TABLE 1.
Clinical studies investigating the EG in the pediatric population.
Study type | EG parameters | n | Mean age | Major findings | |
Pediatric heart surgery | |||||
Nussbaum et al. (2015) | Longitudinal cohort study | PBR (SDF imaging) | 40 patients (36 with CPB, 4 without CPB) | CPB group: 8.9 months [0.2–29] w/o CPB: 9 months [0.2–31] | Increase in PBR after surgery on CPB |
Bruegger et al. (2015) | Prospective cohort study | Serum syndecan-1, HA | 42 | 7 months (2.9–23) | Increase of circulating HA and syndecan-1 associated with the ischemic impact |
Pesonen et al. (2016) | 2 double blinded placebo-controlled trials | Plasma syndecan-1 | 40 (1st trial), 45 (2nd trial) | 1st trial: 7 days (1–27), 2nd trial: 0.37 years (0.15–1.36) | Lower syndecan-1 plasma levels after high-dose steroid treatment in complex heart surgery |
de Melo Bezerra Cavalcante et al. (2016) | Prospective cohort study | Plasma syndecan-1 | 289 | 3.0 years (SD: ± 4.4) | Association of higher syndecan-1 levels with poorer outcomes and postoperative acute kidney disease |
Ferrer et al. (2018) | Prospective cohort study | urinary syndecan-1 | 86 | < 2.0 years: 61.2% | Higher postoperative urine syndecan-1 levels in patients with acute kidney injury |
Bangalore et al. (2021) | Prospective cohort study | Plasma HS | 27 | 4.9 months (1–22 months) | Association of circulating HS with metabolic acidosis, renal dysfunction and capillary leak after CPB |
Pediatric trauma | |||||
Richter et al. (2019) | Prospective cohort study | Plasma syndecan-1, angiopoetin-1 and angiopoetin-2 | 64 (52 trauma, 12 controls) | Trauma: 9.7 years (6.2–13.6), controls: 5 years (1.8–15) | Higher angiopoetin-2 levels associated with worse clinical outcome, pos. correlation of syndecan-1 and angiopoetin-2 |
Russell et al. (2018) | Prospective cohort study | Plasma syndecan-1 and hcDNA | 211 (149 trauma, 62 controls) | Trauma: 8.3 years (4.6–12.3), controls 6.24 ±6.2 years | Highest syndecan 1 levels correspond to highest hcDNA levels and poor outcome |
Pediatric inflammatory and infectious diseases | |||||
Kawasaki disease (KD) | |||||
Ohnishi et al. (2019) | Prospective cohort study | Plasma syndecan-1, HA | 103 (70 complete KD, 18 febrile controls, 15 afebrile controls) | CAL (coronary artery lesions): 27 months (3–121), CAL negative: 18.5 (1–88) | Higher syndecan-1 and HA levels in KD compared to febrile and afebrile controls |
Luo et al. (2019) | Prospective cohort study | Plasma syndecan-1 | 203 (119 KD, 43 healthy children, 40 children with febrile disease) | 26 months (16.0–43.75) | Higher syndecan-1 levels in KD compared to matched febrile and afebrile controls |
COVID-19/PIMS | |||||
Fraser et al. (2021) | Case report | Plasma HA | 1 pt., 20 controls | 15 years [IQR 8] | Increased HA in a patient suffering from PIMS compared to controls |
Malaria | |||||
Yeo et al. (2019a) | Retrospective analysis of frozen samples of a prospective cohort study | Urinary GAGs | 85 | Uncomplicated Malaria: 3.1 years (0.5–7.8), complicated malaria: 3.6 years (0.6–7.2) | Higher urine excretion of GAGs in malaria groups compared to healthy children |
Lyimo et al. (2020) | Cross-sectional study | PBR (IDF imaging), plasma sulfated GAGs | 119 (healthy: 31, non-malaria fever NMF: 7, uncomplicated malaria UM: 12, severe malaria SM: 69) | Healthy: 2.5 years (0.8–4.3), NMF: 2.28 years (1.0–4.), UM: 5.5 years (1.1–10.1), SM: 4.1 years (0.6–10.0) | Increased PBR in patients with SM; sulfated GAGs higher in patients with complicated malaria compared to UM; positive association between HA and PBR |
Diabetes mellitus | |||||
Nussbaum et al. (2014) | Observational study | Glycocalyx thickness (SDF imaging) | 14 patients, 14 controls | patients: 13.6 [9.9–14.4], controls: 11.6 [9.7–14] | Reduced EG thickness in diabetic children compared to controls; inverse correlation of EG with blood glucose levels |