COMMENTARY |
National Institute of Child Health and Human Development
National Institutes of Health
Department of Health and Human Services
Bethesda, MD 20892-2425
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Every now and then, in a pharmaceutical world dominated by agents that are "me-toos" or "variations on a theme," there appears a truly new molecular entity that offers an entirely new approach to treating a disorder that previously had only partially effective therapies or, sometimes, no effective therapy at all. The article by Attallah Kappas1 in this issue describes such a potential advance: tin-mesoporphyrin. This truly new entity was developed specifically by Kappas and his colleagues to block the action of heme oxygenase in converting hemoglobin to bilirubin. By shutting off the production of bilirubin at its source rather than removing it by exchange transfusion or phototherapy after it is formed, this agent has the potential to revolutionize management of jaundice from any cause just as Rh immune globulin did for preventing Rh hemolytic disease of the newborn when introduced in the 1960s.
What is remarkable (and lamentable) is that
Address correspondence to Duane Alexander, MD, National Institute of Child Health and Human Development, National Institutes of Health, Department of Health and Human Services, 31 Center Dr, Room 2A03, MSC 2425, Bethesda, MD 20892-2425. E-mail: da43w@nih.gov
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Z.-W. Xia, C.-E Li, Y.-X. Jin, Y. Shi, L.-Q. Xu, W.-W. Zhong, Y.-Z. Li, S.-C. Yu, and Z.-L. Zhang Reduction of Bilirubin by Targeting Human Heme Oxygenase-1 Through siRNA Experimental Biology and Medicine, April 1, 2007; 232(4): 495 - 502. [Abstract] [Full Text] [PDF] |
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G. R. Gourley, Z. Li, B. L. Kreamer, and M. R. Kosorok A Controlled, Randomized, Double-Blind Trial of Prophylaxis Against Jaundice Among Breastfed Newborns Pediatrics, August 1, 2005; 116(2): 385 - 391. [Abstract] [Full Text] [PDF] |
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