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Biomedical subjects

C Hammerman

Publications and source records attributed to C Hammerman.

At least 55 records · Page 3Linked to original sources
PubMed1997

Gilbert syndrome and glucose-6-phosphate dehydrogenase deficiency: a dose-dependent genetic interaction crucial to neonatal hyperbilirubinemia.

Severe jaundice leading to kernicterus or death in the newborn is the most devastating consequence of glucose-6-phosphate dehydrogenase (EC 1.1.1.49; G-6-PD) deficiency. We asked whether the TA repeat promoter polymorphism in the gene for uridinediphosphoglucuronate glucuronosyltransferase 1 (EC 2.4.1.17; UDPGT1), associated with benign jaundice in adults (Gilbert syndrome), increases the incidence of neonatal hyperbilirubinemia in G-6-PD deficiency. DNA from term neonates was analyzed for UDPGT1 polymorphism (normal homozygotes, heterozygotes, variant homozygotes), and for G-6-PD Mediterranean deficiency. The variant UDPGT1 promoter allele frequency was similar in G-6-PD-deficient and normal neonates. Thirty (22.9%) G-6-PD deficient neonates developed serum total bilirubin >/= 257 micromol/liter, vs. 22 (9.2%) normals (P = 0.0005). Of those with the normal homozygous UDPGT1 genotype, the incidence of hyperbilirubinemia was similar in G-6-PD-deficients and controls (9.7% and 9.9%). In contrast, in the G-6-PD-deficient neonates, those with the heterozygous or homozygous variant UDPGT1 genotype had a higher incidence of hyperbilirubinemia than corresponding controls (heterozygotes: 31.6% vs. 6.7%, P < 0.0001; variant homozygotes: 50% vs. 14.7%, P = 0.02). Among G-6-PD-deficient infants the incidence of hyperbilirubinemia was greater in those with the heterozygous (31.6%, P = 0.006) or variant homozygous (50%, P = 0.003) UDPGT1 genotype than in normal homozygotes. In contrast, among those normal for G-6-PD, the UDPGT1 polymorphism had no significant effect (heterozygotes: 6.7%; variant homozygotes: 14.7%). Thus, neither G-6-PD deficiency nor the variant UDPGT1 promoter, alone, increased the incidence of hyperbilirubinemia, but both in combination did. This gene interaction may serve as a paradigm of the interaction of benign genetic polymorphisms in the causation of disease.

Cohort Studies↗
PubMed1997

Decision-making in the critically ill neonate: cultural background v individual life experiences.

OBJECTIVES: In treating critically ill neonates, situations occasionally arise in which aggressive medical treatment prolongs the inevitable death rather than prolonging life. Decisions as to limitation of neonatal medical intervention remain controversial and the primary responsibility of the generally unprepared family. This research was designed to study response patterns of expectant mothers towards treatment of critically ill and/or malformed infants. DESIGN/SETTING: Attitudes were studied via comprehensive questionnaires divided into three sections: 1-Sociodemographic data and prior personal experience with perinatal problems; 2-Theoretical philosophical principles used in making medical ethical decisions; and 3-Hypothetical case scenarios with choices of treatment options. SUBJECTS AND RESULTS: Six hundred and fifty pregnant women were studied. Maternal birthplace (p = 0.005) and level of religious observance (p = 0.02) were strongly associated with the desire for maximally aggressive medical intervention in the hypothetical case scenario. Specific personal experiences such as infertility problems, previous children with serious mental or physical problems were not correlated with the selection of different treatment choices. Of the theoretical principles studied, only the desire to preserve life at all costs was significantly associated with the choice for maximal medical treatment (p = 0.003). CONCLUSIONS: Maternal ethnocultural background and philosophical principles more profoundly influenced medical ethical decision-making than did specific personal life experiences.

Adult↗
PubMed1996

Conjugated bilirubin in neonates with glucose-6-phosphate dehydrogenase deficiency.

We used a system capable of measuring conjugated bilirubin and its monoconjugated and diconjugated fractions in serum to assess bilirubin conjugation in 29 glucose-6-phosphate dehydrogenase (G6PD)-deficient, term, male newborn infants and 35 control subjects; all had serum bilirubin levels > or = 256 mumol/L (15 mg/dI). The median value for diconjugated bilirubin was lower in the G6PD-deficient neonates than in control subjects (0.06 (range 0.00 to 1.84) vs 0.21 (range 0.00 to 1.02) mumol/L, p = 0.006). Diglucuronide was undetectable in 11 (38.9%) of the G6PD-deficient infants versus 3 (8.6%) of the control subjects (p = 0.015). These findings imply a partial defect of bilirubin conjugation not previously demonstrated in G6PD-deficient newborn infants.

Bilirubin↗
PubMed1996

Contribution of haemolysis to jaundice in Sephardic Jewish glucose-6-phosphate dehydrogenase deficient neonates.

We determined the contribution of haemolysis to the development of hyperbilirubinaemia in glucose-6-phosphate dehydrogenase (G-6-PD) deficient neonates and G-6-PD normal controls. Blood carboxyhaemoglobin (COHb), sampled on the third day of life, was measured by gas chromatography, corrected for inhaled carbon monoxide (COHbC), and expressed as a percentage of total haemoglobin concentration (Hb). Serum bilirubin was tested as clinically necessary. 37 non-jaundiced (peak serum total bilirubin (PSTB) < or = 255 mumol/l) and 20 jaundiced (PSTB > or = 257 mumol/l) G-6-PD-deficient neonates were compared to 31 non-jaundiced and 24 jaundiced controls with comparable PSTB values, respectively. COHbC values for the entire G-6-PD deficient group were higher than in the controls (0.75 +/- 0.17% v 0.62 +/- 0.19%, P < 0.001). COHbC and PSTB values did not correlate in the G-6-PD-deficient group (r = 0.15, P > 0.05) but did in the controls (r = 0.58, P < 0.001). COHbC values were increased to a similar extent in the G-6-PD-deficient, non-jaundiced (0.72 +/- 0.16%), the G-6-PD-deficient, jaundiced (0.80 +/- 0.19%) and the control, jaundiced (0.75 +/- 0.18%) subgroups, compared to the control, non-jaundiced subgroup (0.53 +/- 0.13%) (P < 0.05). Although present in G-6-PD deficient neonates, increased haemolysis was not directly related to the PSTB.

Carbon Monoxide↗
PubMed1996

Intravenous immune globulin in neonatal immune hemolytic disease: does it reduce hemolysis?

We studied the effect of intravenous immune globulin (IVIG) on hemolysis in term, hyperbilirubinemic, Coomb's positive infants utilizing measurement of carboxyhemoglobin fraction corrected for inhaled carbon monoxide (COHbc), a sensitive indicator of hemolysis. COHbc values were determined before and after IVIG infusion. In those babies who responded with a decrease in serum total bilirubin (n = 19), no exchange transfusions were required and COHbc levels decreased significantly by 24 h post-IVIG from 1.37 +/- 0.31 to 1.12 +/- 0.26% tHb (p < 0.0001). There were no corresponding decreases in COHbc levels (1.989 +/- 0.54 to 1.82 +/- 0.48% tHb; p > 0.05) among those whose serum bilirubin levels did not decrease in response in to IVIG (n = 7), and all of these infants required exchange transfusions. Furthermore, the extent of the decrease in COHbc was related to the degree of decrease in serum bilirubin levels, such that the percentage decrease of bilirubin at 24 h was directly correlated with the percentage decrease of COHbc at 24 h (p = 0.007). We conclude that IVIG, when successful, inhibits hemolysis in these infants.

Erythroblastosis, Fetal↗
PubMed1996

Intravenous immune globulin in neonatal ABO isoimmunization: factors associated with clinical efficacy.

OBJECTIVE: Intravenous immune globulin (IVIG) reduces jaundice in many but not all cases of neonatal isoimmunization. We sought to elucidate the type of infant most likely to benefit from IVIG administration by attempting to define pretreatment parameters associated with both clinical symptomatology and therapeutic responsiveness to IVIG. METHODS: Term, healthy Coombs-positive infants were studied prospectively. IVIG was administered if, despite phototherapy, serum bilirubin reached > or = 222 mumol/l (13 mg/dl) at < or = 24 h of age and/or > or = 274 mumol/l (16 mg/dl) at > 24 h of age. Clinical data including serial serum total bilirubin levels, rate of bilirubin rise on day 1 of life, serial corrected carboxyhemoglobin levels (a sensitive indicator of hemolysis) and total hemoglobin (tHb) levels were collected. RESULTS: Infants were classified as IVIG responders (n = 18), those in whom total serum bilirubin levels either remained stable or decreased following IVIG administration; IVIG nonresponders (n = 5), those who developed a total serum bilirubin of > or = 2 mg/dl greater than pre-IVIG bilirubin levels within the first 24 h after IVIG administration, or nontreated, those not meeting IVIG treatment criteria (n = 13). Four of the five nonresponders proceeded to require exchange transfusion vs. none of the others (p < 0.001). Four of the five nonresponders had a pretreatment rate of bilirubin rise of > or = 1 mg/dl/h as compared with only 1 of 18 responders and none of the nontreated (p < 0.001). Pretreatment tHb levels were also different (13.2 +/- 1.3 vs. 15.5 +/- 2.3 vs. 17.7 +/- 2.4 g/dl for nonresponders vs. responders vs. nontreated infants, respectively; p < 0.005). The highest pretreatment COHbc levels were seen in the nonresponders (1.8 +/- 0.7 vs. 1.4 +/- 0.3 vs. 0.9 +/- 0.3% tHb, respectively). CONCLUSIONS: Our 3 groups represent a spectrum of hemolysis, ranging from severe to moderate to mild. This spectrum appears to relate not only to the severity of hemolysis, but also to the therapeutic responsiveness to IVIG. We speculate that some or all of the factors identified can be used prospectively to predict the subsequent clinical course of ABO-incompatible infants and to facilitate optimal management.

ABO Blood-Group System↗
PubMed1995

Oxygen saturation during and after feeding in healthy term infants.

In instrumented infants, 'normal' feeding occasionally causes respiratory changes, however, the extent of 'acceptable' oxygen desaturation is undocumented. We studied O2 saturation in healthy full-term neonates under totally natural feeding conditions unencumbered by any mechanical devices. Infants' O2 saturation was monitored continuously for 10 min of nutritive sucking and for 5 min after feeding. Twenty-one infants were studied, including 11 breast- and 10 bottle-fed infants. The distribution of saturation measurements was calculated and compared during feed vs. postfeed periods for both groups of infants. None of the infants had decreased saturation with feeding when compared to the prefeeding baseline. However, most of the infants in both groups did experience significantly lower O2 saturations after than during feeding (18 and 29% of the postfeed readings were < 90% in breast- and bottle-fed infants). Mean O2 saturations dropped from 96 +/- 2% (during feed) to 93 +/- 2% (postfeed) in breast-fed and from 95 +/- 2% (during feed) to 92 +/- 4% (postfeed) in bottle-fed infants. These findings elucidate the physiology of normal infant feeding and should be taken into account when monitoring term infants with oxygen saturation.

Blood Gas Monitoring, Transcutaneous↗
PubMed1995

Patent ductus arteriosus. Clinical relevance of prostaglandins and prostaglandin inhibitors in PDA pathophysiology and treatment.

This article presents a comprehensive review of the patent ductus arteriosus which so often affects the premature neonate. Included are a discussion of the unique anatomy and physiology of the ductus, a review of the mechanisms involved in normal closure, and factors leading to persistent patency. Various therapeutic options also are discussed, including some new and innovative approaches.

Ductus Arteriosus↗
PubMed1995

Continuous versus multiple rapid infusions of indomethacin: effects on cerebral blood flow velocity.

OBJECTIVE: Therapeutic administration of indomethacin for patent ductus arteriosus (PDA) closure has been documented to decrease cerebral blood flow velocity which may be harmful to the vulnerable premature neonate. We have therefore compared the effects of administering indomethacin by rapid injection versus slow, continuous indomethacin infusion at the same total therapeutic dose on middle cerebral artery (MCA) systolic and diastolic flow velocity, resistance index, and cerebral blood flow (as reflected by the integrated area under the curve). METHODS: Premature neonates (< 1750 g) documented echocardiographically to have a PDA were randomized to receive indomethacin either by three rapid injection doses or by continuous intravenous infusion over the ensuing 36 hours, providing an equivalent total dose. Echocardiograms and transcranial color flow mapping of the MCA flow velocity were measured at baseline and serially following initiation of therapy in both groups. Effects on cerebral blood flow velocity are presented. RESULTS: Eighteen infants [rapid injection-1.2 +/- 0.3 kg (n = 9) and continuous-1.1 +/- 0.2 kg (n = 9)] were studied. In the rapid injection treated infants decreased flow velocity in the MCA as manifested by abrupt, significant decreases in systolic (to 70 +/- 8% baseline) and diastolic (to 65 +/- 13% baseline) flow velocity and area under the curve (to 60 +/- 10% of baseline) were evident by 4 minutes and progressed to 30 minutes after treatment initiation. These changes were not observed in the group treated with continuous indomethacin. Both therapeutic modalities were equally successful in closing the ductus, although the numbers are too small to definitively determine therapeutic efficacy. CONCLUSIONS: Slow, continuous infusion eliminated the decrease in cerebral flow velocity and appears to be effective in closing the PDA.

Blood Flow Velocity↗
PubMed1994

Asphyxia-related infant mortality rates.

We present an epidemiological study of asphyxia-related infant mortality. Via linkage of birth and death certificates, infant mortality data were analyzed for all infants born in Israel from 1985 through 1988. During this period, there were 397,083 live births in Israel, and 4392 infants subsequently died within the first year of life (total infant death rate of 11.1/1000 live births). Of the deaths, 176 (4.0%) were associated with a diagnosis of perinatal asphyxia, resulting in an overall asphyxia-related infant mortality rate of 0.44/1000 live births. The percent of deaths attributable to asphyxia was calculated by birthweight, maternal age, and birth order and was compared with overall infant mortality rates analyzed for the same variables. Interesting results include the following: (1) Asphyxia-related mortality within the low birthweight group was proportional to overall birthweight-specific mortality for that group; (2) birthweight more than 4.5 kg disproportionately increased the risk of asphyxia-related mortality; and (3) perinatal asphyxia did not add to the risk of mortality subsequent to teenage pregnancy.

Adolescent↗
PubMed1994

Neonatal screening for glucose-6-phosphate dehydrogenase deficiency: sex distribution.

Eight hundred and six newborn infants at high risk for glucose-6-phosphate dehydrogenase (G-6-PD) deficiency were screened; 30.2% of the boys and 10.4% of the girls had severe G-6-PD deficiency. Surprisingly, 14% of the enzyme deficient girls had a father from a low risk ethnic group. Girls of high risk mothers should be screened for G-6-PD deficiency regardless of paternal origin.

Fathers↗
PubMed1994

Influence of disease state on oxygen transport in newborn piglets.

Optimally, oxygen delivery (DO2) should be sufficient to provide for adequate oxygen consumption (VO2) while avoiding O2 toxicity. Physiologically a critical level of DO2 has been described, below which decreases in oxygen supply begin to impair VO2, leading to venous hypercarbia and tissue acidosis. We predicted that this critical level would be influenced by factors such as underlying disease state and oxygen needs. Newborn piglets were exposed either to hypoxia (n = 6) or to group-B beta-hemolytic streptococcal sepsis (n = 6). Hemodynamic parameters were measured; DO2 and VO2 were calculated and compared within and between the groups. 'Critical DO2' was defined as the point at which decreases in DO2 began to produce concomitant decreases in VO2. This was observed at 9 ml/kg/min in hypoxic vs. 21 ml/kg/min in septic piglets. The 'critical Vsat' was defined as the venous O2 saturation beyond which tissue acidosis, as defined by base excess, developed. 'Critical VsatS' were 17% for hypoxic vs. 21% for septic animals. In summary, septic newborn piglets had higher critical DO2 and critical Vsat than hypoxic piglets, implying that they became oxygen supply dependent and developed tissue acidosis at higher levels of DO2 and Vsat, respectively.

Animals↗