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The modalities currently employed to screen for type 2 diabetes mellitus (T2DM)/prediabetes are HbA1c, fasting plasma glucose (FPG), and 2-hour plasma glucose (PG) during an oral glucose tolerance test (OGTT). The purpose of this review is to highlight the positive qualities and pitfalls of these diagnostic modalities and reflect on the most reasonable and effective approach to screen high risk youth. Given its inherent preanalytical advantages, glycated hemoglobin (HbA1c) continues to be the preferred diagnostic modality used by pediatricians to screen high risk youth. However, when the three aforementioned tests are performed in youths of different races/ethnicities, discrepant results for T2DM/prediabetes are observed. The prevalence rates for T2DM vary from 0.53% in Chinese youth (including youth of all body mass indexes) to 18.3% in high-risk, overweight, obese Korean youth. Moreover, the FPG is abnormal (>100 less than <126 mg/dL) in 15% of Korean youth versus 8.7% of Chinese youth. The prevalence rates for prediabetes are 1.49% in Chinese youth versus 21% in Emirati youth (HbA1c, 5.7%-6.4%). The coefficient of agreement, k, between these screening tests for T2DM are fair, 0.45-0.5 across all youth. However, using HbA1c as a comparator, the agreement is weak with FPG (k=0.18 in German youth versus k=0.396 in Korean youth). The American Diabetes Association (ADA) Standards of Medical Care Guidelines define "high risk youth" who need to be tested for T2DM and/or prediabetes. OGTT and HbA1c do not always detect T2DM in similar individuals. HbA1c may not be an ideal test for screening Hispanic and African American youth. FPG and OGTT are suitable screening tests for youth of ethnic minorities and those with cystic fibrosis or hemoglobinopathies. Performing all three tests either together or sequentially may be the only way to encompass all youth who have aberrations in different aspects of glucose homeostasis.

Objective Persistent hypoglycemia (PH) beyond 3 days of life warrants investigation which includes a critical sample. We report our case series of five neonates who presented with PH as the first sign of congenital hypopituitarism. Design This is a case series. Methods/Results This is a case series of five neonates evaluated at our academic institution in a 3-year period (2013-2016), who presented with persistent severe hypoglycemia and were subsequently diagnosed with congenital hypopituitarism. All neonates were full term (mean gestational age 39.8 ± 1.4 weeks) born by caesarian section with a mean weight of 3.5 ± 0.16 kg and a mean length of 51.2 ± 1.2 cm at birth. All five neonates had PH beyond 3 days with an average blood glucose (BG) <35 mg/dL at presentation, requiring a mean glucose infusion rate (GIR) of 7.22 ± 1.98 mg/kg/min. The average BG during the critical sample was 42 ± 0.16 mg/dL (three patients). The mean duration of requirement of the glucose infusion was 6.2 ± 3 days during the immediate neonatal period. Diagnosis of the hypopituitarism took 2-52 days from the initial presentation of hypoglycemia. Besides growth hormone (GH) deficiency, cortisol deficiency was diagnosed in all the five neonates. Neuroimaging findings in all the neonates were consistent with pituitary stalk interruption syndrome (hypoplastic anterior pituitary, ectopic posterior pituitary [EPP] and interrupted pituitary stalk). Conclusions Hypoglycemia is a common metabolic complication affecting an infant in the immediate neonatal period. Delay in the diagnosis of hypopituitarism presenting as hypoglycemia is the result of the lack of awareness among neonatologists and/or pediatricians. We propose that providers be cognizant that PH can be the only presentation of hypopituitarism in the neonatal period. Therefore, having a high index of suspicion about this condition can avoid a delay in the evaluation, diagnosis and treatment of hypopituitarism.

Diagnosis of adrenal insufficiency (AI) in infants can be difficult. While a low random cortisol can signal AI, often confirmatory tests are required when clinical suspicion is strong but the cortisol levels are equivocal. Several studies have demonstrated that in sick preterm infants, there is relative adrenal insufficiency (RAI) defined as an inadequate cortisol production relative to the degree of stress or illness, a condition which can last for several weeks, while in term infants the adrenal axis is mature at birth (Bagnoli F, Mori A, Fommei C, Coriolani G, Badii S, et al. ACTH and cortisol cord plasma concentrations in preterm and term infants. J Perinatol 2013;33:520-4). Adrenocorticotrophic hormone (ACTH) and corticotrophin releasing hormone (CRH) stimulation tests have been validated in infants in several studies. In light of recent reports of false-negative results of stimulation tests, it is imperative to highlight the pitfalls of these tests. The purpose of this communication is to bring attention to the accuracy of timing of these tests in infants.

PURPOSE/OBJECTIVE:Premature adrenarche (PA) often leads to polycystic ovary syndrome (PCOS). Higher anti-mullerian hormone (AMH) levels are reported in PCOS. We studied the androgen profile and AMH profiles in Hispanic girls with PA (aged 5-8 years) and age and body mass index (BMI) matched controls. METHODS:Retrospective review of electronic medical records of girls who met the inclusion criteria for premature adrenarche were done. RESULTS:PA girls (n=76) were matched to control girls (n=12) for age (mean±standard deviation) (6.7±1 years vs. 6.2±1.3 years) and BMI (20±10 kg/m2 vs. 17.8±2.7 kg/m2). Dehydroepiandrostenedione sulfate (63.3±51.3 μg/dL vs. 29.8±17.3 μg/dL, P&lt;0.001) and testosterone levels (11.4±4.8 ng/dL vs. 8.2±2.9 ng/dL, P=0.001) were significantly higher in the PA group than controls. AMH values (&lt;14 years: reference range, 0.49-3.15 ng/mL) were 3.2±2.2 ng/mL vs. 4.6± 3.2 ng/mL respectively in the PA and control groups and were not different (P=0.4). AMH did not show a correlation with bone age (P=0.1), and testosterone (P=0.9) in the PA group. 17-hydroxyprogesterone levels (17-OHP ng/dL) were 39.5±30.5 ng/dL vs. 36.8±19.8 ng/dL in PA versus control girls. The concentration of 17-OHP was not statistically different between the control and PA groups. CONCLUSION/CONCLUSIONS:Higher AMH was not observed in PA girls and no correlation with BA and androgen levels was observed.

OBJECTIVE:To study the effect of using a one time high dose "stoss therapy" of vitamin D2 (ergocalciferol: VD2) on indices of insulin sensitivity {whole body sensitivity index: WBISI} and secretion {insulinogenic index: IGI} measured during an oral glucose tolerance test (OGTT) in obese adolescents with VDD (25 OHD; serum metabolite of vit D: < 30 ng/dL). SUBJECTS AND METHODS/METHODS:In a randomized placebo controlled cross over design 20 obese adolescents with vitamin D deficiency (VDD) had baseline OGTT. Arm A received one time high dose 300,000 IU of ergocalciferol and Arm B received placebo. After 6 weeks the adolescents were reassigned to Arm A if they were in Arm B and vice versa. 25OHD, calcium, parathyroid hormone, comprehensive metabolic panel, urine calcium creatinine ratio were measured at each study visit. OGTTs to assess indices of sensitivity and secretion were done at baseline, 6 weeks and 12 weeks respectively. RESULTS:Adolescents were obese and insulin resistant (mean ± SD: mean age = 15.1 ± 1.9 years; BMI: 32.7 ± 9.8; homeostatic model of insulin resistance: HOMA-IR: 4.2 ± 2.8). Stoss therapy with VD2 increased 25OHD from baseline (16.7 ± 2.9 to 19.5 ± 4.5; p = 0.0029) when compared to the placebo. WBISI (2.8 ± 1.9) showed a trend towards improvement in Rx group (p = 0.0577) after adjustment for covariates. IGI (3 ± 2.2) showed an improvement in both Rx and placebo groups. CONCLUSIONS:Our study demonstrated that using a high dose of VD2 (300,000 IU) did not have any beneficial effect on insulin sensitivity (whole body sensitivity index {WBISI}) and secretory indices (insulinogenic index {IGI}) in obese adolescents. High dose "stoss therapy" of VD2 did not appear to have any beneficial effect on glucose homeostasis on obese adolescents.

BACKGROUND AND OBJECTIVE/OBJECTIVE:Adiposity in pre- and postnatal life may influence menarcheal age. Existing evidence is primarily cross-sectional, failing to address temporality, for which the role of adiposity in early life remains unclear. The current study sought to systematically review longitudinal studies evaluating the associations between birth weight and infant/childhood weight status/weight gain in relation to menarcheal age. METHODS:PubMed, EMBASE, Web of Science, Global Health (Ovid) and CINAHL were systematically searched. Selected studies were limited to English-language articles presenting multi-variable analyses. Seventeen studies reporting risk estimates for birth weight (n = 3), infant/childhood weight gain/weight status (n = 4) or both (n = 10), in relation to menarcheal age were included. RESULTS:Lower vs. higher birth weight was associated with earlier menarche in nine studies and later menarche in one study, while three studies reported a null association. Greater BMI or weight gain over time and greater childhood weight were significantly associated with earlier menarche in nine of nine and six of seven studies, respectively. CONCLUSIONS:Studies suggested that lower birth weight and higher body weight and weight gain in infancy and childhood may increase the risk of early menarche. The pre- and postnatal period may thus be an opportune time for weight control interventions to prevent early menarche, and its subsequent consequences.

Introduction: Hyperosmolar hyperglycemic state (HHS) seen in uncontrolled Type 2 diabetes (T2DM) is characterized by severe hyperglycemia (>600 mg/dl), hyperosmolality (> 330 mOsm/kg), and mild/no ketosis(l). As compared to diabetic ketoacidosis (DKA), in HHS insulin action may be inadequate to facilitate glucose utilization by insulin sensitive tissues but sufficient for the prevention of lipolysis and ketogenesis. A mixed picture (HHS+ DKA) is usually characterized by glucose > 600 mg/dL, pH < 7.3, bicarbonate < 15 mEq/L and serum osmolality > 320 mOsm/kg(2). Actual incidence of this mixed picture (HHS+ DKA) in pediatric diabetes is not well known. Objective: a. Description of the clinical presentation and therapeutic challenges encountered in adolescents who presented with a mixed picture (HHS+ DKA); b. Define the metabolic aberrations encountered during their hospitalizations. Case Series: Patients # 1 & 2 had new onset T2DM and # 3 had T1 DM for two years. Patient ages were (mean +/- SD) 15+/-3.5 years and weight 84 +/-35 kg. Patient # 1 and 2 were African American while patient # 3 was Hispanic. They presented in severe dehydration (15-20%) and altered mental status. Initial labs: glucose 1552 +/-309 mg/dL, serum osmolality 439 +/-112 mOsm/kg, pH 7.1 +/-0.1; bicarbonate 10.3 +/-2.9 mEq/L; alanine aminotransferase (ALT) 43+/- 28 U/L, aspartate aminotransferase (AST) 44 +/-23 U/L; amylase 122 +/-87 U/L, serum creatinine 2 +/-1.2 mg/dL. Management: * Patients' fluid requirements in first 48 hrs: total 17.6 +/-8.3 L (maintenance and deficit correction 5.5 +/-1.3 & 12 +/-7 L respectively). Low dose insulin drip (0.05-0.08 U/kg/hr) was used to correct hyperglycemia and acidosis after initial resuscitation. *Severe hypernatremia (corrected sodium 168 +/-17 mEq/L) and hyperchloremia (130 +/-20 mEq/L) with maximum corrected sodium of 184 mEq/L (Patient # 1) was seen which required use of hypotonic fluids (%

Background:Y chromosome material is detected in 6% of Turner syndrome patients by karyotype (1). Y/autosome translocation in Turner syndrome is associated with a) female genitalia or signs of virilization; b) gonadal dysgenesis and a 7-30% future risk of gonadoblastoma (2). We present an atypical phenotype of a Turner syndrome female with 45,X/45,X,dic(Y;5)(p11.3; p15.3). Clinical case: A 9-year and 10-month-old girl presented with short stature (height: 121 cm, -3.2 SD; weight: 37.6 kg, 75%) and Turner syndrome habitus: wide short neck, broad chest, with no signs of virilization, no cardiac defects, no hepatosplenomegaly and with mild learning disability. Lab evaluation: LH 1.14 (<=2.91 U/L); FSH 50.9 (0.72-5.33 U/L); estradiol <2 (

EMBASE:617153110

ISSN: 0163-769x

CID: 2631962