Pediatric Endocrinology, Diabetes and Metabolism最新文献

Childhood obesity is a major complex and multifaceted public health challenge with significant short- and long-term health consequences. It is also associated with a significant reduction in quality of life and poorer mental health outcomes. In general, obesity occurs when energy intake exceeds energy expenditure. In children, however, the former can be interpreted as when a child has a body mass index (BMI) at or above the 95th percentile for children of the same age, sex, and ethnicity on growth charts. Obesity in children is influenced by a complex interplay of genetic, environmental, socio-economic, and behavioural factors. The relationship between a child's behaviour and childhood obesity is multifaceted and influenced by various factors, including dietary habits, physical activity levels, sedentary behaviours, family dynamics, socio-economic status, and environmental factors. Effective strategies for preventing and managing childhood obesity require a comprehensive, multi-sectoral approach that addresses individual, family, community, and educational institutes. Thus, addressing childhood obesity requires a comprehensive approach that addresses not only biological and environmental factors but also behavioural factors that influence children's eating behaviours, physical activity levels, sleep patterns, and emotional well-being. Early intervention and ongoing support are crucial for promoting healthy growth and development and reducing the burden of childhood obesity on individuals, families, and societies. This review discusses factors that influence the child's behaviour and the relationship between the child's behaviour and childhood obesity.

Introduction: For 35 years, recombinant human growth hormone (rhGH) has been successfully used worldwide to treat children with short stature related to growth hormone deficiency (GHD). Growth hormone therapy requires an individual approach to the patient due to varying responses to the treatment. Excessive body weight is one of the factors influencing the response.

Aim of the study: To evaluate the impact of excessive body mass on rhGH therapy effectiveness in GHD children.

Material and methods: 165 short-statured children with isolated GHD (mean age 10.72 ±3.33 years), treated with rhGH for at least one year (mean follow-up 4.32 ±1.80 years), were separated into 3 groups based on their BMI standard deviation score (SDS). Bone age, height, weight, insulin-like growth factor 1 level, and rhGH dose were obtained up to 10 years with one-year intervals.

Results: The mean change in height SDS in the first year was 0.52 ±0.41 SD and 0.60 ±0.32 SD for normal and excessive body weight children, respectively. The mean height velocity, based on the height SDS measured over the consecutive 5 years, was 0.44±0.25 SD/year for the normal-weight group and 0.32 ±0.24 SD/year for the excessive body weight group (p < 0.1).

Conclusions: Excess body weight has a significant impact on rhGH therapy outcomes. This correlates with the height increase in the first year of observation; however, long-term observation has shown that children diagnosed with overweight or obesity achieve significantly worse results compared to their normal-weight peers.

Introduction: To investigate the hypothesis that the presence of prenatal maternal stress, increased level of prenatal testosterone, and low level of vitamin D3 in pregnancy is associated with the development of ADHD-like symptoms in toddlers (< 2 years old).

Material and methods: The study group comprised 53 pregnant women and 53 infants of these pregnancies. The population cohort of 53 pregnant women were recruited at their 35th to 37th week of pregnancy and investigated prospectively. The participants were selected through targeted selection. Maternal experience of stressful life events was assessed by stress standardised questionnaires, prenatal testosterone was determined in the mothers' saliva by using the immune enzymatic (ELISA) method, and maternal plasma D vitamin was measured using the ECLIA method, during pregnancy. When the age of the offspring was 6 months and then less than 2 years, the mothers completed the child behaviour and temperament checklist.

Results: A small but statistically significant association was found between the common symptom complex of ADHD and the level of testosterone and vitamin D3, in the presence of prenatal maternal stress. Multiple regression analysis showed that maternal stressful events during pregnancy significantly predicted ADHD behaviours in offspring.

Conclusions: The study supported the hypothesis that prenatal maternal stress, increased level of prenatal testosterone, and low level of vitamin D3 during pregnancy increases the risk of development of ADHD-like symptoms in toddlers (< 2 years old). Also, the obtained results support the hypothesis that the influence of prenatal factors causes ADHD-like symptoms in offspring through a programming effect.

Hypoglycemic encephalopathy (HE) is a type of encephalopathy resulting from extremely low blood glucose level. Symptoms are not specific and can be misdiagnosed very often. It can occur during deep and/or prolonged hypoglycemia, which may be a result of inadequately controlled diabetes. Here, we report a case of an 11-year old male patient diagnosed with type 1 diabetes mellitus treated with the use of insulin pump who was admitted to the Pediatric Neurology Department because of multiple incidents of seizures. Boy was found unconscious by his mother. The blood glucose level on the glucometer was 35 mg/dl. It turned out that the reason of hypoglycemia was inadequate insulin dosing. He was given intravenous glucose by the ambulance service without improvement in the state of consciousness. Brain MRI revealed in both cerebral hemispheres, symmetrically, elevated white matter signal, mainly in the subcortex and cortex of the frontal and occipital and parietal lobes with features of diffusion restriction. EEG revealed generalized slow brain activity, without obvious epileptiform. Boy was provided with a variety of antiepileptic drugs. Unfortunately, none of them yielded with satisfactory results so far and the patient is still suffering from drug-resistant epilepsy. In conclusion, glucose is one of the key metabolic agents for the proper brain function and any imbalances in its blood level may impair the neuronal computation. Thus, it is extremely important, especially among diabetic patients, to control glucose blood level and avoid any disturbances, as they may lead to severe consequences, such as HE and drug-resistant epilepsy.

The clinical onset of type 1 diabetes (namely stage 3 type 1 diabetes [T1D]) is preceded by a relatively prolonged pre-symptomatic phase featured by islet autoimmunity [1] with (Stage 2 T1D) or without (Stage 1 T1D) dysglycaemia. While islet autoimmunity is the hallmark of the underlying autoimmune process, very little evidence is available for the metabolic changes that accompany the loss of functional beta cell mass. Indeed, a steep decline of C-peptide - a surrogate marker of beta cell function - is measurable only ~6 months before the onset of Stage 3 T1D [2]. Disease modifier drugs have, there-fore, a very limited window of intervention because we lack of effective methods to track beta cell function over time and to identify early changes of insulin secretion that precedes dysglycaemia [3, 4] and clinically symptomatic diabetes. Herein, we will revise current approaches to longitudinally track beta cell function over time before the onset of Stage 3 T1D, which might be suitable for monitoring the risk for diabetes progression as well as the effectiveness of disease modifier treatments.

Introduction: In view of the modifications in the endocrine society guidelines on evaluation and management of children with congenital adrenal hyperplasia (CAH), we performed a review of children and adolescents with CAH.

Material and methods: An audit of 35 children with CAH presenting to the pediatric endocrinology clinic between January 2014 to November 2021 was conducted by formulating ten audit questions. The areas of focus included: genital reconstructive surgery, neonatal screening for CAH, stress dosing, need for adrenocorticotrophic hormone (ACTH) stimulation test, growth promoting therapy, bone age assessment, adrenal imaging, bone mineral density assessment, adequacy of hormone replacement and appropriate management of non-classical CAH.

Results: Conservative approach to genitoplasty in female children increased from 42.9% to 88.9%. Newborn screening identified 4 babies including two asymptomatic males averting saltwasting crisis. Stress dosing of steroids were advised in all and emergency usage of injectable glucocorticoids was warranted in two children. Gonadotropin-releasing hormone (GnRH) analogue therapy improved the final median predicted height by 7 cm in 5 children. Twenty-three (65.7%) had bone age assessment with 14 (40%) having advanced bone age. ACTH stimulation test, Adrenal imaging, dual energy X-ray absorptiometry (DEXA) scan were done in accordance with the guideline. One child with nonclassical CAH was initiated on hydrocortisone replacement for advanced bone age.

Conclusions: A shift to conservative surgical management of females, utility of neonatal screening for CAH, judicious use of growth promoting therapy is highlighted. Need for bone age testing, emergency hydrocortisone provision is warranted in our series.

Compared with healthy children, peers with type 1 diabetes mellitus (DM1) have an increased risk of developing advanced atherosclerosis and cardiovascular disease (CVD). Glycaemic control is the most important modifiable risk factor for CVD in DM1. Currently, monitoring of glycaemic control relies on glycosylated haemoglobin levels (HbA1c), self-monitoring of blood glucose (SMBG), and the use of continuous glucose monitoring (CGM) systems. The flow-mediated dilatation (FMD), pulse wave velocity (PWV), ankle-brachial index (ABI), and carotid intima-media thickness (cIMT) may be used to assess the risk of CVD, by estimating the process of atherosclerosis in peripheral vessels. Aim of the study: To summarize the current literature on the correlation of metabolic control in young people with DM1, assessed by key metrics from CGM reports, and the development of atherosclerosis and the incidence of CVD. Conclusions: Chronic hyperglycaemia is an independent risk factor for vascular changes. The effect of glycaemic control - assessed on the basis of parameters obtained from CGM reports - on the risk of CVD in DM1 has been analysed in few studies, especially in the paediatric population.