{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T05:41:48Z","timestamp":1774330908343,"version":"3.50.1"},"reference-count":20,"publisher":"American Academy of Pediatrics (AAP)","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1998,5,1]]},"abstract":"<jats:p>Background. \u2009Hyperbilirubinemia in new-borns with glucose-6-phosphate dehydrogenase (G6PD) deficiency is a serious clinical problem because of the severity and unpredictability of its course. An innovative approach to this problem is suggested by previous experience with Sn-mesoporphyrin (SnMP), a potent inhibitor of bilirubin production, in moderating neonatal hyperbilirubinemia caused by ABO incompatibility, immaturity, and unspecified mechanisms.<\/jats:p><jats:p>Objective.\u2003To compare the effectiveness of the preventive and therapeutic uses of SnMP in ameliorating the course of bilirubinemia of G6PD-deficient neonates.<\/jats:p><jats:p>Methods.\u2003Neonates born at the Metera Maternity Hospital, Athens, Greece, and found to be G6PD-deficient by cord blood testing were stratified by sex and gestational age (210\u2013265 days and &amp;gt;265 days) and randomized in pairs to receive SnMP (6 \u03bcmol\/kg birth weight, intramuscularly) either on the first day of life (preventive use) or if and when the plasma bilirubin concentration (PBC) level reached an age-specific threshold level for intervention (therapeutic use). In the case of failure of SnMP to control the rise of PBC levels, the protocol defined precisely the threshold PBC levels for switchover to phototherapy (PT) and, if necessary, exchange transfusion. PBC was measured daily until a declining value was obtained and the case was closed.<\/jats:p><jats:p>Results.\u2003A total of 86 G6PD-deficient neonates were randomized: 42 in the preventive arm and 44 in the therapeutic arm. Of the latter, 20 (45%) reached PBC levels requiring therapeutic intervention and thus received SnMP. Regardless of the trial arm, none of the 86 neonates required PT, whereas in a previous study in the same population, 33% of G6PD-deficient neonates required PT. In the intrapair sequential analysis, the favored arm was decided on the criterion of the age at closure of the case being shorter by at least 1 day. After plotting 30 untied pairs in the sequential analysis graph, the preventive use of SnMP proved to be the favored arm, and the trial was stopped. At this point, there were 2 unpaired neonates, 12 tied pairs, 22 pairs in which the preventive use of SnMP was favored and 8 pairs in which the therapeutic use of SnMP was favored. In the group analysis, infants in the preventive group, compared with those in the therapeutic group, had a lower maximum PBC level (8.2 \u00b1 3.1 and 10.9 \u00b1 2.8 mg\/dL, respectively), which was reached at an earlier age (63.5 \u00b1 34.8 and 82.2 \u00b1 24.7 hours, respectively) as well as a lower closing PBC level (7.2 \u00b1 2.9 and 9.6 \u00b1 2.5 mg\/dL, respectively) and an earlier age at closing (89.1 \u00b1 35.6 and 110.8 \u00b1 23.6 hours, respectively). Moreover, a PBC level of \u22658.0 mg\/dL, a level at which jaundice is clearly visible, was not reached by 52% of the neonates in the preventive arm and 16% of the neonates in the therapeutic arm.<\/jats:p><jats:p>Conclusions.\u2003In G6PD-deficient neonates, a single dose of SnMP administered preventively or therapeutically entirely supplanted the need for PT to control hyperbilirubinemia. The preventive use of SnMP offers practical advantages in populations with a high enough prevalence of G6PD deficiency to justify cord blood screening.<\/jats:p>","DOI":"10.1542\/peds.101.5.e1","type":"journal-article","created":{"date-parts":[[2004,8,13]],"date-time":"2004-08-13T23:44:32Z","timestamp":1092440672000},"page":"e1-e1","source":"Crossref","is-referenced-by-count":45,"title":["Control of Hyperbilirubinemia in Glucose-6-Phosphate Dehydrogenase-deficient Newborns Using an Inhibitor of Bilirubin Production, Sn-Mesoporphyrin"],"prefix":"10.1542","volume":"101","author":[{"given":"Timos","family":"Valaes","sequence":"first","affiliation":[{"name":"Metera Maternity Hospital, Athens, Greece; and"},{"name":"New England Medical Center, Boston, Massachusetts."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"George S.","family":"Drummond","sequence":"additional","affiliation":[{"name":"From Rockefeller University Hospital, New York, New York;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Attallah","family":"Kappas","sequence":"additional","affiliation":[{"name":"From Rockefeller University Hospital, New York, New York;"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"417","published-online":{"date-parts":[[1998,5,1]]},"reference":[{"key":"2021121010114812200_B1","doi-asserted-by":"crossref","first-page":"297","DOI":"10.1016\/S0140-6736(61)91476-3","article-title":"Glucose-6-phosphate dehydrogenase deficiency: a new aetiological factor of severe neonatal jaundice.","volume":"1","author":"Doxiadis","year":"1961","journal-title":"Lancet."},{"key":"2021121010114812200_B2","doi-asserted-by":"crossref","first-page":"545","DOI":"10.1136\/adc.39.208.545","article-title":"The clinical picture of glucose-6-phosphate dehydrogenase deficiency in early infancy.","volume":"39","author":"Doxiadis","year":"1964","journal-title":"Arch Dis Child."},{"key":"2021121010114812200_B3","doi-asserted-by":"crossref","first-page":"448","DOI":"10.1203\/00006450-196909000-00008","article-title":"Incidence and mechanism of neonatal jaundice related to G-6-PD deficiency.","volume":"3","author":"Valaes","year":"1969","journal-title":"Pediatr Res."},{"key":"2021121010114812200_B4"},{"key":"2021121010114812200_B5"},{"key":"2021121010114812200_B6","doi-asserted-by":"crossref","first-page":"273","DOI":"10.1111\/j.1651-2227.1996.tb14013.x","article-title":"The impact of phototherapy in the management of neonatal hyperbilirubinemia: comparison of historical cohorts.","volume":"85","author":"Valaes","year":"1996","journal-title":"Acta Paediatr."},{"key":"2021121010114812200_B7","doi-asserted-by":"crossref","first-page":"6466","DOI":"10.1073\/pnas.78.10.6466","article-title":"Prevention of neonatal hyperbilirubinemia by tin protoporphyrin IX, a potent competitive inhibitor of heme oxidation.","volume":"78","author":"Drummond","year":"1981","journal-title":"Proc Natl Acad Sci USA."},{"key":"2021121010114812200_B8","doi-asserted-by":"crossref","first-page":"142","DOI":"10.1172\/JCI111394","article-title":"An experimental model of postnatal jaundice in the suckling rat. 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