SDS gain and AH SDS were dose dependent, with greater growth being observed for the GH(67) than the GH(33) randomization group; however, there were no differences between the once-and twice-daily GH(67) regimens. (C) 2014 S. Karger AG, Basel.

Objective: To compare clinical status after three years of treatment and socio-demographic conditions at onset in children with diabetes born to immigrant parents with children to Swedish born parents. Design: Observational nationwide population based cohort-study on prospectively recorded registry data.

Setting: All children with diabetes in Sweden and their parents between 2000 and 2010.

Patients: 879 children with diabetes born to immigrant parents out of a total of 13 415 children, the immigrant cohort. To these we added 2627 children with diabetes of Swedish born parents, matched for gender, age and year of onset, the Swedish cohort.

Main outcome: The immigrant children had a higher median HbA1c, 69 mmol/mol (8.5 %), compared to their Swedish peers 62 (7.8 %), p = 0.002, and the 75th percentile of 72 (8.8 %) vs 70 (8.5 %). There was however no difference in frequency of severe events of hypoglycemia or keto-acidosis between the two cohorts (p = 0.258). A linear regression model with HbA1c as dependent variable pointed out insulin units per kg BW as the main reason for inferior metabolic control, OR 11.410, CI 95% 7.418_15.402, p < 0.001.

Conclusions: Children with diabetes born to immigrant parents have worse metabolic status three years after disease onset.

Aim: The aim of the present study was to compare clinical and socio-demographic conditions at the onset of Type1 diabetes in children born to immigrant families and children born to Swedish families, and to assess whether those conditions had an impact on metabolic status.

Methods and design: This was an observational nationwide population-based matched cohort study on prospectively recorded registry data of all children with diabetes in Sweden and their families during 2000-2010. Out of a total of 13415 children from the Swedish Childhood Diabetes Registry (SWEDIABKIDS), 879 children born to immigrant parents were collected. To these we added 2627 children with Swedish-born parents, matched for gender, age and year of onset of Type1 diabetes.

Results: The proportion of low capillary pH (<7.30) at onset was higher in the immigrant cohort [25.8% vs. 16.4% in the Swedish cohort (P<0.001)]. HbA(1c) was also higher [95mmol/mol (10.8%) vs. 88mmol/mol (10.2%), respectively (P<0.001)]. In a logistic regression model with low pH as the dependent variable, we were unable to reveal any significant association to socio-demographic factors, but the odds ratio for HbA(1c) was 0.983 (95%CI 0.976-0.991) and for plasma glucose was 0.953 (95%CI 0.933-0.973).

Conclusion: Children born to immigrant parents have lower capillary pH and higher HbA(1c) at diabetes onset. Immigrant families harbour lower socio-demographic living conditions, but this fact does not seem to influence the inferior metabolic condition at diabetes onset.

Aims: To evaluate the associations between physical activity (PA) and metabolic control, measured by glycated hemoglobin (HbA1c), in a large group of children and adolescents with type 1 diabetes.

Methods: Cross-sectional analysis of data from 4655 patients, comparing HbA1c values with levels of physical activity. The data for the children and adolescents were obtained from the Swedish pediatric diabetes quality registry, SWEDIABKIDS. The patients were 7-18 years of age, had type 1 diabetes and were not in remission. Patients were grouped into five groups by frequency of PA.

Results: Mean HbA1c level was higher in the least physically active groups (PA0: 8.8% +/- 1.5 (72 +/- 16 mmol/mol)) than in the most physically active groups (PA4: 7.7% +/- 1.0 (60 +/- 11 mmol/mol)) (p < 0.001). An inverse dose-response association was found between PA and HbA1c (beta: -0.30, 95%CI: -0.34 to -0.26, p < 0.001). This association was found in both sexes and all age groups, apart from girls aged 7-10 years. Multiple regression analysis revealed that the relationship remained significant (beta: -0.21, 95% CI: -0.25 to -0.18, p < 0.001) when adjusted for possible confounding factors.

Conclusions: Physical activity seems to influence HbA1c levels in children and adolescents with type 1 diabetes. In clinical practice these patients should be recommended daily physical activity as a part of their treatment.