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Zahlreiche Medien haben restriktive Diäten bei Diabetes mellitus populär gemacht und berichtet, dass Kohlenhydrate die Ursache für Blutzuckerspitzen, extrem hohe Insulin-Dosierungen und Gewichtszunahme sind. In der vorliegenden Arbeit berichten wir über zwei Fälle von Kindern mit Diabetes mellitus Typ 1, bei denen die Einhaltung einer streng kohlenhydratreduzierten Diät Wachstumsstörungen zur Folge hatte. Zwei präpubertäre Patienten mit Typ-1-Diabetes zeigten bei der Kontrolluntersuchung während der Honeymoon-Phase eine fehlende Gewichtszunahme und geringe Wachstumsgeschwindigkeit. Die Ernährungsanalyse ergab, dass eine kohlenhydratarme Diät begonnen worden war, um eine Reduzierung der postprandialen Blutzuckerspitzen zu erreichen. Nach Zufuhr entsprechender Kohlenhydratmengen begannen das Gewicht und die Körpergröße der beiden Patienten zu steigen. Es liegen nur wenige veröffentlichte Daten vor, die dafür sprechen, die Kohlenhydratzufuhr nicht zu begrenzen; darum berichten wir in der vorliegenden Arbeit über zwei Fälle von Kindern mit Typ-1-Diabetes, bei denen die Einhaltung einer solchen Ernährungsform zu Wachstumsstörungen geführt hat. Besonders hervorheben möchten wir, dass dabei die Schulung der Familien von Kindern mit Typ-1-Diabetes zu diesem Aspekt eine wichtige Rolle spielt, vor allem wenn sich die Kinder gerade in der Honeymoon-Phase befinden oder diese zu Ende geht.

Variety of media have popularized restrictive diets in diabetes mellitus reporting that carbohydrates are the cause of glycemic excursion, excessive insulin dosage, and weight gain. We report 2 cases of children with type 1 diabetes where adherence to restricted carbohydrate diets caused growth failure. Two prepubertal patients with type 1 diabetes presented at follow-up visit during the honeymoon period with no weight increase and low height velocity. Dietetic evaluation revealed a low-carbohydrate diet had been introduced in an attempt to achieve less postprandial excursions in the blood glucose readings. The 2 patients started to improve weight and height when the appropriate amount of carbohydrates was given. There are few published data to support not to restrict carbohydrate; therefore, we report 2 cases of children with type 1 diabetes where adherence to this diet caused growth failure. We want to emphasize the importance of educating families of children with type 1 diabetes on this aspect, particularly when they are in the honeymoon phase or this one is concluding.

Context: Poor sensitivity of IGF binding protein (IGFBP)-3 assessment in the work-up of GH deficiency (GHD) has been ascribed to the equal affinity of IGFBP-3 for IGF-I and IGF-II and to IGFBP-3 proteolysis. Objective: The objective of this study was to determine the IGF-II GH dependency and IGFBP-3 proteolysis in patients with GHD from childhood to young adulthood. Design: This study was cross-sectional. Setting: This was a national multicenter study performed in university hospitals. Patients:One hundred thirty-one subjects (chronological age, 1.3–25 yr), 72 patients with GHD and 59 subjects with idiopathic short stature, were studied. Interventions: IGF-I, IGF-II, and IGFBP-3 serum concentrations were measured by immunoradiometric assay. IGFBP-3 circulating forms were assessed by Western immunoblot (WIB) analysis. MainOutcomeMeasures:Mainoutcomemeasuresweresensitivity and specificity of IGF-I, IGF-II, and IGFBP-3 measurements. Results:SensitivityandspecificityofIGFBP-3measurementwere27 and 100%, respectively. IGFBP-3 sensitivity was 46% in young adulthood. Sensitivity and specificity of IGF-I were 69 and 81%, respectively. Sensitivity and specificity of IGF-II assessment were 23 and 97%, respectively. IGFBP-3 WIB revealed the presence of the intact form and the major 29-kDa fragment in both GHD and subjects with idiopathic short stature. In patients with GHD, WIB showed the presence of an additional smaller IGFBP-3 fragment migrating at approximately 18 kDa. Conclusions: Our results suggest that in children and young adults with GHD, the low GH dependency of IGF-II together with IGFBP-3 proteolytic activity yielding the 18-kDa fragment concur to reduce the sensitivity of IGFBP-3 assessment, ultimately making it too inaccurate as a screening test in the work-up of GHD. (J Clin Endocrinol Metab 90: 6028–6034, 2005)

Epidemiologic studies have demonstrated an association between intrauterine growth retardation and a greater risk of chronic disease, including coronary heart disease, hypertension, stroke, and type 2 diabetes in adulthood. An adverse intrauterine environment may affect both growth and development of the organism, permanently programming endocrine and metabolic functions. One of the mechanisms of programming is the epigenetic modification of gene promoters involved in the control of key metabolic pathways. The aim of this review is to provide an overview of the experimental evidence showing the effects of early exposure to suboptimal environment on epigenome. The knowledge of the epigenetic markers of programming may allow the identification of susceptible individuals and the design of targeted prevention strategies.

Introduction Anticonvulsant drugs taken by pregnant women to prevent seizures are among the most common causes of potential harm to the fetus. While the immediate harmful effects manifesting as congenital abnormalities are well known, the long-term effects on growth of children exposed in utero to antiepileptic drugs are still uncertain. Case presentation A 7-year-old boy presented to our clinic with severe short stature. His height was 110.4 cm (−2.4 standard deviation score), with a target height of 177 cm (+0.35 standard deviation score). Height corrected for target height was −2.75 standard deviation score. He presented with mild dysmorphic facial features, hypospadias and postnatal onset of severe growth retardation. Biochemical and endocrine tests were in the normal range. The child was exposed in utero to both carbamazepine and phenobarbital. Conclusion This case report shows for the first time that prenatal exposure to antiepileptic drugs may induce postnatal onset of severe growth retardation, suggesting the need for growth and endocrine monitoring of offspring exposed in utero to anticonvulsant drugs.