NeoReviews -- E-Letters for Wong et al., 8 (2) 77-84

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Tin Mesoporphyrin for neonatal hyperbilirubinemia: Ayman Habiba (6 January 2009)

Response to Dr. Habiba: Ronald J Wong, David K Stevenson (6 January 2009)

Tin Mesoporphyrin for neonatal hyperbilirubinemia 6 January 2009

Ayman Habiba,
Pediatrician
Cape Breton Regional Hospital, Sydney, NS, Canada
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Re: Tin Mesoporphyrin for neonatal hyperbilirubinemia

aahhabiba{at}yahoo.com Ayman Habiba

Tin Mesoporphyrin interrupts the production of bilirubin by inhibiting heme oxgenase. As hemolysis continues, more heme is produced as a result of the breakdown of hemoglobin. In the presence of an inhibitor of heme oxygenase, heme cannot be recycled into biliverdin, iron, and carbon monoxide. Unlike traditional methods of treating neonatal hyperbilirubinemia - such as phototherapy and exchange transfusion - tin mesoporphyrin can therefore, at least in theory, result in the accumulation of the precursor (heme). Is there any updated information regarding the fate of excess heme under such circumstances ? Is there any evidence of a deleterious effect of such an accumulation of heme ? Or are there alternative metabolic pathways through which it is degraded ? While it appears that tin mesoporhyrin can effectively control hyperbilirubinemia, what is the latest evidence regarding its effeciveness in the prevention of kernicterus ?. Dr Ayman Habiba, MD FAAP aahhabiba@yahoo.com Pediatrician Cape Breton Regional Hospital Sydney B1P 1P3 Nova Scotia Canada 902 567 6268
Conflict of Interest:
None declared

Response to Dr. Habiba 6 January 2009

Ronald J Wong,
Senior Research Scientist
Stanford University School of Medicine,
David K Stevenson
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Re: Response to Dr. Habiba

rjwong{at}stanford.edu Ronald J Wong, et al.

Dr. Habiba raises an important point regarding the fate of the accumulated heme as a result of the inhibition of heme oxygenase (HO), especially since heme is a pro-oxidant and its accumulation may lead to deleterious effects. Early studies in Dr. Kappas� Laboratory by Simionatta CR, et al (J Clin Invest 75:513-21, 1985) and in Dr. Stevenson�s laboratory by Hintz SR, et al in 1987 (J Pediatr Gastroenterol Nutr 6:302-6, 1987) have shown that the excess heme is excreted into the bile in proportion to the degree of inhibition of HO by tin protoporphyrin (SnPP).
With regard to the latest evidence of the effectiveness of SnMP in preventing kernicterus, there is an ongoing phase 2b multicenter single- dose blinded randomized placebo-controlled dose escalation safety and efficacy trial sponsored by InfaCare Pharmaceuticals, Corp. evaluating the use of SnMP (or Stannsoporfin) in neonates with hyperbilirubinemia. In addition, because of the recent report (Morris BH, et al N Engl J Med 359:1885-96, 2008) by the National Institute of Child Health and Development (NICHD) Neonatal Research Network that aggressive phototherapy may increase the mortality of extremely very low birth weight (ELBW) infants (≤750 grams), the need to identify an alternative treatment method(s) that may be safer and/or more effective in reducing total bilirubin levels through the use of HO inhibitors and, hence, prevent neurodevelopmental impairments in ELBW infants is warranted.
Conflict of Interest:
None declared