*Co esponding au ho : Ezenwaeze, Malachy Nwaeze
Copy igh © 2025 Au ho (s) e ain he copy igh o his a icle. This a icle is published unde he e ms o he C ea i e Commons A ibu ion Liscense 4.0.
Pha macogenomics and P egnancy Pha macokine ics: Towa d P ecision D ug
The apy in Obs e ics
Malachy Nwaeze Ezenwaeze 1, *, Syl es e Onuegbunam Nweze 2 and Chibugo Ndidiamaka Nwankwo 3
1 Depa men o Pha macology and The apeu ics, Enugu S a e Uni e si y o Science and Technology College o Medicine.
2 Depa men o Obs e ics and Gynaecology, Enugu S a e Uni e si y Teaching Hospi al /College o Medicine.
3 Depa men o Paedia ics, Albe a Child en Hospi al, Calga y, Canada.
Wo ld Jou nal o Biology Pha macy and Heal h Sciences, 2025, 23(03), 514-522
Publica ion his o y: Recei ed on 20 Augus 2025; e ised on 25 Sep embe 2025; accep ed on 29 Sep embe 2025
A icle DOI: h ps://doi.o g/10.30574/wjbphs.2025.23.3.0874
Abs ac
Backg ound: P egnancy p o oundly eshapes d ug disposi ion h ough physiologic changes in abso p ion, dis ibu ion,
me abolism, and exc e ion. Ma e nal, placen al, and e al genomes add addi ional laye s o a iabili y, c ea ing
challenges o sa e and e ec i e pha maco he apy in obs e ics. Objec i e: To syn hesize cu en e idence on how
pha macogenomics and p egnancy ela ed pha macokine ics can be in eg a ed o op imize d ug he apy in obs e ics,
and o highligh clinical, sa e y, and esea ch implica ions.
Me hodology: This na a i e e iew d aws om clinical guidelines (e.g., CPIC, ACOG, FDA), sys ema ic assessmen s,
pha macokine ic and pha macogenomic s udies, and implemen a ion epo s. Key he apeu ic domains we e examined,
including analgesia/anes hesia, an iepilep ics, an imic obials, and an idep essan s, wi h a ocus on p egnancy induced
pha macokine ic emodeling and geno ype d i en a iabili y.
Resul s: P egnancy inc eases CYP2D6 and CYP3A ac i i y, dec eases CYP1A2 ac i i y, and enhances glucu onida ion,
leading o al e ed d ug exposu e ha may mask o ampli y pha macogenomic e ec s. Clinically, CYP2D6 geno ype
signi ican ly impac s opioid sa e y in he pe ipa um and lac a ion pe iod, while HLA-B15:02 and HLA-A31:01
geno ypes s ongly p edic ca bamazepine/oxca bazepine induced cu aneous eac ions. NAT2 polymo phisms modi y
isoniazid me abolism and oxici y isk, while CYP2C9 and UGT a ian s in luence sul ame hoxazole exposu e. CYP2C19
and CYP2D6 a ian s a ec an idep essan e icacy and ole abili y, wi h p egnancy u he al e ing d ug clea ance.
Implemen a ion s udies demons a e ha p e-emp i e pha macogenomic es ing (e.g., HLA geno yping in Thailand)
educes ad e se ou comes, while clinical decision suppo ools acili a e ansla ion in o p ac ice.
Conclusion: Pha macogenomics, when combined wi h he physiologic eali ies o p egnancy and lac a ion, p o ides a
pa hway owa d p ecision pha maco he apy in obs e ics. High- alue oppo uni ies al eady exis , including a oidance
o CYP2D6-dependen p od ugs in b eas eeding and p e-emp i e HLA es ing o ca bamazepine/oxca bazepine.
Fu u e p io i ies include in eg a ing ma e nal–placen al– e al genomics, de eloping p egnancy-speci ic dosing
algo i hms, and ensu ing equi able implemen a ion ac oss di e se popula ions.
Keywo ds: Pha macogenomics; Pha macokine ics; Obs e ic Pha maco he apy; P ecision Medicine
1. In oduc ion
Medica ion use du ing p egnancy is pe asi e. Recen es ima es sugges ha 93.9 % o p egnan women ake a leas
one medica ion du ing ges a ion, wi h an a e age o 4.2 medica ions pe p egnancy [1]. Use o p esc ip ion medica ions
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du ing p egnancy also shows wide a iabili y ac oss s udies, wi h p e alence a es anging om 27 % o 93 % [2].
Commonly used he apeu ic classes include analgesics, an ibio ics, an ihype ensi es, an iepilep ics, and
an idep essan s e lec ing he b ead h o acu e and ch onic condi ions encoun e ed in obs e ic ca e [3].
Al hough medica ions a e o en essen ial o ma e nal and e al heal h, p egnancy imposes p o ound physiologic
changes ha complica e op imal pha maco he apy. The ges a ional s a e is cha ac e ized by inc eased plasma olume,
al e ed hepa ic enzyme ac i i y (such as induc ion o supp ession o a ious CYP enzymes), enhanced enal glome ula
il a ion, and shi s in p o ein binding, all o which can signi ican ly in luence d ug abso p ion, dis ibu ion, me abolism,
and exc e ion [4,5]. These dynamic al e a ions may lead o sub he apeu ic exposu e o ele a ed d ug le els (and
oxici y) i dosing is no app op ia ely adjus ed.
O e laying hese p egnancy speci ic changes, in e indi idual gene ic a ia ion u he modula es d ug esponse.
Polymo phisms in genes encoding cy och ome P450 enzymes, d ug anspo e s (such as ABCB1, SLCO1B1), and
immune ela ed pa hways in luence pha macokine ics, pha macodynamics, and suscep ibili y o ad e se d ug eac ions
[3,6]. Fo ins ance, CYP2D6 geno ype signi ican ly al e s he me abolic con e sion o codeine o mo phine a clinically
impo an issue o ma e nal analgesia and isk o opioid exposu e o he neona e [7]. Gene ic a ian s in luencing ola e
me abolism o d ug anspo ha e also been implica ed in di e en ial e a ogenic isks associa ed wi h ce ain
an iepilep ic agen s [8,9].
Recen sys ema ic e iews con inue o highligh ex ensi e p egnancy-associa ed pha macokine ic shi s ye also
unde sco e he pe sis en lack o p egnancy- ailo ed dosing guidelines [5,10]. Because obs e ic p esc ibing equen ly
elies on ex apola ion om nonp egnan popula ions, his p ac ice may poo ly cap u e he in e play be ween ma e nal
geno ype and al e ed ges a ional physiology. The unde ep esen a ion o p egnan women in pha macogenomic ials
pe pe ua es unce ain y and po en ial inequi ies in he apy [11,12].
Gi en hese challenges, a uly pe sonalized obs e ic he apeu ic pa adigm mus mo e beyond “one size i s all” models
owa d in eg a ion o bo h gene ic and p egnancy speci ic de e minan s o d ug esponse. A p ecision medicine
amewo k g ounded in pha macogenomics holds p omise o op imizing ma e nal ea men e icacy, minimizing d ug
ela ed ad e se e en s, and p o ec ing e al de elopmen . To ealize his ision, coo dina ed e o s a e needed o
expand pha macogenomic es ing in p egnan popula ions, conduc longi udinal pha macokine ic s udies ac oss
ges a ion, and de elop obus , p egnancy adap ed clinical decision suppo ools [3,13,14].
2. Pha macokine ic emodeling in p egnancy
P egnancy induces subs an ial physiological and biochemical changes ha emodel pha macokine ics. These include
inc eases in plasma olume, ca diac ou pu , and glome ula il a ion a e, as well as al e a ions in hepa ic enzyme
ac i i y. Recen in i o and modeling s udies show ha CYP2D6 and CYP3A ac i i ies inc ease in p egnancy, while
CYP1A2 ac i i y dec eases; glucu onida ion (phase II me abolism) is o en enhanced. Collec i ely, hese changes can
al e d ug exposu es independen o geno ype, meaning ha pha macogenomic e ec s may be masked o magni ied
[15,16].
Fo example, a p obe s udy using dex ome ho phan in p egnan women showed ha CYP2D6 ac i i y was 43% highe
du ing p egnancy compa ed wi h pos pa um, and CYP3A ac i i y was 92% highe , whe eas CYP1A2 ac i i y was
educed. Vi amin A supplemen a ion did no modi y hese changes, al hough highe endogenous e inoic acid le els
co ela ed wi h CYP2D6 ac i i y (17). In i o wo k wi h p ima y human hepa ocy es exposed o p egnancy ela ed
ho mones con i med a dose dependen inc ease in CYP3A4 p o ein and ac i i y o subs a es such as midazolam,
ni edipine, and bup eno phine, wi h a iabili y depending on CYP3A5 backg ound [18].
Physiologically based pha macokine ic (PBPK) models p edic ha CYP1A2 ac i i y declines p og essi ely ac oss
p egnancy, alling o 70%, 44%, and 30% o baseline in he i s , second, and hi d imes e s, espec i ely. In con as ,
CYP2D6 and CYP3A4 ac i i ies inc ease h oughou ges a ion [19]. Measu emen o endogenous bioma ke s, such as
he plasma 4β-hyd oxycholes e ol/choles e ol a io, also con i ms inc eased CYP3A ac i i y in p egnancy, wi h
ges a ional age dependen a ia ion [20].
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2.1. Th ee genomes and a placen a
Figu e 1 D ug disposi ion and esponse in p egnancy
D ug esponse in obs e ics e lec s he in e play o ma e nal, placen al, and e al genomes:
Ma e nal geno ype: Va ian s in CYP2D6, NAT2, UGTs, and HLA can in luence d ug me abolism and ad e se d ug
eac ions. PBPK modeling o dolu eg a i , which is me abolized by UGT1A1, p edic ed ha ma e nal UGT1A1 poo
me abolize s would ha e 1.6- old highe ma e nal and co d blood exposu es han ex ensi e me abolize s, al hough
s anda d dosing emained e ec i e ac oss geno ypes [21].
Placen al biology: The placen a exp esses me abolic enzymes and anspo e s ha shape e al exposu e. Quan i a i e
p o eomics demons a ed ha e lux anspo e s such as P-gp and BCRP dec ease wi h ges a ional age, while some
up ake anspo e s, including OCT3 and OAT4, inc ease [22]. Recen e iews con i m ha Phase II enzymes and
anspo e exp ession shi dynamically ac oss ges a ion, highligh ing gaps in ou unde s anding o ma e nal–placen al
d ug handling [16]. A ascula ized placen a on a chip model has u he demons a ed he easibili y o s udying
ansplacen al anspo o la ge molecules and biologics [23].
Fe al geno ype: Al hough a ely conside ed clinically, e al polymo phisms may con ibu e o immune media ed
eac ions o al e ed de elopmen al d ug esponses. This emains a esea ch on ie , wi h limi ed applica ion in ou ine
ca e [14,25].
A p esen , mos pha macogenomic decisions in p egnancy a e based on ma e nal geno ype, while placen al anspo e
biology and e al genomics emain la gely in es iga ional.
3. The Obs e ic Pha macogenomics Landscape by The apeu ic Domain
3.1. Analgesia and anes hesia: CYP2D6 and opioid sa e y in he pe ipa um and lac a ion
Pos pa um pain managemen is common, opioids may be needed in some pa ien s bu pose unique isks in lac a ion
when p od ugs depend on CYP2D6 ac i a ion (e.g., codeine, amadol). Ul a apid CYP2D6 me abolize s can gene a e
high mo phine (o O-desme hyl amadol) concen a ions, which pass in o b eas milk and may cause in an seda ion,
espi a o y dep ession, o a ely dea h. Regula o y and p o essional guidance has he e o e shi ed away om
codeine/ amadol in b eas eeding [26–29]. The Uni ed S a es Food and D ug Adminis a ion (FDA) added a
con aindica ion o codeine/ amadol in ce ain pedia ic se ings and ecommended agains use in b eas eeding
because in an ha m can occu and mos mo he s will no know hei CYP2D6 s a us [26]. The Ame ican College o
Obs e icians and Gynecologis s (ACOG) and anes hesia socie ies echo his, p io i ize mul imodal non opioid analgesia
and a oid codeine/ amadol du ing b eas eeding [27].
I ecommends ha , i an opioid is necessa y pos pa um, p e e agen s no elian on CYP2D6 bioac i a ion (e.g.,
mo phine), use he lowes e ec i e dose o he sho es du a ion and suppo wi h obus non opioid mul imodal
s a egies [28]. Also o documen any known CYP2D6 geno ype in he elec onic heal h eco d and o a oid p od ug
opioids al oge he in he b eas eeding pe iod i a pa ien is a known ul a apid me abolize [28,29]. Heal h-sys em
e alua ions obse ed u iliza ion changes a e he 2017 FDA communica ion, and case epo s include a b eas ed in an
dea h linked o ma e nal codeine use, ein o cing a conse a i e app oach wi h p od ug opioids in lac a ion [26,28].
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3.2. An iepilep ics: p e en ing li e h ea ening cu aneous eac ions (HLA-B15:02 / HLA-A31:01)
Ca bamazepine (CBZ) and oxca bazepine (OXC) a e some imes used in women o ep oduc i e age. Ce ain HLA
geno ypes con e high isk o se ious cu aneous ad e se eac ions (SCAR), including S e ens Johnson synd ome/ oxic
epide mal nec olysis (SJS/TEN) [29–31].
The CPIC guideline gi es s ong ecommenda ions o a oid CBZ/OXC in HLA-B15:02 ca ie s and o conside
al e na i es o enhanced cau ion in HLA-A31:01 ca ie s [30,31]. Implemen a ion s udies (e.g., Thailand’s na ional
policy) show ha p e-emp i e HLA-B 15:02 es ing educes SCAR by s ee ing he apy away om CBZ/OXC in ca ie s
an ins uc i e model o obs e ic clinics managing epilepsy o igeminal neu algia in p egnancy o p econcep ion
[32,33].
Whe e an iepilep ic he apy is indica ed in p egnancy, p econcep ion pha macogenomics es ing is ideal; i una ailable,
conside HLA es ing be o e ini ia ing CBZ/OXC in a - isk ances ies. Pha macogenomics guides sa e y ( isk o SCAR)
a he han e a ogenici y; e a ogenic isk emains a sepa a e conside a ion in an iepilep ic selec ion [30–33].
3.3. An imic obials: La ge Pha macokine ic Shi s and Eme ging Pha macogenomic In e sec ions
Sys ema ic e iews emphasize ha p egnancy equen ly al e s an imic obial pha macokine ics, ypically leading o
inc eased clea ance and expanded olume o dis ibu ion. These physiological changes can esul in subop imal d ug
concen a ions, necessi a ing dose adjus men s o achie e he apeu ic a ge s. Fo ins ance, β-lac am an ibio ics o en
equi e dose in ensi ica ion du ing la e p egnancy o main ain e ec i e plasma concen a ions [34].
Pha macogenomic ac o s can u he complica e his a iabili y:
Isoniazid (INH) and NAT2 Ace yla ion: Gene ic polymo phisms in he NAT2 gene ca ego ize indi iduals as slow,
in e media e, o apid ace yla o s. Slow ace yla o s may expe ience ele a ed INH concen a ions, inc easing he isk o
hepa o oxici y, while apid ace yla o s migh ha e sub he apeu ic le els, isking ea men ailu e. P egnancy can al e
INH clea ance; howe e , NAT2 geno ype emains a signi ican de e minan . In eg a ing pha macogenomic da a wi h
p egnancy adjus ed dosing could op imize he apy, pa icula ly in high ube culosis bu den egions [35,36].
T ime hop im Sul ame hoxazole (TMP-SMX) and CYP2C9/UGT Polymo phisms: Sul ame hoxazole is me abolized by
CYP2C9 and UGT enzymes. Va ian s such as CYP2C9*2/*3 can educe clea ance and ele a e oxici y isk. TMP-SMX is
u ilized in HIV p ophylaxis and u ina y ac in ec ions du ing p egnancy. While pha macokine ic s udies indica e
inc eased clea ance in la e ges a ion, pha macogenomic di e ences may s ill in luence ma e nal oxici y o d ug–d ug
in e ac ions wi h an i e o i als [37].
3.4. An idep essan s and O he CNS Agen s: Geno ype and Physiology
Beyond p egnancy, CYP2D6 and CYP2C19 geno ypes in luence he me abolism and dosing o many SSRIs and icyclic
an idep essan s. Du ing p egnancy, inc eased CYP2D6 ac i i y and a iable CYP2C19 ac i i y can u he al e d ug
exposu e, impac ing bo h e icacy and elapse p e en ion in mood and anxie y diso de s [3,39]. Clinicians should
in eg a e a ailable geno ype in o ma ion wi h close symp om moni o ing and, whe e easible, he apeu ic d ug
moni o ing (TDM).
Fo example, se aline is commonly used in p egnancy o dep ession and anxie y. CYP2C19 poo me abolize s ha e
highe plasma concen a ions and g ea e isk o dose ela ed ad e se e ec s, whe eas ul a apid me abolize s may
ha e sub he apeu ic exposu e. Pha macokine ic s udies demons a e ha se aline clea ance inc eases du ing la e
p egnancy, o en necessi a ing dose escala ion o main ain symp om con ol. Thus, a CYP2C19 ul a apid me abolize
may be pa icula ly ulne able o ea men ailu e in p egnancy unless TDM o symp om guided i a ion is applied.
Con e sely, poo me abolize s may s ill expe ience ele a ed exposu e despi e p egnancy induced clea ance changes,
emphasizing he impo ance o combining pha macogenomics wi h clinical moni o ing [39,40].
Fo icyclic an idep essan s like no ip yline and ami ip yline, CYP2D6 geno ype s ongly in luences dosing ou side
p egnancy, and inc eased CYP2D6 ac i i y in p egnancy can u he lowe plasma concen a ions, ein o cing he need
o TDM and pha macogenomics in o med dose adjus men s [38,40].
Clinical Implica ions is ha when pha macogenomic in o ma ion is a ailable, i should be laye ed on o p egnancy
physiology. In case o ul a apid CYP2C19 me abolize s, he e will be highe isk o elapse i se aline dose is no
op imized he e o e close moni o ing o al e na i e SSRI may be wa an ed [39]. In case o poo me abolize s, conside
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lowe s a ing dose and igilan moni o ing o ad e se e ec s, e en du ing p egnancy [39,40]. In all geno ypes,
an icipa e inc eased clea ance du ing la e ges a ion and eassess dosing pos pa um as me abolism no malizes [45-47].
Table 1 Key Pha macogenes in Obs e ic Pha maco he apy
Gene(s)
D ug(s)
P egnancy Conside a ions
Pha macogenomic Implica ions
CYP2D6
Codeine, T amadol
(p od ugs)
↑ CYP2D6 ac i i y in
p egnancy; isk o in an
exposu e ia b eas milk in
lac a ion
Ul a- apid me abolize s p oduce excessi e
ac i e me aboli es → neona al
seda ion/ espi a o y dep ession; a oid
codeine/ amadol in b eas eeding; p e e
non-CYP2D6 opioids (e.g., mo phine)
HLA-B15:02,
HLA-A31:01
Ca bamazepine,
Oxca bazepine
P egnancy does no mi iga e
SCAR isk; p econcep ion o
ea ly es ing ideal
S ong CPIC ecommenda ion o a oid
CBZ/OXC in ca ie s; conside al e na i es;
isk applies ega dless o p egnancy s a us
NAT2
Isoniazid
P egnancy al e s INH
clea ance bu no geno ype
e ec ; TB he apy common
in high-bu den se ings
Slow ace yla o s → ↑ isk o hepa o oxici y;
apid ace yla o s → ↓ exposu e and possible
ea men ailu e; PGx may guide
indi idualized dosing
CYP2C9,
UGT1A6/9
Sul ame hoxazole
(TMP-SMX)
Inc eased clea ance in la e
p egnancy; used o HIV
p ophylaxis and UTIs
Reduced- unc ion CYP2C9 alleles (*2, *3) o
UGT a ian s → ↑ isk o ad e se e ec s (e.g.,
hype sensi i i y, hepa o oxici y); geno ype
may e ine isk s a i ica ion
CYP2C19,
CYP2D6
SSRIs (e.g., se aline,
pa oxe ine),
icyclics
↑ CYP2D6 ac i i y and
a iable CYP2C19 ac i i y
du ing p egnancy; isk o
educed an idep essan
e icacy
Geno ype in luences me abolism (e.g., poo
s ul a apid me abolize s); conside PGx +
he apeu ic d ug moni o ing o dose
op imiza ion
4. Lac a ion Pha macogenomics: T ansla ing Ma e nal Geno ype o In an Exposu e
Lac a ion in oduces a second “pa ien ,” he in an , equi ing ca e ul conside a ion o pha macogenomic (PGx) ac o s
in medica ion choices. CYP2D6 dependen p od ug opioids, such as codeine and amadol, a e pa icula ly conce ning
due o a iable ac i a ion o po en me aboli es and po en ial ans e in o b eas milk. Ma e nal CYP2D6 ul a- apid
me abolize s (UMs) can con e codeine in o mo phine a highe a es, leading o inc eased isk o in an seda ion and
espi a o y dep ession [41,42]. The FDA has issued wa nings agains b eas eeding du ing ea men wi h codeine o
amadol due o hese isks [43]. Fo amadol speci ically, Lac Med summa izes he FDA/manu ac u e s ance agains
b eas eeding exposu e and discusses sa e al e na i es [42].
5. Implemen a ion: F om Geno ype o Bedside in Obs e ics
5.1. Timing and Tes Pa ame e s (When and Wha o Tes )
P econcep ion o ea ly p ena al isi s a e ideal o ob ain du able pha macogenomic da a (e.g., CYP2D6, HLA-B, HLA-A),
enabling sa e choices should new indica ions a ise la e (e.g., in apa um analgesia, in ec ions) [44]. Ta ge ed es ing
is wa an ed when s a ing high- isk d ugs (e.g., ca bamazepine/oxca bazepine in a - isk ances ies) o when a
lac a ing pe son equi es analgesia and has a known isky geno ype [44,45].
5.2. Applica ion o Resul
The Clinical Pha macogene ics Implemen a ion Conso ium (CPIC) p o ides ac ionable, d ug speci ic ables mapping
geno ype, pheno ype, and ecommenda ion (dose change, al e na i e, o a oidance) [44,45]. In eg a ing hese in o he
elec onic heal h eco d (EHR) wi h clinical decision suppo is easible and has suppo ing esou ces [44].
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5.2.1. Laye ing P egnancy Physiology on Top o Geno ype
E en wi h geno ype guided selec ion/dosing, p egnancy associa ed pha macokine ic changes can push exposu es
below a ge s. Combining PGx wi h s age o p egnancy pha macokine ic knowledge (e.g expec highe CYP2D6 ac i i y
and highe enal clea ance), he apeu ic d ug moni o ing whe e a ailable, and pos pa um eassessmen as physiology
no malizes a e he key [46].
P ac ical pe ipa um pha macogenomic algo i hms can guide sa e and e ec i e medica ion use. Fo pos pa um
analgesia in a b eas eeding pa en , managemen should begin wi h non-opioid mul imodal he apy, a oiding codeine
and amadol. I an opioid is necessa y, non-CYP2D6-p od ug op ions should be p e e ed, wi h conse a i e dosing,
counseling, and documen a ion o any CYP2D6 geno ype, suppo ed by clinical decision ules [45]. When ini ia ing o
swi ching an iepilep ic he apy, popula ions wi h app eciable HLA-B 15:02 equency should unde go es ing be o e
ecei ing ca bamazepine o oxca bazepine, and ca ie s should a oid hese medica ions, wi h al e na i e an iepilep ic
d ugs selec ed acco ding o obs e ic neu ology guidance [47].
Sa e y, e hics, and equi y conside a ions a e essen ial in pe ipa um pha macogenomics. In o med consen should
encompass he ull ange o pha macogenomic implica ions, including inciden al indings and po en ial impac s on
amily membe s, such as sha ed HLA isks [45]. Equi y equi es o e ing es ing wi hou using ace as a p oxy, while
ensu ing ha panels a e alida ed ac oss di e se popula ions o p e en widening dispa i ies [45]. Da a s ewa dship
in ol es s o ing pha macogenomic esul s as li e ime da a, which can e ain ele ance o u u e p egnancies and non-
obs e ic ca e. Ta ge ed es ing, such as HLA-B 15:02 sc eening be o e ca bamazepine in high p e alence g oups, has
been shown o be bo h clinically impac ul and cos e ec i e [45,47].
6. Resea ch P io i ies
Fu u e esea ch in obs e ic pha macogenomics should p io i ize se e al domains. Fi s , he e is a need o de elop
ma e nal placen al e al iad models ha cla i y how placen al anspo e s and e al geno ypes modula e ma e nal
d ug exposu e and e al ou comes [46]. Second, p egnancy speci ic pha macogenomic dosing s a egies mus mo e
beyond ex apola ion om non-p egnan popula ions by in eg a ing pha macogenomics wi h physiologically based
pha macokine ic (PBPK) modeling and alida ing hese app oaches h ough p agma ic clinical ials. Thi d, lac a ion
pha macokine ics and pha macogenomics equi e u he in es iga ion o quan i y milk o plasma ans e and in an
d ug exposu e ac oss ma e nal pha macogenomic pheno ypes, ex ending esea ch beyond opioids. Fou h, eal wo ld
implemen a ion should ocus on embedding pha macogenomic in o ma ion in o elec onic heal h eco ds, including
obs e ic-speci ic clinical decision suppo ools and ou comes acking [45]. Finally, di e si y in s udy popula ions mus
be imp o ed by expanding ep esen a ion o A ican, Asian, and admixed ances ies in obs e ic pha macogenomics
esea ch [46].
7. Conclusion
Pha macogenomics is a p ac ical le e o sa e , mo e e ec i e obs e ic pha maco he apy when pai ed wi h he
physiologic eali ies o p egnancy and lac a ion. High alue oppo uni ies al eady exis (e.g., a oiding codeine/ amadol
in b eas eeding, p e-emp i e HLA es ing o CBZ/OXC), and b oade in eg a ion ia CPIC-aligned decision suppo can
imp o e ca e now while he e idence base o o he d ug classes g ows.
Compliance wi h e hical s anda ds
Acknowledgmen s
We ex end ou g a i ude o all whose s ead as suppo and encou agemen we e in aluable o he comple ion o his
e iew.
Disclosu e o con lic o in e es
The au ho s decla e no con lic o in e es .
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520
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