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Bronchopulmonary dysplasia and intrauterine growth restriction
Correspondence
Bronchopulmonary dysplasia and intrauterine growth restriction
Still Pictures
We do not have the rights to reproduce this image on the web.
The pathogenesis of bronchopulmonary dysplasia (BPD) is known to be multifactorial. We would like to add a further factor, not mentioned in the Seminar by John Kinsella and colleagues (April 29, p 1421),1 that modulates the risk and pathogenesis of BPD. Intrauterine growth restriction increases the risk of BPD and prolongs the duration of mechanical ventilation in preterm infants younger than 32 weeks of gestation.2 These findings have been confirmed in populationbased studies.3,4 Preterm infants younger than 28 weeks and born small for gestational age are known to be at especially high risk compared with age-matched infants without obvious signs of impaired intrauterine growth.3,4 The main mechanisms to explain how intrauterine growth restriction modulates the risk of a BPD have been described in animals. For example, in experimentally growthrestricted preterm lambs, impaired growth of terminal airways and gas exchange units has been shown. Furthermore, growth restriction leads to reduced expression of surfactant protein mRNA and could induce increased inflammatory activation.5 We declare that we have no conflict of interest. This work was supported in part by the National Genome Network Germany (NGFN 01 GS0401).
*Ludwig Gortner, Irwin Reiss, Anne Hilgendorff [email protected] Saarland University Hospital, Department of Paediatrics and Neonatology, 66421 Homburg, Germany (LG); Erasmus MC-Sophia, Department of Pediatric Surgical Intensive Care, Rotterdam, Netherlands (IR); and Ludwig-MaximilianUniversity, Department of Neonatology, Klinikum Groß-Hadern, München, Germany (AH) 1
28
Kinsella JP, Greenough A, Abman SH. Bronchopulmonary dysplasia. Lancet 2006; 367: 1421–31.
2
3
4
5
Gortner L, Wauer RR, Stock GJ, et al. Neonatal outcome in small for gestational age infants: do they really better? J Perinat Med 1999; 27: 484–89. Lal MK, Manktelow BN, Draper ES, Field DJ. Chronic lung disease of prematurity and intrauterine growth retardation: a populationbased study. Pediatrics 2003; 111: 483–87. Reiss I, Landmann E, Heckmann M, Misselwitz B, Gortner L. Increased risk of broncholpulmonary dysplasia and increased mortality in very preterm infants being small for gestational age. Arch Gynecol Obstet 2003; 269: 40–44. Gortner L, Hilgendorff A, Bahner T, Ebsen M, Reiss I, Rudloff S. Hypoxia-induced intrauterine growth retardation: effects on pulmonary development and surfactant protein transcription. Biol Neonate 2005; 88: 129–35.
The health-worker migration crisis The thoughtful analysis by Bob Bond and Barbara McPake (April 29, p 1448)1 is timely and raises several issues, some of which I highlight here. First, to rein in migration from poor countries, policymakers must simultaneously calibrate demand, supply, price, and global professional mobility. The latter is easier said than done. Ethics, trade, global relations, and the globalisation engine will not support drastic migration controls without hurting other global achievements. For instance, we cannot suddenly lock out medical talent while competing for other talent.2,3 Second, policies within the Organisation for Economic Cooperation and Development (OECD) cannot fix the source countries’ push factors. Health workers from such countries could remain at home and simply quit the profession, leading to internal brain loss,4 or will continue to migrate in smaller numbers to largely non-OECD destinations (a form of “background migration” that may also occur in OECD countries given the global freedom of and market for professionals). Third, the migration crisis is partly induced by OECD supply shortages which in turn have been powerfully influenced by organised medical associations such as the American
Medical Association (AMA). Several times in the past 50 years, the AMA and even some medical deans resisted medical school expansions which have contributed to swings in physician supply in the USA.5 Such incidental resistances, often based on professional power ideologies and perceptions, can make workforce planning difficult, and thus undermine the ability of policymakers and their researchers to “grasp” the science of lagged effects of physician supply interventions. We should not expect any magic bullets from national OECD countries’ policies. I declare that I have no conflict of interest.
Onyebuchi A Arah [email protected] Department of Social Medicine, Academic Medical Center, University of Amsterdam, PO Box 22700, 1100 DE, Amsterdam, Netherlands 1
2
3
4
5
Pond B, McPake B. The health migration crisis: the role of four Organisation for Economic Cooperation and Development countries. Lancet 2006; 367: 1448–55. Kapur R, McHale J. Give us your best and brightest: the global hunt for talent and its impact on the developing world. Washington, DC: Center for Global Development, 2005. Florida R. The flight of the creative class: the new global competition for talent. New York: HarperCollins, 2005. Ogbu UC, Arah OA. The metrics of the physician brain drain. N Engl J Med 2006; 354: 528–30. Blumenthal D. New steam from an old cauldron—the physician-supply debate. N Engl J Med 2004; 350: 1780–87.
Department of Error Sambrook P, Cooper C. Osteoporosis. Lancet 2006; 367: 2010–18—In this Seminar (June 17), the fourth sentence of the eighth paragraph of the section on antiresorptives (p 2014) should have read: “Ibandronate is approved in the European Union for the treatment of postmenopausal osteoporosis. In the USA, it is approved for the treatment and prevention of osteoporosis in postmenopausal women.”
www.thelancet.com Vol 368 July 1, 2006
Bronchopulmonary dysplasia and intrauterine growth restriction
Still Pictures
We do not have the rights to reproduce this image on the web.
The pathogenesis of bronchopulmonary dysplasia (BPD) is known to be multifactorial. We would like to add a further factor, not mentioned in the Seminar by John Kinsella and colleagues (April 29, p 1421),1 that modulates the risk and pathogenesis of BPD. Intrauterine growth restriction increases the risk of BPD and prolongs the duration of mechanical ventilation in preterm infants younger than 32 weeks of gestation.2 These findings have been confirmed in populationbased studies.3,4 Preterm infants younger than 28 weeks and born small for gestational age are known to be at especially high risk compared with age-matched infants without obvious signs of impaired intrauterine growth.3,4 The main mechanisms to explain how intrauterine growth restriction modulates the risk of a BPD have been described in animals. For example, in experimentally growthrestricted preterm lambs, impaired growth of terminal airways and gas exchange units has been shown. Furthermore, growth restriction leads to reduced expression of surfactant protein mRNA and could induce increased inflammatory activation.5 We declare that we have no conflict of interest. This work was supported in part by the National Genome Network Germany (NGFN 01 GS0401).
*Ludwig Gortner, Irwin Reiss, Anne Hilgendorff [email protected] Saarland University Hospital, Department of Paediatrics and Neonatology, 66421 Homburg, Germany (LG); Erasmus MC-Sophia, Department of Pediatric Surgical Intensive Care, Rotterdam, Netherlands (IR); and Ludwig-MaximilianUniversity, Department of Neonatology, Klinikum Groß-Hadern, München, Germany (AH) 1
28
Kinsella JP, Greenough A, Abman SH. Bronchopulmonary dysplasia. Lancet 2006; 367: 1421–31.
2
3
4
5
Gortner L, Wauer RR, Stock GJ, et al. Neonatal outcome in small for gestational age infants: do they really better? J Perinat Med 1999; 27: 484–89. Lal MK, Manktelow BN, Draper ES, Field DJ. Chronic lung disease of prematurity and intrauterine growth retardation: a populationbased study. Pediatrics 2003; 111: 483–87. Reiss I, Landmann E, Heckmann M, Misselwitz B, Gortner L. Increased risk of broncholpulmonary dysplasia and increased mortality in very preterm infants being small for gestational age. Arch Gynecol Obstet 2003; 269: 40–44. Gortner L, Hilgendorff A, Bahner T, Ebsen M, Reiss I, Rudloff S. Hypoxia-induced intrauterine growth retardation: effects on pulmonary development and surfactant protein transcription. Biol Neonate 2005; 88: 129–35.
The health-worker migration crisis The thoughtful analysis by Bob Bond and Barbara McPake (April 29, p 1448)1 is timely and raises several issues, some of which I highlight here. First, to rein in migration from poor countries, policymakers must simultaneously calibrate demand, supply, price, and global professional mobility. The latter is easier said than done. Ethics, trade, global relations, and the globalisation engine will not support drastic migration controls without hurting other global achievements. For instance, we cannot suddenly lock out medical talent while competing for other talent.2,3 Second, policies within the Organisation for Economic Cooperation and Development (OECD) cannot fix the source countries’ push factors. Health workers from such countries could remain at home and simply quit the profession, leading to internal brain loss,4 or will continue to migrate in smaller numbers to largely non-OECD destinations (a form of “background migration” that may also occur in OECD countries given the global freedom of and market for professionals). Third, the migration crisis is partly induced by OECD supply shortages which in turn have been powerfully influenced by organised medical associations such as the American
Medical Association (AMA). Several times in the past 50 years, the AMA and even some medical deans resisted medical school expansions which have contributed to swings in physician supply in the USA.5 Such incidental resistances, often based on professional power ideologies and perceptions, can make workforce planning difficult, and thus undermine the ability of policymakers and their researchers to “grasp” the science of lagged effects of physician supply interventions. We should not expect any magic bullets from national OECD countries’ policies. I declare that I have no conflict of interest.
Onyebuchi A Arah [email protected] Department of Social Medicine, Academic Medical Center, University of Amsterdam, PO Box 22700, 1100 DE, Amsterdam, Netherlands 1
2
3
4
5
Pond B, McPake B. The health migration crisis: the role of four Organisation for Economic Cooperation and Development countries. Lancet 2006; 367: 1448–55. Kapur R, McHale J. Give us your best and brightest: the global hunt for talent and its impact on the developing world. Washington, DC: Center for Global Development, 2005. Florida R. The flight of the creative class: the new global competition for talent. New York: HarperCollins, 2005. Ogbu UC, Arah OA. The metrics of the physician brain drain. N Engl J Med 2006; 354: 528–30. Blumenthal D. New steam from an old cauldron—the physician-supply debate. N Engl J Med 2004; 350: 1780–87.
Department of Error Sambrook P, Cooper C. Osteoporosis. Lancet 2006; 367: 2010–18—In this Seminar (June 17), the fourth sentence of the eighth paragraph of the section on antiresorptives (p 2014) should have read: “Ibandronate is approved in the European Union for the treatment of postmenopausal osteoporosis. In the USA, it is approved for the treatment and prevention of osteoporosis in postmenopausal women.”
www.thelancet.com Vol 368 July 1, 2006