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J A Widness

Publications and source records attributed to J A Widness.

At least 73 records · Page 4Linked to original sources
PubMed1994

Direct relationship of fetal carboxyhemoglobin with hemolysis in alloimmunized pregnancies.

Because carbon monoxide (CO) is a byproduct of heme degradation and because placental diffusing capacity of CO is limited, we hypothesized that the concentration of CO transported in fetal blood as carboxyhemoglobin (HbCO) would correlate with the severity of fetal hemolytic disease. Fetal blood was obtained by cordocentesis and HbCO was measured by gas chromatography. The two primary study groups included control fetuses (n = 26) and fetuses of Coombs-positive mothers before in utero transfusion (n = 15). Compared with controls, fetuses with hemolytic disease had higher HbCO levels (0.0111 +/- 0.0014 versus 0.0159 +/- 0.0072 fraction of total Hb, mean +/- SD, p < 0.002). In contrast, HbCO levels in simultaneously sampled maternal blood samples were not different in the control and alloimmune groups [0.0110 +/- 0.0025 (n = 20) versus 0.0115 +/- 0.0021 (n = 11)]. There was a significant inverse correlation observed between fetal HbCO and Hb concentrations in the group with hemolytic disease (r = -0.73, p < 0.002) but not in controls. In fetuses with hemolytic disease, HbCO and bilirubin were highly correlated (r = 0.88, p < 0.0001). Data from four anemic fetuses who were Coombs negative, three of whom had no evidence of hemolysis, indicated normal HbCO and normal plasma bilirubin levels. A fourth fetus with anemia had viral sepsis and elevated HbCO and plasma bilirubin levels. We conclude that elevated HbCO levels detected in fetuses of nonsmoking mothers with erythrocyte alloimmunization are likely the result of accelerated hemolysis.

Bilirubin↗
PubMed1994

The reactivation of fetal hemoglobin synthesis during anemia of prematurity.

Increased fetal Hb (HbF) synthesis has been shown to occur during fetal hypoxemia and severe anemia. To determine whether increased HbF synthesis occurs during anemia of prematurity, the levels of HbF synthesis were correlated with the degree of anemia and plasma erythropoietin levels. Thirteen newborn infants born at 29.2 +/- 1.7 wk of gestation were studied at a postconceptional age 36.0 +/- 1.1 wk. Hb levels ranged from 65 to 78 g/L. Blood samples were incubated in an amino acid mixture containing [3H]leucine and chromatographed allowing the separation and quantitation of the alpha, beta, and gamma (A gamma T, G gamma, and A gamma I) chains. Erythropoietin was determined by RIA. The mean HbF synthesis was 77.9 +/- 8.9% of total Hb synthesis (range: 61 to 91%). Plasma erythropoietin concentrations were 21.4 +/- 6.4 mU/mL. There was no correlation between the total Hb or HbF synthesis and the level of erythropoietin. There was, however, a significant inverse correlation between the Hb level and HbF synthesis (p < 0.01). Nine infants who had received transfusions during the first few days of life had a mean HbF that was 53.5 +/- 15.2% of total Hb, whereas their HbF synthesis was 78.4 +/- 7.6%. Four of the infants never received transfusions; the total circulating HbF and HbF synthesis in these infants were 87.7 +/- 7.7% and 76.8 +/- 12.7%, respectively. This study shows that there can be a reactivation of HbF synthesis during severe anemia of prematurity.

Anemia, Neonatal↗
PubMed1993

A system approach to pharmacodynamics. Plasma iron mobilization by endogenous erythropoietin in the sheep fetus; evidence of threshold response in spontaneous hypoxemia.

At present, nearly all infants with birth weights of < 1 kg receive blood transfusions for treatment of clinical signs of tissue hypoxia resulting from anemia of prematurity. In contrast to the successful use of recombinant human erythropoietin (rhEp) in adults, treatment of anemic neonates with rhEp to stimulate red cell production and reduce the need for transfusions that pose serious infectious and immunologic risk has not been effective. The present study investigates the pharmacodynamics (PD) of endogenous erythropoietin (Ep) in sheep fetuses to determine possible causes for the poor rhEp response in early development. The dynamic relationship between plasma Ep and plasma iron resulting from spontaneous hypoxemic episodes is investigated by PD system analysis. The erythropoietic effect of Ep is measured in terms of the mobilization of plasma iron needed in the production on new erythrocytes. A hysteresis minimization approach is employed to determine the intrinsic PD dose-response relationship (transduction) of Ep. The dose-response relationship shows a well-defined threshold level that has to be exceeded before Ep begins to show a significant effect on plasma iron. It is postulated that the threshold mechanism may serve a useful purpose during early development by reducing the risk of the fetus developing a pathological degree of polycythemia and hyperviscosity in the relatively hypoxemic fetal environment. At the same time, the threshold serves the purpose of providing a needed response to more severe pathologic hypoxemic episodes. The occurrence of anemia during subsequent postnatal life when PaO2 levels increase markedly may be the inevitable, but unfortunate corollary of a continuation of this mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effect of intravenous beta-sympathomimetic tocolysis on human fetal serum erythropoietin levels.

OBJECTIVE: The major stimulus for erythropoietin production is tissue hypoxia. We sought to investigate the relationship of beta-sympathomimetic administration for tocolysis and fetal serum erythropoietin. STUDY DESIGN: Umbilical cord blood was obtained from infants whose mothers received intravenous beta-sympathomimetic tocolysis and who were delivered at < or = 34 weeks' gestation. Serum erythropoietin was measured by radioimmunoassay. On the basis of the presumed 2- to 4-hour half-life of fetal erythropoietin, the infants were divided into two groups. In group 1 (n = 16) beta-sympathomimetic therapy was discontinued < 24 hours before delivery; in group 2 (n = 11) it was discontinued > or = 24 hours before delivery. RESULTS: Group 1 fetuses had significantly higher erythropoietin levels than did group 2 fetuses (37.3 vs 13.9 mU/ml, p = 0.02). The duration of beta-sympathomimetic tocolysis and the maximum infusion rate were not different. The two groups did not differ in gestational age, birth weight, route of delivery, presence of labor, or duration of first or second stage of labor. CONCLUSIONS: We speculate that intravenous beta-sympathomimetic tocolytic therapy stimulates fetal erythropoietin production by decreasing fetal oxygenation as a result of the reversible fetal metabolic effects of the tocolysis. These data suggest that beta-sympathomimetic tocolysis should be undertaken cautiously if fetal compromise is suspected, fetal well-being should be assessed carefully if tocolysis is undertaken, and treatment should be discontinued promptly if a clear benefit is not realized.

Erythropoietin↗
PubMed1993

Restoration of fetal red blood cells and plasma proteins after a moderately severe hemorrhage in the ovine fetus.

OBJECTIVE: We hypothesized that the fetus, in response to a moderately severe hemorrhage, would restore its plasma volume and red blood cells so that plasma volume would be returned to normal within 24 hours and red blood cell mass would be restored in 5 to 7 days. STUDY DESIGN: Time-dated pregnant sheep (five control and six hemorrhage, gestational age 124 +/- 1 [SE] days) were subjected to a 10-day protocol. Fetal blood volume, plasma volume, red blood cell mass, and plasma protein mass were measured on protocol days 1, 3, 4, 6, 8, and 10. Fetal plasma erythropoietin and plasma iron concentrations were measured daily. On protocol day 3 the hemorrhage animals underwent a 120 ml fetal hemorrhage over 2 hours. Statistical analysis was by three-factor analysis of variance. RESULTS: Control animals had a progressive increase in blood volume, plasma volume, plasma protein mass, and red blood cell mass throughout the 10-day protocol. The 2-hour hemorrhage removed 39.8% +/- 1.2% of the prehemorrhage blood volume. During the 7-day posthemorrhage recovery period fetal blood volume and red blood cell mass in the animals that were hemorrhaged expanded in parallel to, but remained below, that of the control animals. There was no difference in the expansion of fetal plasma volume or plasma protein mass between the two groups. After hemorrhage there was a nonsignificant increase in the fetal reticulocyte index in the animals undergoing hemorrhage. In response to the hemorrhage, erythropoietin levels increased and remained marginally elevated, whereas plasma iron levels decreased in the hemorrhaged animals relative to controls during the 7-day recovery period. CONCLUSIONS: The normal expansion of plasma volume and plasma protein mass that occurs with fetal growth was not altered by a large fetal blood loss. However, in spite of a transient increase in plasma erythropoietin levels the fetuses undergoing hemorrhage did not restore their red blood cell mass or blood volume. These observations suggest that the ovine fetus is able to withstand a significant loss of red blood cells, but fetal transfusion may be needed to restore fetal red blood cell mass after a moderate-to-severe fetal hemorrhage.

Animals↗
PubMed1993

The relationship between fetal arterial oxygen saturation and heart and skeletal muscle myoglobin concentrations in the ovine fetus.

Myoglobin, a hemoprotein found in abundance in the muscle of postnatal animals, increases in concentration in response to hypoxia, thereby protecting tissue from damage. Fetuses exposed to intrauterine hypoxemia are also susceptible to organ damage, but the response of fetal muscle myoglobin to hypoxemia is unknown. To study whether fetal muscle myoglobin concentrations are elevated following intrauterine hypoxemia, we exposed eight chronically catheterized late gestation sheep to a wide range of fetal oxygen levels over 15 to 30 days and correlated the level of fetal oxygenation with heart and skeletal muscle myoglobin concentrations measured at sacrifice. A lower level of fetal oxygenation, expressed as the integrated area under the arterial saturation (SaO2)-time curve, was associated with greater myocardial myoglobin concentration (r = 0.90; P < 0.01). This relationship was not observed for skeletal muscle (r = 0.43; P = ns). A lower level of fetal oxygenation was associated with lower myoglobin:iron (w/w) ratio in skeletal muscle (r = 0.71; P < 0.03), implying less incorporation of iron into myoglobin. A similar relationship was not apparent for cardiac tissue. The higher myocardial myoglobin concentrations found in the more hypoxic fetuses were consistent with previous observations in postnatal animals. This likely represents an intracellular compensatory mechanism for sustaining short-term mitochondrial oxygen delivery in a critical organ with a high rate of oxygen consumption. The lack of myoglobin responsiveness to hypoxia in fetal skeletal muscle may be due to its much lower oxygen consumption rate and activity level.

Animals↗
PubMed1993

Erythropoietin in human fetuses with immune hemolytic anemia and hydrops fetalis.

OBJECTIVE: To determine whether plasma erythropoietin is increased in fetuses with anemia due to Rh isoimmunization. METHODS: Hemoglobin and erythropoietin were measured in samples obtained by funipuncture from 15 fetuses with Rh isoimmunization (gestational age 26.2 +/- 5.0 weeks, mean +/- standard deviation) and from 13 control fetuses (23.1 +/- 6.7 weeks). Hemoglobin and erythropoietin also were determined in umbilical cord blood collected at birth from 20 term fetuses delivered by elective cesarean. RESULTS: Fetuses with Rh isoimmunization had lower hemoglobin and higher plasma erythropoietin measurements than mid-gestation controls (6.1 +/- 3.9 versus 10.7 +/- 1.5 g/dL and 105.5 +/- 168.1 versus 12.5 +/- 3.1 mU/mL, P < .05, respectively). Hemoglobin and plasma erythropoietin increased with gestational age in control fetuses. There was an inverse association between hemoglobin and plasma erythropoietin in control and Rh-isoimmunized fetuses (r = -0.56, P < .005). Using multiple linear regression, hemoglobin and gestational age were associated independently with plasma erythropoietin (overall F2,25 = 12.3, multiple r2 = 0.49, P < .001). Despite marked decreases in hemoglobin, fetuses below 24 weeks' gestation had minimal increases in plasma erythropoietin compared to fetuses above that gestational age. Mildly anemic Rh-isoimmunized fetuses (hemoglobin 11.6 +/- 2.0 g/dL) delivered vaginally had significantly higher erythropoietin levels in umbilical cord plasma than Rh-isoimmunized fetuses with comparable hemoglobin (10.9 +/- 3.5 g/dL) delivered by elective cesarean without labor (1246 +/- 856 versus 106 +/- 66 mU/mL, respectively, P < .05). CONCLUSION: Fetuses with anemia at mid to late gestation respond with increases in plasma erythropoietin, but these changes are substantially attenuated before 24 weeks' gestation.

Anemia, Hemolytic, Autoimmune↗
PubMed1992

Pharmacokinetics and pharmacodynamics of erythropoietin during therapy in an infant with renal failure.

We treated an infant with anemia and chronic renal failure with recombinant human erythropoietin (300 to 750 U/kg subcutaneously per week) and iron (6 mg/kg enterally) from 1 to 4 months of age. A suboptimal pharmacodynamic response was seen at the lower dose. This may have been due to developmental erythropoietin pharmacokinetic differences, that is, relatively greater neonatal plasma clearance and steady-state volume of distribution compared with those in adults.

Anemia↗
PubMed1992

Fetal iron and cytochrome c status after intrauterine hypoxemia and erythropoietin administration.

Chronic fetal hypoxemia stimulates erythropoiesis and may result in a redistribution of fetal iron from plasma into erythrocytes. We studied the response of fetal plasma erythropoietin (Ep) to hypoxemia, the role of Ep in stimulating erythropoiesis in utero, and the effect of augmented erythropoiesis on fetal plasma Ep and iron and tissue cytochrome c concentrations in 19 chronically instrumented late-gestation fetal sheep. The fetuses were stimulated to produce 28 erythropoietic responses after exposure to 1) acute hypoxemia (1-5 days), 2) chronic hypoxemia (greater than 7 days), and/or 3) administration of 1,500 U recombinant human Ep concurrently during normoxemia. Plasma Ep peaked less than 12 h after the onset of hypoxemia or Ep bolus. Plasma iron decreased 24-48 h later and returned to baseline 48-96 h after normalization of Ep levels to baseline. The plasma iron response was directly related to the erythropoietin stimulus (r = 0.79, P less than 0.001) and inversely related to liver iron concentration at death (r = -0.84, P less than 0.001). Nine fetuses with depleted liver iron concentrations at autopsy had significantly lower heart and skeletal muscle iron concentrations compared with animals with 10% of control liver iron remaining. Skeletal muscle and heart iron and cytochrome c concentrations were significantly correlated. Ep has a potent biological effect on fetal erythropoiesis and iron metabolism. Augmented fetal erythropoiesis, mediated by Ep, results in decreased plasma iron, hepatic storage iron, and skeletal and cardiac muscle iron and cytochrome c. The model potentially explains the iron abnormalities found in newborn infants after fetal hypoxia.

Animals↗
PubMed1992

A sensitive and specific erythropoietin immunoprecipitation assay: application to pharmacokinetic studies.

Previous pharmacokinetic studies with radiolabeled erythropoietin have relied on results of nonspecific methods to derive pharmacokinetic parameters. Dependence on nonspecific protein precipitation or total radioactivity may result in falsely high determinations of plasma radiolabeled erythropoietin and erroneous determinations of pharmacokinetic elimination and distribution parameters. In the present study pharmacokinetic parameters were derived by using a specific, sensitive, and reproducible immunoprecipitation assay for biologically active iodine 125-labeled recombinant human erythropoietin (125I-rhEp) and compared with those obtained by using nonspecific protein precipitation with trichloroacetic acid (TCA). Tracer amounts of 125I-rhEp were administered by bolus injection to six newborn lambs. Plasma-precipitable radioactivity assayed by the immunoprecipitation method became progressively lower with time relative to those observed with the TCA method. Pharmacokinetic parameters derived from the immunoprecipitation assay demonstrated significantly more rapid plasma and elimination clearances, shorter terminal half-life, shorter mean body residence time, and shorter distribution time when compared with the TCA assay (p less than 0.01). Volume of distribution was not different. Comparison of immunoprecipitation and TCA assay results from gel permeation fractions of iodinated erythropoietin demonstrated that immunoprecipitation assay results provide a better evaluation of biologically active hormone as determined by comparisons with SDS-PAGE and erythropoietin radioreceptor data. We conclude that 125I-rhEp pharmacokinetic parameters derived by using the immunoprecipitation assay more accurately reflect physiologic conditions than do those derived by using TCA precipitation.

Animals↗
PubMed1992

Developmental differences in erythropoietin pharmacokinetics: increased clearance and distribution in fetal and neonatal sheep.

Although erythropoietin (Ep) is considered the primary hormone responsible for erythrocyte production throughout development, the administration of recombinant human Ep (rhEp) to premature human neonates has, thus far, been ineffective in the prevention and treatment of their anemia. To determine if developmental pharmacokinetic differences might in part be responsible for this lack of efficacy, Ep pharmacokinetic studies were carried out in four groups of sheep: late gestation fetal, neonatal, adult and pregnant. After i.v. bolus injection of tracer amounts of the biologically active [125I]rhEp, plasma [125I]rhEp was measured using a sensitive and specific Ep immunoprecipitation assay. Pharmacokinetic parameters were derived using noncompartmental system analysis. Significantly greater clearances, shorter half-lives, shorter residence times, greater distribution volumes and greater Ep production rates were found in the fetal and neonatal groups compared to pregnant and nonpregnant adults (P less than .01). These developmental differences likely reflect more rapid metabolism and greater distribution of Ep in less mature individuals. As such, they could result in a reduction in Ep's erythropoietic effect similar to that reported in premature infants. We speculate that treatment of anemic premature neonates using rhEp doses shown to be effective in adults may be inadequate.

Animals↗
PubMed1991

Management of fetal hemolytic disease by cordocentesis. I. Prediction of fetal anemia.

Between January 1985 and November 1990, 128 pregnancies complicated by maternal red blood cell alloimmunization were referred to our Fetal Diagnosis and Treatment Unit. We examined the premise that an evaluation of fetal blood would accurately identify fetuses at risk of requiring antenatal transfusion therapy. Two hundred seventy-two diagnostic cordocenteses were performed. Criteria for the timing of repeat cordocenteses were developed retrospectively on the basis of the fetal hematocrit values, reticulocyte counts, and direct Coombs' test results of the first 84 pregnancies. These criteria were tested and confirmed prospectively on the next 44 pregnancies. On the basis of the first blood sample, four hematologic patterns (and their distributions) were identified in the 98 antigen-positive fetuses. Pattern 1: fetuses at low risk of having significant antenatal anemia (hematocrit less than 30%) (n = 11, 11%). These fetuses had normal hematocrit values and reticulocyte counts coupled with negative or trace-positive direct Coombs' test. No fetus in this group had significant antenatal anemia. Pattern 2: fetuses at intermediate risk of having anemia (n = 29, 31%). Pattern 2 fetuses had normal hematocrit values and either direct Coombs' titers of more than trace less than or equal to 2+ and normal reticulocyte counts or low reticulocyte counts (less than 2.5th percentile for gestation). Twenty-one percent (n = 6) of fetuses in pattern 2 had significant antenatal anemia. Patterns 3 and 4: fetuses at greatest risk of having severe anemia. These fetuses had normal hematocrit values associated with either reticulocyte counts greater than 97.5th percentile for gestation or a direct Coombs' test greater than or equal to 3+ (pattern 3, n = 49, 50%) or both, or a mild anemia (greater than 30% but less than 2.5th percentile for gestation) (pattern 4, n = 9, 10%). Eighty percent (n = 39) of fetuses with pattern 3 and 90% (n = 8) with pattern 4 developed a hematocrit value less than 30%. We conclude that evaluation of fetal hemolytic disease with a fetal blood specimen permits the identification of fetuses at high risk of having antenatal anemia.

Amniocentesis↗
PubMed1991

Lack of maternal to fetal transfer of 125I-labelled erythropoietin in sheep.

We administered tracer quantities of biologically active 125I-labelled recombinant human erythropoietin by intravenous bolus injection to seven late gestation pregnant ewes. Maternal and fetal blood was sampled over the subsequent six hours and assayed for erythropoietin-specific radioactivity. Despite the expected increase in maternal plasma immunoprecipitable 125I-labelled erythropoietin radioactivity, fetal plasma levels remained unchanged throughout the study. In addition, erythropoietin receptors were not detected in ovine and human placental tissue. We conclude that biologically active 125I-labelled erythropoietin does not cross the placenta from mother to fetus in measurable quantities in sheep, and likely in humans. Thus, these data indicate the levels of erythropoietin measured in fetal plasma are reflective of fetal, and not maternal, erythropoietin production and elimination.

Animals↗
PubMed1991

Management of fetal hemolytic disease by cordocentesis. II. Outcome of treatment.

Forty-eight of 128 pregnancies complicated by maternal red blood cell alloimmunization (49%) received a total of 142 intravascular transfusions (range, 1 to 7) for treatment of severe anemia (hematocrit, less than or equal to 30%). Thirteen fetuses (27%) had hydrops when therapy was initiated. The overall survival rate was 96%. Eighty-five percent of survivors received two or more transfusions before delivery. The mean gestational age at initiation of therapy was 28 weeks (range, 18 to 36 weeks). Bleeding from uterine and umbilical cord puncture sites was not of clinical significance. The most common complication was fetal bradycardia (8%). Simple intravascular transfusion resulted in the replacement of fetal red blood cells with adult red blood cells and suppression of fetal erythropoiesis. By the completion of the second transfusion, on average, less than 1% of circulating red blood cells were fetal. Within 3 weeks of the second transfusion, the mean reticulocyte count was less than 1%. The rate at which the fetal hematocrit declined after a transfusion (exclusive of the first) was inversely related to gestational age (r = -0.84, p less than 0.0001), permitting a 4- to 5-week interval between transfusions after 32 weeks' gestation. A total of 78% of surviving neonates were delivered at term. Neonates transfused more than once antenatally required less phototherapy (75.8 +/- 54 vs 165 +/- 101 hours, p less than 0.003) and, when delivered at term, fewer hospital days (4.8 +/- 2 vs 8.6 +/- 6 days, p = 0.01) compared with those transfused once. We conclude that the treatment of fetal anemia by intrauterine simple intravascular transfusion permits a term delivery in the majority of cases and is associated with high perinatal survival and low perinatal morbidity.

Blood Transfusion, Intrauterine↗
PubMed1990

Direct relationship of antepartum glucose control and fetal erythropoietin in human type 1 (insulin-dependent) diabetic pregnancy.

In the present study the antepartum relationship between maternal diabetic glucose control and fetal hypoxaemia was examined in 44 Type 1 (insulin-dependent) diabetic and 23 non-diabetic control pregnancies. Maternal HbA1C was used to assess maternal integrated blood glucose control while fetal metabolic control was evaluated by antepartum glucose, insulin, and C-peptide determinations in amniotic fluid at elective caesarean delivery. Fetal hypoxaemia was assessed indirectly by fetal umbilical vein plasma erythropoietin level at delivery. A prospectively developed statistical pathway model was used to examine the relationship of these variables. In applying forced stepwise multiple regression with this model, we observed in the diabetic subjects that mean maternal HbA1C during the last month of pregnancy correlated significantly with fetal umbilical venous erythropoietin at delivery (r = 0.57, p less than 0.001). Additional significant contributions to umbilical venous erythropoietin were found for amniotic fluid glucose and amniotic fluid insulin when these two independent variables were added in stepwise fashion (p less than 0.01). We conclude that in diabetic pregnancy, antepartum control of maternal hyperglycaemia is a significant factor associated with fetal hypoxaemia. We speculate that this effect is mediated through perturbations which accelerate fetal metabolism and which is expressed by amniotic fluid levels of glucose and insulin.

Amniotic Fluid↗
PubMed1990

Postnatal changes in serum immunoreactive erythropoietin in relation to hypoxia before and after birth.

To assess the immediate postnatal changes of serum immunoreactive erythropoietin (EP) in infants born after acute or chronic fetal hypoxia, and to estimate the rate of EP disappearance, we studied EP concentration, measured by double-antibody radioimmunoassay, in cord venous plasma and in serum at a mean age of 8 hours in a control group (n = 9) and in three patient groups: (1) infants with polycythemia (n = 10), (2) infants born to mothers with preeclampsia of pregnancy, without (n = 22) or with (n = 11) acidosis at birth, and (3) infants with acute birth asphyxia (n = 19), seven of whom had postnatal hypoxia. In all patient groups, cord venous EP was elevated in comparison with values in control infants. No change was found in EP level between birth and 8 hours in control infants (geometric mean in cord and 8-hour sample: 20 and 16 mU/ml, not significant) or in acutely asphyxiated infants with postnatal hypoxia (122 and 72 mU/ml, not significant), whereas the EP level decreased in all other groups: infants with polycythemia (123 to 24 mU/ml, p less than 0.001), nonacidotic infants (78 to 26 mU/ml, p less than 0.001) and acidotic infants (176 to 38 mU/ml, p less than 0.001) of the preeclampsia group, and acutely asphyxiated infants without postnatal hypoxia (58 to 30 mU/ml, p less than 0.001). The mean (+/- SD) half-time of EP disappearance was 2.6 +/- 0.5 hours in infants with polycythemia and 3.7 +/- 0.9 hours in infants of the preeclampsia group.

Acidosis↗
PubMed1990

Abnormal iron distribution in infants of diabetic mothers: spectrum and maternal antecedents.

Because chronic hypoxemia causes a redistribution of iron from serum and storage pools into an expanding erythrocyte mass, and because infants of diabetic mothers are often hypoxemic in utero and have a high prevalence of polycythemia at birth, we studied iron distribution in 43 term infants of diabetic mothers. Twenty-four infants were at an appropriate size for gestational age; 19 were large for gestational age. At birth, 28 infants (65%) had abnormal serum iron profiles; eight had decreased ferritin concentrations only (stage 1), nine had decreased ferritin and increased total iron-binding capacity values (stage 2), and 11 had these serum findings plus elevated free erythrocyte protoporphyrin concentrations (stage 3). The hypoglycemic infants who were large for gestational age (n = 14) had a higher prevalence of abnormal iron profiles than euglycemic infants who were appropriate in size for gestational age (n = 20; 93% vs 50%; p = 0.009). Progressively abnormal iron profiles were associated with higher glycosylated fetal hemoglobin values, greater degrees of macrosomia, increased hemoglobin and erythropoietin concentrations, and increased erythrocyte/storage iron ratios. Erythropoietin concentrations were inversely linearly correlated with serum iron values (n = 32, r = -0.54; p = 0.003). The combined erythrocyte and storage iron pools were significantly lower in infants with abnormal iron values whose mothers were diabetic, particularly in infants of women with confirmed diabetic vasculopathy. We speculate that these findings are likely due to (1) increased fetal iron utilization during compensatory hemoglobin synthesis in response to chronic hypoxemia and (2) reduced iron transfer during late gestation complicated by diabetes.

Birth Weight↗