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Peran Kadar Troponin I Sebagai Prediktor Penyakit Jantung Bawaan Neonatus dengan Riwayat Asfiksia Sedang dan Berat Dinar Handayani Asri; Yulidar Hafidh; Sri Lilijanti Widjaja
Sari Pediatri Vol 23, No 4 (2021)
Publisher : Badan Penerbit Ikatan Dokter Anak Indonesia (BP-IDAI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.14238/sp23.4.2021.215-21

Latar belakang. Penyakit jantung bawaan (PJB) merupakan sepertiga kelainan kongenital pada neonatus. Prevalensi PJB di Asia 9,3 dari 1000 kelahiran hidup. Penegakan diagnosis maupun prediksi PJB pada neonatus dengan kondisi tidak stabil terbatas sehingga dipertimbangkan penggunaan biomarker kardiak Troponin I yang paling sensitif dan spesifik pada injuri miokard.Tujuan. Menganalisis peran kadar troponin I sebagai prediktor penyakit jantung bawaan neonatus dengan riwayat asfiksia sedang dan berat.Metode. Desain penelitian potong lintang dalam uji prognostik. Hasil pengolahan data berupa narasi, tabel, dan grafik. Karakteristik dasar subjek penelitian terdiri atas berat badan lahir, kategori asfiksia, faktor penyerta yaitu sepsis dan pneumonia, jenis PJB. Hubungan bivariat antara kedua variabel dianalisis uji chi square. Hasil bermakna jika p<0,05. Analisis data dengan program SPSS (SPSS statistik 25). Hasil. Dari 25 sampel didapatkan 20 sampel PJB. Pada kelompok PJB, asfiksia merupakan faktor risiko yang signifikan dengan nilai p 0,004. Nilai cut off troponiin I yang didapat sebagai prediktor kejadian PJB pada neonatus dengan riwayat asfiksia sedang dan berat, yaitu 58,5 ng/l, dengan nilai sensitivitas 80%, spesifisitas 80%. Hasil uji chi square didapatkan nilai p 0,023 dengan Odd rasio sebesar 16 (dengan 95% CI 1,38-185,4). Kesimpulan. Terdapat peran kadar troponin I sebagai prediktor PJB pada neonatus dengan riwayat asfiksia sedang dan berat.

Cell-Free Regenerative Therapy for Pulmonary Hypertension: Human Breastmilk Stem Cell Secretome Restores Endothelial Barrier Integrity and BMPR2 Signaling Under Hypoxic Stress Sri Lilijanti Widjaja; Mylco Trisaputa Ahmadwirawan; Dina Luthfiyah
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 10 No. 5 (2026): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v10i5.1582

Background: Pulmonary hypertension (PH) is a severe vascular disorder characterized by chronic hypoxia-induced endothelial dysfunction, leading to aberrant remodeling and right ventricular failure. The human breastmilk-derived stem cell (hBSC) secretome contains bioactive factors that may promote endothelial regeneration. However, the temporal dynamics of secretome-mediated repair on critical structural and signaling molecules remain poorly understood. Methods: An in vitro experimental study was conducted using human umbilical vein endothelial cells (HUVECs) exposed to severe hypoxia (1% O₂, 10% CO₂, 37°C) to replicate PH-associated endothelial dysfunction. Cells were divided into four groups: normoxia control, hypoxia control, and hypoxia treated with hBSC secretome for 24 and 72 hours. Expression of bone morphogenetic protein receptor type 2 (BMPR2) and vascular endothelial cadherin (VE-cadherin) was quantified via ELISA. CCK-8 assays evaluated cellular viability. Data were analyzed using one-way ANOVA and least significant difference (LSD) post-hoc tests. Results: Hypoxia significantly diminished cell viability and reduced BMPR2 and VE-cadherin expression compared to normoxia (p<0.001). Administration of hBSC secretome significantly restored BMPR2 and VE-cadherin levels at both 24 and 72 hours (p<0.001), surpassing normoxic baselines. BMPR2 expression plateaued between 24 and 72 hours, while VE-cadherin expression demonstrated sustained functional recovery. Conclusion: The hBSC secretome actively reverses hypoxia-induced endothelial injury through rapid, time-dependent modulation of BMPR2 signaling and VE-cadherin junctional integrity, presenting a viable cell-free therapeutic target for PH.

Prostaglandin E1 Dose and Duration as Determinants of Adverse Outcomes in Neonates with Duct-Dependent Congenital Heart Disease: A Systematic Review and Meta-Analysis Dina Luthfiyah; Muhammad Ali Shodikin; Sri Lilijanti Widjaja
Scientific Journal of Pediatrics Vol. 3 No. 2 (2025): Scientific Journal of Pediatrics
Publisher : Phlox Institute: Indonesian Medical Research Organization

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.59345/sjped.v3i2.261

Introduction: Prostaglandin E1 (PGE1) infusion remains the cornerstone of medical stabilisation in neonates with duct-dependent critical congenital heart disease (DD-CCHD), yet contemporary guidance on optimal dose and duration is not informed by quantitative synthesis of recent evidence. Methods: A systematic review and meta-analysis were conducted in accordance with the PRISMA 2020 and MOOSE statements. PubMed/MEDLINE, ScienceDirect, OpenAlex and Europe PMC were searched (1st January 2014 – 30th April 2026) for original observational studies reporting PGE1 dose and/or duration with at least one adverse outcome in neonates (≤28 days) with DD-CCHD. The Newcastle–Ottawa Scale (NOS) and GRADE were applied. The primary outcome was the pooled prevalence of any PGE1-related adverse event using the Freeman–Tukey arcsine transformation under a DerSimonian–Laird random-effects model with the Hartung–Knapp–Sidik–Jonkman variance adjustment. The secondary, hypothesis-generating outcome was the pooled standardised mean difference (Hedges g) between higher- and lower-dose strata via the Chinn conversion. Heterogeneity, leave-one-out sensitivity, prespecified subgroup analyses, meta-regression and Egger regression were performed. Results: Ten observational studies enrolling 1,060 neonates were included. The pooled prevalence of any PGE1-related adverse event was 0.617 (95% confidence interval [CI] 0.509–0.724; I² = 87.6%). The secondary pooled Hedges g was 0.085 (95% CI −1.93 to 2.10), reflecting directional heterogeneity. Apnoea ranged from 9% to 52%, with a clear dose-related signal in two studies (relative risk approximately 1.97, p = 0.037; relative risk approximately 0.44, p = 0.015). Egger's intercept was 0.58 (p = 0.81), indicating no asymmetry. Meta-regression on median initial dose suggested dose-related apnoea risk. Conclusion: In neonates with DD-CCHD, approximately 62% experienced at least one PGE1-related adverse event. Initiation at 0.005–0.010 µg/kg/min should be regarded as the contemporary clinical default, with structured surveillance for apnoea and fever within 48 hours, gastrointestinal intolerance after 7–10 days and skeletal toxicity after 28 days.

Cell-Free Regenerative Therapy for Pulmonary Hypertension: Human Breastmilk Stem Cell Secretome Restores Endothelial Barrier Integrity and BMPR2 Signaling Under Hypoxic Stress Sri Lilijanti Widjaja; Mylco Trisaputa Ahmadwirawan; Dina Luthfiyah
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 10 No. 5 (2026): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v10i5.1582

Background: Pulmonary hypertension (PH) is a severe vascular disorder characterized by chronic hypoxia-induced endothelial dysfunction, leading to aberrant remodeling and right ventricular failure. The human breastmilk-derived stem cell (hBSC) secretome contains bioactive factors that may promote endothelial regeneration. However, the temporal dynamics of secretome-mediated repair on critical structural and signaling molecules remain poorly understood. Methods: An in vitro experimental study was conducted using human umbilical vein endothelial cells (HUVECs) exposed to severe hypoxia (1% O₂, 10% CO₂, 37°C) to replicate PH-associated endothelial dysfunction. Cells were divided into four groups: normoxia control, hypoxia control, and hypoxia treated with hBSC secretome for 24 and 72 hours. Expression of bone morphogenetic protein receptor type 2 (BMPR2) and vascular endothelial cadherin (VE-cadherin) was quantified via ELISA. CCK-8 assays evaluated cellular viability. Data were analyzed using one-way ANOVA and least significant difference (LSD) post-hoc tests. Results: Hypoxia significantly diminished cell viability and reduced BMPR2 and VE-cadherin expression compared to normoxia (p<0.001). Administration of hBSC secretome significantly restored BMPR2 and VE-cadherin levels at both 24 and 72 hours (p<0.001), surpassing normoxic baselines. BMPR2 expression plateaued between 24 and 72 hours, while VE-cadherin expression demonstrated sustained functional recovery. Conclusion: The hBSC secretome actively reverses hypoxia-induced endothelial injury through rapid, time-dependent modulation of BMPR2 signaling and VE-cadherin junctional integrity, presenting a viable cell-free therapeutic target for PH.

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