Ischemia modified albumin as a marker of hypoxia in preterm infants in the first week after birth

Background: Tissue hypoxia remains a leading cause of morbidity and mortality in preterm infants. Current biomarkers often detect irreversible hypoxic cellular injury (i.e. lactate) and are non-specific. A new biomarker is needed which detects tissue hypoxia before irreversible damage occurs.Aims: To investigate the relation between serum ischemia modified albumin (IMA), a marker of hypoxia; and analytic variables, patient related variables and conditions associated with hypoxia, in preterm infants.Study design: Retrospective cohort study.Subjects: Infants with a gestational age &lt; 30 weeks and/or birth weight &lt; 1000 g.Outcome measures: We collected two remnant blood samples in the first week after birth and measured IMA. IMA/albumin ratio (IMAR) was used to adjust for albumin. We assessed correlations between IMA(R) and analytic variables (albumin, lipemia- and haemolysis index); mean-2 h SpO2; mean-2 h variability of regional splanchnic oxygen saturation (rsSO2), measured using near-infrared spectroscopy; and patent ductus arteriosus (PDA).Results: Sixty-five infants were included. Albumin, the lipemia- and haemolysis index correlated negatively with IMA (r:-0.620, P&lt;0.001; r:-0.458, P&lt;0.001; and r:-0.337, P=0.002). IMAR correlated negatively with SpO2 (rho:-0.614, P&lt;0.001). Lower rsSO2 variability correlated with higher IMAR values (rho:-0.785, n=14, P=0.001 and rho:-0.773, n=11, P=0.005). Infants with a hemodynamic significant PDA (hsPDA) had higher IMAR values than infants without PDA (0.13 [0.11–0.28], n=16 vs. 0.11 [0.08–0.20], n=29, P=0.005 and 0.11 [0.09–0.18], n=13 vs. 0.09 [0.06–0.17], n=37, P=0.026).Conclusions: When adjusted for albumin, the lipemia- and haemolysis index, IMAR has potential value as a marker for systemic hypoxia in preterm infants, considering the associations with SpO2, variability of rsSO2, and hsPDA.</p

Ischemia modified albumin as a marker of hypoxia in preterm infants in the first week after birth

Background: Tissue hypoxia remains a leading cause of morbidity and mortality in preterm infants. Current biomarkers often detect irreversible hypoxic cellular injury (i.e. lactate) and are non-specific. A new biomarker is needed which detects tissue hypoxia before irreversible damage occurs.Aims: To investigate the relation between serum ischemia modified albumin (IMA), a marker of hypoxia; and analytic variables, patient related variables and conditions associated with hypoxia, in preterm infants.Study design: Retrospective cohort study.Subjects: Infants with a gestational age &lt; 30 weeks and/or birth weight &lt; 1000 g.Outcome measures: We collected two remnant blood samples in the first week after birth and measured IMA. IMA/albumin ratio (IMAR) was used to adjust for albumin. We assessed correlations between IMA(R) and analytic variables (albumin, lipemia- and haemolysis index); mean-2 h SpO2; mean-2 h variability of regional splanchnic oxygen saturation (rsSO2), measured using near-infrared spectroscopy; and patent ductus arteriosus (PDA).Results: Sixty-five infants were included. Albumin, the lipemia- and haemolysis index correlated negatively with IMA (r:-0.620, P&lt;0.001; r:-0.458, P&lt;0.001; and r:-0.337, P=0.002). IMAR correlated negatively with SpO2 (rho:-0.614, P&lt;0.001). Lower rsSO2 variability correlated with higher IMAR values (rho:-0.785, n=14, P=0.001 and rho:-0.773, n=11, P=0.005). Infants with a hemodynamic significant PDA (hsPDA) had higher IMAR values than infants without PDA (0.13 [0.11–0.28], n=16 vs. 0.11 [0.08–0.20], n=29, P=0.005 and 0.11 [0.09–0.18], n=13 vs. 0.09 [0.06–0.17], n=37, P=0.026).Conclusions: When adjusted for albumin, the lipemia- and haemolysis index, IMAR has potential value as a marker for systemic hypoxia in preterm infants, considering the associations with SpO2, variability of rsSO2, and hsPDA.</p

Supplementary Material for: Cerebral and Renal Oxygen Saturation Are Not Compromised in the Presence of Retrograde Blood Flow in either the Ascending or Descending Aorta in Term or Near-Term Infants with Left-Sided Obstructive Lesions

Background: In infants with left-sided obstructive lesions (LSOL), the presence of retrograde blood flow in either the ascending or descending aorta may lead to diminished cerebral and renal blood flow, respectively. Objectives: Our aim was to compare cerebral and renal tissue oxygen saturation (rSO2) between infants with LSOL with antegrade and retrograde blood flow in the ascending aorta and with and without diastolic backflow in the descending aorta. Methods: Based on 2 echocardiograms, the study group was categorized according to the direction of blood flow in the ascending and descending aorta. We measured cerebral and renal rSO2 using near-infrared spectroscopy and calculated fractional tissue oxygen extraction (FTOE). Results: Nineteen infants with LSOL, admitted to the NICU between 0 and 28 days after birth, were included. Infants with antegrade blood flow (n = 12) and infants with retrograde blood flow in the ascending aorta (n = 7) had similar cerebral rSO2 and FTOE during both echocardiograms. Only during the first echocardiogram, infants with retrograde blood flow in the ascending aorta had lower renal FTOE (0.14 vs. 0.32, p = 0.04) and tended to have higher renal rSO2 (80 vs. 65%, p = 0.09). The presence of diastolic backflow in the descending aorta was not associated with cerebral or renal rSO2 and FTOE during the first (n = 8) as well as the second echocardiogram (n = 10). Conclusions: Retrograde blood flow in the ascending aorta was not associated with cerebral oxygenation, while diastolic backflow in the descending aorta was not associated with renal oxygenation in infants with LSOL

A role for MLH3 in hereditary nonpolyposis colorectal cancer

We investigated a possible role of the mismatch-repair gene MLH3 in hereditary nonpolyposis colorectal cancer by scanning for mutations in 39 HNPCC families and in 288 patients suspected of having HNPCC. We identified ten different germline MLH3 variants, one frameshift and nine missense mutations, in 12 patients suspected of HNPCC. Three of the 12 also carried a mutation in MSH6

Effect of balloon atrial septostomy on cerebral oxygenation in neonates with transposition of the great arteries

<p>BACKGROUND: The aim of this study was to determine the effect of balloon atrial septostomy (BAS) on cerebral oxygenation in neonates with transposition of the great arteries (TGA).</p><p>METHODS: In term neonates with TGA, regional cerebral tissue oxygen saturation (r(c)SO(2)) was measured using, near-infrared spectroscopy (NIRS) for a period of 2 h, before BAS, after BAS, and 24 h after BAS. In neonates who did not require BAS on clinical,grounds, r(c)SO(2) was measured within 24h of admission and 24h later.</p><p>RESULTS: BAS was performed in 12 of 21 neonates. r(c)SO(2) increased from a median of 42% (before) to 48% at 2 h after BAS (P <0.05), as did transcutaneous arterial oxygen saturation (spO(2)) (from 72% to 85%, P <0.01). r(c)SO(2) increased further during the next 24 h (from 48% to 64%, P <0.05), whereas spO(2) remained stable. Although beginning from a lower baseline (42 vs. 51%, P <0.01), r(c)SO(2) Was higher in neonates treated with BAS, as compared with neonates not treated with BAS, 24h after the procedure (64 vs. 58%, P <0.05); spO(2) was, however, similar between the two groups.</p><p>CONCLUSION: BAS improves cerebral oxygen saturation in neonates with TGA. Complete recovery of cerebral oxygen saturation occurred only 24h after BAS.</p>