-
The Executive Committee hassolicited the opinions of theSection
membership with thegoal of creating a Strategic Plan toguide our
efforts. Survey questionswere sent and 55 responses werereceived
which represented 27% ofour members. The ExecutiveCommittee is now
proceeding toimplement these actions, but it isimportant that we
continue to haveinput from the membership of theSection.
The AAP has powerful advocacyavenues. The Department of
FederalAffairs employs lobbyists and ana-lysts to represent the
needs of chil-dren to our legislative bodies. Some
of our membersrequested thatattention be paidto the problem of
unavailability ofsome of the medications we use dueto
pharmaceutical company supplyissues. Many of us are concernedabout
adequate compensation toour programs for the multidiscipli-nary
staff our patients require. Thefuture of our workforce and
incen-tives for pediatricians to enter ourfield was also
mentioned.
Solutions to these issues do notcome quickly. However, the
AAPDepartment of Federal Affairs is fullyaware of the subspecialty
issuesregarding payment and training offuture pediatric
endocrinologists.
The Academy successfully advo-cated for increased Medicaid
pay-ment for pediatricians in theAffordable Care Act,
includingensuring that the payment increaseapplies to pediatric
subspecialists.Additionally, the Academy stronglyadvocates for
funding programs toimprove the subspecialty workforceincluding the
Children’s HospitalGraduate Medical EducationProgram (CHGME) and
the PediatricSubspecialty Loan RepaymentProgram. The AAP also
continues towork with the administration andthe states to advocate
for the needsof children in the implementation ofthe Affordable
Care Act (ACA) andprovide resources to pediatriciansand parents
regarding the ACA.Drug shortages are another area thataffect many
pediatric subspecialistsand the Academy continues to workon the
implementation of threepediatric drug and device laws andend
shortages of important drugs forchildren. Lastly, the AAP is an
advo-cate for basic and translational pedi-atric research funding
as well as theimportance of including children inclinical research.
The AAP closelytracks the National Children’s Studyand
translational research activitiesat the National Institutes of
Health.For more information about activi-ties going on in the AAP
Departmentof Federal Affairs, we encourage section members to read
theFebruary 2014 Washington Reporton Academic and
SubspecialtyAdvocacy. The report will be sentalong with this
newsletter, but is also
Volume 23 • Spring 2014
The Section on
ENDOCRINOLOGYNewsletter
Section on Endocrinology Newsletter Copyright © 2014 American
Academy of Pediatrics
Continued on Page 2
IN THIS ISSUEChairperson’s Column
.....................................................................................
1-22014 AAP Council & Section Elections are Underway!
....................................... 2Gonadotropins, sex
steroids and gonadotropin-releasing analogs: A practical approach
to the assessment of a child with early onset of secondary sex
characteristics
......................................................................
3-9Editor’s Comments:
............................................................................................
9Not a Member? Joining is Easy!
..........................................................................
9“Pediatric fellowship information for dummies”!
....................................... 10-11New
Members...................................................................................................
11Book Review: Auxology Studying Human Growth and Development
............... 12TODAY Study Publications Summarized from June
2013 Diabetes Care Journal Feature
....................................................................
13-14Federal Legislative Update
................................................................................
14EQIPP: Growth Surveillance
..............................................................................
15Executive Committee
.......................................................................................
16Endocrinology Meeting Schedule
......................................................................
16
Chairperson’s ColumnWhere Are We Heading?
Irene N. Sills, FAAP
-
available to members in electronic form
atwww.aap.org/subspecialty.
The Section Executive Committee is also taking a role
inadvocating for issues of importance to pediatric
endocri-nologists. Dr. Jane Lynch has written a resolution to
beconsidered at the Annual Leadership Forum (ALF) thatstates that
the AAP supports policies that ensure thatinsurance plans cover
adequate numbers of glucosestrips for children with diabetes. The
resolution was dis-cussed and voted on during the ALF March 13 –
16, 2014.If there are other issues that you feel should be
consid-ered and addressed by the Section Executive Committee,please
let us know.
The survey included questions about which PediatricEndocrinology
topics should receive attention for educa-tion to the primary care
pediatrician. The diagnosis andearly management of precocious
puberty was onefavored, therefore, Drs. Paul Kaplowitz and Clifford
Blochhave begun work on such a Clinical Report for the
AAPmembership. Growth and short stature was also a favoredtopic and
we need a volunteer to investigate the existingstatements and
ascertain if a need exists for a new reportor an update of an
earlier report. There were many others mentioned and the Committee
would welcomeothers of you who agree to be involved.
AAP has become a leader in providing resources for Maintenance
of Certification (MOC). PREPENDOCRINOLOGY Self-Assessment has
become a suc-cessful way to obtain MOC part 2 credit. The
Educationin Quality Improvement for Pediatric Practice
(EQIPP)courses allow physicians to collect and analyze practicedata
over time to document improved quality of care andmeets MOC part 4
requirements. STEP Up Diabetes Care– Screening, Testing, Education
and Prevention is cur-rently available and a course on Growth
Surveillance andGrowth Failure will be available in the near
future. Visithttp://eqipp.aap.org/ for information on
availablecourses and to receive notification when upcomingcourses
will be available. One suggestion from the surveywas to develop an
EQIPP module on congenital hypothy-roidism.
Lastly, the Executive Committee feels and the survey sup-ports
that it is time to improve our Section website.Wonderful
suggestions include a comprehensive list ofPediatric Endocrinology
meetings, links to relevant AAPclinical statements and reports,
information about mem-bers and memberships, FDA updates, links to
otherendocrinology/diabetes organizations, and updates onMOC
certification. However, the Executive Committee issearching for a
group of interested individuals and this
may be a valuable way for you to contribute to our
organ-ization.
As the Section Chairperson, I am always interested toknow what
you think. Please e-mail me [email protected] with any comments,
critiques,requests, or news.
Page 2 Section on Endocrinology - Spring 2014
Chairperson’s Column Continued from Page 1
2014 AAP Council
& Section Elections are Underway!
WHAT:Elect the future leaders of your AAP Councils &
Sections and vote on any applicable bylaw referendums
WHY:To exercise your right to vote as a member and toinfluence
the direction of the Council or Section inthe future
WHEN:March 1 -31, 2014. The elected Council leaderswill take
office on July 1, 2014. The elected Sectionleaders will take office
on November 1, 2014.
WHERE:http://www2.aap.org/elections to view the
on-line ballot and biographical information onthe candidates (if
available). Use your AAP ID and password to log in. If you’ve
signed up forhealthychildren.org you will need to use youremail
address.
Note:If you are a member of more than one Council orSection, you
will see ballots only for the council(s)and section(s) conducting
elections this year.
Any questions about this service may be directedto Yolanda
Mackey Amjad, Manager, Council andSection Programs, Department of
SubspecialtyPediatrics, 847/434-4079 or [email protected].
Thank you in advance for your participation!
-
Section on Endocrinology - Spring 2014 Page 3
Glossary of Terms
Sexual precocity: early onset of sec-ondary sexual
characteristics of anytype without reference to an estab-lished
cause.
Central precocious puberty (CPP):early onset of secondary sexual
characteristics derived from GnRHand gonadotropin dependentgonadal
activity. Central precocious puberty may also be referred to
asgonadotropin dependent preco-cious puberty.
Physiology of Sexual Maturation
Puberty is a developmental phase inthe continuum of the
maturation ofthe reproductive axis across the lifes-pan. The
hypothalamic-pituitary-gonadal axis (HPGA), which is drivenby
hypothalamic gonadotropin-releasing hormone (GnRH), is activein
utero and early infancy. In the firstfew months after birth, the
activity ofthe GnRH pulse generator decreasesuntil it enters a
relative quiescentstate by 4 months of age, oftenreferred to as the
inhibitory phase.This juvenile pause lasts throughoutchildhood
until 8 to 9 years of age. It has been postulated that the
rela-tively quiescent state of the repro-ductive system during
theprepubertal years is the result of acombination of two
mechanisms:first and most importantly, an intrin-sic central
nervous system (CNS)inhibition responsible for maintain-ing GnRH
and gonadotropin secre-tion at low levels and minimalpulsatility;
second and to a lesserdegree, an increased sensitivity ofthe HPGA
to sex steroid negativefeedback1,2.
The underlying mechanism that dic-tates when the inhibitory
phase, alsodescribed as a “neurobiologicalbrake”, ends is unknown3.
The linkbetween a critical amount of somaticgrowth and the central
initiation ofpuberty has been in the literature fordecades and is
thought to dependon a hypothalamic somatometer,analogous to a
clock34. In the eyes ofthe clinician, this link is best
illus-trated when the level of physicalmaturation is aligned with
indices ofphysical progression such as skeletalbone age,
nutritional state andgrowth velocity. For example, a boneage of 13
years in a 10 year old malewould make one anticipate midpu-bertal
characteristics that may notnecessarily reflect the
chronologicalage of the patient. Another exampleis the overweight
girl with tallerstature who is more likely to reachand progress
through pubertal mat-uration at a faster pace than her
nor-mal-weight counterparts.
At the onset of the pubertal phase,the reactivation of the
reproductiveaxis is believed to result from thegradual decrease of
the CNSinhibitory tone and decreased sensi-tivity to sex steroid
feedback. As aresult, there is increased pulsatilesecretion of
GnRH, heightened pitu-itary responsiveness to GnRH, risingsecretion
of gonadotropins predom-inantly at night5, especially luteiniz-ing
hormone (LH), and enhancedgonadal production of sex steroidsmainly
represented by circulatingestradiol and testosterone
concen-trations. These gonadal hormoneswill induce the
morphologicalchanges of puberty.
Gonadarche and Adrenarche
When pubertal maturation isassessed, there is an overlap of
twodistinct maturation processes. Onerelates to adrenarche
reflected by thedevelopment of body odor, pubicand axillary hair.
The other relates togonadarche with breast develop-ment in girls
and testicular enlarge-ment in boys, the initial clinical signsof
true puberty.
Adrenarche is expected to occur after8 years in both boys and
girls but theonset is subject to wide individualvariations.
Progressive increase inthe secretion of weak androgens bythe
adrenal glands, in particulardehydroepiandrosterone (DHEA)and its
sulfate (DHEAS), occurs untiladult values are reached at about
15years of age or in the mid- to latepubertal years 6.
Precociousadrenarche will occur before the ageof 8 years, usually
between 5 and 7years and is a common reason forreferral to a
pediatric endocrinologyclinic6. It is thought to be a normalvariant
of development as long asthe growth velocity is in the prepu-bertal
range, the bone age is at mostonly mildly advanced (
-
Page 4 Section on Endocrinology - Spring 2014
results in full reproductive potential:spermatogenesis in males
and ovu-latory menstrual cycle in female.
From a clinical standpoint, it isimportant to assess the
develop-mental stages of adrenarche andgonadarche separately and as
accu-rately as possible. This strategyassists in distinguishing
various clin-ical entities including the focus ofthis article,
central precociouspuberty.
Timing of sexual maturation
Based on the Third National Healthand Nutrition Examination
Survey(NHANES III), in boys, the medianage for the onset of genital
develop-ment was approximately 9.2 yearsfor non-Hispanic black
boys,approximately 10.0 years for non-Hispanic white boys, and 10.3
yearsfor Mexican American boys. Thethreshold for pubertal
developmentin boys is 9 years10 and the first stageof puberty in
boys is characterizedby testicular enlargement or Tannerstage 2
genitalia, assessed as testic-ular volume > 3 ml in volume or
2.5cm in length [Marshall WA, TannerJM. Variations in the pattern
ofpubertal changes in boys. Arch DisChild 1970; 45: 13-23. Prader,
A.Testicular size: Assessment and clin-ical importance. Triangle
1966;7:240-243.]
In girls, the threshold for breastdevelopment is 8 years
regardless ofethnicity12,13. It has been found thatthe median age
for the onset ofbreast development was approxi-mately 9.5 years for
non-Hispanicblack girls, approximately 9.8 yearsfor Mexican
American girls, andapproximately 10.4 years for non-Hispanic white
girls. As studied byTanner et al.11,14 the onset of pubertyin girls
is typically characterized bythe development of thelarche orTanner
stage 2, which is best evalu-ated by both inspection and
palpa-tion.
For all practical purposes, sexualmaturation, distinct from
simpleadrenarche, should be consideredprecocious if secondary sex
charac-teristics appear before 8 years of agein girls and before 9
years of age inboys. One has to bear in mind how-ever that early
puberty can be elusiveif there are competing physical
char-acteristics such as obesity.
In boys, the accumulation of supra-pubic fat can obscure the
examina-tion of the genitalia and makepuberty staging
difficult.Furthermore, extreme obesity in themale can paradoxically
be associ-ated with delayed onset of puberty,which will not be
discussed here.
One of the major challenges in ascer-taining pubertal maturation
in girlsis recognizing that adipose tissuecan masquerade as early
breastdevelopment, particularly in thecontext of rising rates of
childhoodobesity15. In contrast, menarche, areadily identifiable
event, is a robustindicator of pubertal progressionthat is not as
dependent on clinicalskills. Thus, despite considerablemedia
coverage suggesting earlieronset of puberty in girls mostlybased on
clinical assessment thatdid not adjust for adiposity, statisti-cal
data points to remarkable stabil-ity of the average age of menarche
inaffluent nations where previous sec-ular trends have plateaued
16.
Based on NHANES III, the averageage at menarche in the US is
12.54years; this data represents a decreaseof �~2½ months over the
previous 25years17. During the same timeperiod, the percentage of
10 to 15-year-old girls in the United Stateswho were above the 85th
percentilefor BMI increased from 16% to27%17, thereby increasing
the likeli-hood of obese preadolescent girlswith central adiposity
to be misla-beled as early pubertal. Most recentresults from NHANES
indicate that
the prevalence of childhood obesityin the United States
remainsunchanged although increases inobesity prevalence may be
occurringamong males 18.
Higher relative weight has beenstrongly associated with
earlierachievement of menarche after con-trolling for age and race.
This findingsupports the long-understood asso-ciation between
sexual maturationand adiposity and the role of rela-tive weight as
a possible explanatoryfactor for the secular trend towardearlier
onset of puberty, which hassince stabilized in the US
popula-tion.
Precocious puberty: Why evaluate?
When a patient presents with a ques-tion of early pubertal
maturation therole of the clinician is to establishwhether this
sexual precocity isgonadotropin dependent or inde-pendent, bearing
in mind that a sig-nificant proportion of patients willpresent with
adrenarche which canbe established after careful
clinicalexamination. One example is the 7year old girl brought in
by hermother because she is “developingtoo fast”. If the physical
examinationreveals only pubic hair and axillaryhair without breast
development,the sexual precocity is likely relatedto adrenarche
rather than earlypuberty.
Central precocious puberty is a clas-sification that can be used
whenthere is a clear link between second-ary sexual characteristics
and GnRHactivated gonadotropins19. Centralprecocious puberty is
much morecommon in girls than in boys. In girlsthe most common
final diagnosis isCPP that is idiopathic or without arecognizable
cause. This centrallymediated precocious puberty usu-ally follows a
sequentially normal,although accelerated pattern of mat-
Gonadotropins, sex steroids and gonadotropin-releasing . . .
Continued from Page 3
Continued on Page 5
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Section on Endocrinology - Spring 2014 Page 5
uration. Approximately 85 % of casesof precocious puberty in
girls and 35% in boys can be attributed to idio-pathic, premature
maturation of theHPGA.20 Despite the high incidenceof centrally
mediated, “idiopathic”precocious puberty, the clinicianmust
diligently search for pathologiccauses, especially in boys. The
ini-tial motivation for the evaluationrests on the possibility that
an iden-tifiable cause for CPP could be treat-able with the
potential of reversal ofsymptoms. Aside from the primaryconcern of
a treatable cause, sec-ondary outcomes considered relateto
potential compromise of finaladult height.
Causes of precocious puberty
GnRH-dependent puberty
Central precocious puberty is con-sidered to be organic when it
is asso-ciated with a lesion of the CNS andas idiopathic when the
magnetic res-onance imaging (MRI) shows noidentifiable lesion of
the centralnervous system. The incidence ofidiopathic forms and the
pattern ofdevelopment of CPP vary accordingto gender. All boys with
CPP and girlswith organic CPP have rapidly pro-gressive forms,
while girls with idio-pathic CPP may have a slowlyprogressive
variant in which pre-dicted height is not altered even after2 years
of spontaneous evolution21.
Any type of intracranial disturbancecan cause organic
precociouspuberty including hamartomas,CNS tumors such as
astrocytoma,ependymoma, pinealomas, andoptic and hypothalamic
gliomas.CNS irradiation may also cause pre-cocious puberty and is
commonlyassociated with growth hormone(GH) deficiency. Other CNS
lesionsinclude hydrocephalus, cysts,trauma, CNS inflammatory
disease,and congenital mid-line defects,such as optic nerve
hypoplasia.
GnRH-independent puberty
The causes of GnRH-independentpuberty include gonadal, adrenal
orectopic sources of hormone produc-tion or may result from
exposure toan exogenous source of sex steroid.Gonadal causes
include McCune-Albright syndrome, familial maleprecocious puberty,
and ovarian ortesticular neoplasms. Adrenal causesinclude
congenital adrenal hyper-plasia (CAH) and tumors. Ectopiccauses
include human-chorionic-gonadotropin secreting tumors. Arelatively
new source of exogenoussteroids in children results
fromcross-contamination from adultsusing testosterone gels or
creams.
Diagnosis
The challenge of diagnosing centralprecocious puberty with a
single LHmeasurementGonadotropins are mostly secretedat night,
therefore a random daytimesample has a limited use althoughseveral
studies have attempted tosupport its utility as an initial
labora-tory screening test for precociouspuberty.23 24
Multiple generations of gona -dotropin assays have improved
sen-sitivity at the lower limits ofdetection. However, in girls
there issignificant overlap between prepu-bertal controls and early
pubertalpatients which further limits the use-fulness of random
gonadotropinscreening. In boys, a cut-off value of0.1 UI/L has been
suggested butthere are limited studies that clearlysupport this
threshold value. 25,26 2623
GnRH stimulation test: A historicalgold standardGnRH is a
decapeptide with a veryshort half-life which has not
beensuccessfully sampled from theperipheral circulation. As a
result,pediatric endocrinologists haverelied for years on the use
of GnRH
for the assessment of gonadotrophs’response by comparing the 1
hour-post-challenge LH and FSH levels tobaseline27. Pituitary
responsivenessin prepubertal children is character-ized by a
preferential release of FSHin response of GnRH. Girls havemore
pronounced FSH release thantheir male counterparts at all stagesof
puberty26. The interpretation ofpubertal status relies on a
semi-quantitative assessment of “prefer-ential LH release” or an LH
to FSHratio greater than 115. The validationof absolute cut-off
values inresponse to stimulation have beenhampered by the rapid
developmentof new assays with greater sensitivity,thereby
generating a moving targetfor normative data15.
GnRH testing refers to stimulatedgonadotropin values at 20-40
min-utes. Long-acting gonadotropinreleasing hormone analogs
havebeen used as a substitute for GnRHbecause of reduced
manufacturingof the synthetic hormone replicat-ing the original
physiologicdecapeptide. GnRH analog stimu-lated values are
collected at 60 min-utes post-injection. Although therehas been no
systematic validation ofthe interchangeability of the testsrecent
summary reports haveincluded data from both methods ofassessment of
the HPGA.
There is no consensus on a hor-monal threshold that defines
earlyCPP as a distinct group from prepu-bertal children. The
development ofnew assays have allowed GnRH ana-log-stimulated LH
concentrationcut-off to drop from >10 to 6 to morerecently 3.3
to 5 mIU/mL28. Thegreatest challenge however residesin the great
variability in assays usedfrom institution to institution,thereby
severely limiting the appli-cability of these cut-off values for
theaverage clinician. What hasremained consistent however, from
Gonadotropins, sex steroids and gonadotropin-releasing . . .
Continued from Page 4
Continued on Page 6
-
both research and clinical data isthat centrally-mediated
puberty ischaracterized by a predominant LHrelease in response to
GnRH stimu-lation. It is our opinion that stimula-tion tests should
combine theabsolute values of both LH and FSHand that LH/FSH ratio
of 1 or greateris consistent with CPP.
Sex steroids and Precocious puberty
In tandem mass spectrometry assayscommercially available,
measurableestradiol >15 pg/mL relatively con-firms advanced
puberty30. Similarly,testosterone assays with detectionlimits of
>10 ng/dL may discriminateprepubertal from early pubertal
lev-els3130. Random estradiol levels mayor may not be measurable at
thepresentation of CPP for several rea-sons. Most commercial
laboratoriesprocess large volumes of adult sam-ples and are
calibrated for higherconcentrations of estradiol. Hencemany routine
assays are not sensi-tive enough to capture low concen-trations of
circulating estradiol asseen in early puberty. In addition tothe
limitation associated with lowhormonal levels, circulating
estra-diol also fluctuates through the daywith higher
concentrations detectedin the morning for early pubertalgirls29.
Bearing in mind the limita-tions associated with these methods,we
recommend using laboratoriesthat provide normal ranges for bothsex
steroids classified by Tannerstage. We also recommend deliber-ate
timing of the sample in earlymorning to provide a better yield,
asit is more likely to reflect overnightgonadotropin activity.
Establishing the diagnosis of cen-tral precocious puberty
The clinician should evaluate forpotential triggering
circumstancesand identify treatable causes. In thisprocess an MRI
of the brain with aspecial focus of the hypothalamicpituitary is
recommended although
the universal application of thisstrategy has been challenged in
thepast 32-34. The discussion with thefamily should emphasize that
thepubertal process is not a disease;rather the early timing may
haverepercussions on overall health,especially if there is a CNS
pathologyat the outset. Once immediatethreats to wellbeing have
been setaside, a discussion about the impactof CPP on final height
can take place,taking into account family historyand with the
support of a bone ageand calculated predicted heightfrom
standardized tables35.
Cases in which the height predictionis consistent with the
genetic back-ground of the child and/or fall withinnormal range, do
not necessarilyrequire treatment on the basis ofheight alone. Girls
with CPP betweenthe ages of 7 to 8 have not beenshown to benefit
from suppressivetherapy with improved height pre-dictions 36,37.
[This statement is con-troversial, based upon the
editor’sexperience.] Further considerationscan be given to the
psychosocialimpact of precocious puberty par-ticularly in girls but
the outcomesappear to be linked to cognitive abil-ities, cultural
norms and familialattitude towards sexual develop-ment16.
There is mounting evidence thatsubclinical estradiol
concentrationsin prepubertal girls have a beneficialeffect on
long-term bone density.This observation may have rele-vance to the
discussion related to theduration of GnRH analog suppres-sive
therapy38. A comprehensive dis-cussion weighing all of
theseparameters can assist the family inmaking an informed decision
forthose cases in which treatment maynot necessarily improve their
heightprediction.
It is now suggested that daytimespontaneous LH
concentrations
may provide a useful laboratoryscreening test in patients that
arebeing evaluated for CPP. Elevatedbasal values may be considered
forfurther evaluation by the gold stan-dard GnRH stimulation test.
Thereis no single level of LH, FSH, or estra-diol with 100%
sensitivity and speci-ficity for CPP. As with all clinical
tests,both clinical presentation and labo-ratory findings should be
taken intoconsideration for the accurate diag-nosis of CPP.
Treatment considerations
Once CPP has been conclusivelyestablished, long-acting
GnRHanalogs provide the most efficacioussuppressive therapy. The
goals ofcurrent therapy with these GnRHanalogs include suppression
ofpubertal progression, delay of onsetof menses and improved final
heightpotential. A discussion about thebone age and the percentage
of adultcompleted height associated withthat bone age can assist
the clinicianand the patient’s family in articulat-ing goals for
treatment. One has tobear in mind that more advancedbone age is
less likely to benefit withimproved final height outcome.
Treatment with long-acting GnRHanalogs implies an initial gona
-dotropin stimulation phase; there-fore an advancement of the bone
ageat the beginning of therapy is antic-ipated in most cases. Great
careshould be undertaken to avoidrepeating this initial
stimulationphase and the risk of impairingheight outcomes. Thus
strict adher-ence to the prescribed schedule ofsuppressive therapy
and commit-ment from the family are requisitesfor a successful
outcome. GnRHanalog treatment in patients with abone age reflecting
more than 95%final height, might further acceleratethe skeletal
maturation with mini-mal hopes of capitalizing on the few
Page 6 Section on Endocrinology - Spring 2014
Gonadotropins, sex steroids and gonadotropin-releasing . . .
Continued from Page 5
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References
1) Kulin HE, Grumbach MM, Kaplan SL. Changing sensitivity of the
pubertal gonadal hypothalamic feedback mechanism in man.Science.
1969;166(3908):1012-1013.
2) Kelch RP, Kaplan SL, Ghumbach MM. Suppression of urinary and
plasma follicle-stimulating hormone by exogenous estro-gens in
prepubertal and pubertal children. J Clin Invest.
1973;52(5):1122-1128.
3) Plant TM. Hypothalamic control of the pituitary-gonadal axis
in higher primates: Key advances over the last two decades.
JNeuroendocrinol. 2008;20(6):719-726.
4) Rosen DS, Kletter GB, Kelch RP. Puberty what to do when the
clock doesn’t ring. Journal of Pediatric Endocrinology
andMetabolism. 1998;5 (3) de Gruyter(Jul 1,):29-41.
5) Cemeroglu AP, Foster CM, Warner R, Kletter GB, Marshall JC,
Kelch RP. Comparison of the neuroendocrine control of puber-tal
maturation in girls and boys with spontaneous puberty and in
hypogonadal girls. J Clin Endocrinol Metab.
1996;81(12):4352-4357.
6) Sizonenko PC, Paunier L. Hormonal changes in puberty III:
Correlation of plasma dehydroepiandrosterone, testosterone, FSH,and
LH with stages of puberty and bone age in normal boys and girls and
in patients with addison’s disease or hypogonadismor with premature
or late adrenarche. J Clin Endocrinol Metab.
1975;41(5):894-904.
7) von Oettingen J, Sola Pou J, Levitsky LL, Misra M. Clinical
presentation of children with premature adrenarche. Clin
Pediatr(Phila). 2012;51(12):1140-1149.
8) Miller WL. The molecular basis of premature adrenarche: An
hypothesis. Acta Paediatr Suppl. 1999;88(433):60-66.
9) Rege J, Rainey WE. The steroid metabolome of adrenarche. J
Endocrinol. 2012;214(2):133-143.
10) Sun SS, Schubert CM, Chumlea WC, et al. National estimates
of the timing of sexual maturation and racial differences amongUS
children. Pediatrics. 2002;110(5):911-919.
11) Marshall WA, Tanner JM. Variations in pattern of pubertal
changes in girls. Arch Dis Child. 1969;44(235):291-303.
12) Rosenfield RL, Lipton RB, Drum ML. Thelarche, pubarche, and
menarche attainment in children with normal and elevatedbody mass
index. Pediatrics. 2009;123(1):84-88.
13) Rosenfield RL, Bachrach LK, Chernausek SD, et al. Current
age of onset of puberty. Pediatrics. 2000;106(3):622-623.
14) Marshall WA, Tanner JM. Variations in the pattern of
pubertal changes in boys. Arch Dis Child. 1970;45(239):13-23.
15) Kasa-Vubu J. Obesity and puberty: The impact of childhood
obesity on central precocious puberty. Pediatric Endocrinology
centimeters of somatic growth left.In that case, if improved
final heightis the principal motivation for thefamily to seek
treatment, proceed-ing with GnRH analog suppressivetherapy is
debatable.
The duration of treatment should bediscussed with patients and
theirfamilies with the understanding thatpuberty may not resume for
severalmonths after discontinuation ofsuppressive therapy and a
longerduration may achieve better finalheight outcomes. In general,
discon-tinuing treatment at the time whenage-matched peers are
initiatingspontaneous puberty is appropriate.Despite the
theoretical risk, there isno evidence thus far that
pubertysuppressive therapy is associatedwith decreased bone density
but
conclusive long-term data is lackinggiven the lifespan
implicationsrelated to bone health.
Biochemical suppression is ade-quate when LH levels are
suppressedbut variability between assaysshould be interpreted with
cau-tion39,40. If testosterone and estra-diol are measured, levels
should bein a prepubertal range for the assayused.41
Clinicians need to be aware that anoptimal index for LH
suppression(random or stimulated) has not yetbeen defined. If the
clinical evalua-tion reveals progression of breast ortesticular
development, increasedgrowth velocity or rapid bone ageadvancement,
these clinical signsare suggestive of insufficient dosing,
lack of compliance with the fre-quency of dosing or treatment
fail-ure. Anyone of these possibilitiesimplies the need for further
assess-ment41, including discontinuationof therapy.
Conclusion
Central precocious puberty resultsfrom the activation of the
HPGAbefore age thresholds that are thesame across major ethnic
groups42,43. The evaluation should focus ondefining the source of
sex steroidsand, if indicated, assessing whetherthe maturation is
centrally-medi-ated. Aside from the possibility ofCNS pathology,
secondary concernsrelate to the potential compromiseof final adult
height and in somecases, the potential of a negative psy-chosocial
impact.
Section on Endocrinology - Spring 2014 Page 7
Gonadotropins, sex steroids and gonadotropin-releasing . . .
Continued from Page 6
Continued on Page 8
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Page 8 Section on Endocrinology - Spring 2014
Reviews. 2007;4(SUPPL. 3):291-299.
16) Parent AS, Teilmann G, Juul A, Skakkebaek NE, Toppari J,
Bourguignon JP. The timing of normal puberty and the age limits
ofsexual precocity: Variations around the world, secular trends,
and changes after migration. Endocr Rev. 2003;24(5):668-693.
17) Anderson SE, Dallal GE, Must A. Relative weight and race
influence average age at menarche: Results from two nationally
rep-resentative surveys of US girls studied 25 years apart.
Pediatrics. 2003;111(4 Pt 1):844-850.
18) Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of
obesity and trends in body mass index among US children and
ado-lescents, 1999-2010. JAMA. 2012;307(5):483-490.
19) Klein KO. Precocious puberty: Who has it? who should be
treated? J Clin Endocrinol Metab. 1999;84(2):411-414.
20) Kelch RP. Management of precocious puberty. N Engl J Med.
1985;312(16):1057-1058.
21) Trivin C, Couto-Silva AC, Sainte-Rose C, et al. Presentation
and evolution of organic central precocious puberty according tothe
type of CNS lesion. Clin Endocrinol (Oxf). 2006;65(2):239-245.
22) Listernick R, Charrow J, Gutmann DH. Intracranial gliomas in
neurofibromatosis type 1. Am J Med Genet. 1999;89(1):38-44.
23) Houk CP, Kunselman AR, Lee PA. Adequacy of a single
unstimulated luteinizing hormone level to diagnose central
precociouspuberty in girls. Pediatrics. 2009;123(6):e1059-63.
24) Neely EK, Wilson DM, Lee PA, Stene M, Hintz RL. Spontaneous
serum gonadotropin concentrations in the evaluation of pre-cocious
puberty. J Pediatr. 1995;127(1):47-52.
25) Neely EK, Hintz RL, Wilson DM, et al. Normal ranges for
immunochemiluminometric gonadotropin assays. J
Pediatr.1995;127(1):40-46.
26) Resende EA, Lara BH, Reis JD, Ferreira BP, Pereira GA,
Borges MF. Assessment of basal and gonadotropin-releasing
hormone-stimulated gonadotropins by immunochemiluminometric and
immunofluorometric assays in normal children. J ClinEndocrinol
Metab. 2007;92(4):1424-1429.
27) Eckert KL, Wilson DM, Bachrach LK, et al. A single-sample,
subcutaneous gonadotropin-releasing hormone test for
centralprecocious puberty. Pediatrics. 1996;97(4):517-519.
28) Carel JC, Eugster EA, Rogol A, et al. Consensus statement on
the use of gonadotropin-releasing hormone analogs in
children.Pediatrics. 2009;123(4):e752-62.
29) Boyar R, Finkelstein J, Roffwarg H, Kapen S, Weitzman E,
Hellman L. Synchronization of augmented luteinizing hormone
secre-tion with sleep during puberty. N Engl J Med.
1972;287(12):582-586.
30) Endocrine Sciences Reference Laboratory. Endocrinology
syllabus.
http://www.esoterix.com/files/Endocrinology_Syllabus_3.22.11.pdf.
Updated 2011.
31) Wang C, Catlin DH, Demers LM, Starcevic B, Swerdloff RS.
Measurement of total serum testosterone in adult men: Comparisonof
current laboratory methods versus liquid chromatography-tandem mass
spectrometry. J Clin Endocrinol Metab.2004;89(2):534-543.
32) Bridges NA, Christopher JA, Hindmarsh PC, Brook CG. Sexual
precocity: Sex incidence and aetiology. Arch Dis
Child.1994;70(2):116-118.
33) Chemaitilly W, Trivin C, Adan L, Gall V, Sainte-Rose C,
Brauner R. Central precocious puberty: Clinical and laboratory
features.Clin Endocrinol (Oxf). 2001;54(3):289-294.
34) Grunt JA, Midyett LK, Simon SD, Lowe L. When should cranial
magnetic resonance imaging be used in girls with early
sexualdevelopment? J Pediatr Endocrinol Metab.
2004;17(5):775-780.
35) Greulich W PI. Radiographic atlas of skeletal development of
the hand and wrist. Second ed. Standford: Stanford University
Press;1959.
36) Cassio A, Cacciari E, Balsamo A, Bal M, Tassinari D.
Randomised trial of LHRH analogue treatment on final height in
girls withonset of puberty aged 7.5-8.5 years. Arch Dis Child.
1999;81(4):329-332.
37) Mul D, Oostdijk W, Otten BJ, et al. Final height after
gonadotrophin releasing hormone agonist treatment for central
preco-cious puberty: The dutch experience. J Pediatr Endocrinol
Metab. 2000;13 Suppl 1:765-772.
38) Neely EK, Bachrach LK, Hintz RL, et al. Bone mineral density
during treatment of central precocious puberty. J
Pediatr.1995;127(5):819-822.
39) Cohen D, Janfaza M, Klein KO. Importance of leuprolide
acetate variable dosing for precocious puberty: A range of
accept-able suppression. J Pediatr Endocrinol Metab.
2009;22(7):629-634.
40) Kunz GJ, Sherman TI, Klein KO. Luteinizing hormone (LH) and
estradiol suppression and growth in girls with central preco-cious
puberty: Is more suppression better? are pre-injection LH levels
useful in monitoring treatment? J Pediatr EndocrinolMetab.
2007;20(11):1189-1198.
Gonadotropins, sex steroids and gonadotropin-releasing . . .
Continued from Page 7
Continued on Page 9
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41) Eugster EA, Clarke W, Kletter GB, et al. Efficacy and safety
of histrelin subdermal implant in children with central
precociouspuberty: A multicenter trial. J Clin Endocrinol Metab.
2007;92(5):1697-1704.
42) Chumlea WC, Schubert CM, Roche AF, et al. Age at menarche
and racial comparisons in US girls. Pediatrics.
2003;111(1):110-113.
43) Rosenfield RL, Bachrach LK, Chernausek SD, et al. Current
age of onset of puberty. Pediatrics. 2000;106(3):622-623.
Section on Endocrinology - Spring 2014 Page 9
Gonadotropins, sex steroids and gonadotropin-releasing . . .
Continued from Page 8
Editor’s Comments:Clifford A. Bloch, MD, FAAP
With the expectation that we as clinicians ought to strive to
practice evidence-based medicine, it is vital thatwe understand
normal, human physiology. Once we fully understand this, we might
appreciate the varia-tions of normal, and finally draw the margins
that define a disease state. When we arrive at that point,
wetypically design studies to determine the consequences of the
untreated disease state v outcomes of intervention thatalters the
course of the disease state.
In this article, Drs Granados and Kasa-Vubu have presented a
brief, clinical overview of the physiology of puberty andits
variants. It highlights some of the gaps in our knowledge in
understanding the physiology of normal puberty andits variants,
thereby blurring the margins between when we ought to consider
puberty to be pathologically early v withinthe physiologic range of
normal. It touches on some of the caveats involved in choosing and
interpreting the hormonaltests that we use to assess puberty,
including use of newer and more sensitive assays. Given the many
variables andpaucity of normative hormone data, it is no wonder
that we lack consensus on the diagnosis of central
precociouspuberty, resulting in a dilemma of whom to treat and whom
not to treat. If we lack consensus, can we ever really prac-tice
evidence-based medicine, or do we still place some stock on the
fabled “art of medicine?” The authors suggestthat we discuss the
diagnosis and goals of intervention with the family, listening to
their perceptions and needs beforemaking any treatment decisions.
This amounts to complete transparency in discussing what we know,
admitting to the uncertainties in what we don’t know, and allowing
the patient and family to participate in any intervention
strategy.
Not a Member?
Joining is Easy!
The Section on Endocrinology accepts “FAST TRACK” applications
for AAP members interested in join-ing the Section. Current members
of the Academy in good standing are eligible to apply online by
usingthe direct link:
http://www.aap.org/en-us/about-the-aap/Committees-Councils-Sections/Pages/Online-Council-Section-Membership-Application.aspx
PLEASE NOTE: You will be added to the section/council (s) within
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Questions? Don’t know your member ID or having trouble with the
online application? Please contact theCustomer Service at
866/THE-AAP1 (866-843-2271) to speak with a representative.
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For those of you who wonder ifYou need to draft another PIF
It’s not “CLER” that “NAS” will spiff“EPA” assessments in a
jiff
As “milestones” now take the stageThe “CCC” is all the rage
If you understand this pageYou’ve done well and been engaged
The new vocab is quite confusingAs are rules that we are
using
Few find the changes to be amusingAnd competencies now are
fusing
New fellows in ERAS successfully matchedWith PhDs and med/peds
also snatchedMatch day snafus were luckily patched
As 2014 plans were being hatched
Leaders of Pedi Endo tossed inIdeas to be shared by Bruce
Boston
Fellows from Portland, Miami & AustinWill enjoy schedules
with less exhaustion
Pedi endocrinologists continue to ageYet Teen DKA will still
rampage
Let’s hope the MCA improves our wageWith workforce data hard to
gage
Here is a “cheat sheet” for the changes in graduate medical
education (GME) that are affecting our training programs. There are
lots of ideas and acronyms floating around the programs this past
year and many of thenext accreditation plans will be outlined in
more detail within the upcoming year.As of 2013, there were a total
of 272 pediatric endocrine fellows (94 PL4/ 85 PL5/ 93 PL6) in
accredited US programswith the majority of programs using ERAS
applications and the NRMP match (as of spring 2012). Applicants
apply inthe fall of their PL2 year with interviews beginning in
December and ending in late April for an early May match day.
Once in fellowship, the fellows meet 3-4x/year to present their
research to a pediatric scholarship oversight commit-tee (PSOC).
New requirements for additional review by a clinical competency
committee (CCC) went into place inJune 2013. “SITE” exams are given
each spring. A yearly ACGME survey combined with board pass rates,
scholarly activity information and other basic descriptors in the
“ADS” annual program director summary are now used to monitor the
fellowship quality and alert the ACGME to local issues.
Board exams are proctored at test centers every 2 years with new
standardized absolute scores (1-300) and pass rateof 83% for
first-time takers.
Page 10 Section on Endocrinology - Spring 2014
“Pediatric fellowship information for dummies!”Jane L. Lynch,
MD, FAAP
Continued on Page 11
-
In the past, curriculum goals and objectives were integral parts
of a dreaded program information form (PIF) whichwas reviewed with
required details of the local fellowship program at an equally
dreaded “ACGME site visit” in cyclesof 2-5 years depending on how
the visit went in order to maintain accreditation. As of 2013,
established pediatric fellowship programs will be evaluated instead
at “CLER” visits in conjunction with their core pediatric residency
program with a focus on curriculum “milestones” which are being
developed to assess fellows on a set of essentialskills and
knowledge based expectations. The competencies describe categories
of professional aspects of trainingwhich will now be used to guide
the list of specific skill sets and professional activities
“entrustable professional activities” or EPA’s considered to be
either common to core training or unique to subspecialty pediatric
endocrinetraining. By standardizing basic expectations for programs
and decreasing the burdens of documentation, it is thegoal that
there will be space for some innovative teaching.
Section on Endocrinology - Spring 2014 Page 11
“Pediatric fellowship information for dummies!” Continued from
Page 10
Sungeeta Agrawal, MD
Nidhi Bansal, MBBS, MPH, FAAP
Katie Barger, MD
Deepti Chaturvedi, MD
Abby Fleisch, MD, FAAP
Shannon French, MD, FAAP
Anthony Gannon, MD, FAAP
Kimberly Henrichs, MD
Katherine Hwu, MD, FAAP
Jake Kushner, MD, FAAP
George Jeha, MD, FAAP
Hillary Lockemer, MD, FAAP
Anamaria Manea, MD
Nivedita Patni, MD
Tracey Patel, MD, FAAP
Stacy Rustico, MD, FAAP
Rajan Senguttuvan, MD
Monica Serrano-Gonzalez, MD
Stephanie Sisley, MD, FAAP
Lydia Snyder, MD, FAAP
Rona Sonabend, MD, FAAP
Stephen Stone, MD
Sunitha Sura, MD
Shadi Tabba, MBBS, FAAP
Teresa Tseng, MD
New Memberssince July 2014
The Section on Endocrinology welcomes the following new
members:
-
AUXOLOGYStudying human growth and developmentMichael Hermanussen
(Ed.)Publisher: Schweizerbart, 2013.Hardcover, 324 pages. ISNB
978-3-510-65278-5
This book is a comprehensive reference book on the auxology of
growth, edited by DrHermanussen, with an extensive list of
interna-tional contributors. It contains text, figures, tables,
andillustrative cartoons in color, and an extensive list of
references.
The book is divided into sections and subsections, numbered as
9.1, 9.2, 9.2, etc. The first section is a briefintroduction into
growth, followed by the next section,“Basics.” This section is
discussion on patterns of growthand a variety of factors that may
influence growth. The 3rd
section is a very brief discussion on body shape, compo-sition
and proportions, followed by a lengthier sectionthat deals with the
effects of genetics, gender, puberty andthe more controversial
topic, “Community Effects onGrowth.” This discusses the “community
effects” on thesize of Swiss conscripts, which this reviewer found
con-fusing. It cites a number of observational studies, spec-ulates
about socio-political environment which mayinfluence height, but
provides no convincing evidence inthe form of prospective,
comparative studies, to supportthe hypothesis that community
affects height independ-ently of factors such as nutrition,
exercise, weight, etc. Inthe subsection of puberty, the subject of
“tempo” is madeunusually complicated. By my understanding,
temposimply refers to the rate of change. Thus, it is fair to
com-pare and contrast the timing and tempo of puberty withthe tempo
of height or the tempo of height SDS, or withthe tempo of skeletal
age. Insulin is discussed as a majordeterminant of intrauterine
growth. However, it is not dis-cussed as a contributor to
post-natal growth, via its effectson metabolism and via
cross-reactivity with the IGF-1receptor. It is discussed briefly in
the context of T1DM, vis a vis insulin deficiency at diagnosis and
insulinreplacement, but is not discussed in
hyperinsulinemicstates.
The sections that follow include an excellent discussionon
height predictions, followed by a less helpful discus-sion of
“Prevention and Health,” and “Auxology of thePast.” The book lives
up to its title about halfway through,as the discussion turns to
the actual “Auxological
Methods” and “Statistical Approaches.” These 2 sectionsare
excellent, discussing the standardization of meas-urements, the
inaccuracies and pitfalls in the variousmethods of measurement,
bone age determination,height prediction models, growth charts,
statistical meth-ods for data smoothing and harmonization of
growthcurves derived from populations of different nationali-ties.
There is a detailed section on knemometry, whichappears to be a
particular interest of the editor, and a sec-tion that discusses
the automation of bone age determi-nation and prediction of height
[the BoneXpert method].The latter subject may be of interest to
American readers,as the method has yet to be approved by the Food
andDrug Administration. This reviewer accessed the refer-enced
website for final height prediction using a
formula:www.willi-will-wachsen.com, but was disappointed atits lack
of functionality. At the back of the book is a seriesof reference
tables of measurements, largely derived fromEuropean population
data. The listing of the referencesat the back of the book is
clumsy, some being out of order.Although there is a glossary of
abbreviations and termi-nology at the back of the book, some of the
abbreviationsare not defined in the text the first time they are
used,while others are not defined or listed anywhere. Thismakes
reading difficult.
I found the first half of this textbook to be a collection ofcut
and paste material with a number of unsubstantiatedand sometimes
perplexing statements presented in theform of text, figures and
cartoons. The strength of thisbook is in the discussion of the
scientific methods inmeasurements of growth, prediction of height,
and inthe compilation of growth charts in a complex and chang-ing
growth environment that includes puberty, the tempoof puberty and
variations in the tempo of growth with ageand illness. It
highlights the statistical methods andpotential flaws in
interpretation of growth data againstthis background.
Page 12 Section on Endocrinology - Spring 2014
Book Review:Auxology Studying Human Growth and Development
Clifford A. Bloch, MD, FAAP
-
The TODAY Study primary outcome results were reported in a June
2012 NEJM article which found that half ofthe youth in the study
were unable to maintain glycemic control when treated with
metformin alone and neededto be put on insulin. The study’s initial
findings also showed that treating youth with both metformin and
rosigli-tazone reduced/delayed the need to transition them to
insulin. Further analysis of the complications and character-istics
of the patients were published in a series of articles in the June
issue of Diabetes Care. The TODAY studyrecruited youth who had met
ADA criteria for Type 2 Diabetes within 2 years of diagnosis and
required a trial run inperiod to assess for compliance and
eligibility before randomly assigning patients to one of three
treatment arms:metformin alone; metformin plus rosiglitazone; and
metformin plus an intensive lifestyle intervention that
includeddiet, exercise and counseling on how to lose weight.
Despite optimal therapy which provided education, medications
including metformin, insulin, ACE inhibitors andstatin therapy and
laboratory monitoring oversight to ensure compliance with therapy,
the study found that youthwith type 2 diabetes were developing
early and rapidly progressing signs of heart and kidney disease,
poor glycemiccontrol and diabetes-related eye disease., even in the
group receiving more intensive two-drug therapy, shown in
pre-viously released results to be the most effective treatment for
maintenance of glycemic control.
Although rosiglitazone is not currently recommended for use as
treatment in youth, the addition of rosiglitazone tometformin as a
treatment not only reduced the need to transition participants to
insulin therapy, it appears to havedone so because it helped to
preserve beta cell function. In the first six months of treatment,
those in the rosiglita-zone plus metformin arm saw a 20 percent
improvement in insulin sensitivity, while the other two treatment
armssaw either a deterioration (metformin alone) or no change
(metformin plus lifestyle), lessening the burden on betacells to
produce insulin. The rate of deterioration of beta cell function in
youth was almost four times higher than hasbeen reported in adults,
researchers found, noting a 20-35 percent decline in beta cell
function per year on average,compared to 7-11 percent for adults
(as reported in previous research). Initial preserved beta cell
function and lowerHbgA1c were factors that reduced the risk of
failing treatment and requiring insulin therapy during the
study.
Both hypertension and kidney disease also progressed rapidly in
the study participants, regardless of treatment arm.The incidence
of hypertension rose from 11.6 percent of participants to 33.8
percent after 3.9 years. Males were at 81percent higher risk for
developing high blood pressure than females, which is consistent
with adult findings in termsof gender differences in hypertension.
As boys grew older, their risk for developing hypertension
increased: for everyadditional year of age at baseline, there was a
14 percent greater risk of hypertension. Weight also played a role
inincreasing risk: for every one unit of increased BMI, there was a
6 percent increased risk for high blood pressure. Therewere no
differences in hypertension risk based on differences in race,
ethnicity or randomized treatment group.
In contrast, gender did not appear to impact the increased
incidence of early kidney disease. The rates of microalbu-minuria
overall rose from 6.3 percent of participants at the beginning of
the study to 16.6 percent of participants. Poorglycemic control was
the major factor which influenced kidney disease progression risks
in participants. For every 1percent rise in A1C (e.g., from 7
percent to 8 percent), there was a 17 percent increased risk of
developing microal-buminuria. 57 participants developed
macroalbuminuria and one-third of those advanced to proteinuria
within the3.9 average duration of study participation. Of the 205
participants who required ACE inhibitors for hypertension orkidney
disease, 79 needed maximal ACE dosing and needed a second
medication added during these 3.9 years of thestudy.
Regardless of which treatment arm they were in, participants
also experienced a worsening of cardiovascular riskswith LDL,
triglycerides and other inflammatory markers all rising during the
first 12 months and then stabilizing overthe next 24 months.
Overall, only 55.9 percent of participants remained at their LDL
goal of less than 100 mg/dl overthe 36 months. The participants in
the study arm with lifestyle interventions did no better for their
LDL goals but didhave less triglyceride elevations.. Whereas LDL
levels rose with increasing A1C levels regardless of treatment
group,
Section on Endocrinology - Spring 2014 Page 13
TODAY Study Publications Summarized from June 2013Diabetes Care
Journal Feature
Jane L. Lynch, MD, FAAP
Continued on Page 14
-
Page 14 Section on Endocrinology - Spring 2014
higher A1C levels were not associated with higher triglyceride
levels in the lifestyle intervention group.
The group treated with metformin and rosiglitazone, conversely,
experienced the largest accumulation of body fatbut maintained the
best glycemic control. The improved weight loss and body
compositions associated with thelifestyle arms were significant
during the initial six months but these effects were
disappointingly minimal by 24 monthswhen compared to metformin.
An accompanying editorial by the Diabetes Care Editor in Chief
William Cefalu, MD lamented. “We are not preparedas a medical
community or as a global society at this time to effectively
address the growing problem of type 2 diabetes in youth.
Excerpted from the American Diabetes Association May 23, 2013
press release.
TODAY Study Publications Summarized from June 2013 . . .
Continued from Page 13
Federal Legislative Update
The February 2014 Washington Report on Academic and
Subspecialist Advocacy in now available! (member log-in required)
www.aap.org/subspecialtyHighlights of the newsletter:
• Medicaid Payment Increase
• Academic and Subspecialty Workforce – including Pediatric
Subspecialty Loan Repayment, Children’s HospitalGME Funding and
Reauthorization
• Health Care Reform Implementation
• Pediatric Drugs and Devices – Drug Shortages, FDA Action on
Reduce Drug Shortages, GAO Report on DrugShortages, Reporting a
Drug Shortage, BPCA and PREA Implementation
• Pediatric Research
• Drug shortages
◦ June 15 – 17, 2014 Legislative Conference in Washington, DC.
Visit www.aap.org/legcon for more informationabout the conference,
including a brochure, scholarships, and how to register.
-
Section on Endocrinology - Spring 2014 Page 15
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Page 16 Section on Endocrinology - Spring 2014
Endocrinology Meeting Schedule
Pediatric Endocrine Society Annual
Meetinghttp://www.pedsendo.org/May 3-6, 2014Vancouver, Canada
Pediatric Academic Societies Annual
Meetinghttp://www.pas-meeting.orgMay 3-6, 2014Vancouver, Canada
American Diabetes
Associationhttp://professional.diabetes.org/HomeContinuingEducationAndMeetings.aspx?hsid=574th
Scientific SessionsJune 13 -17, 2014San Francisco, CA
ICE/ENDO 2014https://www.endocrine.org/endo-2014June 21-24,
2014McCormick Place WestChicago, IL
40th Anniversary Conference of the InternationalSociety of
Pediatric and Adolescent
Diabeteshttp://www.ispad.org/2014/homeDiversity in
DiabetesSeptember 3-6, 2014Toronto, Canada
AAP National Conference and
Exhibitionhttp://www.aapexperience.org/October 11-14, 2014San
Diego, CA
84th Annual Meeting of the American Thyroid
Associationhttp://www.thyroid.orgOctober 29-November 2, 2014Hotel
Del CoronadoCoronado, CA
AAP Section
on Endocrinology
ExecutiveCommittee
2014 - 2015
ChairpersonIrene N. Sills, MD, FAAP
Executive CommitteeClifford A. Bloch, MD, FAAP
Samuel J. Casella, MD, MSc, FAAPJose L. Gonzalez, MD, JD, MSEd,
FAAP
Jane L. Lynch, MD, FAAPKupper A. Wintergerst, MD, FAAP
Immediate Past ChairpersonPaul B. Kaplowitz, MD, PhD, FAAP
Newsletter EditorsClifford A. Bloch, MD, FAAP
Jane L. Lynch, MD, FAAP
StaffLaura N. Laskosz, MPH
Journal Production SpecialistMark A. Krajecki
Statements and opinions
expressed in this publica-
tion are those ofthe authors
and not necessarily those of
the American Academy of
Pediatrics or the Section on
Endocrinology.