Endocrinology/Diabetes Copyright (c) 2013 University of Massachusetts Medical School All rights reserved. http://escholarship.umassmed.edu/peds_endocrinology Recent documents in Endocrinology/Diabetes en-us Fri, 17 May 2013 11:20:57 PDT 3600 Double Diabetes: The Search for a Treatment Paradigm in Children and Adolescents http://escholarship.umassmed.edu/peds_endocrinology/40 http://escholarship.umassmed.edu/peds_endocrinology/40 Tue, 14 May 2013 08:41:07 PDT Discusses double diabetes -- the coexistence of features of both type 1 and type 2 diabetes in the same individual -- with a comprehensive discussion of the various aspects of this disorder and a focus on the search for a treatment paradigm in children and adolescents.

]]> Benjamin U. Nwosu Diabetes Mellitus, Type 1 Diabetes Mellitus, Type 2 Obesity Adolescent Child Double Diabetes: The Evolving Treatment Paradigm in Children and Adolescents http://escholarship.umassmed.edu/peds_endocrinology/39 http://escholarship.umassmed.edu/peds_endocrinology/39 Thu, 04 Apr 2013 08:24:07 PDT The global pandemic of obesity in children and adolescents has resulted in a new expression of diabetes mellitus designated as double diabetes. The entity encompasses the autoimmune load of Type 1 Diabetes and the metabolic load of Type 2 Diabetes. There is no consensus on the best therapeutic modality for this new expression of diabetes mellitus. Optimal therapeutic options must address the coexistence of both metabolic and autoimmune components of diabetes mellitus in the patient. There have also been calls to revise the current classification of diabetes mellitus to take into account the surging prevalence of double diabetes in children and adolescents.

]]> Benjamin U. Nwosu Diabetes Mellitus, Type 1 Diabetes Mellitus, Type 2 Obesity Adolescent Child Serum 25-hydroxyvitamin D levels do not correlate with asthma severity in a case-controlled study of children and adolescents http://escholarship.umassmed.edu/peds_endocrinology/38 http://escholarship.umassmed.edu/peds_endocrinology/38 Thu, 23 Aug 2012 06:55:56 PDT Background: There is no consensus on the association between vitamin D and asthma.

Objective: To determine the relationship between 25-hydroxyvitamin D [25(OH)D] levels and asthma symptom severity in children and adolescents.

Methods: A retrospective, case-control study of 263 subjects of ages 2–19 years with asthma who were compared to 284 non-asthmatic controls of similar ages. Subjects were excluded if they had diseases of calcium or vitamin D metabolism or were receiving calcium or vitamin D supplementation. Serum 25(OH)D was measured in all subjects. Asthma symptom severity, usually stratified into 6 steps, was stratified into five steps [1–5] based on the number and dose of controller medications used as outlined by the National Heart, Lung, and Blood Institute’s guidelines. Mean 25(OH)D values were compared between the asthmatic patients and controls, as well as among the five steps of asthma symptom severity. Results were adjusted for age, sex, BMI, race and severity of asthma symptoms.

Results:There was no difference in 25(OH)D between asthmatic patients and controls (28.64±10.09 vs. 28.42±11.47, p=1.0). However, there was a significant difference in 25(OH)D between obese and non-obese asthmatic patients (23.33±7.67 vs. 30.16±10.20, p

Conclusions: There were no differences in mean 25(OH)D levels between asthmatic patients and controls. Mean 25(OH)D level was significantly lower in both the obese asthmatic patients and obese controls. Asthma severity had no relationship to mean 25(OH)D levels.

]]> Jennifer Menon et al. Vitamin D Asthma Is vitamin D deficiency a feature of pediatric celiac disease? http://escholarship.umassmed.edu/peds_endocrinology/37 http://escholarship.umassmed.edu/peds_endocrinology/37 Wed, 20 Jun 2012 13:10:10 PDT Background: Celiac disease (CD) is an autoimmune enteropathy characterized by villus atrophy and malabsorption of essential nutrients. Vitamin D deficiency has been described in autoimmune diseases, but its status in prepubertal children with CD has not been adequately studied.

Objective: To determine the vitamin D status of prepubertal children with CD.

Study design: A retrospective study of prepubertal children aged 3–12 years with CD (n=24) who were compared to prepubertal, non-CD children of the same age (n=50). Children were included in the study if they had a diagnosis of CD by intestinal biopsy, and were not on a gluten-free diet (GFD). Patients were excluded if they had diseases of calcium or vitamin D metabolism, or were receiving calcium or vitamin D supplementation or had other autoimmune diseases. All subjects had their serum 25-hydroxyvitamin D [25(OH)D] level measured.

Results: There was no difference in 25(OH)D level between the CD and non-CD children (27.58±9.91 vs. 26.20±10.45, p=0.59). However, when the patients were subdivided into obese and non-obese groups, the non-obese CD patients had a significantly higher 25(OH)D level than the obese normal children (28.39±10.26 vs. 21.58±5.67, p=0.009). In contrast, there was no difference in 25(OH)D level between non-obese CD patients and non-obese normal children (28.39±10.26 vs. 30.64±12.08, p=0.52). The season of 25(OH)D measurement was not a significant confounder (p=0.7).

Conclusions: Our data showed no difference in 25(OH)D levels between normal children and those with CD when adjusted for body mass index.

]]> Jeffrey Villanueva et al. Celiac Disease Vitamin D Deficiency Child The increased incidence of congenital hypothyroidism: fact or fancy? http://escholarship.umassmed.edu/peds_endocrinology/36 http://escholarship.umassmed.edu/peds_endocrinology/36 Fri, 11 May 2012 07:55:55 PDT OBJECTIVE: The incidence of congenital hypothyroidism (CH) detected by newborn screening in the US has increased significantly since the early 1990s. We defined the characteristics associated with the increased incidence.

PATIENTS: A cohort of children with CH born during an earlier period of low incidence (1991-94) was compared with a cohort born during a later period when the incidence of CH had doubled (2001-04).

MEASUREMENTS: Screening was performed with T4 as the primary marker and thyroid stimulating hormone (TSH) on selected specimens. Follow-up on hypothyroid children determined whether they had permanent or transient hypothyroidism. Cases were classified based on laboratory results: initial TSH ≥100 mU/l was 'severe,' initial TSH/l but ≥20 mU/l was 'mild' and initial TSH/l with subsequent abnormal TSH was 'delayed'.

RESULTS: The overall incidence of CH almost doubled between the two time periods, from 1:3010 to 1:1660. Excess cases were found in the mild and delayed categories, with no increase in severe cases. The proportion of transient cases was

CONCLUSION: The rising incidence of CH in Massachusetts is confined to mild and delayed cases. Our findings suggest that this rise is attributable to enhanced detection rather than an absolute increase in numbers.

]]> Marvin L. Mitchell et al. Child Cohort Studies Congenital Hypothyroidism Female Follow-Up Studies Humans Incidence Infant Infant, Newborn Male Massachusetts Neonatal Screening Severity of Illness Index Up-Regulation What causes the insulin resistance underlying obesity? http://escholarship.umassmed.edu/peds_endocrinology/35 http://escholarship.umassmed.edu/peds_endocrinology/35 Mon, 30 Apr 2012 08:04:40 PDT PURPOSE OF REVIEW: The association between obesity and insulin resistance is an area of much interest and enormous public health impact, with hundreds of articles being published in the last year focused on the possible mechanisms that underlie this association. The purpose to this review is to highlight some of the key recent literature with emphasis on emerging concepts.

RECENT FINDINGS: The specific link between visceral adipose tissue accumulation and insulin resistance continues to be discerned. Visceral adiposity is correlated with accumulation of excess lipid in liver, and results in cell autonomous impairment in insulin signaling. Visceral adipose tissue is also prone to inflammation and inflammatory cytokine production, which also contribute to impairment in insulin signaling. The expansion of visceral adipose tissue and excess lipid accumulation in liver and muscle may result from limited expandability of subcutaneous adipose tissue, due to the properties of its extracellular matrix and capacity for capillary growth.

SUMMARY: Recent studies underscore the need to better understand the mechanisms linking visceral adiposity with liver fat accumulation, the mechanisms by which ectopic fat accumulation cause insulin resistance, and the mechanisms by which the size of adipose tissue depots is determined.

]]> Olga T. Hardy et al. Insulin Resistance Obesity Educating diabetes camp counselors with a human patient simulator: A pilot study http://escholarship.umassmed.edu/peds_endocrinology/34 http://escholarship.umassmed.edu/peds_endocrinology/34 Fri, 27 Apr 2012 10:09:08 PDT Purpose.  The purpose of this study was to pilot test the feasibility and efficacy of a novel method of teaching camp counselors hypoglycemia management.

Design and Methods.  During orientation, counselors were assigned to the experimental (n= 21) or control (n= 15) group and received hypoglycemia education. The experimental group received supplemental education with a human patient simulator (HPS).

Results.  Baseline demographics, knowledge, and self-efficacy were similar between groups. The experimental group had a significantly larger gain in diabetes knowledge than the control group. Within-participant change in self-efficacy did not differ by group. We observed a significant effect modification, with larger treatment-related differences in the small subgroup with no previous diabetes exposure.

Practice Implications.  This feasibility study demonstrated the ease of teaching diabetes management to camp counselors using HPS.

]]> Susan Sullivan-Bolyai et al. Diabetes Mellitus, Type 1 Hypoglycemia Counseling Patient Simulation Manikins Stroke in a child with Adams-Oliver syndrome and mixed diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome http://escholarship.umassmed.edu/peds_endocrinology/33 http://escholarship.umassmed.edu/peds_endocrinology/33 Wed, 18 Apr 2012 12:48:28 PDT Diabetes mellitus complicated by mixed diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome presents a special challenge to physicians. There is no standard protocol for the management of mixed hyperglycemic hyperosmolar syndrome and diabetic ketoacidosis in children. The commonest cause of neurological deterioration during an episode of diabetic ketoacidosis is cerebral edema, whereas hyperosmolality often leads to thrombosis. The risks for these complications are further increased in diseases associated with vasculopathies. We present the first case of complex cerebral arteriovenous thrombosis leading to stroke in a child with Adams-Oliver syndrome, a genetic condition that is associated with abnormal vasculogenesis. He presented with new-onset double diabetes complicated by a combination of diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome. Magnetic resonance imaging, magnetic resonance angiography, and magnetic resonance venography provided evidence for an ischemic stroke. Children and adolescents who present with a combination of hyperglycemic hyperosmolar syndrome and diabetic ketoacidosis should be monitored for neurologic deficits and must be investigated for both stroke and cerebral edema in the event of neurological deterioration.

]]> Benjamin U. Nwosu et al. Adams Oliver syndrome Diabetic Ketoacidosis Hyperglycemic Hyperosmolar Nonketotic Coma Diabetes Mellitus, Type 1 Diabetes Mellitus, Type 2 Stroke Does Hepatic Dysfunction Worsen Glucose Homeostasis by Impairing Vitamin D Metabolism? http://escholarship.umassmed.edu/peds_endocrinology/32 http://escholarship.umassmed.edu/peds_endocrinology/32 Thu, 12 Apr 2012 11:23:59 PDT The Management of diabetes mellitus (DM) remains an enigma even though the symptoms of the disease had been described more than 3000 years ago. This is because the central therapeutic goal of DM therapy, euglycemia, is influenced by complex physiologic and pathologic processes, some of which are clearly understood, while others are less clear. Suboptimal glycemic control is a recognized risk factor for acute and chronic complications of diabetes including microvascular and macrovascular diseases. The central question for this editorial is whether mild hepatic dysfunction could impair vitamin D metabolism and secondarily lead to sub-optimal glycemic control.

]]> Benjamin U. Nwosu Liver Diseases Diabetes Mellitus Vitamin D Deficiency Blood Glucose Hepatic dysfunction is associated with vitamin D deficiency and poor glycemic control in diabetes mellitus http://escholarship.umassmed.edu/peds_endocrinology/31 http://escholarship.umassmed.edu/peds_endocrinology/31 Mon, 12 Mar 2012 08:27:12 PDT Background/Aims: The effect of the rising prevalence of nonalcoholic fatty liver disease on the 25-hydroxylation of pre-vitamin D in the liver, and consequent glycemic control in children with diabetes mellitus is not known. Our aim was to determine whether mild hepatic dysfunction was associated with impaired 25-hydroxylation of pre-vitamin D, and if this vitamin D deficiency was associated with impaired glycemic control in children and adolescents with type 1 diabetes (TIDM) and type 2 diabetes (T2DM).

Methods: We analyzed simultaneously measured HbA1c, ALT, AST, and 25OHD levels and clinical parameters in 121 children and adolescents with T1DM (n=81) and T2DM (n=40). The subjects, ages 11–21 years, all had diabetes of >6 months duration. Multivariate linear regression was used to analyze the associations, while comparisons between subgroups were made using two-tailed Student’s t-test.

Results: Vitamin D deficiency (25OHD/mL (37.5 nmol/L) was more prevalent in T2DM patients (47.5%) compared to T1DM patients (18.5%). Subjects with T2DM had significantly elevated transaminases (AST 39.3±2.0 vs. 22.4±1.4, p

Conclusions: The association of elevated ALT with vitamin D deficiency suggests that hepatic dysfunction could impair vitamin D metabolism and negatively impact glycemic control in youth with T2DM.

]]> Benjamin U. Nwosu et al. Vitamin D Deficiency Diabetes Mellitus Fatty Liver Serum Concentrations of Organochlorine Pesticides and Growth among Russian Boys http://escholarship.umassmed.edu/peds_endocrinology/30 http://escholarship.umassmed.edu/peds_endocrinology/30 Fri, 02 Mar 2012 13:08:13 PST Background: Limited human data suggest an association of organochlorine pesticides (OCPs) with adverse effects on children's growth.Objective: We evaluated the associations of OCPs with longitudinally assessed growth among peripubertal boys from a Russian cohort with high environmental OCP levels.

Methods: A cohort of 499 boys enrolled in the Russian Children's Study between 2003 and 2005 at 8-9 years of age were followed prospectively for 4 years. At study entry, 350 boys had serum OCPs measured. Physical examinations were conducted at entry and annually. The longitudinal associations of serum OCPs with annual measurements of body mass index (BMI), height, and height velocity were examined by multivariate mixed-effects regression models for repeated measures, controlling for potential confounders.

Results: Among the 350 boys with OCP measurements, median serum hexachlorobenzene (HCB), β-hexachlorocyclohexane (βHCH), and p,p´-dichlorodiphenyldichloroethylene (p,p´-DDE) concentrations were 159 ng/g lipid, 168 ng/g lipid, and 287 ng/g lipid, respectively. Age-adjusted BMI and height z-scores generally fell within the normal range per World Health Organization standards at entry and during follow-up. However, in adjusted models, boys with higher serum HCB, βHCH, and p,p´-DDE had significantly lower mean [95% confidence interval (CI)] BMI z-scores, by -0.84 (-1.23, -0.46), -1.32 (-1.70, -0.95), and -1.37 (-1.75, -0.98), respectively, for the highest versus lowest quintile. In addition, the highest quintile of p,p´-DDE was associated with a significantly lower mean (95% CI) height z-score, by -0.69 (-1.00, -0.39) than that of the lowest quintile.

Conclusions: Serum OCP concentrations measured at 8-9 years of age were associated with reduced growth, particularly reduced BMI, during the peripubertal period, which may affect attainment of optimal adult body mass and height.

]]> Jane S. Burns et al. Hydrocarbons, Chlorinated Pesticides Hexachlorobenzene Growth and Development Body Mass Index Russia Dioxin and polychlorinated biphenyl concentrations in mother's serum and the timing of pubertal onset in sons http://escholarship.umassmed.edu/peds_endocrinology/29 http://escholarship.umassmed.edu/peds_endocrinology/29 Tue, 06 Dec 2011 06:56:11 PST BACKGROUND: Animal studies have demonstrated that timing of pubertal onset can be altered by prenatal exposure to dioxins or polychlorinated biphenyls (PCBs), but studies of human populations have been quite limited.

METHODS: We assessed the association between maternal serum concentrations of dioxins and PCBs and the sons' age of pubertal onset in a prospective cohort of 489 mother-son pairs from Chapaevsk, Russia, a town contaminated with these chemicals during past industrial activity. The boys were recruited at ages 8 to 9 years, and 4 years of annual follow-up data were included in the analysis. Serum samples were collected at enrollment from both mothers and sons for measurement of dioxin and PCB concentrations using high-resolution mass spectrometry. The sons' pubertal onset--defined as pubertal stage 2 or higher for genitalia (G) or pubic hair (P), or testicular volume >3 mL--was assessed annually by the same physician.

RESULTS: In multivariate Cox models, elevated maternal serum PCBs were associated with earlier pubertal onset defined by stage G2 or higher (4th quartile hazard ratio = 1.7 [95% confidence interval = 1.1- 2.5]), but not for stage P2 or higher or for testicular volume >3 mL. Maternal serum concentrations of dioxin toxic equivalents were not consistently associated with the sons' pubertal onset, although a dose-related delay in pubertal onset (only for G2 or higher) was seen among boys who breast-fed for 6 months or more.

CONCLUSIONS: Maternal PCB serum concentrations measured 8 or 9 years after sons' births--which may reflect sons' prenatal and early-life exposures--were associated with acceleration in some, but not all, measures of pubertal onset.

]]> Olivier Humblet et al. Dioxins Polychlorinated Biphenyls Puberty Male Russia Sexual Maturation Pseudohypoparathyroidism in Children http://escholarship.umassmed.edu/peds_endocrinology/28 http://escholarship.umassmed.edu/peds_endocrinology/28 Tue, 06 Dec 2011 06:37:59 PST Summary: Albright hereditary osteodystrophy (AHO) is a genetic syndrome characterized by a distinctive set of developmental and skeletal defects that may easily be misdiagnosed as exogenous obesity in children. There are very few publications detailing the comprehensive management of children and adolescents with this disorder. This chapter provides a comprehensive discussion of the various aspects of this disorder. At the end, the reader should be able to: (1) List the clinical features of Albright hereditary osteodystrophy, (2) Identify the genetic and molecular abnormalities of AHO, (3) List the clinical features of pseudohypoparathyroidism type 1a (PHP 1a), (4) Describe the management of children and adolescents with PHP 1a.

Citation: Benjamin U. Nwosu (2011). Pseudohypoparathyroidism in Children, Contemporary Aspects of Endocrinology, Evanthia Diamanti-Kandarakis (Ed.), ISBN: 978-953-307-357-6, InTech, Available from: http://www.intechopen.com/articles/show/title/pseudohypoparathyroidism-in-children

]]> Benjamin U. Nwosu Pseudohypoparathyroidism Fibrous Dysplasia, Polyostotic Child Adolescent Pediatrics for Parents Podcast Show 107: Short Stature (Audio File) http://escholarship.umassmed.edu/peds_endocrinology/27 http://escholarship.umassmed.edu/peds_endocrinology/27 Wed, 19 Oct 2011 07:27:33 PDT Interview (mp3 audio file, 13 MB, 29 minutes) by Benjamin Nwosu, MD with Rich Sagall, MD, editor and host of the "Pediatrics for Parents Podcast", October 24, 2010. Dr. Nwosu was interviewed about an article that he and Mary Lee, MD, wrote on the diagnosis and treatment of short and tall stature in children.

Citation: Nwosu, BU. Interview with Rich Sagall, MD, editor and host, “Pediatrics for Parents Show 107- Short Stature”, Pediatrics for Parents Podcast. October 24, 2010. Available from iTunes and http://pedsforparents.libsyn.com/2010/10.

]]> Benjamin U. Nwosu Adolescent Body Height Child Growth Growth Disorders Endocrine parameters of cystic fibrosis: back to basics http://escholarship.umassmed.edu/peds_endocrinology/26 http://escholarship.umassmed.edu/peds_endocrinology/26 Tue, 18 Oct 2011 13:10:51 PDT Dramatic changes in the life expectancy of cystic fibrosis (CF) patients are occurring, creating a cohort of aging individuals experiencing long-term complications of this chronic disease. The two most common of these complications include CF-related diabetes and CF bone disease. The clinical implications of each have become better understood, as have potential therapies. However, data obtained from the basic science studies of both diseases have not been widely recognized. In this review, we focus on the known and hypothesized pathogenesis of these two disorders. Additionally, the molecular underpinnings of CF will be explained along with the potential interactions with endocrine disease phenotypes.

]]> Michael S. Stalvey et al. Aging Animals Bone Diseases, Endocrine Cystic Fibrosis Diabetes Mellitus Disease Progression Female Humans Male Cystic Fibrosis http://escholarship.umassmed.edu/peds_endocrinology/25 http://escholarship.umassmed.edu/peds_endocrinology/25 Tue, 18 Oct 2011 13:04:38 PDT Citation: Stalvey, M., Mueller, C., and Flotte, T. “Cystic Fibrosis”, in Domino FJ, ed., The 5-Minute Clinical Consult 2011. Lippincott Williams & Wilkins, 19th Edition, p. 340-341, 2010.

A preview of this chapter is available via Google Books.

]]> Michael S. Stalvey et al. Cystic Fibrosis Childhood Diabetes Explosion http://escholarship.umassmed.edu/peds_endocrinology/24 http://escholarship.umassmed.edu/peds_endocrinology/24 Tue, 18 Oct 2011 13:04:36 PDT Summary: A century ago, the incidence of both Type 1 (T1D) and Type 2 (T2D) was very low. Worldwide epidemics of both T1D and T2D have placed tremendous burdens on both affected individuals and society. Disproportionate resources are spent on complications of the diseases. Although multiple etiologies have been promulgated, for T1D, causative factors and the precise mechanisms leading to the disease remain elusive. In contrast, the rising incidence of T2D in children is closely associated with the obesity explosion which is strongly linked to an increased food supply and decreased physical activity. The rising incidence of obesity has reached pandemic proportions with more than a billion people affected worldwide. Focus needs to be directed to understanding the complex interaction between genes, the environment, and the immune system culminating in T1D and tackling the obesity epidemic. This chapter will discuss the emergence of the diabetes explosion, the proposed pathogenic mechanisms, and potential interventions.

Citation: Stalvey, M., Schatz, D. “Childhood Diabetes Explosion” in Controversies in Treating Diabetes: Clinical & Research Aspects. Ed LeRoith, D., Vinik, A. Humana Press, p. 179-200, 2008, DOI: 10.1007/978-1-59745-572-5_10.

Partial preview of chapter available via Google Books.

]]> Michael S. Stalvey et al. Diabetes Mellitus, Type 1 Diabetes Mellitus, Type 2 Obesity Epidemics Hyperinsulinism of Infancy: Localization of Focal Forms http://escholarship.umassmed.edu/peds_endocrinology/23 http://escholarship.umassmed.edu/peds_endocrinology/23 Tue, 18 Oct 2011 13:04:34 PDT Summary: Congenital hyperinsulinism is the most common cause of persistent hypoglycemia in infants and children (1). Infants with severe forms of the disorder (formerly termed nesidioblastosis) present with hypoglycemia in the newborn period and are at high risk of seizures, permanent brain damage, and retardation. Infants with congenital hyperinsulinism may have either focal or diffuse abnormalities of the pancreatic β cells. In cases with diffuse disease, an underlying defect in the β-cell adenosoine triphosphate (ATP)-dependent potassium channel may be present, caused by recessive loss of function mutations of the two genes encoding the KATP channel, SUR1 or Kir6.2 (1,2). These mutations may also cause focal hyperinsulinism in which there is an area of β-cell adenomatosis due to loss of heterozygosity for the maternal 11p region and expression of a paternally derived KATP channel mutation (3). Most of the cases with severe hyperinsulinism do not respond to medical therapy with diazoxide, octreotide (Fig. 27B.1), or continuous feedings and require near-total pancreatectomy to control hypoglycemia. However, cases of focal hyperinsulinism can be treated effectively with partial pancreatectomy. The surgical approach and therapeutic outcome for the infants depends on preoperatively distinguishing between focal and diffuse forms of hyperinsulinism. This chapter describes the focal lesions of hyperinsulinism, the pancreatectomy procedure, previous methods of determining the site of focal lesions, and the rationale for using positron emission tomography (PET) scans with 18F-fluoro-L-DOPA.

Citation: Hardy O, Stanley C. PET for localization of focal forms of hyperinsulinism of infancy. In Pediatric PET Imaging. Springer. New York. (2006), p. 479-484, DOI: 10.1007/0-387-34641-4_27.

]]> Olga T. Hardy et al. Hyperinsulinism Neonatal Endocrinology http://escholarship.umassmed.edu/peds_endocrinology/22 http://escholarship.umassmed.edu/peds_endocrinology/22 Tue, 18 Oct 2011 13:04:33 PDT Summary: This chapter covers common endocrine conditions and some of the more unusual endocrine disorders of newborns.

Citation: Catlin EA and Lee MM. “Neonatal Endocrinology,” in McMillan JA (Ed-in-chief), DeAngelis CD, Feigin RD, and Jones MD, Jr, eds. Oski’s Pediatrics: Principles and Practice, 4th ed., Philadelphia: Lippincott, Williams & Wilkins, 2006, 411-423.

A partial preview of this chapter is available via Google Books.

]]> Elizabeth A. Catlin et al. Endocrinology Infant, Newborn Endocrine Disorders of the Newborn http://escholarship.umassmed.edu/peds_endocrinology/21 http://escholarship.umassmed.edu/peds_endocrinology/21 Tue, 18 Oct 2011 13:04:31 PDT Citation: Lee MM, Moshang T. “Endocrine Disorders of Newborn” In Avery GV, Flethcer MA and MadDonald MG, eds. Avery's Neonatology: Pathophysiology and Management of the Newborn, 6th Edition. Philadelphia: Lippincott Williams & Wilkins, 2005, p.914-938.

A partial preview of this chapter is available via Google Books.

]]> Mary M. Lee et al. Endocrinology Infant, Newborn