OBJECTIVE -The purpose of this study was to assess glycemic control and complications of type 1 diabetes in children and adolescents in Tanzania. RESEARCH DESIGN AND METHODS -This demographic and clinical survey in-cluded 99 children aged between 5 and 18 years attending Muhimbili National Hospital Clinic for Diabetes. A structured questionnaire was used for evaluating socioeconomic data and for estimation of the prevalence of acute complications occurring over the last 6 months. The prevalences of retinopathy and diabetic nephropathy were determined by fundus ophthalmoscopy and by microalbuminuria, respectively.RESULTS -All of these children were treated with a conventional insulin regimen. The mean Ϯ SD duration of diabetes was 4.76 Ϯ 3.58 years. Only 1 child (1%) had good glycemic control (A1C Ͻ7.5%), 60 children (60.6%) had moderate glycemic control (A1C 7.5-10%), 14 children (14.1%) had poor glycemic control (A1C Ͼ10 -12.5%), and 24 children (24.2%) had very poor glycemic control (A1C Ͼ12.5%). At onset of diabetes, 75% of children presented with diabetic ketoacidosis (DKA); 89 children (89.80%) had at least one episode of DKA, and 55 children (55.67%) had symptomatic hypoglycemic episodes. Microalbuminuria was present in 29 (29.3%) and retinopathy in 22 (22.68%) children.CONCLUSIONS -Although there are some methodological limitations, this survey highlights the difficulties of achieving good metabolic control and the high prevalence of acute and chronic complications in Tanzanian children with type 1 diabetes. These results clearly show that major efforts are needed to improve quality of care in children with type 1 diabetes in Tanzania. Diabetes Care 30:2187-2192, 2007T ype 1 diabetes is one of the most frequent chronic disease in children and represents a public health challenge globally. Its burden is huge in developing countries owing to the lack of a basic means for reaching reasonable glycemic control. Because of the unavailability of reliable epidemiological data, the natural history of type 1 diabetes, including its complications, is largely unknown (1). With the few data available on subSaharan African children, incidence in Tanzania was estimated to be 1.5/ 100,000 (2), and an increase in incidence in Sudan from 9.5/100,000 in 1991 to 10.3/100,000 in 1995 has been reported (3). The prevalence is higher in Western countries (4,5), suggesting the possibility of missed diagnosis in sub-Saharan Africa. In fact, the problem of missed diagnosis of childhood diabetes, although not unique to developing countries (6), is certainly much more common than in developed countries (7). In a Sudanese study, it was reported that 10% of children were not admitted at the time of diagnosis, being admitted only after they developed diabetic ketoacidosis (DKA) or hypoglycemia (3). This situation contributes to omission of patients in the registry as well as to the possibility of death before diagnosis, especially for those aged Ͻ5 years. In sub-Saharan Africa, most children present with DKA at the time of diagnosis (8,...

A significant increase in the prevalence of end-stage renal disease (ESRD) has been reported over the last three decades, paralleling the increasing prevalence of obesity and insulin resistance, also in the pediatric population. Overweight, obesity and the metabolic syndrome, which frequently coexist, contribute substantially to cardiovascular disease and ESRD. A higher body mass index, the presence of type 2 diabetes, hypertension and, of particular importance, reduced insulin sensitivity (IS), have recently emerged as strong independent risk factors for chronic kidney disease and ESRD. Of particular concern, the long-term cardiovascular impact of obesity, although deferred to adult life, has its origins in childhood. Clustering of cardiovascular risk factors is seen in children and adolescents with the highest degree of reduced IS, suggesting that adult consequences of obesity on target organs, including the kidney, are more likely to develop in these young people. This review will discuss the association between obesity and the risk of kidney disease, focusing on the way in which obesity and its metabolic complications may lead to renal involvement and injury, with particular regard to childhood. It is beyond the scope of this article to examine kidney disease as a component of syndromes that result in obesity in childhood.

No abstract

SummaryIn 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.

Obese boys and girls presented an earlier onset of puberty and completion of puberty and an impaired height gain during puberty.

No abstract

Obese adults have shorter telomeres than their normal-weight counterparts, while this phenomenon is not present in childhood.

Oxidant-antioxidant status was investigated in a group of severely obese prepubertal children in comparison with healthy subjects and in relation to a dietary restriction-weight loss program. All subjects underwent anthropometric measurements and determination of lipid profile, lag phase, malondialdehyde (MDA), and vitamin E. Compared with controls, obese children had a significantly higher body mass index (BMI) (28.97 +/- 2.42 vs. 16.03 +/- 1.88 kg/m2; P = 0.0002) and waist-to-hip ratio (WHR) (0.89 +/- 0.03 vs. 0.80 +/- 0.01; P = 0.0004); lag phase and vitamin E levels were significantly decreased [24.05 +/- 16.21 vs. 43.16 +/- 10 min (P = 0.004) and 21.12 +/- 14.96 vs. 35.54 +/- 13.62 micromol/liter (P = 0.02), respectively], whereas MDA was significantly increased (0.90 +/- 0.31 vs. 0.45 +/- 0.24 nmol/mg; P = 0.001). Both lag phase and MDA significantly correlated with BMI [respectively, r = -0.34 (P = 0.004) and r = 0.57 (P = 0.002)] and WHR [respectively, r = -0.63 (P = 0.0001) and r = 0.38 (P = 0.04)]. Oxidant status normalized after 6 months of dietary restriction [lag phase, 59.11 +/- 14.74 min (P = 0.002); MDA, 0.47 +/- 0.09 nmol/mg (P = 0.003)], which was associated with a reduction of BMI (27.34 +/- 1.87 kg/m2; P = 0.003), WHR (0.87 +/- 0.02; P = 0.001), and fat mass (34.49 +/- 2.68%; P = 0.008), but returned to baseline levels together with fatness indexes after another 6 months of free diet. Altered oxidant-antioxidant status is already present in prepubertal severely obese children and is reversible with a dietary restriction-weight loss program, which should be highly encouraged and maintained over time in this age group.