100 tahun lagi@Bo Sindroma Metabolik Pada Kehamilan OES i 38 Vy On Dr. dr. M ADRIANES BACHNAS, SpOG, Subsp. K. Fm + Ketva Divs! Fetomaternal, Bagian Obstetri dan Ginekologi FK Universitas Sebelas Maret/ RSUD Dr. Moewardi, Solo + Sekretaris Himpunan Kedokteran Fetomaternal (HKFM) Indonesia ‘+ Ketua Pokja USG Perkumpulan Obstetri dan Ginekologi Indonesia (POG!) ‘+ Anggota Komisi Kurikulum Kolegium Obstetri dan Ginekologi indonesia, Pokja PAKIAS POGI, Pokja Intensive Care POG!© @60 HKFM How is metabolic syndrome diagnosed? * OBESE Metabolic syndrome is diagnosed when you have three or more ofthese conditions: * DM + Central or abdominal obesity (measured by waist circumference) * HIPERTENSI Men - greater than 40 inches * DISLIPIDEMIA (2) Women - greater than 3Sinches + High trislycerides -150 milligrams per deciliter (mg/L) or more, or you're taking ‘medicine for high triglycerides ‘What is Metabolic Syndrome? + Low HDL cholesterol, or you're taking medicine for low HDL cholesterol Men - Less than 40 mgiiL. Women - Less than 50 mg/dl. + High blood pressure ~ 130/85 millimeters of mercury (mm Hg) or more, or you're taking ‘medicine for high blood pressure + High fasting alucose (blood sugar) -100 mgfiL or more, or you're taking medicine for high blood glucose BEST TO DEFINE PRIOR TO PREGNANCY6 4. METABOLIC SYNDROME Teepe as scsi ts LOW HDL (GOOD) CHOLESTEROL Cmte, PYOTR NS STRONG ENVIRONMENT DRIVE: LIFE-STYLE: DIET + EXERCISEPERUBAHAN HORMONAL SELAMA KEHAMILAN Progesterone Ttine of mmuce poner notedia gat Progesteron ‘Sein poston yd Beta 3:1 prin niin Penne tanspor GLUT aman placenta lactogen PLS or done socattopinhemoce (SED, lava sma rein hPL avai secret ad syteinftion lacs ll rad es, (Ghcue eaten td ane 2 Lpstsisand it msbicaton, ‘etating FFA‘ trea covation Placental growth hormone PGH: PpGH Facute cmp Stipa ‘See tne ted Wy 101 Placental Corconophia Releasing ioweca pCRH ape bei pea ‘etal > ni tans inductee AIRS rection Tre ‘nea esitace mater ae prepay toa ne DAE TNF 1 SS rec ater! ce ee twelnated placer TNFa epson of ‘ecm lana pests ees etl oi Ee) Repti of yates ofplaet progeterone pronty Cocnbatonts apes tier store Fes restnce Prepency a eptin estan + ‘Ghrelin Highly epee ie fest instr Haptic crepes ation and pico vpaleindicicn Heovtte cn of ery ‘ee ‘Adiponetia ‘ay prodecedand sect tytn WAT Asoc parce ty tbe pleats + Replton of prove bemeontas + Dasease pce prodctin and Epopenis ypoutgoeesaemas pret marer of CDM Mainly protacedby betes WAT — infetion amend el of hee preg women ed (GOM> op ep placental aya wpe cetrba scene ft rpstion HREM Esterogen Leptin Gherelin AdiponectinDTS ethLIPID PROFILE SS Cholesterol <200 200-239 | 240 mg/dl mg/dl mg/dl Triglycerides <150 150-199 | 200-499 mg/dl mog/di mg/dl HOL 60 35-45 35 cholesterol _mgidl mg/dl mg/dl LoL 60-130 | 130-159 ‘| 160-189 cholesterol _magidi mg/dl mg/dl Cholesterol) 4.0 5.0 60 HDL ratio diketahui sebelum kehamilan tidak lazim diperiksa saat kehamilan TG (mmov) HOL (mmoln) LOL (mmott) TC (mmoll) tidak ada patokan baku kira-kira naik 2x nilai normalOx. Dyslipidemia in Pregnancy sto 206 | aia sats Me. ACE et nase In a large European community-based cohort study comprising nearly 4000 non- diabetic otherwise healthy women with a mean age of 30.9 + 4.9, investigators found that elevated[TG levels, but not TC levels, during the first trimester|were independently associated with adverse outcomes for both the mother and the without proteinuria and preeclampsia in the mother, and preterm babies who are too large for e. Authors suggest that lifestyle modification with a focus on reduction in weight and increase in physical activity in these women may avert hypertensive complications and preterm birth in these women.2"13 characterized by high TG, small dense LDL, and low HDL-C levels - confers an increased risk of adverse pregnancy outcomes as well as cardiovascular risk later in life. Co-morbid conditions of preeclampsia, gestational hypertension and diabetes, as well as maternal obesity may accentuate these unfavorable changes patterns and clinical outcomes. signifies the importance of early detection and risk modification of dyslipidemia during pregnancy. Further studies are needed to delineate the role of anti- hyperlipidemic therapies in pregnant women with dyslipidemia.sat ons Cosa Secon Ete | ua 0 A222 oom Dyslipidemia Management in Pregnancy: Why Is It not ®) @ 6 @© Covered in the Guidelines? So he Joanna Leva & Mace Banach ‘erent AteroscleassRcorts 24, 547-586 (2022) | Cte this arcs 1405 Accoses | Catone | 10 Arma | Maca Recent Findings ‘Among many available groups of lipid-lowering drugs only bile acid sequestrans are approved forthe treatment of dyslipidemia during pregnancy. Eaetimibe and fenofibrate right be considered if benefits outweigh the potential risk. Statins ae stil contraindicated 140 mg/L. Then advise OGTT for three hours. 2. O'Sullivan test is one-hour glucose after 50 grams of oral glucose intake. 3. Screening for GDM advises OGTT with 50 grams of glucose. 4. Check the one-hour glucose level, which is called the O'Sullivan test. 5. Screening should be done between 24 to 28 weeks of gestation. 6. fone hour sample is >140 mg/L, then taking a 3-hour 100-grams of glucose(OGTT) is necessary. 1, Normal pregnancy is associated with increased insulin resistance, especially in the second and third trimesters. Gestational Diabetes mellitus (GDM) | 200 180 | 150 120 100 80 | 507 liaise poutve COM easan compared wih Caper and Coustan cor Wich WHO 1996" | =126(7.0) TSgOGTT Not | =140(78) Not rae cared th Compania fu} id} Acos™2il | 28563) YoogoGTT=te0(100) " =185(66) ‘Canadian 205(53) 75g OGTT2I91(106) = 16069) Diabetes ‘Assocation ta ct tong laa gucone 270 neal [RRs | FED ReOGTTseOTOO FER | Ae) [eroutvineamratsconganatensteoe pape at requires ‘hcene mecuneent wiht FPO she other ind bo enienort BOSE Nat eaared 75 OOTT Wa m Rat requred | 1 tenured) Sirematy eet srg pans fucose 80.9 mn 128 Mo #0ne value suicient for diagnosis, ##Two or more values required for diagnosis Teg mgiayahar oemgnasenginPogyhecee oa ‘iFTwo oF more values required for diagnosis, #t##One value Is sufcent for agnosis variasi: keuntungan dan kelebihan - persentase terjaring - false positif - false negatif - kemudahan: angka drop outThe association between maternal HbAIc and adverse outcomes in gestational diabetes March 2023 . Erontirs in Endocrinology 14 Dt: 19.3389/fendo.2023.105899 License - CC.BY 40 xia Zhang -Qi Wu @ Lu Qi- Show all9 authors - @ Munuza Parfaite ‘ockgroun The ote of HOATC In women wih gestational Sabet metus (COM 's si uncieaparicuany ith Ain population. im To mvestgat the ‘between MbAIc an adverse pregnancy outcomes wae astesved. Rest ‘Comgaredto women wh Hokle + SOX, BATE was Bonicanty atte wi) ‘macrosomia (90R 263,95XC1 61431), pregrancy induced hypertension {208 26 95XC157 410, preterm bth (OR 164,95XC! 105258, ad peiary ‘Cesarean section primary C-section, aR 49,9SXCi109,203) in COM women | th HoAte 255% whe sgiicaty associated wih PI (OR 19195%C1124204) im women wth HOA 515.4% The assoclaton between ‘okt an adverse outcomes varied with maternal ge, pre-prognancy Mt and GWG. tn women aged 329 years, teres sigrfcant association between HBATE tnd primary C-section when HOAtC was 51-54% and #5.SK. n women oped 29° 3 years ana HAT 25.5% MOAIc was sgnficaty associated wih macrosomia. In women aged 35 years, thee sgnfeat association Between HaAIe and ‘rete bth when MBAIe was 515.4% and macrosomia ana PM when HOATE 253%. nre-pegrant normal-weight woman, HDA‘ was Snir a 1 @ 8 © GDM HbA1C >5.5 PIH Preterm birth Macrosomia C-Section> Am J Obstet Gynecol. 2014 Dec;211(6):641.e1-7. dok: 10.1016), ajog.2014.06.016, Epub 2014 Jun6. Use of hemoglobin Aic as an early predictor of _ gestational diabetes mellitus ‘Alex Fong *, Allison E Serra 2, Lauryn Gabby *, Deborah A Wing ?, Kathleen M Berkowitz ASfiliations. + expand PMID: 24912095 DO: 10.1016) j09.2014.06.016 Abstract ‘Objective: The purpose ofthis study was to assess an early hemoglobin Ate (HabATe) value from '57-6.4% as an early predictor of progression to gestational diabetes (GDM). Sy dein Arto cor yn prod en a wen ret gl sattonowr 2 yrs noha anes ceoung Hate paremed a <2 west owen venom pecs anaes hates oh oe 3x GDM RISK Stade The nay otcone ar OO Geom. Secon ces Rese ery ‘ute mater weghtonn Sth deena meats Worentnonvesncvaunst — IA] C 57.803. wan compe wih ose wh a geet 57% Raut: Ney one-hidof tove patents inthe HgbA 87-64% geup 272%) emecencarne — >I FG A Seracpmer ot Gu corp nan 874m Het 7% nos ao, 39, 0% 1-0. corters et 20-7) Th 2 rare raed ser a ao, 24) att ‘ssn on, erarnc oe marin pester ae on ae derstood renng Tt ero aie Siteescein a ee rescaled ae MnweaR, Meena cron mobos. ‘Conclusion: More than 10% of patients in our cohort had an early screening Hobie value of 57- 6.4%. Women inthis group havea significantly higher risk of progression to GDM compared with _wornen with normal HgbAc values and should be considered for closer GOM survellance and possible interventionFETAL SURVEILLANCE — DIABETES IN PREGNANCY WAIT FOR SPONTANEOUS Denke DELIVERY UNTIL 41 WEEKS Very rarely neonatal adverse event (02 transfer 63, need {3 - supply G, failed in many processes Pregnancy loss: 10%-30% Noticable US: BIOMETRY US: 65, ¥5, AF, PR —_ progressiveness pci +S: Fetal tone, tes : ~ fetol breathing, : Cee {etal movement, ae (Wea s AF index, y “re Us: DOPPLER VELOCY Us: DOPPLER VELOCY (/P RATIO (A.UMB-MCA) A.UTERINA Fetal Hypoxia ee maternal vasculopathy a REE Sudden fetal weeks Fetal Acidemia death preeclampsia DIA ABD-HEAD >2.6 cm he {EFW4000g (INA) >4500 placental changes Fetal + . Sei ee eae Metabolism — ( oaerasmorareo | steleren fetal hyperinsulinemia ~ — Failure Cerny) PERINATAL Us: BIOMETRY i SCENIC aaa Dy birth defect a ~~ Cm | _controt__. SONE Us: 11-13 Weeks wer) (oor) ” (__msuun-ora —) Dogg ==> <_, y a ‘ 5: 18. MADR: Us: 18-22 Weeks HOR l WAIT FOR SPONTANEOUS LIVERY UNTIL 41 WEEKS ror) (_umwaLow o0se aspinn ) (_DEUVERY UNTIL 41 WEEKShd aW i hye)KRITERIA DIAGNOSIS DAN TERAPI: REVISI HKFM See cee UMUR KEHAMILAN saan Onset awa saat keharnilan s/d Te nrc Cog of 112 minggu pasea melahirkan Soe dence HIPERTENSI KRONIS SUPER IMPOSED PE PROTEHNURIA OBESE ANTI HIPERTENSIChronic Hypertension in Pregnancy Ellen W. Seely =) and Jetfrey Ecker Originally published 18 Mar 2014 | ntps:/do\org/10.1161/CIRCULATIONAHA.113.003908 | Circulation. 2014;129:1254-1261 “Table. mmediate Maternal and Fetal Complications of HOP increase risk for mortality 2-3x Table 2. Complications of Chronic Hypertension in Pregnancy ‘The Great Obstetrics Syndrome’Preeclampsia ‘The most prevalent complication in pregnancy in women with chronic hypertension isthe development of Preeclampsia. In the general population, the risk of preeclampsia is 3% to 5%, yet among women with chronic hypertension, 17% to 25% develop superimposed preeciampsia.**"" In a study of 763 women with chronic hypertension that reported a 25% rate of superimposed preeclampsia, rates were higher"? in women with >4-year duration of hypertension and with diastolic blood pressures of 100 to 110 mm Hg compared with <100 mm Hg. In a ‘more recent study of 822 women with chronic hypertension enrolled in a trial of antioxidants for the prevention of preeclampsia, the risk of superimposed preeclampsia was 22%. Of note, 44% of this 22% developed superimposed preeclampsia before 34 weeks of gestation, a rate that stands in contrast to patterns seen in women without chronic hypertension, who more commonly develop preeclampsia closer to term.'? Preeclampsia is more commonly observed in blacks than whites, but whether this is due to the greater prevalence of underlying chronic hypertension in blacks or to greater underying propensity for preeclampsia is controversial.“ Preeciampsia is a major contributor to preterm birth and cesarean delivery in women with chronic hypertension because of its association with induced early delivery, placental abruption, and fetal growth abnormaiities."°*® Accordingly, women with chronic hypertension with ‘superimposed preeclampsia have worse birth outcomes than women with chronic hypertension without superimposed preeclampsia."2" 17-25% > PE >4th >100 MMH diastolic before pregnant‘Because preeciampsia is managed diferently from worsening chronic hypertension, tis important to distinguish these 2 entities. There is a continuing search for improved tests to both predict and diagnose preeclampsia. Chief among the candidate tests studied are angiogenic markers, including soluble fms-like tyrosine kinase 1 (sFit-1) and placental grovah factor. A post hoc analysis of blood collected as part ofa study examining the utity of calcium ‘supplementation to prevent recurrent preeclampsia demonstrated higher levels of sFit-1 and reduced levels of placental growth factor in those women who developed preeclampsia compared with those who did not. sFit-1, for ‘example, was reported tobe elevated as eary asthe second trimester in women who went on to develop preeclampsia."” From these and other supportive results,'*"® sFit-1 was proposed as a potential predictive marker for the development of preeclampsia. However, in a prospective study that excluded women with chronic hypertension, SFi-1 measured in the fis trimester had a poor postive predictive value (<10%) forthe development of preeclampsia.” On the basis of current data, these markers are not recommended for clinical use at this time." It is possible that future work and analyses may show that, although these markers do not appear to be useful in a general Population, they may function more effectively as predictors of preeclampsia among a group whose risk for primary or recurrent preeclampsia is chronic hypertension. sFit-1 > best prognosticator for PE developemt on HT O) 1 @ 8 ©Fetal Growth Restriction Sr ‘American, Canadian, and New Zealand population data demonstrate a 10% to 20% prevalence of fetal growth restriction, defined as absolute or estimated weight less than the 10th percentile for gestational age-based population ‘norms, in pregnancies in women with chronic hypertension.**"° A similar association remained even after adjustment {for age, body mass index, smoking, parity, and diabetes mellitus in an analysis of the Danish National Birth Cohort. In that analysis, “definite chronic hypertension" was associated with a §.5- and 1.5-fold risk for preterm and term small- for-gestational-age birth, respectively (95% confidence intervals [Cis], 3.29.4 and 1.0-2.2).*! A more recent analysis. using growth curves customized for fetal sex and maternal height, weight, parity, and ethnicity suggests that the risk ‘may be higher, 41% and 21% among women with and without superimposed preeclampsia, respectively. '? 1.5 times higher risk for SGA 2 times higher risk in HT >PE sup. Placental Abruption ‘Because fetal growth abnormalities are often thought of as manifestations of placental dysfunction, it is interesting to ‘note that placental abruption —premature separation of the placenta from the underlying myometrium resulting in pain, bleeding, and, potentially clinical significant interruption of fetal gas and nutrient exchange—is more common in ‘women with chronic hypertension. National Center for Health Statistics data from 1995 to 2002 demonstrated that ‘women with chronic hypertension had a frequency of placental abruption of 1.569% compared with 0.58% in ‘nonhypertensive women (adjusted relative risk, 2.4; 95% Cl, 2.9-2.5).” In the Sibai et al"? study of women with chronic hypertension mentioned above, the overall rate of abruption was 1.5%, with higher rates in those with superimposed preeclampsia (3%) than those without (1%). A more recent analysis ofa large Swedish birth registry found rates of abruption of 1.1% versus 0.4% when women with and without chronic hypertension, respectively, were compared.®* 2.4 times higher risk for Abruptio Placenta 2 times higher risk in HT >PE sup.Hypertension in Pregnancy: Diagnosis, Blood Pressure Goals, and Pharmacotherapy: A ‘Scientific Statement From the American Heart Association Prepregnancy Care coarse ie Prenatal care of women with chronic hypertension should begin before pregnancy to provide counseling about the pregnancy risks discussed above and to optimize antihypertensive regimens before conception. The majority of women who enter pregnancy with chronic hypertension have hypertension of unknown origin. Evaluation for secondary ‘causes of hypertension should follow recommendations of the Seventh Report of the Joint National Commission? and, when indicated, should occur before pregnancy because such evaluation may involve radiation exposure or require surgical intervention. Women with chronic hypertension should also be evaluated as indicated according to Seventh Report of the Joint National Commission for end-organ damage before pregnancy because end-organ damage may affect pregnancy outcomes or help stratify the risk of developing specific obstetric complications. A 24-hour urine collection for protein determination before pregnancy may assist in the diagnosis of superimposed preeclampsia and provides prognostic information because women with prepregnancy proteinuria have an increased risk for fetal growth restriction.'? Finally, as discussed below, antihypertensive agents may need to be changed to another class before conception. Lifestyle Modification Lifestyle modifications such as sodium restriction,® weight reduction, ”* and implementation of the Dietary Attempts to ‘Stop Hypertension (OASH) diet have been demonstrated to improve blood pressure control in many nonpregnant individuals. Given the need for volume expansion in pregnancy, strict sodium restriction in hypertensive women planning pregnancy is of concern, and new dietary sodium restriction is not recommended by the Canadian guidelines.®° However, both weight reduction and the DASH diet are reasonable to recommend for such women. ACOG recommends weight reduction in overweight/obese women with hypertension before pregnancy.®" Whether such recommendations implemented before pregnancy, however prudent, result in improved pregnancy outcomes among hypertensive women is unknown, however, and needs to be studied. Anti-hypertensive drugs, DASH, weight reduction HKFM1@ 8 © Blood Pressure Goals in Pregnancy ie HKFM Sa Studies suggest that the primary benefit of antinypertensive treatment of hypertension pregnancy i the reduction of ‘maternal morbity by limiting episodes of severe hypertension. Antihypertensive treatment has not been shown to ‘reduce superimposed preeclampsia, placental abruption, or growth restriction o to improve neonatal outcome. *2 There 's concer that overly aggressive antihypertensive treatment may decrease fetoplacental perfusion and increase the Fisk for fetal growth restriction. large meta-analysis, for example, suggests that treatment of hypertension in pregnancy may be associated with increased fetal growth restriction. As a result blood pressure goals are higher during pregnancy than they are outside of pregnancy, and medication dosages may need tobe adjusted downward Particularly in the second trimester when pregnancy-associated nadirs of blood pressure ae typically encountered. The ‘exact goal ranges for blood pressures during pregnancy in women with chronic hypertension are not established because, at this pont, there are no randomized studies to support one goal over anther. As a resi, blood pressure {goa for pregnancy for women with chronic hypertension are often not specified in guidelines or ifr among guidelines. ACOG recommends that blood pressures in women with uncomplicated hypertension be maintained between 120/80 and 160/105 mm Hg.' The Society of Obstetricians and Gynaecologists of Canada clinical practice uidelines target systolic blood pressure of 130 to 155 mm Hg and diastolic blood pressure of 80 to 105 mm Hg in ‘women without comorbid conditions and systolic blood pressure of 130 to 139 mm Hg and dastolc pressure of 80 to '89 mm Hg in women with comorbid conditions (such as type 1 diabetes melitus)° Some experts recommend stopping antinypertensives during pregnancy, as long as pressures fal below these threshold. For women with chronic hypertension who enter pregnancy not on antihypertensive treatment, ACOG recommends initiating antinypertensive treatment when blood pressures are consistently >160 mm Hg systolic and/or >105 mm Hg diastolic. “The Society of Obstetric Medicine of Australia and New Zealand guidelines indicate a defintve recommendation for antinypertensive treatment when blood pressure is 2160 mm Ha systolic or 2100 mm Hag diastolic and that treatment Cf blood pressure between 140 and 159 mm Hg systolic or 90 and 99 mm Hg dastoic is common practice with good ‘outcomes. Thus, ther is variability in goal range for blood pressure in pregnancy. When blood pressures fll below these ranges, there is a recommendation to taper the antihypertensive and eventually to stop the antihypertensive i blood pressure remains within the goal range. There are no evidence-based regimens for tapering antihypertensive ‘medications in pregnancy. Thus, the tapering regimen needs to take into consideration factors related tothe particular medication used, dose, and timing in pregnancy Ve, Keeping in mind the physiological decrease in blood pressure at the end ofthe fst trimester) We recommend tapering antihypertensives when blood pressures consistently fall below 130/80 mm Hg, a threshold consistent with Canadian guidelines. »° Tight control: diastolic < 85 mmHg ES eT vee TES ET aT a, ere. Tee ote(O)s] ER C7 asooDEFINIS!I OBESITAS a normal BM| is 18.5 to 24.9 kg/m?; Weight (pounds) overweight is a BMI of 25 to 29.9 kg/m?; 2,910 190150 170 190 210 290 250 270 200 310 39050, / |" obesityis a BMI of 30 kg/m? or greater. class I (BMI: 30 to 34.9 kq/m?), class Il (BMI: 35 to 39.9 kg/m2), and 7" sv 2 class Ill (BMI: 40-plus kg/m?). i i 3. 87 Z Weight } 9 ; Body Mass _ __(in kg) 7 7 Index Height® r (in m) “"" DIUKUR SEBELUM UK 12 MINGGU ©9067 9 %0 100 10 120 190 140 150 160 Weight a)a World Health SE Organization Figure 5: Projected rates of obesity40 Percent 20 10) US obesity Prevalence of obesity among adults ‘aged 20 and over, by sex and age: United States, 2013-2014 ius! NOTES: Totals were agoacusted by he direct metros to ‘te 2000 US. consus population using he age wus 20-28, 40-69, and 60 ond over. Croce estimates ore 37.9% or a, 35.2% for men, and 40.5% for wonen, SOURCE: COG/NCHS, Natorol Heath and Nuon Examination Survey, 2013-2014. 40% wanita usia reproduksiMany Indonesians Getting Fatter Pare een et ee eer ae terryResearch report Obesity trends and determinants in Indonesia * Cornelia Roemling*, Matin Qaim Department of Agricultural Economics and Rural Development, Georg-August-University of Goettingen, Platz der Goettinger Sieben 5, 37073 Goettingen, Germany anand change i Mt by gender snd weaton. Ol esitas di Indonesia: meningkat signifiakan open 58 2012) 1005-013, Year ‘Male Female Urban ‘ural Urban Rural Mean ‘sD Mean sD Mean ‘sD Mean ‘sD 1993 2180 321 2048 248 277 392 21.05 321 2000 2186 347 20st 276 2320 44 2179 359 2007 2248 375 2143 320 23.90 449 2289 4s ‘change 1993-2000 ose 023 123 078 ‘Change 2000-2007 119 on vat 115 Source: (FL, IFLS3, ILS. Note: Change signifies the average change in mean from 1993 to 2000 and from 2000 to 2007. Panel A: Asian cut-off values Panel B: International cut-off values a — Underweight 8338 80 © 4 20 ° 1993 2000 20071993, 2000 2007 Source: IFLS1, IFLS3, IFLS4Research report = Obesity trends and determinants in Indonesia * open 58 2012) 1005-1013, Cornelia Roemling*, Matin Qaim Department of Agricultural Economics and Rural Development, Georg-August-University of Goettingen, Platz der Goettinger Sieben 5, 37073 Goettingen, Germany 1, E oy 0 1 Underweight & oF 1 Normal weight ial @ Preobese 32 [|g mobese 2 of e Kerja Kantoran va ¥ of off Share of individuals in BMI categories (%). 10 persen kurang tse: SEEEEE ES 2000 REEEEEE 2007 SEEEEEE coe Male Female Male Female Male _ Female giz Underweight 1671 1729. 1666 1447-1367 1095 4591 5495 403 22.48 double burden —Nermatweight 5245 3071 5878 (RISKESDAS) Obese 100 © 100 = 100PERCENTAGE OF OBESITY IN SOUTH-EAST ASIA Malaysia 229993 15% 10% 5% 4000 ¢ 170429) ‘pone Birth weight > 4500 20 (14-30) < ooo! Childhood obesity 232026) = 95 ‘Foe 95 concern FW eae eal weigh VF ito Kron: OR oe Ime VAAC vaginal bh ar cee {Rev Obstet Gynecol 2008;1(4):170-178)= {EQ Sa eT obsty — oo |sacpmanena oe / Mast cell Mimacrophage, __ Neutrophil | Pronto OP race “hn Induction of (pro)-inflammatory cytokine TNF-a, IL-6, IFN-Y, IL-1B Inflamasi Koagulasi HKFM Hypertrophic adipocytes Induction of Tissue Factor (TF)@6o Placenta Uterine environment Pregnancy MetS Epigenetic changes Gee Metabolic & | Gut Microbiota pregnancy . reonaternnsteny outcomes insulin-resistant Miscarriages, PE, GDM, and hyperlipidemic state Stillbirth, PTB Poor nacre came WY v= Uterine environment Epigenetic changes condo: "inca Changes in gut microbiota myocardial infarction CVD disease Mother & offspring & heart failure2X In utero programming PR Eee Telomer yang pendek Usia sel yang buruk Penuaan sel yang cepat sel organ janin yang burukwed owe Later in life Qe BMI Fat mass oe perma reeenny, Visceral fat oe ee aey 8M! Metabolic consequences: he rae > * Risk for type I! diabetes 4 Risk for cardiovascular disease Ayviscoral tat Risk for metabolic syndrome © First pregnancy —_jyetabolic consequences: tM > preecampsa Berat badan yang eee 4 Hypercholesterolemia cenderung menetap dan bertambah dari satu kehamilan ke kehamilan berikutnya ae a eesHOW? — Excess Weight Excessive Carbohydrate Intake Sedentary Lifestyle Genetics t Sleep Apnea Polycystic Ovarian Disease Increased blood clots risk, Resistance Cardiomyopathy Neurological Changes: Urinary Frequency, Lightheadedness, Bloating, Heartbum, Constipation and ED _ Elevated Hypertension Increase of Blood (High Blood Intra-Abdominal — gypar Pressure) Fat —_ m cas HKFM Atherosclerosis: Contributes to Heart Attacks, Strokes and _—— Peripheral Vascular Disease Inflammation of the liver and cirrhosis. Elevated Triglycerides Low HDL - “Good Cholesterol”@8o 0.14 0.12 = 0.10 § 0.08 £ 0.06 2 0.04. 0.02 Pregravid Early Late Pregnancy pregnancy sensitivitas sensulin yang semakin buruk signifikan seiring bertambah berat badanHealthy Range: 1.0 (0.5-1.4) Less than 1.0 means you are insulin-sensitive which is optimal Above 1.9 indicates early insulin resistance. Above 2.9 indicates significant insulin resistance. HOMA-IR Blood Code Calculation Insulin Glucose ulU/ml (mU/L) (mg/dL) HOMA-IR 0 x 0 = 0 The HOMA-IR calculation requires U.S. standard units. To convert from international SI units: Insulin: pmol/L to ulU/ml, divide by (+) 6 Glucose: mmol/L to mg/dL, multiply by (x) 18 HOMA IR ee Niel ai. INA: GDP/IP > LI SIMA G:Table 1. Diagnostic Glucose Values for Gestational Diabetes in the United States Fasting (mg per dl One hour (mg per dl Two hours (mg per dl. Three hours (mg per dl. Diagnostic test {mmolpert) __ {mmol peri) [mmol per Uy) [mmol pert) 100-9 OGTT 95 (5.25) 180 (10.00) 155 (8.60) 140 (7.75) Carpenter and Coustan’® {two or more abnormal) 75-9 OGTT 126 (7.00) = 140 (7.75) = World Health Organization”* (one or more abnormal) 75-9 OGTT 95(5.25) 180 10.00) 155 6.60) - American Diabetes Association” (two or more abnormal) OGTT = oral glucose tolerance test Information from references 14 through 17.Gestational diabetes FPG or 75-g, 2-hr OGTT at 6-12 weeks postpartum ¥ Yearly assessment of glycemic status Diabetes mellitus Impaired fasting glucose or IGT or both Normal | | | Refer for diabetes management Consider referral for management Assess glycemic status ‘Weight loss and physical activity every 3 years counseing as needed Weight loss and physical activity Consider metformin if combined oer pemeriksaan post impaired fasting glucose and IGT partum Medical nutrition therapy@ 6 @® ARF INSULIN RESISTANCE AND PREECLAMPSIA | ‘TABLE Midgestation fasting glucose, insulin, insulin resistance, and subsequent preeclampsia ‘Measure. Preeclampsia, %* Normal, %° Odds ratio (95% Cl) Adjusted odds ratio (95% Cl) Glucose =75th percentile m6 265 1.7 (1.0-27) 1.5(0.9-2.5) Insulin =75th percentile 40.5 253 20(13-32) (10-3) Gl cance rena HOW R, Honest model asesnert fran rear, UCN, arte rn serety Check ex ‘= 85 women; 9 = 582 women, Adu orc or tic up, ty mass inex an od presse a sti ry, teaert gap, and gettin ape at sng “Hath Insulin retance and preeclampsia. Am J Obstet Gye 2011 peningkatan risiko preeklamsiaThe gestational age must be between 11 weeks and 13 weeks and six days. Sagittal section of the uterus must be obtained and the cervical canal and internal cervical os identified. identify each uterine artery along the side of the cervix and uterus at the level of the internal os Sampling gate 2 mm to cover the whole vessel and ensuring that the angle of insonation less than 30°, Three similar consecutive waveforms are obtained the PI must be measured and the mean PI of the left and right arteries be calculated.BASCHAT pees eae PREECLAMPSIA SCREENING Increased risk for pre-eclampsia ALGORITHM Determination of primary profiles contributing to increased risk Initiate risk profile specific therapy by)t6 weeks? gestation Low-dose aspirin | Low-dose aspirinImplications of maternal obesit ‘* TYPE 2M ‘+ Maternal and childhood obesity Long term risk -s0a!ofserng luce meostasis + Cardiovascular disease * SGA/LGA Neonatal * >NICU admission © Birth injuries + Infection e>cs Obstetric <3, o VTE PIH/ Preeclampsia GDM Maternal*Apa yang dapat dilakukan? Prevent excessive gestational weight Focus on maternal gain insulin resistance LOW CALORIE DIET ~~“ Ey rN ane ar Ns > (aah 180 minutes/week 4 4kg Advice Group Group + No reduction in GWG [ [ (Outeomes to Outcomes to | 6 months 6 months post-partum post-partumRECOMMENDED CARE - OBESITY Risk Factor Recommended Care Increased risk of neural tube defect * Preconception folic ac supplementation (4 mg daily ideally 3 months prior to pregnancy through the frst trimester) Increased risk of hypertensive disorders of pregnancy, including preeclampsia Increased risk of gestational diabetes (GDM) Increased risk of unexplained stillbirth Increased risk of anesthesia complications Failure to lose weight after delivery is associated with subsequent adverse maternal health problems, including complications of future pregnancies ‘+ Maternal serum AFP (15-20 weeks) ‘* Detailed fetal anatomy survey (18-20 weeks) ‘* Baseline 24-hour urinalysis in second trimester ‘Baseline liver and renal function tests in second trimester Blood pressure and urine dip for protein at each prenatal visit ‘© There is no effective way to prevent preeclampsia ‘© Consider early screening with 1-hour nonfasting 50-g glucose load test (GIT) at 16-20 weeks. If positive, check a definitive 3-hour 100-g glucose tolerance test (GTM) to confirm the diagnosis of GDM. If negative, repeated GLT at the usual gestational age of 24-28 weeks '* Consider weekly antepartum fetal testing with NST and/or BPP beginning at 36 weeks, especially in women with a BMI = 40 kg/m (although this has ‘not been shown to definitively improve perinatal outcome) '* ACOG recommends a prelabor or early intrapartum anesthesia consultation for all women with a BMI = 40 kg/m? '* Consider early epidural placement in labor ‘* Recheck epidural placement if the patient is transferred to the operative room for cesarean delivery because of increased risk of migration of the epidural catheter ‘+ Continue nutrition counseling and exercise program after delivery '* Consider consulting a weight loss specialist to optimize postpartum weight loss before attempting another pregnancy ‘= If complicated by GDM, check 2-hour 75-g GTT at or after 6-week Lee rere ryGB @BO Obesity is a HIGH-RISK Pregnancy aE Thank you for your kind attention...