Type 1 Diabetes in Adults: Principles and Practice

282 Pages·2007·4.22 MB·English

by  Serge Jabbour

Type 1
Diabetes
in Adults
PRInCIPlES And PRACtICE
Edited by
Serge Jabbour
Thomas Jefferson University, Philadelphia, Pennsylvania, USA
Elizabeth A. Stephens
Providence Portland Medical Center, Portland, Oregon, USA
Associate Editors
Irl B. Hirsch
University of Washington, Seattle, Washington, USA
Satish Garg
University of Colorado Health Sciences Center, Denver, Colorado, USA
Barry J. Goldstein
Thomas Jefferson University, Philadelphia, Pennsylvania, USA
Matthew C. Riddle
Oregon Health & Science University, Portland, Oregon, USA
Jabbour_978-0849326226_TP.indd 2 10/18/07 3:29:50 PM
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Type1diabetesinadults:principlesandpractice/editedbySergeJabbour...[etal.].
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1.Diabetes. I.Jabbour,Serge. II.Title:Typeonediabetesinadults.
[DNLM:1.DiabetesMellitus,Type1. 2.Adult.WK810T990752007]
RC660.T9682007
616.4(cid:2)62–dc22 2007023324
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Preface
At a time of dramatic increases in the prevalence of obesity, it is appropriate that type 2
diabetes has received a great deal of attention by the endocrinology community. Clearly,
themanagementofinsulinresistanceandcardiovascularriskisacriticalissue.However,
it is equally important to acknowledge and address type 1 diabetes, whose prevalence
is also increasing and whose management remains complex. Currently it is estimated
that 10–15% of those with diabetes have type 1, and often the diagnosis is challenging
since many of those previously thought to have type 2 diabetes actually have late-onset
type1diabetes(alsotermedlatentautoimmunediabetesinadults,orLADA).Overthelast
decadethetoolsforthemanagementoftype1diabeteshavealsoevolvedandsothereis
an opportunity to more closely replicate normal physiologic insulin secretion with either
basal–bolusinsulintherapyorcontinuoussubcutaneousinsulininfusions.Besidesinsulin,
therearenowsomeaddedtherapiessuchaspramlintide.Whiletheseadvancementsallow
ustobettermanageourpatientswithtype1diabetes,theyalsoaddcomplexity.Anupdated
texttoaddresstheconceptsbehindthecareofthepersonwithtype1diabetesiswarranted
toreviewtheseissuesforendocrinologistsandprimarycareproviderswithaninterestin
diabetes.
Toachievethisgoal,wehavedividedourtextbookintofourseparatesections:
(cid:1)
In the first section, we review the pathogenesis of type 1 diabetes, including
polyglandularautoimmunity,andexpandourunderstandingofLADA.
(cid:1)
In the second section, we discuss in detail the management of type 1 diabetes,
including blood glucose monitoring; diabetes education, nutrition, and special
situations;insulin;andpramlintidetherapies.
(cid:1)
In the third section, we review the complications of diabetes: Hyperglycemia
and tissue damage, including data from DCCT/EDIC, retinopathy, nephropathy,
neuropathy,andhypoglycemia.
(cid:1)
In the fourth and last section, we discuss special settings and situations such as
pregnancy, psychology, including depression and eating disorders, and pancreas
andislettransplantation.
iii
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iv Preface
Wewouldliketoacknowledgethementoringofoursenioreditors,Dr.IrlHirsch,Dr.
SatishGarg,Dr.BarryJ.Goldstein,andDr.MatthewRiddle.
Wehopeyoufindthistexttobeinformativeandpracticalinyourday-to-dayman-
agement oftype1diabetespatientsandallthecomplexissuesthatariseintheircare.
SergeJabbour
ElizabethA.Stephens
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Contents
Preface .... iii
Contributors .... vii
1.PathophysiologyofType1Diabetes ...................................... 1
L.F.Meneghini
2.LatentAutoimmuneDiabetesinAdults .................................. 17
R.G.NaikandJ.P.Palmer
3.BloodGlucoseMonitoring:GlycatedHemoglobin,Fructosamine,
Meters,andSensors ..................................................... 33
T.S.Bailey
4.DiabetesEducation,Nutrition,Exercise,andSpecialSituations ........... 53
JoAnnAhern
5.InsulinTherapyinAdultswithType1DiabetesMellitus .................. 67
M.F.Magee,J.J.Reyes-Castano,andC.M.Nassar
6.PramlintideandOtherAdjunctiveTherapies ............................ 109
C.H.Wysham
7.Hyperglycemia-InducedTissueDamage:PathwaysandCauses ........... 127
K.K.Hood,H.A.Keenan,andA.M.Jacobson
8.DiabeticRetinopathy .................................................... 143
J.M.CropseyandM.S.Fineman
9.DiabeticNephropathy ................................................... 157
Y.Woredekal
10.Neuropathy ............................................................. 173
J.L.Edwards,A.A.Little,andE.L.Feldman
11.HypoglycemiainType1Diabetes ........................................ 195
V.J.BriscoeandS.N.Davis
v
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vi Contents
12.DiabetesandPregnancy ................................................. 213
K.W.Hickey,J.G.Umans,andM.Miodovnik
13.PsychologicalAspectsofType1DiabetesinAdults ....................... 231
B.A.Boyer,V.Myers,andD.Lehman
14.Beta-CellReplacement:PancreasandIsletTransplantation ............... 247
R.PaulRobertson
Index .... 263
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Contributors
JoAnnAhern AnimasCorporation,WestChester,Pennsylvania,U.S.A.
T.S.Bailey AdvancedMetabolicCare&Research,Escondido,California,U.S.A.
B.A.Boyer InstituteforGraduateClinicalPsychology,WidenerUniversity,Chester,
Pennsylvania,U.S.A.
V.J.Briscoe VanderbiltSchoolofMedicine,DivisionofDiabetes,Endocrinologyand
Metabolism,VanderbiltUniversity,Nashville,Tennessee,U.S.A.
J.M.Cropsey WillsEyeInstitute,Philadelphia,Pennsylvania,U.S.A.
S.N.Davis VanderbiltSchoolofMedicine,DivisionofDiabetes,Endocrinologyand
Metabolism,VanderbiltUniversity,Nashville,Tennessee,U.S.A.
J.L.Edwards DepartmentofNeurology,UniversityofMichigan,AnnArbor,
Michigan,U.S.A.
E.L.Feldman DepartmentofNeurology,UniversityofMichigan,AnnArbor,
Michigan,U.S.A.
M.S.Fineman WillsEyeInstitute,Philadelphia,Pennsylvania,U.S.A.
K.W.Hickey GeorgetownUniversityHospital,Washington,DC,U.S.A.
K.K.Hood SectiononBehavioralandMentalHealthResearch,SectiononGenetics
andEpidemiology,JoslinDiabetesCenter,HarvardMedicalSchool,Boston,
Massachusetts,U.S.A.
A.M.Jacobson SectiononBehavioralandMentalHealthResearch,JoslinDiabetes
Center,HarvardMedicalSchool,Boston,Massachusetts,U.S.A.
H.A.Keenan SectiononVascularCellBiology,JoslinDiabetesCenter,Harvard
MedicalSchool,Boston,Massachusetts,U.S.A.
D.Lehman InstituteforGraduateClinicalPsychology,WidenerUniversity,Chester,
Pennsylvania,U.S.A.
A.A.Little DepartmentofNeurology,UniversityofMichigan,AnnArbor,
Michigan,U.S.A.
vii
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viii Contributors
M.F.Magee MedStarDiabetes&ResearchInstitutesatWashingtonHospitalCenter
andGeorgetownUniversitySchoolofMedicine,Washington,DC,U.S.A.
L.F.Meneghini DiabetesResearchInstitute,UniversityofMiamiLeonardM.Miller
SchoolofMedicine,Miami,Florida,U.S.A.
M.Miodovnik WashingtonHospitalCenter,Washington,DC,U.S.A.
V.Myers PenningtonBiomedicalResearchCenter,LouisianaStateUniversity,
Louisiana,U.S.A.
R.G.Naik BombayHospitalandMedicalResearchCenter,Mumbai,India
C.M.Nassar MedStarDiabetes&ResearchInstitutesatWashingtonHospitalCenter,
Washington,DC,U.S.A.
J.P.Palmer DVAPugetSoundHealthCareSystem,UniversityofWashington,Seattle,
Washington,U.S.A.
J.J.Reyes-Castano MedStarDiabetes&ResearchInstitutesatWashingtonHospital
Center,Washington,DC,U.S.A.
R.PaulRobertson PacificNorthwestResearchInstitute,UniversityofWashington,
Seattle,Washington,U.S.A.
J.G.Umans MedstarResearchInstitute,Hyattsville,Maryland,U.S.A.
Y.Woredekal SUNYDownstateMedicalCenter,Brooklyn,NewYork,U.S.A.
C.H.Wysham WashingtonStateUniversity,Spokane,Washington,U.S.A.
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1
Pathophysiology of Type 1 Diabetes
L.F.Meneghini
DiabetesResearchInstitute,UniversityofMiamiLeonardM.MillerSchoolofMedicine,
Miami,Florida,U.S.A.
INTRODUCTIONANDBACKGROUND
Type 1 diabetes mellitus (T1DM) is characterized by defects in beta-cell function that
eventuallyresultinabsoluteinsulindeficiency,requiringinsulinreplacementtherapiesto
ensure survival and limit the complications of hyperglycemia. Type 1A or autoimmune
diabetes, which accounts for 85% to 90% of T1DM, is characterized by the presence of
autoantibodies to several islet cell molecules, including insulin, GAD, and IA-2, as well
asbyinfiltrationoftheisletsanddestructionofbetacellsbymononuclearcells(insulitis).
Althoughthepresenceofinsulitisrequiresatissuespecimenfordiagnosis,autoantibodies
on the other hand can be measured from serum and are detectable years prior to the
onsetofhyperglycemia.Alongwithgeneticscreeningandassessmentofstimulatedinsulin
secretion,autoantibodiescanalsobeusedtopredictthedevelopmentofT1DMinat-risk
populations.
Althoughthereisa10-to15-foldincreaseinthelifetimeriskofdevelopingthedisease
forfirst-degreerelativesofsubjectswithT1DMcomparedtothegeneralpopulation,over
85%ofpatientswhodevelopautoimmunediabetesdosointheabsenceofapositivefamily
history. Several genetic factors that increase the risk of developing autoimmune diabetes
have been identified; the best characterized and studied are the DR3/DR4 alleles in the
MHC (HLA) complex. It is still unclear what triggers the initial immunologic attack on
the beta cell, but a combination of both genetic and environmental factors is likely to be
involved.Onceautoantibodiesaredetectableintheserum,manyofthesepatientswillgo
ontodevelopinsulitisandbeta-celldestructioneventuallyleadingtometabolicinstability,
hyperglycemia, and possibly ketoacidosis. The mechanisms underlying the progression
of the autoimmune attack on the beta cells have been extensively assessed in the rodent
model, but unfortunately remain incompletely understood in humans, where access to
injured tissue (pancreatic islet cells) and other factors have limited our ability to better
address the pathology of diabetes. In this chapter, we will review the natural history
and the development of the metabolic abnormalities that characterize the progression of
autoimmune diabetes and try to link these clinical observations to possible pathogenetic
factors. We will conclude by describing the relationship of T1DM to other autoimmune
syndromesthatsharesimilargeneticpredisposition.
1