Bilirubin binding and neonatal acidosis.

1981 ◽  
Vol 27 (11) ◽  
pp. 1872-1874 ◽  
Author(s):  
M Perlman ◽  
J Kapitulnik ◽  
S H Blondheim ◽  
A Alayoff ◽  
A Russell

Abstract Plasma of neonates with severe metabolic acidosis secondary to fetal hypoxia bound less bilirubin than that of neonates without acidosis, as determined by Sephadex gel filtration. There was a significant correlation between the amount of bilirubin adsorbed by Sephadex and the base deficit. The method used ruled out any influence of plasma pH per se on binding. Our results suggest that organic anions that accumulate in the plasma of asphyxiated acidotic neonates may compete with bilirubin for binding sites on albumin.

2008 ◽  
Vol 27 (7) ◽  
pp. 539-546 ◽  
Author(s):  
KE Hovda ◽  
D Jacobsen

Fomepizole is now the antidote of choice in methanol poisoning. The use of fomepizole may also change the indications for hemodialysis in these patients. We have addressed this change in a review of articles on methanol poisonings. Review of the literature (through PubMed®) combined with our own experiences from two recent methanol outbreaks in Estonia and Norway. The efficiency of dialysis during fomepizole treatment was reported in only a few reports. One recent study challenged the old indications, suggesting a new approach with delayed or even no hemodialysis. Methanol-poisoned patients on fomepizole treatment may be separated into two categories: 1) The critically ill patient, with severe metabolic acidosis (base deficit >15 mM) and/or visual disturbances should be given buffer, fomepizole and immediate hemodialysis: dialysis removes the toxic anion formate, and assists in correcting the metabolic acidosis, thereby also reducing formate toxicity. The removal of methanol per se is not important in this setting because fomepizole prevents further production of formic acid. 2) The stable patient, with less metabolic acidosis and no visual disturbances, should be given buffer and fomepizole. This treatment allows for the possibility to delay, or even drop, dialysis in this setting, because patients will not develop more clinical features from methanol poisoning when fomepizole and bicarbonate is given in adequate doses. Indications and triage for hemodialysis in methanol poisonings should be modified. Delayed hemodialysis or even no hemodialysis may be an option in selected cases.


2004 ◽  
Vol 69 (5) ◽  
pp. 1137-1148 ◽  
Author(s):  
Gennady V. Oshovsky ◽  
Willem Verboom ◽  
David N. Reinhoudt

Ureidocavitand 1 and thioureidocavitand 2 bind in CH3CN organic anions such as acetate, propionate, butyrate, etc. with K values of 2-8 × 105 l mol-1 and 2-9 × 106 l mol-1, respectively, as was determined with isothermal microcalorimetry (ITC). Bringing together four (thio)urea binding sites on a molecular platform gives rise to about 2000 times higher binding constants, compared with those of the corresponding single binding sites. Glucose- and galactose-containing thioureidocavitands 5 and 6 bind acetate in 1:1 CH3CN/water with a K-value of 2.15 × 103 l mol-1.


2020 ◽  
pp. 000313482095692
Author(s):  
Marina L. Reppucci ◽  
Eliza H. Hersh ◽  
Prerna Khetan ◽  
Brian A. Coakley

Background Gastrointestinal (GI) perforation is a risk factor for mortality in very low birth weight (VLBW) infants. Little data exist regarding pretreatment factors and patient characteristics known to independently correlate with risk of death. Materials and Methods A retrospective review of all VLBW infants who sustained GI perforation between 2011 and 2018 was conducted. Birth, laboratory, and disease-related factors of infants who died were compared to those who survived. Results 42 VLBW infants who sustained GI perforations were identified. Eleven (26.19%) died. There were no significant differences in birth-related factors, hematological lab levels at diagnosis, presence of pneumatosis, or bacteremia. Portal venous gas ( P = .03), severe metabolic acidosis ( P < .01), and elevated lactate at diagnosis ( P < .01) were statistically more likely to occur among infants who died. Discussion Portal venous gas, severe metabolic acidosis, and elevated lactate were associated with an increased risk of mortality among VLBW infants who develop a GI perforation. Further research is required to better identify risk factors.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Grace Mzumara ◽  
Stije Leopold ◽  
Kevin Marsh ◽  
Arjen Dondorp ◽  
Eric O. Ohuma ◽  
...  

Abstract Background Severe metabolic acidosis and acute kidney injury are major causes of mortality in children with severe malaria but are often underdiagnosed in low resource settings. Methods A retrospective analysis of the ‘Artesunate versus quinine in the treatment of severe falciparum malaria in African children’ (AQUAMAT) trial was conducted to identify clinical features of severe metabolic acidosis and uraemia in 5425 children from nine African countries. Separate models were fitted for uraemia and severe metabolic acidosis. Separate univariable and multivariable logistic regression were performed to identify prognostic factors for severe metabolic acidosis and uraemia. Both analyses adjusted for the trial arm. A forward selection approach was used for model building of the logistic models and a threshold of 5% statistical significance was used for inclusion of variables into the final logistic model. Model performance was assessed through calibration, discrimination, and internal validation with bootstrapping. Results There were 2296 children identified with severe metabolic acidosis and 1110 with uraemia. Prognostic features of severe metabolic acidosis among them were deep breathing (OR: 3.94, CI 2.51–6.2), hypoglycaemia (OR: 5.16, CI 2.74–9.75), coma (OR: 1.72 CI 1.17–2.51), respiratory distress (OR: 1.46, CI 1.02–2.1) and prostration (OR: 1.88 CI 1.35–2.59). Features associated with uraemia were coma (3.18, CI 2.36–4.27), Prostration (OR: 1.78 CI 1.37–2.30), decompensated shock (OR: 1.89, CI 1.31–2.74), black water fever (CI 1.58. CI 1.09–2.27), jaundice (OR: 3.46 CI 2.21–5.43), severe anaemia (OR: 1.77, CI 1.36–2.29) and hypoglycaemia (OR: 2.77, CI 2.22–3.46) Conclusion Clinical and laboratory parameters representing contributors and consequences of severe metabolic acidosis and uraemia were independently associated with these outcomes. The model can be useful for identifying patients at high risk of these complications where laboratory assessments are not routinely available.


1974 ◽  
Vol 2 (1) ◽  
pp. 52
Author(s):  
T. Valaes ◽  
J. Kapitulnik ◽  
N. A. Kaufman ◽  
S. H. Blondheim

1989 ◽  
Vol 8 (3) ◽  
pp. 243-245 ◽  
Author(s):  
F.P. Gijsenbergh ◽  
M. Jenco ◽  
H. Veulemans ◽  
D. Groeseneken ◽  
R. Verberckmoes ◽  
...  

A rare case of butylglycol intoxication in a suicide attempt is reported. Coma and hypotension were present on admission and severe metabolic acidosis arose subsequently. Forced diuresis and haemodialysis led to an uneventful outcome.


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