Ajaliste esilekutsutud sünnituste vs. spontaanselt alanud sünnituste mõju võrdlus laste õpiedukusele 12 aasta vanuses

Eesti Arst 2023; 102(8):415–41

Kaksikraseduste kulg ja perinataalne tulemus TÜ Kliinikumi naistekliinikus aastatel 2003–2007

Uuringu eesmärgiks oli võrrelda spontaanselt ja kunstliku viljastamise tulemusena tekkinud kaksikraseduste kulgu ning tüsistuste esinemist, samuti hinnata kaksikute sünnitusviisi ning perinataalset tulemust aastatel 2003–2007 TÜ Kliinikumi naistekliinikus. Kaksikraseduste kulg oli sarnane sõltumata viljastumisviisist: tüsistustest esinesid kõige sagedamini aneemia, ähvardav enneaegne sünnitus, rasedusest tingitud hüpertensioon ja preeklampsia. Sünnitusjärgsetest probleemidest oli esikohal verekaotus > 1000 ml. Vaginaalselt sünnitas 39,3%; keisrilõike teel 57,9% ning kombineeritult 2,7% naistest. Peamiseks perinataalseks probleemiks oli enneaegne sünd sellest tulenevate tüsistustega. Teisena sündinud kaksik oli rohkem ohustatud asfüksiast, kuid tema seisundit sünnil mõjutas pigem enneaegsus kui sünnitusviis. Perinataalne suremus kaksikutel oli viis korda suurem võrreldes kõikide sündidega Eestis samal ajaperioodil. Eesti Arst 2009; 88(3):164−17

Rasedus pärast elundisiirdamist

1956. aastast, mil rasestus esimene siiratud elundiga naine, on peatselt möödas 60 aastat. Elundisiirdamine suurendab viljatute naiste rasestumise tõenäosust ning täiustunud meditsiinilised teadmised võimaldavad ka siirikutega naistel raseduse edukat kulgu. Kõige rohkem on kirjeldatud rasedusi neerusiirikuga naistel, kuid see on võimalik ka pärast maksa, südame, kopsude, peensoole või isegi mitme elundi samaaegset siirdamist. Eestis on elundisiirdamisjärgseid rasedusi olnud väga vähe, kuid siirdamiste hulga suurenemine on muutnud teema aktuaalseks ka siinse arstkonna jaoks.Artikli eesmärk on selgitada, milline on seos elundisiirdamise ja viljakuse vahel, kas ja kuidas mõjutavad rasedusaegsed immunoloogilised muutused siiratud elundit, millised on sagedasemad tüsistused siirikutega rasedatel ning mida on teada immunosupressiivse ravi mõjust loote arengule.Eesti Arst 2016; 95(2):98–10

Enneaegse sünnituse ja enneaegse vastsündinu perinataalperioodi ravijuhend

Eesti Arst 2017; 96(7):422–43

Rasedusaegne aordi dilatatsiooni ja bikuspiidse aordiklapi operatsioon Turneri sündroomiga patsiendil. Haigusjuhu kirjeldus

Rasedusaegne südameoperatsioon kätkeb endas suurt riski nii emale kui ka lootele. On kirjeldatud vaid üksikud aorditüve ja aordiklapi operatsioone raseduse ajal. Kirjanduse andmetel on loote suremus ekstrakorporaalse vereringe kasutamisel 20%. Operatsiooniaegne hüpotermia halvendab uteroplatsentaarset perfusiooni ja soodustab emaka kontraktsioonide teket. Hüperkaleemia emal võib põhjustada lootel bradükardiat ja düstressi. Artiklis on kirjeldatud raseduse kulgu Turneri sündroomiga 31-aastasel patsiendil, kellel aordianeurüsm diameetriga 5 cm ning bikuspiidne aordiklapp diagnoositi esimest korda raseduse ajal. Patsiendile tehti raseduse 13. nädalal Bentalli operatsioon (aordiklapi ja üleneva aordi proteesimine). Rasedus jätkus ning patsient sünnitas raseduse 36. nädalal keisrilõike teel poja sünnikaaluga 1950 g, Apgari hinded olid 8 ja 9 palli. 5 kuu vanusena kaalus laps 6,5 kg ja oli normaalse emotsionaalse arenguga. Ka naise tervis on hea.Eesti Arst 2015; 94(6):365–36

Extensive shift in placental transcriptome profile in preeclampsia and placental origin of adverse pregnancy outcomes

One in five pregnant women suffer from gestational complications, prevalently driven by placental malfunction. Using RNASeq, we analyzed differential placental gene expression in cases of normal gestation, late-onset preeclampsia (LO-PE), gestational diabetes (GD) and pregnancies ending with the birth of small-for-gestational-age (SGA) or large-for-gestational-age (LGA) newborns (n = 8/group). In all groups, the highest expression was detected for small noncoding RNAs and genes specifically implicated in placental function and hormonal regulation. The transcriptome of LO-PE placentas was clearly distinct, showing statistically significant (after FDR) expressional disturbances for hundreds of genes. Taqman RT-qPCR validation of 45 genes in an extended sample (n = 24/group) provided concordant results. A limited number of transcription factors including LRF, SP1 and AP2 were identified as possible drivers of these changes. Notable differences were detected in differential expression signatures of LO-PE subtypes defined by the presence or absence of intrauterine growth restriction (IUGR). LO-PE with IUGR showed higher correlation with SGA and LO-PE without IUGR with LGA placentas. Whereas changes in placental transcriptome in SGA, LGA and GD cases were less prominent, the overall profiles of expressional disturbances overlapped among pregnancy complications providing support to shared placental responses. The dataset represent a rich catalogue for potential biomarkers and therapeutic targets.Peer reviewe

Stanniocalcin-1 Hormone in Nonpreeclamptic and Preeclamptic Pregnancy : Clinical, Life-Style, and Genetic Modulators

Context and Objectives: The study represents the first comprehensive analysis of Stanniocalcin-1 (STC1) hormone in human pregnancy, assessing clinical, lifestyle, and genetic determinants of circulating STC1 at term. Design, Setting, and Participants: Participants included women with (n = 50) and without (n = 316) preeclampsia (PE) at delivery, recruited in the REPROgrammed fetal and/or maternal METAbolism (REPROMETA) study (2006-2011, Estonia). Genetic association analysis combined PE cases (n = 597) and controls (n = 623) from the REPROMETA and Finnish Genetics of Preeclampsia Consortium (2008-2011) studies. Main Outcome Measure(s): Maternal postpartum plasma STC1 was measured by ELISA (n = 366) and placental STC1 gene expression by TaqMan quantitative RT-PCR (n = 120). Genotyping was performed using Sequenom MassArray. Results: Significantly higher STC1 plasma level was measured for the PE (median, 1952 pg/mL; 1030-4284 pg/mL) compared with non-PE group (median, 1562 pg/mL; 423-3781 pg/mL; P = 3.7 = 10 = 4, Mann-Whitney U test). Statistical significance was enhanced after adjustment for cofactors (linear regression, P = 1.8 x 10(-6)). STC1 measurements were negatively correlated with maternal smoking. Prepregnancy body mass index had a positive correlation with STC1 only among PE patients (r = 0.45; P =.001). The strongest genetic association with hormone concentrations was detected for STC1 single nucleotide polymorphisms rs3758089 (C allele: minor allele frequency, 5%; linear regression: beta = 249.2 pg/mL; P =.014) and rs12678447 (G allele: minor allele frequency, 7%; beta = 147.0 pg/mL; P =.082). rs12678447 placental genotypes were significantly associated with STC1 gene expression (P =.014). The REPROMETA/Finnish Genetics of Preeclampsia Consortium metaanalysis suggested an increased risk to develop late-onset PE for the rs12678447 G allele carriers (P =.05; odds ratio = 1.38 [0.98 -1.93]). Conclusions: Increased STC1 hormone represents a hallmark of late-onset PE. STC1 gene variants modulate placental gene expression and maternal hormone levels.Peer reviewe

Mid-gestational gene expression profile in placenta and link to pregnancy complications.

Despite the importance of placenta in mediating rapid physiological changes in pregnancy, data on temporal dynamics of placental gene expression are limited. We completed the first transcriptome profiling of human placental gene expression dynamics (GeneChips, Affymetrix®; ~47,000 transcripts) from early to mid-gestation (n = 10; gestational weeks 5-18) and report 154 genes with significant transcriptional changes (ANOVA, FDR P<0.1). TaqMan RT-qPCR analysis (n = 43; gestational weeks 5-41) confirmed a significant (ANOVA and t-test, FDR P<0.05) mid-gestational peak of placental gene expression for BMP5, CCNG2, CDH11, FST, GATM, GPR183, ITGBL1, PLAGL1, SLC16A10 and STC1, followed by sharp decrease in mRNA levels at term (t-test, FDR P<0.05). We hypothesized that normal course of late pregnancy may be affected when genes characteristic to mid-gestation placenta remain highly expressed until term, and analyzed their expression in term placentas from normal and complicated pregnancies [preeclampsia (PE), n = 12; gestational diabetes mellitus (GDM), n = 12; small- and large-for-gestational-age newborns (SGA, LGA), n = 12+12]. STC1 (stanniocalcin 1) exhibited increased mRNA levels in all studied complications, with the most significant effect in PE- and SGA-groups (t-test, FDR P<0.05). In post-partum maternal plasma, the highest STC1 hormone levels (ELISA, n = 129) were found in women who had developed PE and delivered a SGA newborn (median 731 vs 418 pg/ml in controls; ANCOVA, P = 0.00048). Significantly higher expression (t-test, FDR P<0.05) of CCNG2 and LYPD6 accompanied with enhanced immunostaining of the protein was detected in placental sections of PE and GDM cases (n = 15). Our study demonstrates the importance of temporal dynamics of placental transcriptional regulation across three trimesters of gestation. Interestingly, many genes with high expression in mid-gestation placenta have also been implicated in adult complex disease, promoting the discussion on the role of placenta in developmental programming. The discovery of elevated maternal plasma STC1 in pregnancy complications warrants further investigations of its potential as a biomarker