Introduction and hypothesis
Pediatric endocrinology deals with the very common diseases of young age and addresses the most prevalent health risks of childhood and adolescence. Only infectious diseases are more common than civilization diseases such as obesity, diabetes, vitamin D and iodine deficiency as well as disorders of the thyroid and gonads , , , , , . In addition, the very fundamental issues of growth and pubertal development constitute the core of pediatric endocrinology and pediatrics in general , , , . Despite these facts, in many countries and many institutions pediatric endocrinology is considered a minor subspecialty of pediatrics and in many cases pediatric hospitals and importantly university children’s hospitals are being led by pediatric oncologists, neonatologists or pediatric cardiologists. These pediatric subspecialties very often are being refinanced considerably better than pediatric endocrinology and diabetes. It is hypothesized that this is the case because pediatric endocrinologists were neither aggressive nor skilled enough to put forward their case once it came to negotiate the refinancing of health care and health services. In addition, many adult physicians do not have pediatric issues such as growth, developmental aspects, civilization diseases at a young age and rare genetic syndromes on their mental agenda. As adult physicians very often are in charge of large hospitals, it is thus no surprise that pediatric endocrinology is being neglected. Finally, patient advocacy groups in the areas of pediatric oncology, neonatology and congenital heart disease are much more visible than those in areas such as Prader-Willi syndrome, Turner syndrome, diabetes or rare diseases .
However, the very large number of children and adolescents affected by civilization diseases such as obesity, diabetes, vitamin D and iodine deficiency as well as by disorders of the thyroid and gonads is a fact and needs to be reported more often and made public constantly by those affected and their families as well as by care takers and pediatric endocrinology specialists. In addition, as, for example, the very fundamental issues of growth and pubertal development constitute the core of pediatric endocrinology and hence pediatrics in general these issues need to be addressed more frequently and more visibly in courses, lectures, textbooks and podcasts to teach medical students, nursing staff, doctors and the public. Indeed, pediatric endocrinology and diabetes needs a public awareness campaign. This is particularly so, as, for example, the number of children affected by obesity, diabetes and thyroid disorders are constantly on the rise in many areas of the world , , .
Not only does pediatric endocrinology play an important role in the day-to-day clinical care for neonates, infants, children and adolescents worldwide and hence is an important topic for training physicians and pediatricians in particular, but it also contributes to scientific knowledge in medicine and pediatrics enormously: it is pediatric endocrinologists who are involved in unraveling cell signaling mechanisms in biology and medicine, conducting clinical trials to improve medical treatments and start prevention trials to prevent civilization diseases such as obesity even on a large scale .
Thus, pediatric endocrinology is the basis of pediatric and adolescent medicine. Pediatric endocrinology is pediatrics. As pediatrics is always directly related to public health and the wellbeing of individuals and societies, pediatrics is public health. Hence, we hypothesize that pediatric endocrinology is pediatrics is public health! If this is true, our journal of pediatric endocrinology is a true pediatric journal and its publications support and address public health. In this issue of the Journal of Pediatric Endocrinology and Metabolism, pediatric public health issues are again being addressed.
The aim of a study on childhood obesity in a single community setting was to assess putative relationships between adipocyte fatty acid-binding protein (FABP4) and total body fat, abdominal fat, body fat distribution, aerobic fitness, blood pressure, cardiac dimensions and increases in body fat over a period of 2 years. A cross-sectional study design studying 170 (92 boys and 78 girls) children aged 8–11 years was employed. Total body fat and abdominal fat (AFM) were measured by dual-energy X-ray absorptiometry (DXA). Maximal oxygen uptake (VO2PEAK) was assessed by indirect calorimetry during a maximal exercise test and scaled to body mass. Systolic and diastolic blood pressure (SBP and DBP) and pulse pressure (PP) were measured. Echocardiography was performed. Frozen serum samples were analyzed for FABP4. Data from this community-based cohort of young children show that increased body fat and abdominal fat, more abdominal body fat distribution, low fitness, more LVM and increased LA, increased SBP and PP were all associated with increased levels of FABP4. Increase in total body fat and abdominal fat over 2 years were associated with increased levels of FABP4. FABP4 may serve as a surrogate marker for critical obesity while its function for the development of obesity complications remains unclear .
Vitamin D supplementation, the development of metabolic syndrome and oxidative stress in obese children have been studied by Grunwald et al. . Evidence suggests that vitamin D deficiency may contribute to the occurrence of oxidative stress which may or may not contribute to the development of cardiovascular disease. This study aimed to determine whether or not treatment of vitamin D deficiency in obese children led to changes in their metabolic profile. In this predominantly Hispanic population of obese children in an urban setting, a relationship between vitamin D deficiency and markers of oxidative stress was detected. In contrast, no association between vitamin D status, adiposity and markers of insulin sensitivity was found. The authors conclude that a differential effect of vitamin D on cardiovascular risk factors such as oxidative stress and insulin resistance is suggested .
The association of low serum 25 hydroxy cholecalciferol (25OHD) levels with high glucose levels and impaired insulin sensitivity may suggest that vitamin D may modulate insulin metabolism directly or via indirect mechanisms. In this study from Egypt, vitamin D deficiency was screened for in pediatric patients with type 1 diabetes (T1D) and the effect of vitamin D supplementation on glycemic control and insulin dosage was analyzed. Fifty patients with T1D (mean diabetes duration of 4.11±2.34 years) were included in a prospective clinical trial. Vitamin D levels ranged from 0.2 to 33 ng/mL. Vitamin D status correlated significantly with daily insulin dose (p=0.030, r=0.306) and HbA1c (p<0.001, r=0.243). Thirty-five patients with low vitamin D levels were allocated for vitamin D supplementation for 3 months. According to the authors, mean HbA1c improved significantly after supplementation (p=0.003). Whether or not vitamin D sufficiency/supplementation directly improves glycemic control in patients with T1D needs to be studied in randomized, controlled clinical trials with sufficient statistical power .
In a cross-sectional analysis of universal vitamin D supplementation in the former East Germany during the first year of life Siafarikas et al. report on the efficacy of 400 IU vitamin D3 supplementation in infants. These findings are being reported as the dosing of vitamin D supplementation is still somewhat controversial. The study was a cross-sectional analysis of data from 3481 term-born children during their first year of life in 1989. No significant clinical signs of rickets was reported in the cohort. 25(OH)D (mean and SEM, total analyses n=572) after birth (n=28) was 36(7) nmol/L, at 1 month 64(4) nmol/L (n=70, p<0.0001), 91(5) nmol/L at 3 months (n=95, p<0.0001), 65(8) nmol/L at 8 months (n=21, p=0.005) and ranged between 33 and 109 nmol/L until 12 months. Less than 0.2% of analyses revealed pathological levels for calcium or phosphate. Alkaline phosphatase levels (n=690) were >1500 U/L (95th percentile) in 3.6%. It is conclude that supplementation with 400 IU of vitamin D3 during the first year of life is safe and provides sufficient 25(OH)D levels in an environment of moderate sun exposure as is the case in Germany .
Congenital hypothyroidism is a common endocrine disorder that can lead to intellectual disability if it is not detected early by neonatal screening and treated rapidly. In this issue of our journal the incidence of congenital hypothyroidism among different ethnic groups in the capital of Macedonia is reported . In this 14-year retrospective cohort study 121,507 newborns in the capital of Macedonia, Skopje, were screened for thyroid-stimulating hormone (TSH) in dry blood spots collected 48–72 h after birth, during the period 2002–2015. A TSH value of 15 mIU/L was used as cutoff point until 2010 and 10 mIU/L thereafter.
Overall incidence of congenital hypothyroidism was 3.8/10,000 (1/2641). Hypothyroidism incidence among Roma neonates (6.7/10,000) was significantly higher (p<0.05) than that detected in Macedonians (3.9/10,000) or Albanians (3.7/10,000) (18). This study shows the reported high incidence of congenital hypothyroidism across ethnic groups. The importance and public health aspect of neonatal screening is emphasized.
Kose et al.  in this issue report upon changes of thyroid hormone serum concentrations in patients receiving ketogenic diet as a therapy for intractable epilepsy. A so-called ketogenic diet high in fat and low in carbohydrates mimics the metabolic state of starvation and is used therapeutically for sever forms of epilepsy. It is known that the generation of triiodothyronine (T3) from thyroxine (T4) decreases during fasting periods. Therefore, thyroid function was studied prospectively in children receiving ketogenic diets for at least 1 year due to pharmacotherapy-resistant epilepsy. A total of 120 patients [63 males, 52.5%; mean age 7.3±4.3 years] were included in the study and seizure control, and side effects, were recorded. Free T3, free T4, and thyroid-stimulating hormone (TSH) levels were measured at baseline and thereafter. Hypothyroidism was diagnosed and L-thyroxine medication was initiated for eight, seven and five patients (20 patients in total, 16.7%) after 1, 3, and 6 months of ketogenic therapy. It is concluded that ketogenic diets can cause thyroid malfunction which may require L-thyroxine treatment. Hence, thyroid function should be monitored regularly in patients with epilepsy who are treated with ketogenic diets.
We hypothesize that pediatric endocrinology and diabetes is pediatrics is public health. Pediatric endocrinology teaching and research have to be strengthened in an interdisciplinary approach involving clinicians, clinical scientists, basic researchers and behavioral and social scientists alike. Refinancing pediatric endocrinology services is a good and well paid off investment into the future of our children. The public and societal institutions have to be made aware that pediatrics in general and pediatric endocrinology in particular support good health of our future generations and hence are crucial for the wellbeing of societies and the individual alike.
Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.
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