In children with type 1 diabetes, a healthy lifestyle is important to control postprandial glycemia and to avoid hyperglycemic peaks that worsen the inflammatory state of vessels and tissues. Glycemic index and glycemic load are two important indexes which assess the quality and quantity of foods consumed during meals. The main macronutrients of the diet have a different effect on postprandial blood glucose levels, so it is important that diabetic children consume foods which determine a slower and steadier glycemic peak. In this review, we present the results of the most recent studies carried out in the pediatric population with T1D, whose aim was to analyze the effects of low-glycemic-index foods on glycemic control. The results are promising and demonstrate that diets promoting low-glycemic-index foods guarantee a greater glycemic stability with a reduction in postprandial hyperglycemic peaks. However, one of the main limitations is represented by the poor adherence of children to a healthy diet. In order to obtain satisfactory results, a possibility might be to ensure a balanced intake of low-, moderate- and high-glycemic-index foods, preferring those with a low glycemic index and limiting the consumption of the high- and moderate-glycemic-index types.

Childhood obesity is increasing all over the world. It is associated with a reduction in quality of life and a relevant burden on society costs. This systematic review deals with the cost-effectiveness analysis (CEA) of primary prevention programs on childhood overweight/obesity, in order to benefit from cost-effective interventions.We screened and evaluated all the studies with a cost-effectiveness analysis on childhood obesity primary prevention program by PUBMED and Google Scholar, using inclusion and exclusion criteria. The quality of the studies was assessed by Drummond’s checklist.Ten studies were included. Two of them examined the cost-effectiveness of community-based prevention programs, four focused only on school-based programs while four more studies examined both community-based and school-based programs. The studies were different in terms of study design, target population, health and economic outcomes. Seventy per cent of the works had positive economic results.The majority of the studies showed effective economic outcomes applying primary prevention programs on childhood obesity. It is important to increase homogeneity and consistency among different studies.

Nutrition during the prenatal period is crucial for the development of insulin resistance (IR) and its consequences in children. The relationship between intrauterine environment, fetal nutrition and the onset of IR, type 2 diabetes (T2D), obesity and metabolic syndrome later in life has been confirmed in many studies. The intake of carbohydrates, protein, fat and micronutrients during pregnancy seems to damage fetal metabolism programming; indeed, epigenetic mechanisms change glucose−insulin metabolism. Intrauterine growth restriction (IUGR) induced by unbalanced nutrient intake during prenatal life cause fetal adipose tissue and pancreatic beta-cell dysfunction. In this review we have summarized and discussed the role of maternal nutrition in preventing insulin resistance in youth.

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis (NMDARe) is the most common cause of nonviral encephalitis, mostly affecting young women and adolescents with a strong female predominance (F/M ratio of around 4:1). NMDARe is characterized by the presence of cerebrospinal fluid (CSF) antibodies against NMDARs, even though its pathophysiological mechanisms have not totally been clarified. The clinical phenotype of NMDARe is composed of both severe neurological and neuropsychiatric symptoms, including generalized seizures with desaturations, behavioral abnormalities, and movement disorders. NMDARe is often a paraneoplastic illness, mainly due to the common presence of concomitant ovarian teratomas in young women. Abdominal ultrasonography (US) is a key imaging technique that should always be performed in suspected patients. The timely use of abdominal US and the peculiar radiological features observed in NMDARe may allow for a quick diagnosis and a good prognosis, with rapid improvement after the resection of the tumor and the correct drug therapy.

The skeletal muscle channelopathies represent a rare group of neuromuscular disorders which are caused by genetic mutations regarding voltage-gated ion channels, which play an important role in muscle membrane depolarization. Muscle channelopathies are broadly divided into 2 main categories: nondystrophic myotonias (NDM) and periodic paralysis (PP). Periodic paralysis (PP) are rare autosomal dominant neuromuscular disorders, characterized clinically by periodic attacks of muscle weakness in concomitance with serum potassium level alterations. It is possible to distinguish normokalemic, hyperkalemic and hypokalemic paralysis. PP is caused by genetic mutations in voltage-gate ion channels like sodium, potassium, and calcium channels, which are determinant for muscle membrane depolarization. The most common genes involved in pathogenesis are CACN1S, SCN4A and KCNJ2, encoding calcium, sodium, and potassium channels (Table 1). Moreover, paralysis related to serum potassium values may also occur in thyreotoxicosis [1], Liddle syndrome, Gitelman syndrome, primary hyperaldosteronism, and acid-base balance disorders. In this case report, we describe a case of transient paralysis and muscular weakness of both upper and lower limbs after a high carbohydrate meal on the day before clinical presentation. Potassium level was normal at the hospital admission, while high levels of creatine phosphokinase, (CPK), Myoglobin, and Aspartate Aminotransferases (AST) was observed.A missense mutation in CACNA1S exon 11 was identified. This case supports the importance of a correct family history, muscular enzyme analysis and genetic study in a normokalemic presentation of periodic paralysis.