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Notice: An overlap in case reports
LETTERS TO THE EDITOR
Notice: An overlap in case reports It was recently brought to the attention of The Journal that an article by Copley et al published in the July 2007 issue of the Journal of Bone & Joint Surgery, American Volume (JBJS-A)1 may have reported some cases of deep venous thrombosis that had been previously reported in an article by Crary et al published in the October 2006 issue of The Journal.2 The editors of The Journal and JBJS-A investigated this patient population by corresponding with the authors of the JBJS-A and Journal articles and the Institutional Review Board and Research Administration at the University of Texas Southwestern. Please see the following reply from Lawson A. B. Copley, MD, corresponding author of the article published in JBJS-A. William F. Balistreri, MD Editor-in-Chief The Journal of Pediatrics Cincinnati Ohio 10.1016/j.jpeds.2007.12.011
REFERENCES 1. Hollmig ST, Copley LAB, Browne RH, Grande LM, Wilson PL. Deep venous thrombosis associated with osteomyelitis in children. J Bone Joint Surg Am 2007;89:1517-23. 2. Crary SE, Buchanan GR, Drake CE, Journeycake JM. Venous thrombosis and thromboembolism in children with osteomyelitis. J Pediatr 2006;149:537-41.
Reply To the Editor: During our study period of January 1, 2002 to December 31, 2004, we reported 13 cases of DVT associated with musculoskeletal infection in children. Eleven of these cases occurred in children with osteomyelitis. After our report was published, we became aware of the article in The Journal by Crary et al that reported 10 cases of DVT associated with osteomyelitis from the same institution (University of Texas Southwestern–Children’s Medical Center of Dallas). Comparing the 2 articles indicates that 8 of the children are described in both. Thus, our report includes 8 children who were previously reported by Crary et al, along with 5 other children with DVT (3 with osteomyelitis, 1 with septic arthritis, and 1 with pyomyositis) within our 3-year study period. I apologize for any confusion that might have arisen as a result of these 8 cases being reported in 2 separate articles.
Iron, oxidant injury, and practice choices in preterm infants To the Editor: Braekke et al1 report no effect of iron therapy on urine oxidant species 1 week after starting therapy. We do not fully agree with “high-dose iron in very low birth weight infants is well tolerated without indication of increased oxidant injury.”2 It is not the production of oxidative species alone but their reaction with iron that, altering redox state, may be primarily responsible for oxidant damage and long-term cellular toxicity.3 Ferrous iron reacts with H2O2, producing hydroxyl radicals, damaging proteins, nucleic acids, and membrane phospholipids.4-6 Animal and basic studies show that neonatal oral intake with elevation in basal iron levels produces higher iron content in the adult substantia nigra pars compacta, with progressive age-related enhancement of oxidative damage, nigrostriatal and dopaminergic neurodegeneration, and longterm cell loss.7,8 Furthermore, the infants studied were 6 weeks old, healthy, receiving fully human milk feedings, vitamin E 15 mg/d (antioxidant), and no potential “oxidants” (no blood transfusion 4 days before study start and withdrawn if infections or transfusion occurred).1 Hence, Braekke et al1 show “no evidence of effect” only on oxidative species in a very short period of time of iron started at 6 weeks of age in a selected population, but not in younger and sicker infants and infants receiving other diets. They do not show “evidence of no effect” nor assess oxidant injury and clinical short- and longterm effects. Effects on clinical outcomes that matter to patients and parents, such as death, long-term effects, and others should guide practice choices. It is extremely important to prevent iron deficiency states. It may be as important to avoid inducing “iron excess.” As long as we do not know the short- and long-term consequences, it seems judicious to avoid neonatal treatments that may induce long-term oxidant injury in preterm infants during the first 2 to 6 weeks of life unless such treatment improves outcomes that matter. Augusto Sola, MD Marta Rogido, MD MANA Atlantic Neonatal Research Institute Atlantic Health System Morristown, New Jersey 10.1016/j.jpeds.2007.09.028
REFERENCES Lawson A. B. Copley, MD Department of Orthopedic Surgery University of Texas Southwestern Dallas, Texas 10.1016/j.jpeds.2007.12.012
Letters to the Editor
1. Braekke K, Bechensteen AG, Halvorsen BL, Blomhoff R, Haaland K, Staff AC. Oxidative stress markers and antioxidant status after oral iron supplementation to very low birth weight infants. J Pediatr 2007;151:23-8. 2. Jobe AH. Iron for preterm infants. J Pediatr 2007;151:A3. 3. Kling PJ. Iron supplementation in prematurity: How much is too much? J Pediatr 2007;151:3-4.
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Notice: An overlap in case reports It was recently brought to the attention of The Journal that an article by Copley et al published in the July 2007 issue of the Journal of Bone & Joint Surgery, American Volume (JBJS-A)1 may have reported some cases of deep venous thrombosis that had been previously reported in an article by Crary et al published in the October 2006 issue of The Journal.2 The editors of The Journal and JBJS-A investigated this patient population by corresponding with the authors of the JBJS-A and Journal articles and the Institutional Review Board and Research Administration at the University of Texas Southwestern. Please see the following reply from Lawson A. B. Copley, MD, corresponding author of the article published in JBJS-A. William F. Balistreri, MD Editor-in-Chief The Journal of Pediatrics Cincinnati Ohio 10.1016/j.jpeds.2007.12.011
REFERENCES 1. Hollmig ST, Copley LAB, Browne RH, Grande LM, Wilson PL. Deep venous thrombosis associated with osteomyelitis in children. J Bone Joint Surg Am 2007;89:1517-23. 2. Crary SE, Buchanan GR, Drake CE, Journeycake JM. Venous thrombosis and thromboembolism in children with osteomyelitis. J Pediatr 2006;149:537-41.
Reply To the Editor: During our study period of January 1, 2002 to December 31, 2004, we reported 13 cases of DVT associated with musculoskeletal infection in children. Eleven of these cases occurred in children with osteomyelitis. After our report was published, we became aware of the article in The Journal by Crary et al that reported 10 cases of DVT associated with osteomyelitis from the same institution (University of Texas Southwestern–Children’s Medical Center of Dallas). Comparing the 2 articles indicates that 8 of the children are described in both. Thus, our report includes 8 children who were previously reported by Crary et al, along with 5 other children with DVT (3 with osteomyelitis, 1 with septic arthritis, and 1 with pyomyositis) within our 3-year study period. I apologize for any confusion that might have arisen as a result of these 8 cases being reported in 2 separate articles.
Iron, oxidant injury, and practice choices in preterm infants To the Editor: Braekke et al1 report no effect of iron therapy on urine oxidant species 1 week after starting therapy. We do not fully agree with “high-dose iron in very low birth weight infants is well tolerated without indication of increased oxidant injury.”2 It is not the production of oxidative species alone but their reaction with iron that, altering redox state, may be primarily responsible for oxidant damage and long-term cellular toxicity.3 Ferrous iron reacts with H2O2, producing hydroxyl radicals, damaging proteins, nucleic acids, and membrane phospholipids.4-6 Animal and basic studies show that neonatal oral intake with elevation in basal iron levels produces higher iron content in the adult substantia nigra pars compacta, with progressive age-related enhancement of oxidative damage, nigrostriatal and dopaminergic neurodegeneration, and longterm cell loss.7,8 Furthermore, the infants studied were 6 weeks old, healthy, receiving fully human milk feedings, vitamin E 15 mg/d (antioxidant), and no potential “oxidants” (no blood transfusion 4 days before study start and withdrawn if infections or transfusion occurred).1 Hence, Braekke et al1 show “no evidence of effect” only on oxidative species in a very short period of time of iron started at 6 weeks of age in a selected population, but not in younger and sicker infants and infants receiving other diets. They do not show “evidence of no effect” nor assess oxidant injury and clinical short- and longterm effects. Effects on clinical outcomes that matter to patients and parents, such as death, long-term effects, and others should guide practice choices. It is extremely important to prevent iron deficiency states. It may be as important to avoid inducing “iron excess.” As long as we do not know the short- and long-term consequences, it seems judicious to avoid neonatal treatments that may induce long-term oxidant injury in preterm infants during the first 2 to 6 weeks of life unless such treatment improves outcomes that matter. Augusto Sola, MD Marta Rogido, MD MANA Atlantic Neonatal Research Institute Atlantic Health System Morristown, New Jersey 10.1016/j.jpeds.2007.09.028
REFERENCES Lawson A. B. Copley, MD Department of Orthopedic Surgery University of Texas Southwestern Dallas, Texas 10.1016/j.jpeds.2007.12.012
Letters to the Editor
1. Braekke K, Bechensteen AG, Halvorsen BL, Blomhoff R, Haaland K, Staff AC. Oxidative stress markers and antioxidant status after oral iron supplementation to very low birth weight infants. J Pediatr 2007;151:23-8. 2. Jobe AH. Iron for preterm infants. J Pediatr 2007;151:A3. 3. Kling PJ. Iron supplementation in prematurity: How much is too much? J Pediatr 2007;151:3-4.
295