Document Detail


Evidence for magnesium deficiency in the pathogenesis of bronchopulmonary dysplasia (BPD).
MedLine Citation:
PMID:  9140865     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Bronchopulmonary dysplasia (BPD) has been defined as a requirement for oxygen for more than 28 days because of chronic pulmonary changes, usually in a premature infant. About 50 per cent of very low birth weight (VLBW) infants who weigh 1 kg at birth and who survive 28 days will develop BPD. Since 80 per cent of fetal accretion of magnesium occurs during the third trimester, this population is also at risk for magnesium deficiency. This paper reviews evidence for a role of magnesium deficiency in the pathogenesis of BPD. Pathology in BPD that may be caused or aggravated by magnesium deficiency is noted. Agents or mediators that are increased in BPD and in BPD include: oxygen free radicals; the inflammatory cytokines interleukin (IL)-1 and IL-6, and tumour necrosis factor-alpha; vaso- and bronchoconstrictors thromboxane A2 (TXA2) and serotonin: vasoconstrictor, endothelin-1 (ET-1); and bronchoconstrictor, histamine. Magnesium deficiency increases the susceptibility of cells and tissues to peroxidation, worsens the inflammatory reaction, reduces the immune response, exaggerates catecholamine release in stress, and diminishes energy metabolism. Possibly because of the danger of magnesium toxicity and the difficulty in studying the preterm VLBW neonate, little is known about magnesium supplementation in this group. Such information must be gained through controlled studies on the effect of antepartum exposure to maternally administered magnesium sulphate on the VLBW infant, through carefully monitored postnatal administration of magnesium in an intensive care setting, or through evaluations of combined pre- and postnatal supplementation.
Authors:
J L Caddell
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Magnesium research : official organ of the International Society for the Development of Research on Magnesium     Volume:  9     ISSN:  0953-1424     ISO Abbreviation:  Magnes Res     Publication Date:  1996 Oct 
Date Detail:
Created Date:  1997-07-03     Completed Date:  1997-07-03     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  8900948     Medline TA:  Magnes Res     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  205-16     Citation Subset:  IM    
Affiliation:
Thomas Jefferson University, Philadelphia, PA 19107-6799, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Bronchopulmonary Dysplasia / etiology*,  metabolism*,  physiopathology
Chemokines
Endothelin-1
Free Radicals / metabolism
Humans
Hydroxyeicosatetraenoic Acids / metabolism
Immunoglobulins
Infant, Newborn
Infant, Very Low Birth Weight
Magnesium Deficiency / complications*,  metabolism,  physiopathology
Nitric Oxide
Substance P
Thromboxane A2 / metabolism
Tumor Necrosis Factor-alpha
Chemical
Reg. No./Substance:
0/Chemokines; 0/Endothelin-1; 0/Free Radicals; 0/Hydroxyeicosatetraenoic Acids; 0/Immunoglobulins; 0/Tumor Necrosis Factor-alpha; 10102-43-9/Nitric Oxide; 33507-63-0/Substance P; 57576-52-0/Thromboxane A2; 73945-47-8/15-hydroxy-5,8,11,13-eicosatetraenoic acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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