Highlights Archive Issues

Volume 15, Number 4, 2007

New technologies in pediatric endocrinology

- Editorial
Susan R Rose
- Imaging techniques
Mohamad Maghnie, Andrea Rossi and Paolo Tortori-Donati
- A new approach to steroid analysis: mass spectrometry
Donald Walt Chandler and Russell Philip Grant
- Microarrays and copy number variation
Stefan J White and Andrew H Sinclair
- Proteomics in endocrine research and practice
Elke Clynen and Liliane Schoofs
- Pharmacogenomics in clinical decision-making
Lars Hansen
- Potential endocrine applications of stem cell technology
Linda Baker Lester
- Commentaries

Volume 14, Number 4, 2006

ENDO 2006
The Endocrine Society's 88th Annual Meeting
Boston, USA 24-26 June, 2006

Sumana Sundararajan, Michael S Racine, and Susan R Rose

ENDO 2006 presented the latest advances in clinical and translational endocrinology. Cutting-edge concepts in hormone biology included stem cell biology, insulin action in the brain, tumor micro-environments, molecular systems of aging molecular scaffolds in signal transduction, and new discoveries in the regulation of folliculogenesis. Themes focused on The Endocrine Brain and Controversies in Endocrinology. The speakers at ENDO 2006 came from around the world to bring the very latest in endocrine clinical care and research to the meeting. Teresa K Woodruff served as Basic Science Program Chair and Jennifer Larsen served as Clinical Program Chair. Despite daily rain, the city of Boston charmed participants with its wonderful museums and delicious cuisine.

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Volume 14, Number 3, 2006

ESPE 2006
45th Annual Meeting of the European Society for Paediatric Endocrinology (ESPE)

Rotterdam, The Netherlands 30 June-3 July 2006
By John Achermann, Fergus Cameron, Chris Cowell, Linda Johnston and Susan R. Rose

Volume 14, Number 2, 2006

Puzzling case
Endocrine effects after brain tumor

Editorial

By Susan R Rose

The puzzling case series allows us to use a challenging patient history to solicit the clinical approach used by a number of experts around the world. Participants in this clinical case 'discussion' did not have the opportunity to view the answers of the other respondants, thus the content and the length of their comments were independent of other participants. Many times there was consensus. However, some differences are evident in clinical approach to the endocrine care of late effects after cancer survival. It is clear that some areas of controversy remain.
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Volume 13, Number 5, 2005

Obesity

- Biology and clinical relevance of the adipocytokines leptin, resistin, adiponectin and visfatin as fat cell products
A. Körner, J. Kratzsch and W. Kiess
- Metabolic improvements in morbidly obese adolescents after gastric bypass surgery
Thomas H. Inge
- Pharmacological aspects of obesity
Sridhar Chitturi and Mark Harris
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Volume 13, Number 4, 2005

ESPE/LWPES 7th Joint Meeting Paediatric Endocrinology
in collaboration with APEG, APPES, JSPE and SLEP

Lyon, France
21-24 September, 2005
By John Achermann, Fergus Cameron and Susan R. Rose
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Volume 13, Number 3, 2005

The Endocrine Society's 87th Annual Meeting:
Pathways to Discovery and Practice

San Diego, CA, USA
4-7 June, 2005
By Michael S. Racine, Sumana Sundararajan, and Susan R. Rose
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Volume 13, Number 2, 2005

Thyroid

Editorial

By Susan R Rose

In this issue of Highlights, we focus on the thyroid. Dr Kirk addresses screening for congenital hypothyroidism (CH) in developing nations. Dr Robson summarizes current knowledge about thyroid hormone (TH) effects on the growth plate, while Dr Weetman addresses treatment options in both adult and pediatric Graves' hyperthyroidism. Finally, Drs Moreno and Visser provide an update of the genes disturbed in different thyroid diseases including congenital thyroid gland or pituitary deficiency, TH synthetic defects, TSH receptor mutations, and TH resistance. In addition, this issue includes a summary from the Turner syndrome Workshop held in Vienna in March, 2005. Of course, girls with Turner syndrome have increased risk for autoimmune hypothyroidism.
Unrecognized congenital hypothyroidism leads to mental retardation. Newborn screening and TH therapy started within 2 weeks of age can normalize cognitive development. The primary thyroid-stimulating hormone screening has become standard in many parts of the world but is not yet universal in some countries. Universal salt iodization can prevent morbidity from iodine deficiency.
In the infant with CH, initial dosage of 10 to 15 mg/kg levothyroxine is recommended. Goals of TH therapy should be to keep total T4 or free T4 in the upper half of the normal range during the first 3y of life and to keep TSH 0.5 to 2mU/l to ensure optimal TH dosage and compliance.
Improvements in screening and therapy have led to improved developmental outcomes in adults with CH who are now in their 20s and 30s. TH regimens used today are more aggressive in targeting early correction of TSH than were those used 20 or even 10 years ago, so current newborns with CH may do even better. Hypothyroidism can be acquired after the newborn screening. When clinical symptoms and signs suggest hypothyroidism, regardless of newborn screening results, serum FT4 and TSH assays should be performed.
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Volume 13, Number 1, 2005
Puzzling case

Editorial

By Susan R Rose

This is the third in a series of puzzling cases of growth disorders. The current puzzling case was developed by Fergus Cameron. The case was provided in parts to experts in pediatric endocrinology. The experts did not see the next part until after their response to the prior part. The resulting "conversation" among the experts provides insight into the thought process in evaluating a difficult clinical case. Both the differences and the similarities in responses are interesting.
We appreciate the contributions of all of the participants.
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Volume 12, Number 5, 2004
43rd Annual Meeting of the European Society for
Paediatric Endocrinology (ESPE)

Editorial

By Susan R Rose

Dr Indi Banerjee and Dr John Achermann have prepared an extensive summary of the 2004 ESPE Meeting held in Basel, Switzerland. Topics emphasized included diabetes and immunology, pancreatic development, child-hood obesity, circadian regulation, pituitary gland development, growthhormone release, growth, Turner syndrome, puberty, and endocrine alteration during illness. Finally, in this issue is the report by Fergus Cameron of the Satellite Symposium SGA Directions and Challenges.
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Volume 12, Number 4, 2004
The evolving phenotype of hypopituitarism

Editorial

By Susan R Rose

In the current issue of Highlights, we take the opportunity to review contributions to the phenotype of hypopituitarism. The "phenotype" is the contribution of clinical appearance, physical examination, growth pattern, and other hormone deficiency.

Bazzolo and co-authors compare birth weight, facial gland size and body proportions, skeletal growth, body composition in growth hormone (GH) deficiency compared to syndromes that may have clinical phenotype in common with GH deficiency: GH resistance, Prader-Willi syndrome, intrauterine growth retardation, hypogonadotropic hypogonadism, Williams syndrome, Turner syndrome, and Noonan syndrome.
The article by Padreira reviews changes with age in pituitary gland size and shape, and in MR imaging.
Then the genotype of pituitary abnormalities in mice is described in the article by Thomas, and Dattani correlates the clinical phenotype in humans with these genetic abnormalities.

It is clear that the majority of patients with hypopituitarism have no genetic mutation (as yet identifiable). However, systematic recording of phenotype of our patients may lead to new insights.
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Volume 12, Number 3, 2004
The Endocrine Society's 86th Annual Meeting (ENDO 2004)

ENDO 2004 Focus:
Obesity, Endocrinology and the Future
Susan R. Rose, M.D.

Cincinnati Children's Hospital Medical Center and University of Cincinnati
E. Chester Ridgway, MD, President of The Endocrine Society, indicated that obesity affects more people than ever before and can lead to devastating health problems such as diabetes and cardiovascular disease. Soon, obesity will surpass tobacco as the leading cause of preventable death in the United States, affecting children as well as adults of all races and nationalities. The Endocrine Society and The Hormone Foundation have launched a campaign, "America Weighs In", to educate the public, the media, and Congress about endocrinology and obesity. A resource guide "Obesity in America: The Endocrine Society's Guide to the Nation's Health Crisis" includes facts about obesity and the latest obesity research. The Annual Meeting Committee included BMK Biller, GS McKnight, PM Stewart, and M Jensen. Theme-related sessions addressed adipocyte biology, energy homeostasis, appetite regulation and management of obesity and related diseases. Theme-related activities raised awareness of lifestyle changes that combat obesity (diet/nutrition, fitness/exercise, and overall health). The ENDO 2004 5K Run/Walk race to benefit The Hormone Foundation was held in Audubon Park, with the Mississippi River at its back, ancient oak trees, ducks in the lagoon, and fresh air and exercise among quiet beauty. New Orleans with its unique blend of French heritage and U.S. southern hospitality is famous for its festive spirit, lively music, 17th century architecture lined with intricate iron balconies, and flavorful cuisine (spicy crawfish, Po-Boy sandwiches, shrimp etouffee, muffalettas, jambalaya, gumbo, Bananas Foster, pecan pralines, hot beignets and café au lait).
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Volume 12, Number 2, 2004
Implications of SGA and insulin resistance

Intrauterine influences on subsequent growth

Neus Potau, Ana Carreňo
Hormonal Laboratory, Hospital Materno-Infantil Vail d'Hebron, Barcelona, Spain

Introduction

By definition, nearly 3% of human infants are born small for gestational age (SGA). Approximately 10—15% of SGA infants maintain a height below -2 SD throughout childhood.The cause of short stature is unknown [1]. An increasing series of pediatric endocrinopathies and metabolic anomalies have been associated with reduced prenatal growth.
Fetal growth is a dynamic process involving a balance between the mechanisms controlling substrate uptake, fetal synthesis of protein and lipids, and fuel oxidation for fetal metabolic requirements. In an analogy to postnatal life, intrauterine growth is determined by the interaction of exogenous (nutrition) and endogenous factors (genetics).
Growth of the fetus occurs at an extremely rapid rate relative to the organism's size in late gestation. However, the factors controlling anabolism, mitosis and differentiation have been only poorly defined. The fetal pancreas is competent as an insulin-producing organ before the second trimester in humans. Thus, insulin could potentially serve as a potent anabolic signal, particularly in late gestation when net synthetic rates of protein and lipid appear to be high.
The fetus is dependent on the transfer of nutrients across the placenta for substrate supply. Interferences with this supply may occur at the level of maternal intake or at the level of uteroplacental blood supply and placental function. It is assumed that most intrauterine growth retardation has its origin in interference in nutrient delivery to the fetus.
Other causes of SGA birth could be genetic in origin (such as deletional mutation in the gene encoding insulin growth factor (IGF )-1 [2]), embryopathies as a result of teratogens or infective agents, or substrate limitations.
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