Cathy Hammerman - Academia.edu (original) (raw)

Papers by Cathy Hammerman

Archives of Disease in Childhood - Fetal and Neonatal Edition, 2006

Pediatric Research, 1984

Myoinositol (INO) may potentiate hormone-induced lung maturation & increase surfactant in lung da... more Myoinositol (INO) may potentiate hormone-induced lung maturation & increase surfactant in lung damage (Ped Re • 17 , 378A,-83; Life Sci 31, 175,-82). Serum INO is high in RDS at birth. INO decreases after bi r th , in part because the diet may contain only

Pediatric Research, 1984

Pediatric Cardiology, 1986

Pretreatment plasma dilator prostaglandin levels were measured in 16 premature infants with paten... more Pretreatment plasma dilator prostaglandin levels were measured in 16 premature infants with patent ductus arteriosus in an attempt to correlate abnormally elevated levels with clinical responsiveness to indomethacin therapy. Nine of the 16 infants responded well to indomethacin, with complete disappearance of their murmurs by 48 h. Eight of these nine infants had elevated baseline 6 keto PGF Ia levels (>500 pg/ml). In contrast, seven of the 16 infants did not respond to indomethacin, and six of these had 6 keto PGFI a within the normal range (<500 pg/ml). PGE2 levels varied in the same general direction, but lacked the specificity and sensitivity of the 6 keto PGF Ia levels. Thus, 6 keto PGFIa levels seem to correlate with, and may eventually be helpful in predicting, clinical indomethacin responsiveness in the premature neonate with patency of the ductus arteriosus .

Pediatric Cardiology, 1986

Prophylactic closure of the patent ductus arteriosus has been recommended as a means of decreasin... more Prophylactic closure of the patent ductus arteriosus has been recommended as a means of decreasing the morbidity of the very low birth weight neonate. This study was undertaken in order to determine potential risk factors involved in the development of the silent ductus, its impact upon both the early cardiorespiratory symptomatology and the subsequent morbidity of the premature neonate, and finally the potential benefit to be derived from prophylatic closure in this presymptomatic stage. Infants with birth weights of 1000 g or less were studied on days 2-3 of life echocardiographically, clinically, and with determination of plasma dilator prostaglandin levels. On entry to the study, those infants with early evidence of silent left-to-right patent ductus arteriosus (PDA) shunting were randomized to receive either prophylactic indomethacin or placebo therapy. Those infants with no evidence of ductal shunting were not treated at all. Infants with silent PDAs had elevated levels of the dilator prostaglandin metabolite 6-keto PGFj,~ on admission, although they had no echocardiographic abnormalities. No other risk factors for PDA development could be identified. Silent PDA infants had an increased incidence of subsequent symptomatic PDAs, and overall morbidity and mortality when compared with those with no evidence of PDA (silent or symptomatic). Prophylactic ductai closure decreased the incidence of subsequent PDA development, but had no effect on overall morbidity and/or mortality.

Archives of disease in childhood. Fetal and neonatal edition, Jan 17, 2015

We performed a systematic review and meta-analysis of all the available evidence to assess the ef... more We performed a systematic review and meta-analysis of all the available evidence to assess the efficacy and safety of paracetamol for the treatment of patent ductus arteriosus (PDA) in neonates, and to explore the effects of clinical variables on the risk of closure. MEDLINE, Scopus and ISI Web of Knowledge databases, using the following medical subject headings and terms: paracetamol, acetaminophen and patent ductus arteriosus. Electronic and manual screening of conference abstracts from international meetings of relevant organisations. Manual search of the reference lists of all eligible articles. Studies comparing paracetamol versus ibuprofen, indomethacin, placebo or no intervention for the treatment of PDA. Data regarding efficacy and safety were collected and analysed. Sixteen studies were included: 2 randomised controlled trials (RCTs) and 14 uncontrolled studies. Quality of selected studies is poor. A meta-analysis of RCTs does not demonstrate any difference in the risk of d...

Clinical Chemistry, 1998

intravenous sites where furosemide has been administered, because contamination of the sample by ... more intravenous sites where furosemide has been administered, because contamination of the sample by even small volumes of furosemide significantly affected thyroxine results. The differences in sensitivity to furosemide interference among assays appear to reflect the serum dilution used in each method. This concern may apply to interference from other drugs (e.g., salicylates and fenclofenac) as well as to other assays (e.g., free triiodothyronine). This study does not address the in vivo effect of furosemide administration on thyroxine measurement. Because oral furosemide may influence measurement of the free thyroxine index (4), the time interval between doses of oral furosemide and blood sampling should be considered in result interpretation. Both the Vitros and AxSYM assays use sample volume:total volume ratios greater than the ratio (0.09) used by the assay in that study (4). Thus, it is likely that the in vivo effect from oral furosemide will be even greater in the Vitros and AxSYM assay systems. Furosemide concentrations of 6.6-73.0 mol/L reported with routine therapeutic doses of furosemide (5) fall within the range of furosemide concentrations examined here. Clinicians thus may need greater awareness to potential interference from drugs such as furosemide when interpreting results from newer free thyroxine assays that use large sample volume:total volume ratios. TSH measurement may be a more useful test for assessing thyroid function in such cases.

The Journal of Pediatrics, 2015

Objective To evaluate the frequency of glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, the... more Objective To evaluate the frequency of glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, the incidence of clinically significant jaundice (any serum total bilirubin value >75th percentile on the hour-specific bilirubin nomogram), and the need for phototherapy in the pooled male Israeli-Arab and Palestinian-Arab population born at the Shaare Zedek Medical Center in Jerusalem, Israel. Study design Quantitative G-6-PD enzyme testing of umbilical cord blood was performed during birth hospitalization. G-6-PD deficiency was defined as any G-6-PD value <7.0 U/gHb. Transcutaneous bilirubin was performed daily during birth hospitalization, with serum total bilirubin testing in those with a transcutaneous bilirubin value >75th percentile. Results Ten of 286 (3.5%) consecutively delivered male Arab newborns had G-6-PD deficiency. Clinically significant jaundice was higher in the population with G-6-PD deficiency compared with normal controls (relative risk, 3.45; 95% CI, 1.24-9.58). Thirty percent of the newborns with G-6-PD deficiency met American Academy of Pediatrics indications for phototherapy according to the high-risk (middle) curve on the phototherapy graph.

The Journal of Maternal-Fetal & Neonatal Medicine, 2014

A: Donor blood glucose-6-phosphate dehydrogenase deficiency reduces the efficacy of exchange tran... more A: Donor blood glucose-6-phosphate dehydrogenase deficiency reduces the efficacy of exchange transfusion in neonatal hyperbilirubinemia. Pediatrics 123, E96-E100 (2009). Intravascular hemolysis following transfusion with glucose-6-phosphate dehydrogenase (G-6-PD)-deficient blood has been documented, although it is not routine to screen donor blood for this condition prior to exchange transfusion. Samanta et al. studied the effect of exchange transfusion with G-6-PD-deficient donor blood on neonates with moderate hyperbilirubinemia to determine the effectiveness of the exchange, postexchange serum total bilirubin levels, the duration of phototherapy and the need for repeat exchange transfusion. A total of 21 newborns were exchanged with G-6-PD-deficient donor blood and 114 with G-6-PD normal blood. Although the percentage decrease in serum total bilirubin from pre-exchange values immediately following the exchange was similar between the groups, during the postexchange period the percentage decrease became less in those exchanged with G-6-PDdeficient blood. Similarly, the duration of postexchange phototherapy and the number of babies requiring repeat exchange transfusion, were higher in those transfused with G-6-PD-deficient blood.

Pediatrics international : official journal of the Japan Pediatric Society, 2013

We read the meta-analysis by Long et al. in which the association between neonatal hyperbilirubin... more We read the meta-analysis by Long et al. in which the association between neonatal hyperbilirubinemia and UDPglucuronosyltransferase (UGT) 1A1 gene polymorphisms was analyzed, with great interest. 1 We were particularly surprised by the authors' conclusion that UGT1A1 TATA promoter polymorphisms were not associated with an increased risk of neonatal hyperbilirubinemia in Asian subjects and that results from Caucasian populations were conflicting. Our surprise emanates from the non-inclusion in the meta-analysis of a study in which the interaction between glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and UGT1A1 (TA)6/(TA)7 heterozygosity or (TA)7/(TA)7 homozygosity led to a dramatic and significant increase in the incidence of neonatal hyperbilirubinemia. 2 In that study, hyperbilirubinemia was defined as serum total bilirubin (STB) Ն15.0 mg/dL (257 mmol/L) during the first week of life. DNA from term neonates born to Sephardic Jewish mothers was analyzed for the UGT1A1 TATA promoter polymorphism and for the G-6-PD Mediterranean mutation. The variant (TA)7 promoter allele frequency was similar among G-6-PDdeficient (n = 131) and normal neonates (n = 240). Overall, 30 G-6-PD-deficient neonates (22.9%) developed hyperbilirubinemia versus 22 normal neonates (9.2%; P = 0.0005). Among those normal for G-6-PD, the UGT1A1 polymorphism had no significant effect on the incidence of hyperbilirubinemia (normal homozygotes, 9.9%; heterozygotes, 6.7%; variant homozygotes, 14.7%, NS). Furthermore, of those with the normal homozygous

Pediatrics, 2014

We recently demonstrated that direct antiglobulin titer (DAT) positive, blood group A or B newbor... more We recently demonstrated that direct antiglobulin titer (DAT) positive, blood group A or B newborns born to group O mothers had a high incidence of hyperbilirubinemia, attributable to increased hemolysis. We reanalyzed our data asking whether increasing DAT strength plays a modulating role in the pathophysiology of the hemolysis and hyperbilirubinemia. Data from previously published DAT-positive, ABO-heterospecific neonates were analyzed for hyperbilirubinemia and hemolysis according to strength of DAT. DAT was measured by using a gel agglutination technique and reported as values ranging from DAT ± to DAT ++++. Hemolysis was evaluated by blood carboxyhemoglobin corrected for inspired, ambient CO (COHbc), and expressed as percent total hemoglobin (tHb). Hyperbilirubinemia was defined as any plasma total bilirubin value >95th percentile on the hour-specific nomogram. Hyperbilirubinemia was more prevalent in those with DAT ++ readings (16 of 20, 80%) than those both DAT ± (37 of 87...

Proceedings of the National Academy of Sciences, 1997

Severe jaundice leading to kernicterus or death in the newborn is the most devastating consequenc... more 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 μmol/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 ...

Postgraduate Medical Journal, 1995

Meningitis is common in neurosarcoidosis.2'3 The CSF always exhibits lymphocytic pleiocytosis, th... more Meningitis is common in neurosarcoidosis.2'3 The CSF always exhibits lymphocytic pleiocytosis, the lowest proportion of lymphocytes reported being 68%.2 A low glucose level is also usual, the lowest CSF level of glucose reported being 18 mg/dl.3 In our case, lymphocytes were not predominant, the polymorph reaction was strong, and the level of CSF glucose was the lowest ever reported. Consequently, neurosarcoidosis must be added to the list of aetiologies of meningitis with neutrophilic pleiocytosis.

Pediatrics, 2012

OBJECTIVE: Predischarge bilirubin screening predicts neonatal hyperbilirubinemia. We evaluated th... more OBJECTIVE: Predischarge bilirubin screening predicts neonatal hyperbilirubinemia. We evaluated the incidence of false-negative bilirubin screening among readmissions for hyperbilirubinemia. METHODS: In healthy term and late preterm, predominantly breastfeeding newborns, predischarge transcutaneous bilirubin values were plotted on the hour of life–specific bilirubin nomogram and confirmed with plasma total bilirubin in those with a transcutaneous reading ≥75th percentile, or between the 41st and 75th percentiles in the presence of predictive icterogenic risk factors. False-negative bilirubin screen was defined as a predischarge bilirubin value ≤75th percentile in a newborn who was subsequently readmitted for phototherapy. RESULTS: Of a total of 25 439 neonates born between 2008 and 2009, 143 (0.56%) were readmitted with a mean plasma total bilirubin of 18.7 ± 1.7 mg/dL at 125 ± 54 hours. False-negative predischarge bilirubin screen was identified in 46 (32.2%). Of these, 6 (4.2%) wer...

Pediatrics, 2011

Standard pharmacologic closure of the patent ductus arteriosus currently involves the administrat... more Standard pharmacologic closure of the patent ductus arteriosus currently involves the administration of 1 of 2 cyclooxygenase inhibitors: either indomethacin or ibuprofen. However, both of these drugs can be associated with potentially significant adverse effects. We present here the cases of 5 preterm infants (gestational age: 26–32 weeks; postnatal age: 3–35 days) with large, hemodynamically significant patent ductus arteriosus who had either failed or had contraindications to ibuprofen therapy. Each of these infants was treated with off-label oral paracetamol (15 mg/kg per dose every 6 hours). Ductal closure was achieved within 48 hours in all the treated infants. No toxicity was observed.

Pediatrics, 2002

Objective. The objective of this study was to evaluate the roles of production and conjugation of... more Objective. The objective of this study was to evaluate the roles of production and conjugation of bilirubin, individually and in combination, in the mechanism of neonatal jaundice. Methods. A cohort of healthy, term male newborns was sampled on the third day of life, coincident with routine metabolic screening, for blood carboxyhemoglobin determination, a reflection of heme catabolism, and for serum unconjugated and conjugated bilirubin fractions, reflecting bilirubin conjugation. The former was determined by gas chromatography, corrected for inspired CO (COHbc), and expressed as percentage of total hemoglobin. Serum bilirubin fractions were quantified by alkaline methanolysis and reverse phase high performance liquid chromatography. The sum of all bilirubin fractions comprised serum total bilirubin (STB). Total conjugated bilirubin (TCB) was comprised of the sum of the conjugated fractions and was expressed as percentage of STB (TCB[%]). A “bilirubin production/conjugation index” (...

Pediatrics, 2004

Background. Although glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is prevalent in Africa... more Background. Although glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is prevalent in African Americans, their risk of associated neonatal hyperbilirubinemia has not been prospectively studied.Objective. To compare hemolysis and the risk of hyperbilirubinemia among African American, G-6-PD-deficient neonates (study group) and G-6-PD-normal control subjects.Methods. Consecutive, healthy, term and near-term, male neonates born to African American mothers comprised the patient cohort. G-6-PD testing was performed with umbilical cord blood samples. Routine management included measurement of the end tidal carbon monoxide level corrected for ambient carbon monoxide level (ETCOc) within 4 hours after delivery (assessment of hemolysis), ≥1 predischarge bilirubin determination, and additional bilirubin testing as clinically indicated. Indications for phototherapy were identical for study patients and control subjects. Neonates were monitored for the first 1 week of life. ETCOc results, ...

Pediatric Research, 2008

Nigerian neonates have a high incidence of bilirubin encephalopathy. Glucose-6-phosphate dehydrog... more Nigerian neonates have a high incidence of bilirubin encephalopathy. Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is prevalent in this population. (TA) 7 promoter polymorphism in the gene encoding the bilirubin conjugating enzyme UDP-glucuronosyltransferase 1A1 (UGT1A1) potentiates hyperbilirubinemia in G-6-PD deficient neonates. We studied (TA) n allele frequency to determine, at least in part, its contribution to the frequency and severity of hyperbilirubinemia. DNA was extracted from umbilical cord blood of sequentially born Nigerian neonates and the (TA) n UGT1A1 promoter sequence determined. The (TA) n allele distribution was compared with reported adults of varying African ancestry and Sephardic Jewish neonates. Among 88 Nigerian neonates, (TA) 6 and (TA) 7 alleles were almost equally distributed (0.46 and 0.43, respectively). Some individuals with (TA) 5 and (TA) 8 sequences were encountered. Allele distribution was similar to that of the African ancestry population but differed from the Sephardic Jewish newborns, in whom the (TA) 6 /(TA) 7 distribution was 0.65/ 0.35. Whereas 45% of Nigerian alleles and 50% of African ancestry alleles, respectively, included a (TA) 7 or (TA) 8 sequence, only 35% of Jewish alleles were (TA) 7 (p Ͻ 0.001), and no (TA) 8 alleles were encountered. The high frequency of (TA) n promoter polymorphism, coupled with G-6-PD deficiency, may contribute to the pathogenesis of extreme neonatal hyperbilirubinemia in Nigeria.

Pediatric Research, 2001

The objective was to compare the contribution to perinatal bilirubinemia of hemolysis and UDP-glu... more The objective was to compare the contribution to perinatal bilirubinemia of hemolysis and UDP-glucuronosyltransferase (UGT) gene promoter polymorphism, seen in Gilbert's syndrome, between glucose-6-phosphate dehydrogenase (G-6-PD)deficient and-normal neonates. Serum total bilirubin (STB) values from 52 G-6-PD-deficient and 166 G-6-PD-normal term, male neonates, sampled within 3 h of delivery (first sample) and on d 3 (second sample), were analyzed in relation to blood carboxyhemoglobin corrected for inspired CO (COHbc), an accurate index of hemolysis, and UGT promoter genotype. COHbc values (% total Hb) were greater in G-6-PD-deficient neonates than controls: first sample 1.00 Ϯ 0.25% versus 0.84 Ϯ 0.24%, p Ͻ 0.0001; second sample 0.83 Ϯ 0.20% versus 0.76 Ϯ 0.19%, p ϭ 0.002. First sample COHbc and STB values did not correlate in either the G-6-PD-deficient or control groups, whereas second sample COHbc values correlated significantly with corresponding STB values in the control population only (r ϭ 0.28, p ϭ 0.0007). At second sampling, there was a higher allele frequency of the variant UGT promoter among those with STB values Ն75 th percentile than those Ͻ75 th among the G-6-PD-deficient neonates (0.60 versus 0.33, respectively, p ϭ 0.025), but not controls (0.31 versus 0.40, respectively, p ϭ 0.24). Among those infants with at least one variant UGT promoter allele, STB values were higher in the G-6-PD-deficient neonates than controls at second sampling only (181 Ϯ 56 M versus 149 Ϯ 46 M, respectively, p ϭ 0.03). Both within and between the G-6-PDdeficient and control groups, our data demonstrate changing and differing contributions of hemolysis and UGT promoter polymorphism to bilirubinemia during the first 3 d of life. (Pediatr Res 50: 532-537, 2001) Abbreviations: COHb, carboxyhemoglobin COHbc, carboxyhemoglobin corrected for inspired carbon monoxide G-6-PD, glucose-6-phosphate dehydrogenase RBC, red blood cell STB, serum total bilirubin tHb, total Hb UGT, UDP-glucuronosyltransferase 1A1

Archives of Disease in Childhood - Fetal and Neonatal Edition, 2006

Pediatric Research, 1984

Pediatric Cardiology, 1986

Archives of disease in childhood. Fetal and neonatal edition, Jan 17, 2015

Clinical Chemistry, 1998

The Journal of Pediatrics, 2015

The Journal of Maternal-Fetal & Neonatal Medicine, 2014

Pediatrics international : official journal of the Japan Pediatric Society, 2013

Pediatrics, 2014

Proceedings of the National Academy of Sciences, 1997

Postgraduate Medical Journal, 1995

Pediatrics, 2012

Pediatrics, 2011

Pediatrics, 2002

Pediatrics, 2004

Pediatric Research, 2008

Pediatric Research, 2001