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http://slidepdf.com/reader/full/80563dba84550346aa9aa64fa6 1/79

1

Hypertensive Disorders inPregnancy (I)

Williams Obstetrics 22nd Edition

Chapter 34

부산백병원 산부인과

조인호

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Index

Diagnosis Etiology

Pathogenesis

Pathophysiology

Prediction and Prevention

Management

Long-term conse!ences

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"estational #ypertension $ 3%&' in ()*+***

,ational Center .or #ealth /tatics+ 2**(0

Pregnancy-related hypertension 1 Pregnancy-related deaths,32*( 명 in /+ ((-

(&0 의 (' 차지

5lac6 7omen are 3%( times to die as 7hite

7omen

#ypertensive disorders remain among the

most signi.icant and intrig!ing !nsolved

problems in obstetrics

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Diagnosis

"estational hypertension

Preeclamsia

Eclamsia

/!perimposed preeclamsia ,on chronichypertension0

Chronic hypertension

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Gestational hypertension

5P8 (4*9*mm#g .or .irst time d!ring pregnancy

o protein!ria

5P ret!rns to normal : (2 7ee6s; postpart!m

<inal diagnosis made only postpart!m

May have other signs or symptoms o.preeclampsia+ .or e=ample+ epigastric discom.ortor thrombocytopenia

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Preeclampsia

￭

Minimum Criteria - 5P8(4*9*mm#g a.ter 2*7ee6s> gestation

- Protein!ria 83**mg924hrs or 8(?dipstic6

￭Increased certainty of preeclampsia

- 5P8(*9((*mm#g

- Protein!ria 2%*g924hrs or 82?dipstic6

- /er!m creatinine @(%2mg9dl !nless 6no7n to be previo!slyelevated

- Platelets :(*****9mm3 - Microangiopathic hemolysis ,Ancreased LD#0

- Elevated BL or B/

- Persistent headache or other cerebral or vis!al dist!rbance

- Persistent epigastric pain

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Preeclampsia Diastolic hypertension 8)mm#g

<etal death rate 1 3 배이상 증가

Worsening protein!ria preterm labor 증가

eonatal s!rvival변화없음

Epigastric or pain #epatocell!r necrosis+ ischemia+ edema that

stretches the "lisson caps!re

B/9BL 상승 1 임신종결의 sign #epatic r!pt!re 1 rare

hrombocytopenia severe vasospasm -@ microangiopathic hemolysis -@

Platelet activation+ aggregation

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/everity o. Preeclampsia

apid increase in 5P .ollo7ed by conv!lsions is !s!ally preceded by

!nrelenting severe headache or visual disturbances%

Di..erentiation bet7een mild F severepreeclampsia can be misleading

-beca!se apparently mild disease may

progress rapidly to severe disease

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Eclampsia

preeclampsia?conv!lsion

/eiG!res that cannot be attrib!ted to other

ca!ses in 7oman 7ith preeclampsia

/eiG!res are generaliGed and may appear

be.ore+ d!ring+ o. a.ter labor

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Chronic hypertension

5P 8(4*9* mm#g be.ore pregnancy ordiagnosed be.ore 2*7ee6s; gestation ,not

attrib!table to gestational trophoblastic

disease0 or

#ypertension .irst diagnosed a.ter

2*7ee6s; gestation and persistent a.ter(27ee6s; postpart!m

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Chronic Hypertension

Chronic hypertension 은 임신후반!지 "#$ %&' % 이( 1 5P decreases d!ring the second and

early third trimesters in both normotensive andchronically hypertensive 7omen

nderlying hypertension 의 원인 Essential .amilial hypertension ,*'0

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Underlying Causes of Chronic hypertensiveDisorder

Essential .amilial hypertension ,hypertensive vasc!lar disease0

Obesity Btrterial abnormalities

enovasc!lar hypertension

Coarctation o. the aorta

Endocrine diordersDiabetes mellit!s

C!shing syndromePrimary aldosteronism

Pheochromocytoma

hyroto=icosis

"lomer!lonephritis ,ac!te and chronic0

enoprival hypertensionChronic glomer!lonephritis

Chronic renal ins!..iciencyDiabetic nephropathy

Connetive tiss!e diseaseL!p!s erythematos!s

/ystemic sclorosis

Periarteritis nodosa

Polycystic 6idney disease Bc!te renal .ail!re

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Chronic Hypertension

Chronic # H ventric!lar hypertrophy+ cardiac

decompensation+ cerebrovasc!lar accidents+

renal damage

임신 ) s!perimposed preeclampsia 가 * + ,- , ./ 2)' !지 0/1 + (I+ /ibai0

2의 3병증4이 56 호78 %

P l i i d

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Preeclampsia superimposed onChronic Hypertension

e7-onset protein!ria8 3**mg924ho!rs in

hypertensive 7omen b!t no protein!ria

be.ore 2* 7ee6s; gestation

B s!dden increase in protein!ria or blood

press!re or platelet co!nt :(**+***9mm3 in

7omen 7ith hypertension and protein!riabe.ore 2*7ee6s; gestation

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Superimposed preeclampsia

Placental abr!ption+ gro7th restriction+preterm delivery+ death 의 29:이 증가

;반<=> ? P!reJ preeclampsia @ AB증상이 CD severe $/ 종종 .etal gro7th

restriction 이 E반FG %

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Incidence and Ris !actor

!lliparo!s 7omen @H I8 % Ancidence 1 )' ,7ide variation0 An.l!ence by

Parity+ race+ ethnicity+ genetic predisposition !lliparo!s

otal 1&%' 9 severe 1 3%3' ,#a!th+ 2***0

is6 .actor Chronic hypertension+ m!lti.etal gestation+maternal old age,@3) yrs0+ obesity+ B.rican-

Bmerican ethnicity

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Incidence and Ris !actor

Maternal 7eight and the ris6 o. preeclampsia isprogressive%

/mo6ing d!ring pregnancy red!ced ris6 o. hypertension

d!ring pregnancy ,5ainbridge+2**) K hang+ (0

Placenta previa also red!ced the ris6 o. hypertension

5MA ,g9m20 Morbidity ,'0

:(%I 4%3

@3) (3%3

"estation

t7in (3

single ) (Sibai, 2000)

I id d Ri ! t

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Incidence and Ris !actor(Eclampsia)

Eclampsia /ome7hat preventable

eceive ad!ate prenatal care

(& ,7illiams Obstetrics ()th edition0 (9&** deliveries ,Par6land #ospitial0

(I3-(I (9(()* deliveries

( (9(&)* deliveries

2***+ ational Nital /tatistics eport+ in / (932)*

(4+ Do!glas and edman in (92***

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Etiology

5asic concepts E=posed to chorionic villi .or the .irst time

E=posed to a s!perab!ndance o. chorionicvilli+ as 7ith t7ins or hydatidi.orm mole

#ave pree=isting vasc!lar disease

"enetically predisposed to hypertensiondeveloping d!ring pregnancy

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Nasc!lar endothelial damage 7ith vasospasm+

trans!dation o. plasma+ and ischemic and

thrombotic se!elae%

C!rrently pla!sible potential ca!se ,2**3+ /ibai0 Bbnormal trophoblastic invasion o. terine vessels

Amm!nological intolerance bet7een maternal and

.etoplacental tiss!es

Maternal maladaptation to cardiovasc!lar or

in.lammatory changes o. normal pregnancy

Diatary de.iciencies

"enetic in.l!ences

"# l $ h #l ti

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"#normal $ropho#lasticInvasion

An normal implantation+ endovasc!lartrophoblasts invade the !terine spiral

arteries

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"#normal $ropho#lastic

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An preeclampsia Ancomplete trophoblastic invasion he magnit!de o. de.ective trophoblastic invasion o.

the spiral arteries correlated 7ith the severity o. thehypertensive disorder ,2***+ MadaGli0

sing electron micorscopy Endothelial damage Ans!dation o. plasma constit!ents into vessel 7alls

Proli.eration o. myointimal cells Medial necrosis Lipid and macrophage acc!m!lates in myointimal

cells

"#normal $ropho#lasticInvasion

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Lipid-laden cells -@ atherosis ,#ertig+ (4)0

Obstr!ction o. the spiral arteriolar l!men by

atherosis may impair placental blood .lo7

Placental per.!sion -@ diminished

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Immunological !actors

heory <ormation o. bloc6ing antibodies o. placental

antigenic sites might be impaired% !mber o. antigenic sites provided by the placenta is

!n!s!ally great compared 7ith the amo!nt o.

antibody+ as 7ith m!ltiple .et!ses% ,5eer+ (&I0 E..ective imm!niGation by a previo!s pregnancy is

lac6ing+ as in .irst pregnancies%

he imm!niGation concept 7as s!pported by their observations that preeclampsia developed lesso.ten in m!ltiparas 7ho had a prior term pregnancy,Mostello+ 2**2K r!pin+ (0

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Early second timester - Developpreeclampsia 7omen Lo7er proportion o. helper cells ,h(0 h2 dominance+ mediated by adenosine+

7hich is .o!nd in higher ser!m level inpreeclamptic compared 7ith normotensive7omen ,oneyama+ 2**20

hese helper lymphocytes secrete speci.ic

cyto6ines that promote implantation+ andtheir dys.!nction may .avor preeclampsia,#ayashi+ 2**4K Whitecar+ 2**(0

Immunological !actors

$he %asculopathy and the

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$he %asculopathy and theIn&ammatory Changes

he decid!a contains an ab!ndance o. cells that+ 7hen activated+ can release no=io!sagents% ,/ta..+ (0 -@ mediators to provo6eendothelial cell in!ry

Preeclamsia d!e to an e=treme state o.activated le!6ocytes in the maternal circ!lation,<aas+ 2***0 Cyto6ines 1 <-a+ interle!6in H o=idative stress

,highly to=ic radicals0

Potential bene.it o. antio=idants to preventpreeclampsia ,Chappell+ (K hang+ 2**20

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'utritional !actors

Dietary de.iciencies and E=cesses over thecent!ries have been blamed as the ca!se o.eclampsia%

/!pplementation 7ith vario!s elements s!ch asGinc+ calci!m+ and magnesi!m to preventpreeclampsia ,Qohn+ 2**20

Obesity+ is a potent ris6 .actor .or preeclampsia

C-reactive protein+ an in.lammatory mar6er+ 7assho7n to be increase in obesity+ 7hich in t!rn7as associated 7ith preeclampsia ,Wol.+ 2**(0

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Genetic !actors

#ereditary hypertension is lin6ed topreeclampsia ,ess+ 2**30

Preeclampsia- eclampsia is highly heritable insisters+ da!ghters+ grandda!ghters+ andda!ghters-in-la7% ,Chesley and Cooper+ (I0

*' concordance in monoGygotic .emale t7inpairs ,ilsson+ 2**40

#LB-D4 J preeclampsia J의 KL:,6ilpatric6+(I0

Pathogenesis

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Pathogenesis%asospasm

Nasc!lar constriction Hresistance and

s!bse!ent hypertension

Maldistrib!tion+ ischemia o. the

s!rro!nding tiss!es H blood .lo7 의 MN

H necrosis+ hemorrhage+ and other end-organ dist!rbances

Pathogenesis

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PathogenesisEndothelial cell activation

n6no7n .actors ,.rom placenta0 are secretedinto the maternal circ!lationH activation and dys.!nction o. the vasc!lar

endotheli!m%

Damaged or activated endothelial cells secretes!bstancesH promote coag!lation and increase the sensitivity to

vasopressorsHchanges in glomer!lar capillary endothelial

morphology

Hincreasd capillary permeability

Helevated blood concentrations

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Ancreased Pressor esponses

ormally+ pregnant 7omen developre.ractoriness to in.!sed vasopressors ,Bbd!l-arim an Bssali+ ((0

5!t+ early preeclampsia 7omen have

increased vasc!lar reactivity to in.!sed

norepinephrine and angiotensin AA ,aab+()0

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Ancreased Pressor esponses

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Ancreased Pressor esponses Prostaglandins

An preeclampsia Endothelialprostacyclin ,P"A20 prod!ction isdecreased

hrombo=ane B2 ,RB20 secretionby platelets isincreased

H Ancreased

sensitivity toin.!sedangiotensin AA

H vasoconstriction

Membrane phospholipid

Arachidonic acid

COX1,2

TXA2 PGI2, PGE2

Phospholipase

A2

Platelet

Increased Pressor Responses

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/ynthesiGed .rom L-arginine by endothelialcells% ,potent vasodilator0

itric o=ide maintains the normal lo7-press!re

vasodilated state characteristic o. .etoplacental

per.!sion ,Myatt+ (20

Preeclampsia is associated 7ith decreasedendothelial nitric o=ide synthase e=pression+

7hich increases cell permeability ,Wang+ 2**40


'itric oxide


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Endothelin-( ,E-(0 1 potent vasoconstrictors

Prod!ced by h!man endotheli!m

Plasma E-( is increased in

normotensive pregnant 7omen+ b!t

7omen 7ith preeclampsia have evenhigher levels ,Bne+ 2**3 K Clar6+ (20

Increased Pressor Responses Endothelins


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Nasc!lar endothelial gro7th .actor ,NE"<0+Placental gro7th .actor ,PA"<0+ 7hich secretion increases in normal pregnancy

Promote angiogenesis And!ce nitric o=ide Nasodilatory prostaglandins

Parado=ically+ NE"< is increased in ser!m .rom7omen 7ith preeclampsia+ b!t its bioavailabilityis decreased ,5a6er+ () K /immons+ 2***0


"ngiogenic actors

Pathophysiology

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PathophysiologyCardiovascular System

Ancreased cardiac a.terload ca!sed byhypertension

Cardiac preload in preeclampsia

Pathologically diminished hypervolemia o.pregnancy

Aatrogenically increased by iv crystalloid or oncoticsol!tion

E=travasion into the e=tracell!lar space+especially the l!ng

Cardiovascular System

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Hemodynamic Changes

Preeclampsia Cardiac o!tp!t elevated be.ore hypertension

developed than normal pregnancy%

With clinical onset o. preeclampsia Mar6ed red!ction in cardiac o!tp!t% Ancreased peripheral resistance%

5y contrast+ "estational hypertension Elevated cardiac o!tp!ts 7ith development o.

hypertension%

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(Hankin, 1984)


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5lood vol!me in term ormal pregnancy 1 )***ml

ot pregnancy 1 3)**ml

Eclampsia 1 3)**ml

#emoconcentration in preeclampsia Nasoconstriction and Endothelial dys.!nction 7ith

vasc!lar permeability%

/evirity J KLO% P지 Q음 %

Whereas+ gestational hypertension have a normal

blood vol!me ,/ilver+ (I0


lood volume

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With severe hemoconcentration+ an ac!te .all inhematocrit s!ggested resol!tion o. preeclampsia

Antravasc!lar compartment in eclamptic 7omen is!s!ally not !nder.illed%

H vasospasm and endothelial lea6age o. plasma has contractedthe space to be .illed%

H At persist some time a.ter delivery 7hen the vasc!lar

endotheli!m repairs%

/ensitive to vigoro!s .l!id therapy to e=pand thecontracted blood vol!me to normal pregnancy levels%

/ensitive to even normal blood loss at delivery%


lood volume

lood and Coagulation

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lood and CoagulationPlatelet

hrombocytopenia H li.e threatening /evere disease 1 : (**+***9!L Platelet co!nt MN -@ indication o. delivery -@ RS 후

3-) days+ T상UV=> WX

Platelet activation+ aggregation+ cons!mption -@“exhausion” -@ thrombocytopenia ,#arlo7+ 2**20

#ELLP syndrome 1 hemolysis ,#0 + elevated liver

enGymes ,EL0+ and lo7 platelets ,LP0 ,Weinstein+ I20

eonatal thrombocytopenia Maternal thrombocytopenia J KL이 없음 % ,Prichard+ (I&0


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P+ aP+ .ibrinogen level ,ro!tine labassessment o. coag!lation0 -@ preeclampsia 의management @ YZ$지 Q음 %

<DP 의 증가 1 !n6no7n ,b!t+ hepaticderangements )[; \=> ]T ,Led!c+ (20 0

hrombophilias 1 clotting .actor de.iciencies -@ early onset

preeclampsia Bntithrombin ^ _`$a b조c@ AB

preeclampsia 의 7*def gh U P음 ,Chang+ (20 <ibronectin

"lycoprotein-vasc!lar endothelial cell basementmembrane

Preeclampsia 의 ij인k> lm

lood and CoagulationCoagulation


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/evere preeclampsia ) LD# 의 증가 nhemolysis 의 증o

Peripheral blood change 1

/chiGocytosis+ spherocytosis+ retic!locytosis

lood and Coagulation!ragmentation Hemolysis

%olume Homeostasis

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%olume HomeostasisEndocrine changes

enin+ angiotensin+ aldosterone T상 임신@p+ 증가

5!t+ preeclampsia @p+ A임신의 T상 level

> MN q 1 a ? retension+ hypertension @ 의B

Q!=taglomer!lar apparat!s @p renin RA가 MN

Bngiotensinogen 이 angiotensin A => conversion

,renin 의 rm 0 이 MN

Bngiotensin AA 의 MN -@ aldosterone 의 MN

이s 상t@e uv$/ preeclampsia 산w@p

a retension 이 xy FG % ,5ro7n+ (II0

%olume Homeostasis

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Deo=ycorticosterone ,DOC0 Bnother potent mineralocorticoid

3rd trimester @ z- 증가 Maternal adrenal gland @p RA가 증가F \이 {

|} plasma progesterone 의 q~임 %

•€> a retension 이‚ hypertension 이 P%e MN$지 Q음

-@ preeclampsia 의 7병과 지y@ ƒZ„ …†^ ‡

ˆ† \=> b %


%olume Homeostasis

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Btrial atri!retic peptide ,BP0 5lood vol% e=pansion @ 의„ atrial 7all

streching @ 의Bp RA1

Nasoactive „ ‰Š + aldosterone+ renin

activity+ angiotension AA+ vasopressin 의action ^ ‹Œ$ sodi!m 과 7ater e=cretion

^ 조Ž8 %

T상 임신@pe 증가$지S preeclampsia )+ 56 증가


%olume Homeostasis

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%olume Homeostasis!luid and Electrolyte Changes

Preclampsia 산w EC< vol% 이 T상산w0G 56 이 증가 %

Pathologic retension 1 endothelial in!ry

Electrolyte concentration do not di..er%

Electrolyte !nbalance 가 *+ ,- Nigoro!s di!retic therapy /odi!m restriction Bdministration o. 7ater 7ith s!..icient o=ytocin to

prod!ce antidi!retisis%

<ollo7ing eclamptic convertion -@ lo7er #CO3

*id

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*idney

enal per.!sion and glomer!lar .iltrationMN ,in preeclampsia0 D!e to vasospasm

5!t+ Cr% Level 의 MN+ ;반<=> $지 Q음 -@ severe „ ,-+ 2-3 배 ‘}가e 8 %

,Pritchard+ (I40

Oligo!ria 가 P+ preeclampsia 산w@Hp

intensive iv .l!id therapy + indication 이 {’%

*id

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*idney

Protein!ria Preeclampsia-eclampsia "#@ ƒZ Late $H 7* % 24hr B 가 ƒZ

Bnatomical changes "lomer!li 1 2*' !지 증가 Glomerular capillary endotheliosis

Capillary endothelial swelling with subendothelial depositsof protein materials

Bc!te renal .ail!re !b!lar necrosis+ cortical necrosis -@ oligo!ria+ an!ria+rapidly develped aGotemia

원인 1 #ELLP synd% + placental abr!ption+ postpart!mhemorrhage

+i

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+iver

Periportal hemorrhagic necrosis in the peripheryo. the liver lob!le /er!m liver enGyme 상승의 원인

on.atal case @p+ “ 0이지 Q음

B!topsy @p ”> 인 #epatic r!pt!re,more rare0+ s!bcaps!lar

hematoma,more common0 ^ ;=– U P음 %

reatment

/!rgical intervention 이 — + li.e saving 가˜ 5lood 9< 이 e' %

Liver transplantation e ™š가˜

/pontaneo!s hepatic r!pt!re 의 mortality 13*'

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+i

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+iver

#ELLP syndrome #emolysis+ Elevated Liver enGyme and Lo7

Platelet

2*' o. severe preeclampsia and eclampsia

Bdverse o!tcome 1 4*'

Other complication Eclampsia ,'0+ Placental abr!ption ,(*'0+ B<

,)'0+ p!lmonary edema ,(*'0+ s!bcaps!lar liverhematoma ,(%'0

/teroid =% - controversial

rain

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rain

Common /=% #eadache+ vis!al dist!rbance $ associated

conv!lsion ,eclampsia0

Bnatomical pathology "ross hemorrhage $ severe hypertension

Chronic hypertension 이 P+ ,- 56 I8

Postmortem cerebral lesion Edema+ hyperemia+ .ocal anemia+ thrombosis+

hemorrhage

rain

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rain

e!roimaging st!dy C

)*' @p abnormal .inding #ypodense cotical area $ petechial hemorrhage

and in.arction site @ Bˆ ,at a!topsy0 MA

”> post% Cerebral artery area @p remar6ablechange 가 7›1 %

Conv!lsion 과 œ<인 KL Conv!lsion 의 2)' + cerebral in.arction area 가

P음 %

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rain

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rain

Cerebral 5lood <lo7 Eclampsia 1 loss o. a!toreg!lation o. cerebral

blood .lo7 ,Bpollon+ 2***0 #yperper.!sion $ similar in hypertensive

encephalopathy%

Ancreased cerebral per.!sion $@ headache (

7 Cerebral vasospasm ^ žŸ지 ¡8 %

rain

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rain

5lindness are

4hr to Idays Te!지 지yO지S 결¢ £q¤ WXFG %

Nis!al dist!rbance More common etinal detachement

otal loss f ¥¦ $지+ Q음

”> one side f involve

U§<¨©+ YZ없음 % ;반<=> prognosis + good+ ( ”;이@ T상=> ª{«

rain

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rain

Cerebral Edema /= Letharge+ con.!sion+ bl!rred vision+ coma

Mental change TeJ brain involvement Te+ %¬TeA„G % ,C+ MA 상 변화 0

/!dden severe blood press!re elevatoin ®¯2„ vasogenic edema > °±$H ²화 5lood press!re control 이 ƒZ8 %

Electroencephalopgraphy Eclampsia ~k의 &)' @p abnormal .inding 이 ‚³´ %

,4Ihr 이 0 )*' 이상은 ( ”;이상 지y$지S + 3 µ¶ 이@ b부R

·{"G %

,teroplacental perusion

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Nasospasm -@ placental per.!sion ¸$ -@ perinatal mortality

and morbidity 증가의 ƒZ„ ZN

Meas!rement /piral a% 1 )**Sm , T상 0+ 2** Sm ,preeclampsia0

Placental blood .lo7 Anaccesibility+ comple=ity+ !ns!itablity

D#B/ s!l.ate-@ estradiol-(&5 ,in placenta0 의clearance rate > ¹jT ,Everett+ (I*0


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Doppler Doppler meas!rement o. blood velocity thro!gh

!terine artery%

-@ estimate !teroplacental blood .lo7

/9D ratio in preeclampsia 1 증가 Bbnormal 7ave .orm -@ .etal indication => c9sec Y

Z8 %

#ELLP synd% 의 (I-3' 1 abnormal 7ave .orm ^ 0

임 % Preeclampsia 산w+ T상산w@ AB mean

resistance 가 º음 %


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Prediction Lots o. attemption to predict preeclampsia in

early pregnancy -@ poor sensitivity+ poor

positive predictive val!e

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oll over test 2I-3276s

Lt% lat% ec!mbent position -@ s!pine position #ypertension (7Oa abnormal

이 ,- + angiotension AA in.!sion @e abnormal 반»^ 0임 %

Positive predictive val!e ,tr!e positive0 1 33'

,De66er+ (* K <riedman and Lindhemier+ (0

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ric acid Decreased renal !ric acid e=cretion -@ elevated

ser!m !ric acid level

Qacobson ,(*0

ric acid level @ )%mg9dL at 2476s K positive predictiveval!e 1 33'

Weerase6era and Peiris ,2**30 /er!m !ric acid levels did not vary signi.icantly be.ore

the detection o. hypertension

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<ibronectin Endothelial cell activation -@ elevated ser!m

cell!lar .ibronectin level ,5r!ba6er+ (20

Clinical st!dy+ Paarlberg ,(I0 Lo7 sensitivity 1 '

Positive predictive val!e 1(2'

Clinical st!dy+ Chavarria ,2**30

(76s-2*76s+ 3&I lo7-ris6 n!lliparas Positive predictive val!e 1 2'

egative predictive val!e 1 I'

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O=idative /tress Lipid pero=ides level 증가 n antio=idants 의 activity

MN -@ preeclampsia 의 prediction 가˜ ,Walsh+

(40

Mar6er Lipid pero=ides1 malondialdehyde

Pro-o=idants 1 iron+ trans.errin+ .erritin+ blood lipids+ "+ .ree

.atty acid+ lipoproteins+ Nit C F E

#yperhomocysteinemia Btherosclerosis 의 ris6 .actor ,non pregnant0

5!t+ midpregnancy ) level 이 º=a preeclampsia 의 ris6

가 T상0G 3-4 배 증가8 % ,D;Bnna+ 2**4K #ietala+ 2**(0

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Cyto6ines eleased by vasc!lar endotheli!m and

le!6ocytes

)* µ 이상의 cyto6ine 이 preeclampsia ) 증

가 Anterle!6in+ < $ a

CP 증가

ot s!..iciently predictive ,/avvido!+ 2**20

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Placental peptides Corticotropin releasing hormone+ chorionic

gonadotropin+ activin B+ inhibin B 5!t+ variation 이 B investigator ¼G 결과가 G

½$H ‚³´ % Bngiogenic .actor 1NE"<+ Pl"<

<irst trimester ) Pl"<+ s<lt( 의 ser!m level 증가

임상<=> (m$‚ 의›이 RR%

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<etal DB Adenti.ication o. <etal DB in marternal

ser!m -@ prediction o. preeclampsia ,hong+

2**(0

이( 1 endothelial activation and in.lammation

이 7*$a .etal cells and cell!lar material 이maternal circ!lation @ RA1 %

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terine Brtery Doppler Nelocimetry /econd trimester $ !teroplacental vac!lar

resistance jT ,by doppler o. !terine artery0

5asic concepts Ampaired trophoblastic invasion o. the spiral

arteries -@ !teroplacental blood .lo7 의 MN

5o7er ,(30

/ensitivity 1 &I' Positive predictive val!e 12I'

Prevention

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Prevention

Dietary Manip!lation /alt restriction -@ ine..ective ,n!ist+ (I0

Prenatal Ca s!pplementation -@ signi.icant

red!ction in 5P and incidence o. preeclampsia

,5r!cher+ (0

5!t+ Levin+ ,(&0 4** n!lliparas -@ calci!m

and placebo ¾¿ -@ preeclampsia J

gestational hypertension 의 incidence + À •Á¹의 차이가 없음 %

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Lo7 dose aspirin *mg aspirin -@ red!ce the incidence o.

preeclampsia K selective RB2 ‹Œ +

dominence o. endothelial prostacyclin

,#a!th+ (I+ Wallenb!rg+ (I0 Caritis+ (IK CLB/P Collaborative "ro!p+

(4K #a!th+ (3+ (IK otchell+ (IK

/ibai+ (3a Lo7-dose aspirin 7as ine..ective in preventing

preeclampsia

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Bntio=idants Davidge+ (2

Mar6edly red!ced antio=idant activity in

preeclampsia 7omen%

Chappel+ ( 2I3 high ris6 7omen

(I-2276s + vit C F E vers!s placebo

/igni.icant red!ction in preeclampsia ,((' 9 (&'0

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진단

질병

양성 음성

양성 a b

음성 c d

Sensitivity : a/ a+c

Specificity : d/b+d

Positive predictive value : a/a+b

Negative predictive value : d/c+d

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