Mother O Positive in 1970 Baby O Negative What. Happens When Child Jaundice

J Pediatr. Author manuscript; available in PMC 2011 Nov 1.

Published in final edited form every bit:

PMCID: PMC2951500

NIHMSID: NIHMS209003

HEMOLYSIS AND HYPERBILIRUBINEMIA IN ABO BLOOD Group HETEROSPECIFIC NEONATES

Michael Kaplan, MB, ChB, Cathy Hammerman, MD, Hendrik J Vreman, PhD, Ronald J Wong, BSc, and David G Stevenson, MD.

Abstract

Objective

We quantified hemolysis and determined the incidence of hyperbilirubinemia in directly antiglobulin titer (DAT) positive, ABO heterospecific neonates and compared variables amongst O-A and O-B subgroups. Study design Plasma full bilirubin (PTB) was determined predischarge and more frequently if clinically warranted, in DAT positive, blood group A or B neonates of group O mothers. Heme catabolism (and therefore bilirubin product) was indexed by blood carboxyhemoglobin corrected for inspired carbon monoxide (COHbc). Hyperbilirubinemia was divers as any PTB concentration >95th percentile on the hr-of-life-specific bilirubin nomogram.

Results

Of 164 neonates, 111 were O-A and 53 O-B. Overall, 85 (51.8%) developed hyperbilirubinemia, which tended to be more prevalent in the O-B than O-A neonates (62.3% vs. 46.eight% respectively, p=0.053). Importantly, more than O-B than O-A newborns developed hyperbilirubinemia at <24 hours (93.9% vs. 48.i%, p<0.0001). COHbc values were globally higher than our previously published newborn values. Babies who developed hyperbilirubinemia had higher COHbc values than the already high values of those non-hyperbilirubinemic, and O-B newborns tended to have higher values than O-A counterparts.

Conclusions

DAT positive, ABO heterospecificity is associated with increased hemolysis and a high incidence of neonatal hyperbilirubinemia. O-B heterospecificity tends to confer even higher gamble than O-A counterparts.

Keywords: Direct antiglobulin titer, bilirubin, ABO heterospecificity, hemolysis, hyperbilirubinemia, carboxyhemoglobin

ABO claret group heterospecific (female parent grouping O, newborn A or B) newborns are at chance for hyperbilirubinemia due to immune based hemolysis (1). The hemolysis occurs when maternal immunoglobulin G anti-A or anti-B antibodies cantankerous the placenta and attach to the rehearsed antigen site on the neonatal red jail cell. Resultant heme catabolism increases bilirubin product. For each molecule of bilirubin produced, equimolecular quantities of carbon monoxide (CO) are produced. Carboxyhemoglobin (COHb) quantification may index the charge per unit of bilirubin production (ii).

The direct antiglobulin titer (DAT) examination is regarded as the cornerstone of diagnosis of immune hemolytic illness of the newborn (ane). Some reports suggest that this exam may exist only a weak predictor of severe hyperbilirubinemia (3,four) and encountered only infrequently among infants readmitted for jaundice (5). Nonetheless, these reports contrast with the prominence of cases of ABO heterospecificity in recent communications on severe hyperbilirubinemia and/or bilirubin encephalopathy (half-dozen–9). Furthermore, blood group incompatibility with a positive DAT is listed by the Subcommittee on Hyperbilirubinemia of the American Academy of Pediatrics (AAP) as a major risk cistron for the evolution of severe hyperbilirubinemia and also every bit a risk cistron for neurotoxicity (ten,11). ABO heterospecificity may therefore have serious consequences.

To capture bilirubin dynamics during the first days of life, the 95^th percentile on the hour of life specific nomogram has been used to ascertain hyperbilirubinemia (12–15). Furthermore, total bilirubin concentrations greater than this percentile may be predictive of severe hyperbilirubinemia. Our objective was to reevaluate the contribution of DAT positive ABO heterospecificity to neonatal hyperbilirubinemia past assessing the incidence of jaundice using this new definition of hyperbilirubinemia. We further assessed the incidence of hyperbilirubinemia occurring <24 hours, which may exist indicative of hemolysis (10), and compared the risk of hemolysis and hyperbilirubinemia between O-A and O-B subgroups. We quantified the degree of hemolysis by measuring blood COHb corrected for inhaled (ambience) CO (COHbc) (2).

METHODS

The study was approved past the Institutional Review Board of the Shaare Zedek Medical Middle. Because of the beneficial nature of the written report which did not involve randomization or administration of a study drug, oral parental consent only was required. The clinical wing of the study was conducted in the well-infant nurseries of the Shaare Zedek Medical Center from January 2006 to April 2007. A sample of sequent (except for the conditions mentioned below) DAT-positive blood grouping A or B infants who were born at ≥37 weeks gestation to mothers with blood grouping O was selected for enrollment in the report shortly subsequently nascence and. To avert any inclusion bias, patients were included earlier any plasma full bilirubin (PTB) results were available. Neonates with whatever obvious condition likely to increase jaundice, other than ABO incompatibility, such severe bruising, sepsis, Down's syndrome, glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, or a positive DAT from whatever cause other than ABO isoimmunization, were excluded. Similarly, DAT positive, ABO heterospecific newborns who were too Rh-positive and born to Rh-negative mothers were excluded because of the difficulty in differentiating a positive DAT acquired by Rh isoimmunization from that caused by ABO heterospecificity. Newborns were not enrolled into the study on weekends, or secular or religious holidays.

Routine management of infants built-in to blood group O mothers at the Shaare Zedek Medical Center was previously described (16). Blood type and DAT tests were routinely performed on cord blood on all infants born to blood grouping O mothers. Results were available inside 24 hours of delivery, and frequently sooner.

Newborns were assessed visually for jaundice at the time of admission to the plant nursery and subsequently at least once per nursing shift. PTB testing was performed on any newborn with jaundice actualization within the first 24 hours, and after that time catamenia as clinically warranted. During routine, predischarge metabolic screening, a PTB determination was performed on DAT positive infants.

All PTB results were plotted on the hr of life specific bilirubin nomogram, and the percentile and risk category adamant. Phototherapy for DAT-positive infants was instituted in accordance with the 2004 AAP guidelines for neonates with risk factors (10). After discharge, follow-upwardly PTB decision was performed when necessary on an outpatient ground at our hospital. Indications for follow up were based on the take a chance category designated by the predischarge PTB concentration, according to the guidelines of the Israel Neonatal Society for the direction of neonatal hyperbilirubinemia and prevention of kernicterus (17).

Blood sampling for COHb determination was performed prior to discharge at the time of routine metabolic screening. Simultaneous with the COHb sampling, a sample of air from the nursery in which the infant was being cared for was nerveless for CO analysis. The timing of metabolic screening was suited to COHb sampling of neonates of smoking mothers, because, by 48 hours, in that location should no longer be whatever event of the smoking on the newborns' COHb concentrations (18).

COHb

Blood for COHb decision (150 μL) was nerveless in custom-prepared capillary tubes containing heparin and saponin, supplied past Stanford Academy. The filled tubes were sealed and the contents mixed, stored at −eighteen°C, and sent on moisture ice to Stanford University. COHb was determined every bit a percentage of total hemoglobin (tHb) in one batch by a gas chromatographic method (eighteen). The tHb latter was measured using the same blood sample by a cyanmethemoglobin method (18). The within-solar day and between-day coefficients of variation for this method for reference blood samples are 3% and 8%, respectively. CO content of the sampled ambience air was measured at Shaare Zedek Medical Eye by using a CO analyzer supplied for this purpose by Stanford Academy and measured COHb values corrected for inspired CO to derive COHbc, as described (eighteen).

Previously published COHbc and tHb values for neonates from this plant nursery that were analyzed using the same methodology and Stanford University laboratory, are supplied for comparison. The reference newborns were not DAT positive or G-half dozen-PD deficient (nineteen,20).

DAT and Blood Type

DAT testing was performed routinely in the blood depository financial institution of the Shaare Zedek Medical Center on umbilical cord blood using an agglutination technique and reported on a calibration of ± to ++++ [DiaMed-IDMicroTyping System, ID-Bill of fare "LISS/Coombs" (DiaMed AG, Cressier s/Morat, Switzerland)]. Blood grouping typing was performed routinely on umbilical cord blood using standard blood bank techniques.

Plasma Total Bilirubin

Routine PTB testing was measured on heparinized, centrifuged, capillary tube samples by absorbance of bilirubin at 455 nm (NEO BIL Model A2 [Digital and Analog Systems, Rome, Italy]).

Data Analysis

Hyperbilirubinemia was defined as any PTB value >95^thursday percentile on the hour-of-life-specific nomogram (12).

COHbc, tHb values and factors relating to hyperbilirubinemia were compared between the O-A and O-B subgroups, and also, within the subgroups, between hyper- and non-hyperbilirubinemic neonates. Categorical variables were compared using χ^two analysis. Continuous variables with a normal distribution were compared using Pupil t test, and in others a Mann-Whitney Rank Sum test was used. The incidence of hyperbilirubinemia was compared past calculating the Relative Hazard (95% confidence interval), in which case significance was defined every bit a 95% confidence interval that did not include 1. For other comparisons, significance was defined equally a p value <0.05.

RESULTS

Ane hundred sixty-iv DAT positive, claret grouping A or B newborns born to claret group O mothers were enrolled between Jan 2006 and Apr 2007 (Table I). Overall, 85 (51.8%) adult a PTB value >95th percentile for hour of life at any point. Age at first PTB >95th percentile was xix ± 11 hr (range i–48 hr, one boosted newborn was readmitted at age fourscore 60 minutes), with respective PTB 9.ix ± 2.5 mg/dL (range 5.i–17.8 mg/dL). Early hyperbilirubinemia (PTB >95th percentile during the kickoff 24 hours) was noted in 56 (34.1% of the cohort, 66.vii% of those with hyperbilirubinemia) and in 27/56 (48.2%) PTB >95th percentile was recorded within the get-go 12 hours. Mean (SD) PTB for the offset reading >95^th percentile for the ≤24 hour group was 8.ix ± 1.ix mg/dL, and that for the ≤12 hour subgroup was eight.4 ± 1.9 mg/dL. Of the remaining 29 hyperbilirubinemic neonates, all but 1 became hyperbilirubinemic between 25–48 hours (31 ± 6 hrs). Phototherapy was administered to 80 neonates of the entire group at an average PTB concentration of 10.6 ± iii.0 mg/dL at mean age 22 ± 17 hr. Of the 53 presenting with hyperbilirubinemia at ≤24 hr of age phototherapy was administered to 51 (mean PTB 9.ii ± 2.0 mg/dL at 13 ± viii hr). All neonates responded to phototherapy. None required intravenous allowed globulin infusion or exchange transfusion.

Table i

Demographic details of the newborns reported for the unabridged grouping and O-A and O-B subgroups.

	Full	O-A	O-B	Significance O-A vs. O-B
Number of neonates (n)	164	111 (67.7%)	53 (32.3%)
Nascency weight (gm. Mean ± SD)	3401 ± 425	3434 ± 450	3342 ± 359	p=0.2
Gestational age (wks)	39 ± 1	39 ± 1	39 ± 1	p=1
Males (%)	44	47	41	p=0.6
Cesarian section (%)	10	9	eleven	p=0.9
Breast feeding (sectional or partial) (%)	88	89	85	p=0.6
Maternal smoking (%)	4	4	six	p=0.8
Jewish:Arab (north)	150 (92%): fourteen (8%)	104 (93%): vii (7%)	46 (87%): 7 (thirteen%)	p=0.vii

A comparison betwixt the O-A and O-B subgroups is summarized in Table 2. Although there was a tendency in the O-B subgroup towards higher adventure of developing hyperbilirubinemia in general, significantly more O-B newborns did develop hyperbilirubinemia within the 1^st 24 hours than O-A counterparts,. The age at which the first PTB value >95^thursday percentile was noted was earlier in the O-B neonates. Similarly, there was a tendency for phototherapy to be commenced before in the OB neonates.

Tabular array 2

Comparison of hyperbilirubinemia and need for phototherapy between neonates with O-A and O-B heterospecificity.

Category	O-A	O-B	Significance
Number of infants	111	53
Hyperbilirubinemia (northward) (Relative Hazard, 95% Confidence Interval)	52 (46.8%)	33 (62.3%)	RR 1.34, 95% CI 0.99–1.77, p=0.053
Historic period at anest PTB >95th centile (h) (mean ± SD)	20.half-dozen ± 11.5	xv.three ± 9.viii*	p=0.035
Hyperbilirubinemia inside anest 24 hr (n)	25/52 (48.1%)	31/33 (93.9%)*	p<0.0001
1st PTB >95th centile (mg/dL)	10.2 ± 2.6	9.3 ± i.9	p=0.17
Phototherapy (n)	48 (43.2%)	33 (62.iii%)	p=0.14
Age at which phototherapy commenced (h) [median (interquartile range)]	21.5 (12–32)	17 (7–27)	p=0.07
PTB at commencement of phototherapy (mg/dL)	xi.2 ± iii.2	9.8 ± 2.four*	p=0.04

COHbc studies for the entire cohort, as well as for the O-A and O-B subgroups, are presented in Tabular array III. Overall, COHbc values were significantly higher than those of a previously reported newborn cohort (19). Both in the entire cohort, equally well as within the O-A and O-B subgroups, those who developed hyperbilirubinemia had higher COHbc values than the already high values of those who did non have whatever documented PTB value >95^thursday percentile. Furthermore, the percentage of newborns developing hyperbilirubinemia increased in tandem with increasing COHbc percentile values (Effigy). In that location was a trend for the O-B subgroup to have COHbc values which were higher than the already high levels of the O-A subgroup.

Incidence of hyperbilirubinemia, defined as any plasma full bilirubin value >95^th percentile on the hour of life specific bilirubin nomogram, graded past corrected carboxyhemoglobin (COHbc) percentile value.

COHbc percentile ranges (% tHb): <50^th percentile, 0.54–i.xix; 50–74^th percentile, 1.20–1.44; 75–ninety^th percentile, 1.45–i.76; >90^th percentile, one.79–ii.62

Table 3

Blood carboxyhemoglobin values, corrected for inspired CO (COHbc) for the unabridged ABO heterospecific grouping, and for the O-A and O-B subgroups individually. For reference, COHbc values for previously reported, healthy, non-hemolyzing neonates are included (xix).

COHbc (% tHb)	Entire ABO Group	O-A	O-B	Reference Group	Significance
Overall
north =	163	111	53	131
COHbc (mean ± SD)	i.24 ± 0.40*	1.20 ± 0.38	ane.32 ± 0.441	0.77 ± 0.19	*p<0.0001, entire group vs. reference group; 1p=0.07, O-B vs. O-A
Hyperbilirubinemia
due north =	85	52	33
COHbc	1.42 ± 0.39	1.40 ± 0.36	1.45 ± 0.45
Non-hyperbilirubinemia
n =	78	59	20
COHbc	1.00 ± 0.25	0.99 ± 0.26	1.04 ± 0.24
Significance	p<0.001	p<0.001	p=0.002

tHb values were 17.4 ± ii.9 g/dL for the cohort. These were lower than our previously reported reference values (19.0 ± 2.4 g/dL, p<0.001) (twenty). Inside the ABO heterospecific cohort, tHb values for the hyperbilirubinemic newborns were lower than for those not-hyperbilirubinemic (16.9 ± 2.ix 1000/dL vs. 18.2 ± 2.7 g/dL, p=0.007). Fifty-fifty in those ABO heterospecific neonates who did not become hyperbilirubinemic, tHb values were lower than those of the reference grouping. Even though the tHb values were somewhat lower for the O-B neonates, the difference between these and the O-A group was non significant (17.0 ± 3.1 chiliad/dL vs. 17.7 ± 2.eight grand/dL, p=0.2).

Discussion

Of the neonatal population delivered at the Shaare Zedek Medical Center, 21% comprise blood group A or B newborns born to group O mothers of which 15% are DAT positive (16). In the present study we documented a 52% incidence of hyperbilirubinemia in the DAT positive subgroup. This incidence is clearly many-fold that of other population groups studied using the identical definition of hyperbilirubinemia. For example, in a multicenter, multinational report of 1370 newborns, eight.viii% adult hyperbilirubinemia (13). In an African American male accomplice, hyperbilirubinemia was documented in 6.7% of 436 G-6-PD normal, command infants and 21.nine% of 64 G-6-PD scarce newborns (xiv). Further calculation to the high hazard nature of these infants is the high incidence of hyperbilirubinemia occurring within the first 24 hours. However, nearly all babies who developed hyperbilirubinemia did and so within the first 48 hours, implying little risk of subsequent hyperbilirubinemia in those discharged after that timeframe. Many of the babies had combinations of conditions listed by the AAP as major risk factors for the development of astringent hyperbilirubinemia: predischarge bilirubin value in the loftier risk zone; hemolysis due to blood group incompatibility with positive DAT; jaundice appearing within the get-go 24 hours, and exclusive chest feeding (ten).

A correspondingly loftier number of newborns met the requirement for phototherapy. We cannot foretell the bilirubin dynamics had phototherapy non been instituted at low concentrations of PTB in accordance with AAP guidelines. It is possible that in some neonates the serum bilirubin concentrations would have leveled off and not met the criteria for phototherapy at a later on age (three,21).

Considering that kernicterus is rarely encountered and exchange transfusion nowadays is unusual, it is non surprising that, despite the high incidence of hyperbilirubinemia, nosotros encountered no cases of this nature. Although our findings are consistent with previous reports demonstrating that few DAT positive, ABO heterospecific neonates will see the criteria for exchange transfusion (three,5), newborns of these blood grouping combinations do announced prominently in contempo series of severe hyperbilirubinemia and kernicterus (half dozen–9). The apparent mild nature of the disease should not cause complacency regarding ABO hemolytic disease.

At that place may be an increased effect of hemolytic conditions on the development of bilirubin induced neurologic dysfunction (22,23). Our elevated COHbc results, comptatible with previously reported data (thirteen, 24–26), confirm the hemolytic nature of DAT positive ABO heterospecificity in general and emphasize the loftier risk nature of these neonates. Despite the overall high rate of hemolysis, not all infants in our series who adult hyperbilrubinemia had loftier levels of COHbc. The percentage of hyperbilirubinemic neonates increased along with increasing COHbc percentile values. We speculate that, in the lower percentile groups, varying degrees of immaturity of the bilirubin conjugating system, or presence of the (TA)₇ promoter variant of the UGT1A1 gene associated with Gilbert syndrome, along with moderately increased heme catabolism, may accept contributed to the hyperbilirubinemia (27). Even so, in those neonates with the highest COHbc levels, all babies developed hyperbilirubinemia. In this latter group, the degree of hemolysis must accept been sufficiently high to overwhelm even the about efficient conjugation procedure.

The literature is inconsistent with regard to the degree of hemolysis and the incidence and severity of hyperbilirubinemia between O-A and O-B subgroups. Several investigators were unable to show whatsoever difference in clinical severity between O-A and O-B hemolytic disease of the newborn, although in the former written report there was a trend towards performing exchange transfusion during the commencement 24 hours more frequently in O-B compared with O-A infants (28–xxx). Similarly, a retrospective assay of ABO hemolytic disease did not find significant relationships betwixt the infants' blood type and clinical effect (31). Sisson (32) and Kaplan (33) reported no meaning differences in severity or response to therapy between the two blood types. An infant whose blood group was A was as likely to be afflicted by ABO hemolytic disease as a blood group B baby (34). However, Bakkeheim et al constitute a significantly increased rate of invasive treatments, including intravenous immune globulin therapy and exchange transfusion, in O-B infants compared with O-A (35). Two studies documented a higher need for exchange transfusion in O-B neonates than in O-A (36, 37).

The reasons for the apparently increased severity of jaundice in the O-B subgroup are not clear. Maternal factors including differing levels of IgG anti-A or anti-B may affect the degree of hemolysis, and variations in IgG subgroup distribution may change macrophage induced RBC clearance. The number of fully developed A or B antigen sites on fetal RBCs may exist different, equally may be the dilutional result of other tissues bearing these surface antigens (38).

Comparisons of these studies are difficult every bit inclusion criteria, definitions, therapeutic indications, and fourth dimension epochs differed from study to written report. In contrast, we categorized our patients using an up to appointment definition of hyperbilirubinemia which takes into business relationship the bilirubin dynamics of the outset days of life (12). Standardized criteria for treatment were employed (10), and the rate of heme catabolism was assessed by a state of the fine art method (2). Selection bias was avoided past including all DAT positive ABO heterospecific newborns at birth, and prior to their becoming jaundiced. Although not all our comparisons achieved statistical significance, O-B heterospecific neonates did appear to be at higher hazard than the O-A subgroup. Hyperbilirubinemia did occur before in the O-B infants and more than O-B newborns developed hyperbilirubinemia within the first 24 hours. This difference was owing to moderately, although not statistically significantly, increased hemolysis. Lack of statistical significance, still, does not preclude an consequence of moderately increased hemolysis resulting in increased bilirubin production. Coupled with immaturity of the bilirubin conjugating system, moderately increased hemolysis may have resulted in a higher incidence of hyperbilirubinemia. A shortcoming of our study was the dependence on visual recognition of early jaundice, and lack of a fixed protocol for PTB determinations during the first 24 hours.

In summary, our study provides information nigh the incidence, severity and mechanism of jaundice in ABO heterospecific neonates. A high charge per unit of hemolysis is a hallmark of DAT positivity with a resultant high incidence of hyperbilirubinemia and especially early hyperbilirubinemia. These factors have the potential of increasing the take a chance of severe hyperbilirubinemia and bilirubin neurotoxicity. Furthermore, O-B heterospecific neonates appear to be at higher chance than their O-A counterparts

Acknowledgments

Supported at Stanford Academy by National Institutes of Health (grants RR00070 and RR025744), the Hess Inquiry Fund, the HM Lui Research Fund, and the Mary L Johnson Enquiry Fund. The authors declare no conflicts of interest.

ABBREVIATIONS

AAP

American Academy of Pediatrics

CO

carbon monoxide

COHb

carboxyhemoglobin

COHbc

carboxyhemoglobin corrected for inspired CO

DAT

direct antiglobulin titer

G-6-PD

glucose-6-phosphate dehydrogenase

PTB

plasma full bilirubin

RBC

scarlet blood cell

tHb

total hemoglobin

Footnotes

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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2951500/