Mehmet Keskin

Insulin Resistance in Obese Children and Adolescents: HOMA-IR Cut-Off Levels in the Prepubertal and Pubertal Periods

Objective: Childhood obesity is associated with an increased risk for insulin resistance. The underlying mechanism for the physiological increase in insulin levels in puberty is not clearly understood. The aim of the present study was to determine the cut−off values for homeostasis model assessment for insulin resistance (HOMA−IR) in obese children and adolescents according to gender and pubertal status. Methods: Two hundred and eight obese children and adolescents (141 girls, 127 boys) aged between 5 and 18 years were included in the study. The children were divided into prepubertal and pubertal groups. A standard oral glucose tolerance test (OGTT) was carried out in all children. A total insulin level exceeding 300 μU/mL in the blood samples, collected during the test period, was taken as the insulin resistance criterion. Cut−off values for HOMA−IR were calculated by receiver operating characteristic (ROC) analysis. Results: In the prepubertal period, the rate of insulin resistance was found to be 37% in boys and 27.8% in girls,while in the pubertal period, this rate was 61.7% in boys and 66.7% in girls. HOMA−IR cut−off values for insulin resistance in the prepubertal period were calculated to be 2.67 (sensitivity 88.2%, specificity 65.5%) in boys and 2.22 (sensitivity 100%, specificity 42.3%) in girls, and in the pubertal period, they were 5.22 (sensitivity 56%, specificity 93.3%) in boys and 3.82 (sensitivity 77.1%, specificity 71.4%) in girls. Conclusions: Since gender, obesity and pubertal status are factors affecting insulin resistance, cut−off values which depend on gender and pubertal status, should be used in evaluation of insulin resistance. Conflict of interest:None declared.

Protein oxidation in obesity and insulin resistance

IntroductionAdvanced oxidation protein products (AOPP) are considered reliable markers to estimate the degree of oxidant-mediated protein damage. Data on oxidative stress in childhood obesity and insulin resistance are limited.ObjectiveThe aim of this study was to investigate the AOPP level as an oxidative stress marker in obesity and insulin resistance. The study included 57 pubertal obese children and adolescents (30 girls and 27 boys) and 20 healthy pubertal children and adolescents (11 girls and 9 boys). Materials and MethodsAll participants in the obesity group underwent an oral glucose tolerance test (OGTT) and two separate groups were formed according to the existence of insulin resistance. ResultsAOPP levels were measured in the obesity and control groups spectrophotometrically. The obesity group consisted of 25 children and adolescents with insulin resistance and 32 subjects without insulin resistance. AOPP levels in the obesity group were found to be significantly higher than those in the control group. Although AOPP levels in the subjects with insulin resistance were higher than the subjects without insulin resistance, there was no significant difference between AOPP levels of subgroups with insulin resistance and without insulin resistance.ConclusionThis study showed protein oxidation in obesity with a novel oxidative stress marker and it also suggests that insulin resistance may play an important role as a source of oxidative stress in the development of other diseases after pubertal years.

Severe Hyperinsulinaemic Hypoglycaemia in a Baby Born to a Mother Taking Oral Ritodrine Therapy for Preterm Labour

Hyperinsulinism of infancy is a major cause of persistent hypoglycaemia in the newborn period. Transient mild self-limiting hyperinsulinaemia and hypoglycaemia have been described in neonates born to mothers taking ritodrine therapy for premature labour. Ritodrine crosses the placental barrier and enters the fetal circulation readily but the mechanism of how it causes hyperinsulinaemia and hypoglycaemia is unclear. We report the case of severe prolonged hyperinsulinaemic hypoglycamia in a neonate born to a mother taking ritodrine therapy from 16 weeks’ gestation for preterm labour. The hyperinsulinaemic hypoglycaemia was managed with oral nifedipine as diazoxide was contraindicated due to fluid overload. Possible mechanisms of ritodrine-induced hypoglycaemia and insulin secretion are discussed.

Thiamine Withdrawal Can Lead to Diabetic Ketoacidosis in Thiamine Responsive Megaloblastic Anemia : Report of Two Siblings

Thiamine responsive megaloblastic anemia syndrome (TRMA), an autosomal recessive disorder caused by the deficiency of thiamine transporter protein, is the association of diabetes mellitus, anemia and deafness. Pharmacological dose thiamine normalizes hematological abnormalities and their effects on the course of diabetes mellitus. We report on 8 years follow up of two siblings with TRMA. They presented in the prepubertal period with diabetic ketoacidosis due to lack of thiamine supplementation for 2 months. Their insulin requirements fell rapidly and disappeared with thiamine therapy. Hematological parameters normalized within 30 days. The diabetic picture is responsive to thiamine treatment in patients with TRMA. Insulin dependent diabetes may occur throughout the pubertal period. If thiamine supplementation is not sufficient, ketoacidosis may develop in patients during the prepubertal period.

Increased Resistin Serum Concentrations in Patients with Type 1 Diabetes Mellitus

Objective: Adiponectin, leptin, and resistin are adipokines which play a significant role in the regulation of lipid and carbohydrate metabolism in patients with type 2 diabetes, while little is known about their role in type 1 diabetes mellitus (T1DM). The aim of this study was to measure serum adiponectin, leptin, and resistin levels and to investigate their relationships with some parameters in patients with T1DM and healthy controls. Methods: Fifty children and adolescents with T1DM (21 boys and 29 girls) and 33 healthy control subjects (18 boys and 15 girls) participated in the study. All subjects were patients followed in the Pediatric Endocrinology and Metabolism Unit of Gaziantep University Faculty of Medicine. None of the subjects had hypertension, obesity, hyperlipidemia, anemia, or infection. Adiponectin, leptin, and resistin levels were analyzed with ELISA. Results: There were no statistically significant differences related with age, sex, pubertal status, or body mass index distribution between the diabetic and control groups. Resistin levels were significantly higher in the diabetic group compared to controls (5.26±3.15 ng/mL vs. 3.50±1.26 ng/mL; p<0.01). Conclusion: Of the three investigated adipokines, only resistin was associated with T1DM. Resistin may play a role in the process of inflammation and also in the pathophysiology of T1DM. Conflict of interest:None declared.

Cohen syndrome with insulin resistance and seizure

Cohen syndrome is a rare, genetic, connective-tissue disorder with the genetic abnormality linked to chromosome 8q22. The diagnosis of Cohen syndrome is based on the recognition of certain clinical findings, which include mental retardation, typical morphologic stigmata (e.g., truncal obesity, hypotonia, short philtrum, prominent frontal incisors, high-arched palate, narrow hands and feet), and characteristic ophthalmologic abnormalities. We report a patient manifesting the typical characteristics of Cohen syndrome with seizure and hyperinsulinemia.

Diabetes mellitus type 1: association with Rett syndrome

Diabetes mellitus type 1 results from the autoimmune destruction of pancreatic beta cell. After describing genetic immunological and metabolic factors, some researchers have hypothesized that environmental factors might trigger the autoimmune process based on epidemiological, anatomical and animal studies. 1 Rett syndrome is now considered to be a neurodevelopmental disorder predominantly occurring in females. 2 There have been recent reports also of affected males, some of whom have an XXY karyotype. 3 Rett syndrome usually occurs sporadically, although rare familial cases have been reported. However, the risk of recurrence is likely to be less than 1%. 4 To our knowledge, our case is the second report of this association in a patient with diabetes mellitus type 1 in addition to Rett syndrome.

Vulvovaginal candidiasis in children and adolescents with type 1 diabetes mellitus.

In this prospective study we investigated the frequency of vulvovaginal candidiasis, the results of yeast cultures and detection of ketoconazole resistance in female children and adolescents with type 1 diabetes mellitus (DM1). The study consisted of 35 patients with DM1 (age 1.7-20 years) and 22 controls (age 1.5-18 years). Age, duration of DM1 and evidence of genital symptoms were recorded initially. After a pelvic examination, two separate swabs and samples for blood glucose and hemoglobin A1c (HbA1c) were taken. One of the swabs was used for direct examination and the second was placed on Sabourauds dextrose agar and incubated. In vitro susceptibility of Candida species to ketoconazole was established by using Etest (AB B1ODISC). Candida species were isolated in 32 of 61 (52.5%) swabs of patients with DM1 and five of 22 (18.2%) of the control group. The predominant Candida species isolated from patients with DM1 were C. albicans (72.7%), C. glabrata (22.7%), C. tropicalis (2.3%), and C. parapsilosis (2.3%). The mean HbA1c in diabetic patients from whom Candida species were isolated was significantly higher than that of patients without Candida infection (p = 0.002). Most of the C. glabrata isolates were significantly resistant to ketoconazole. During the follow-up of patients with DM1, genital candidiasis is generally overlooked. It should not be forgotten that species other than C. albicans might cause genital candidiasis.

Relationship between cord blood levels of IGF-I and ferritin in healthy term neonates.

OBJECTIVE We hypothesize that the balance of maternal and fetal insulin-like growth factor-I (IGF-I) concentrations contributes to the regulation of substrate distribution between mother and fetus, and may thus mediate the maintenance of blood ferritin concentration in the fetus. Therefore, the relationship between cord blood IGF-I to ferritin concentration was investigated. INFANTS AND METHODS Twenty-six term neonates were recruited. Anthropometric measures were recorded and umbilical cord blood samples were collected at birth. We studied serum concentrations of IGF-I in relation to blood ferritin and anthropometric data in term neonates. To assess the importance of the correlation of ferritin with both IGF-I and all other parameters, multiple linear regression analysis was carried out, with ferritin as the dependent variable and IGF-I and anthropometric parameters as independent variables. RESULTS The mean concentrations of cord blood IGF-I and ferritin levels were 45.2 +/- 36.8 ng/ml and 225.5 +/- 124.2 ng/ml, respectively, at birth. A positive correlation was observed between IGF-I and ferritin concentrations of term neonates (r = 0.53, p = 0.005). IGF-I emerged as a significant predictor of ferritin concentration (beta = 1.79, p = 0.005) contributing to 28% of its variability. CONCLUSIONS We showed a relationship between cord blood IGF-I and ferritin levels in term neonates, suggesting that even within an unremarkable population, fetal ferritin level may be influenced by IGF-I. Moreover, we speculated that IGF-I might also be important in the regulation of placental transport of ferritin.

Rhabdomyosarcoma with coexistent diabetes insipidus and cerebral salt wasting as postoperative complication

Correspondence: Professor Selim Kurto ğ lu, Erciyes Üniversitesi T ı p Fakültesi, Çocuk Sa ğ l ı ğ ı ve Hastal ı klar ı Anabilim Dal ı , 38039 Kayseri, Turkey. Email: selimk@erciyes.edu.tr Received 10 December 2003; revised 5 January 2005; accepted 14 January 2005. Children with acute or chronic central nervous system damage may develop a distinctive syndrome of salt wasting. The disorder has been associated with head trauma, central nervous system surgery, tumor or meningitis. The postulated sequence of events could be described as follows: a humoral substance released in response to a brain injury causes impairment in renal tubular salt transport, with resultant diminution in effective vascular volume. A diminished effective vascular volume leads to stimulation of antidiuretic hormone (ADH) release despite the suppressive effect of hyponatremia. ADH in turn impairs urine dilution and causes hyponatremia. 1