The adverse effects of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) are not limited to the related infectious disease. In children and adolescents, serious risks due to the ...coronavirus disease 2019 (COVID-19) pandemic are also related to its indirect effects. These include an unbalanced diet with an increased risk of weight excess or nutritional deficiencies, increased sedentary lifestyle, lack of schooling, social isolation, and impaired mental health.Pediatricians should be aware of the side effects of the COVID-19 pandemic on children's diet, physical mental health and advise the families according to their nutritional needs and financial resources. Moreover, the lack of a targeted therapy able to offer protection against the deleterious effects of SARS-CoV-2 infection should require a greater effort by scientific societies to find a more effective prevention strategy. In this context, much interest should be given to nutritional support, able to contrast malnutrition and to stimulate the immune system.
Summary
What is already known about this subject
There is emerging evidence suggesting that childhood obesity may influence the timing/tempo of puberty and growth patterns.
An earlier onset of ...puberty generally occurs in obese girls, whereas conflicting data are available for boys.
Obese children tend to be taller during pre‐puberty but lose this growth advantage during puberty.
What this study adds
Obese boys and girls present an earlier onset of puberty and completion of puberty, with a shorter duration of puberty compared to normal‐weight peers.
Obese children tend to have a similar adult height compared to normal‐weight children.
Background
There is emerging evidence suggesting that childhood obesity may influence the timing of puberty and growth patterns. However, there are scant and controversial data in this field.
Objective
To assess whether puberty and physical growth vary in obese when compared to normal‐weight children.
Methods
One hundred obese pre‐pubertal children (44 boys; mean age (±SD): 9.01 ± 0.62 years; 56 girls; 8.70 ± 0.57 years) were compared to 55 normal‐weight controls (27 boys; 9.17 ± 0.26 years; 28 girls; 8.71 ± 0.62 years). All study participants were followed prospectively with 6‐monthly follow‐up visits. At each study visit, height, weight, body mass index (BMI) and pubertal stage were assessed.
Results
Obese children entered puberty and achieved later stages of puberty earlier than controls (onset of puberty: boys: 11.66 ± 1.00 vs. 12.12 ± 0.91 years, P = 0.049; girls: 9.90 ± 0.78 vs. 10.32 ± 1.70, P = 0.016; late puberty: boys: 13.33 ± 0.71 vs. 14.47 ± 1.00 years, P < 0.001; girls: 11.54 ± 0.99 vs. 12.40 ± 1.02, P = 0.001). Pre‐pubertal BMI standard deviation score (SDS) was inversely associated with both age at the onset of puberty (β = −0.506, P < 0.001) and age at late puberty (β = −0.514, P < 0.001). Obese children also showed an earlier age at peak height velocity (PHV) (boys: 12.62 ± 0.82 vs. 13.19 ± 0.96 years, P = 0.01; girls: 11.37 ± 0.89 vs. 12.77 ± 0.76, P < 0.001) and a lower PHV (boys: 7.74 ± 1.49 vs. 9.28 ± 1.64 cm year−1, P < 0.001; girls: 7.60 ± 1.64 vs. 8.29 ± 1.03, P = 0.03). Height SDS progressively declined over the study period in the obese group (P for trend <0.001), whereas there were no significant changes in the control group (P for trend = 0.5).
Conclusions
Obese boys and girls presented an earlier onset of puberty and completion of puberty and an impaired height gain during puberty.
In the last years, a growing body of literature indicates an association between valproic acid therapy and weight gain. Weight gain during valproate treatment can be observed within the first 3 ...months of therapy and women seem to be more susceptible than men. The mechanism through which valproic acid may induce a weight gain is still controversial. The scope of this paper is to investigate the possible causal link between treatment and weight gain in epileptic patients. Systematic review of published epidemiological studies has been done in order to evaluate the real extent of this side effect of valproic acid and its clinical implications, such as an increased risk of insulin resistance and other secondary metabolic abnormalities. The knowledge of the potential of valproic acid to cause significant changes in body weight will help in appropriate selection and modification of antiepileptic therapy to minimize the risk for weight abnormalities. Measurements of body weight before initiation of valproic acid therapy should be done as part of the monitoring of patients with epilepsy to detect changes before there are serious adverse consequences; an increase of 2 kg of body weight after 1 month of treatment should imply considerations to change antiepileptic drug therapy.
Many antiepileptic drugs (AEDs) are associated with hematological disorders that range from mild thrombocytopenia or neutropenia to anemia, red cell aplasia, until bone marrow failure. Fortunately, ...potentially fatal hematological disorders such as aplastic anemia are very rare. This review investigates hematological effects associated with classic and newer AEDs: a PubMed search indexed for MEDLINE was undertaken to identify studies in adults, children and animals using the name of all anticonvulsant drugs combined with the terms “hematological disease” and “hematological abnormalities” as key words. The most common hematological alterations occur with older AEDs than newer. Indeed, careful hematological monitoring is needed especially using carbamazepine, phenytoin and valproic acid. The pathogenetic mechanisms are still unknown: they seem to be related to an immunological mechanism, but drugs pharmacokinetics and pharmacodynamics interactions may also play an important role. Further research is needed to assess the real pathogenetic mechanism at the basis of hematological complications caused by AEDs.
•Avoid anticonvulsants as valproic acid, phenobarbital and phenytoin during pregnancy for risk of cognitive impairment in the offspring.•Anticonvulsant drug monotherapy should be preferred during ...pregnancy to reduce possible adverse effects.•It is important to use the lowest efficacy dose of anticonvulsant drugs during pregnancy.•More researches are needed for the safety of newer anticonvulsant drugs for epileptic women during pregnancy.
In utero exposure to antiepileptic drugs (AEDs) may affect neurodevelopment causing postnatal cognitive and behavioral alterations. Phenytoin and phenobarbital may lead to motor and learning dysfunctions in the pre-exposed children. These disorders may reflect the interference of these AEDs with the development of hippocampal and cerebellar neurons, as suggested by animal studies. Exposure to valproic acid may result in inhibition of neural stem cell proliferation and/or immature neuron migration in the cerebral cortex with consequent increased risk of neurodevelopmental impairment, such as autistic spectrum disorders. A central issue in the prevention of AED-mediated developmental effects is the identification of drugs that should be avoided in women of child-bearing potential and during pregnancy. The aim of this review is to explore the possible link between AEDs and neurodevelopmental dysfunctions both in human and in animal studies. The possible mechanisms underlying this association are also discussed.
Diabetic nephropathy (DN) is one of the major microvascular complications of diabetes and one of the leading causes of death among patients with diabetes. DN is characterized by excessive amassing of ...extracellular matrix with thickening of glomerular and tubular basement membranes and increased amount of mesangial matrix, which ultimately progress to glomerulosclerosis and tubulo-interstitial fibrosis. The high intracellular glucose environment due to an increased cellular uptake of glucose activates several pathways related to the production of advanced glycation endproducts, cytokines, chemokines, growth factors, reactive oxidative species, which are all final mediators of renal damage in human and experimental diabetes. Several growth factors have been implicated in the pathogenesis of DN, through complex intra-renal systems. Transforming growth factor beta, connective tissue growth factor, vascular endothelial growth factor, growth hormone and insulin-like growth factors are among those best known and investigated. There are also data, even though limited, on the involvement of other two growth factors, epidermal growth factor and platelet derived growth factor, in the pathogenesis of DN. These growth factors, which are generally expressed in the normal kidney and whose levels increase in relation to diabetes, have been implicated in the control of renal matrix composition, cell hypertrophy, proliferation and survival, modulation of cells of the immune system, and enzymes involved in glucose metabolism. The development of specific inhibitors of growth factors has provided further evidence for the involvement of growth factors in the development and progression of DN and further studies might help in developing new potential therapeutical interventions.
Diabetic autonomic neuropathy (DAN) represents a major complication of diabetes mellitus but there is considerable uncertainty about its incidence, prevalence, pathogenesis, diagnosis, and prognosis. ...There are conflicting opinions about the pathogenesis of DAN: the ‘classical hypothesis’ has been supplemented by some new insights. Clinical symptoms of autonomic neuropathy do not generally occur until long after the onset of diabetes. DAN seems to be detectable even in asymptomatic children and adolescents with diabetes and is associated with the most serious consequences, such as cardiovascular dysfunction. Because of its association with a variety of adverse outcomes, including cardiovascular deaths, cardiovascular autonomic neuropathy is the most clinically important and well-studied form of DAN. No form of therapy in DAN has been identified that provides unequivocal, safe, and effective stabilization or reversal of the condition, just a near normal control of blood glucose in the early years after the onset of diabetes that may delay the development of clinically significant nerve impairment. This article reviews recent developments in knowledge of epidemiology, pathogenesis, clinical symptoms, diagnosis, and therapy of DAN.
Background. Skipping breakfast has been associated with a higher risk of obesity and cardiovascular (CV) risk factors. However, it is not known if skipping breakfast is also correlated with CV risk ...factors independently from obesity. The mechanisms explaining the role of skipping breakfast on promoting fat accumulation as well as CV risk are not known. Hormones, in particular, insulin-like growth factor-1 (IGF-1), may potentially play a role in the metabolic profile of breakfast skippers. Aim. This cross-sectional study aims to test, in a sample of overweight/obese children, the hypotheses that skipping breakfast is associated with a worse metabolic profile and that IGF-1 levels are associated with this unfavorable metabolic profile. Methods and Results. We enrolled 112 overweight/obese prepubertal children (3–12 years). Anthropometric characteristics (height SDS, weight SDS, and body mass index (BMI) z-score) were measured. Blood samples were collected to evaluate glucose and lipid metabolisms and hormone profile (growth hormone (GH), IGF-1, insulin, and cortisol). The triglycerides/high-density lipoprotein (HDL) cholesterol ratio was calculated as a predictor of cardiovascular risk. Children were divided into two groups according to breakfast habits: consumers (≥5 weekly; N = 76) and skippers (≤4 weekly; N = 36). Glycaemia, total and low-density lipoprotein (LDL) cholesterol, triglycerides (p<0.05), and triglycerides/HDL cholesterol ratio (p<0.001) were higher, while HDL cholesterol was lower (p<0.01) in skippers as compared to consumers. IGF-1 concentrations were inversely correlated with LDL cholesterol (r = −0.279, p=0.013) and directly correlated with HDL cholesterol (r = 0.226, p=0.047). IGF-1 correlated positively with HDL cholesterol (r = 0.266, p=0.045) in consumers and correlated negatively with LDL cholesterol (r = −0.442, p=0.024) in skippers. Breakfast consumption among prepubertal overweight/obese children showed a better lipid profile in comparison with those who skipped breakfast OR: 0.165 (95% CI: 0.053–0.518), p=0.001; these latter odds of the increased triglycerides/HDL cholesterol ratio was 6.1-fold higher. Conclusions. Breakfast skippers show a worse lipid profile when compared to breakfast consumers. IGF-1 might play a role as an independent modulator of lipid metabolism.
Concomitantly with the increasing prevalence of childhood obesity, the prevalence of metabolic syndrome (MS) is rising among children and adolescents, leading to fears for future epidemics of type 2 ...diabetes mellitus and cardiovascular disease in the young. This makes the accurate identification and the appropriate treatment of children and adolescents with MS an important priority for health care systems. This review will focus on the management of each component of MS, including the nonalcoholic fatty liver disease (NAFLD), which is currently considered as the hepatic component of the syndrome. The most relevant target of treatment of MS in children and adolescents is the abdominal obesity. To this end, we will discuss the efficacy of dietary approaches, possibly coupled with regular physical activity, on eliciting visceral fat reduction. We will also highlight several aspects of the treatment of the high triglyceride/low high-density lipoprotein cholesterol phenotype, including the use of non-pharmacological measures, and indications for instituting drug therapies. Part of this review will address treatment of glucose abnormalities, including the benefits of lifestyle modification alone, and the potential adjunctive role of hypoglycemic drugs. The treatment of hypertension in children with MS also requires a multifaceted approach and the available data of this topic will be examined. The remainder of this review will address treatment to reverse NAFLD and prevent progression to end-stage disease.
Background
The recent introduction of microarrays for genetic analyses has allowed higher etiological diagnostic rates in patient with intellectual disability (ID), autism spectrum disorders (ASD), ...epilepsy and multiple congenital anomalies (MCA), because of its resolution. This approach still results of high complexity and some limitations have been reported. In fact, it discloses several variants of unknown significance (VOUS) or incidental findings. In all cases, a massive amount of data is generated, because of this, the analysis and the interpretation is very difficult and often without a definitive conclusion.
Method
We analysed an Italian cohort of 343 patients with ID, MCA and ASD by array‐comparative genomic hybridization. The purpose of this work was to consider the proportion of the chromosomal abnormalities in such cohort and to assess the distribution of the different type of the chromosomal abnormalities concerning their pathogenic significance, their origin and their correlation to these clinical phenotypes.
Results
Array‐comparative genomic hybridization analysis revealed 76 positive results. Abnormalities were detected in 27.8% of patients with ID, 11.1% with ASD, 10.7% with epilepsy and 19.4% with multiple congenital anomalies. The anomalies were classified in three major groups: group 1 (27 patients) with pathogenic alterations (P group); group 2 (34 patients) with VOUS potentially pathogenic (PP group); and group 3 (13 patients) with VOUS potentially benign (PB group). As expected, comparing the diagnostic groups, we observed a greater number of deletions in the P group and that all the abnormalities of the PB group were inherited.
Conclusions
Our retrospective study resulted in confirming the high detection rate of microarrays. CNV classification remains a complex procedure. The difficulty in CNV classification points out the importance of the patient selection, helping the interpretation of the molecular cytogenetic results.
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