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Lung injury in vivax malaria: Pathophysiological evidence for pulmonary vascular sequestration and posttreatment alveolar-capillary inflammation

Anstey, Nicholas M., Handojo, Tjandra, Pain, M. C. F., Kenangalem, Enny, Tjitra, E., Price, Ric N. and Maguire, Graeme (2007). Lung injury in vivax malaria: Pathophysiological evidence for pulmonary vascular sequestration and posttreatment alveolar-capillary inflammation. Journal of Infectious Diseases,195(4):589-596.

Document type: Journal Article
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ISI LOC 000243565800018
Title Lung injury in vivax malaria: Pathophysiological evidence for pulmonary vascular sequestration and posttreatment alveolar-capillary inflammation
Author Anstey, Nicholas M.
Handojo, Tjandra
Pain, M. C. F.
Kenangalem, Enny
Tjitra, E.
Price, Ric N.
Maguire, Graeme
Journal Name Journal of Infectious Diseases
Publication Date 2007
Volume Number 195
Issue Number 4
ISSN 0022-1899   (check CDU catalogue open catalogue search in new window)
Start Page 589
End Page 596
Place of Publication Chicago
Publisher University of Chicago Press
HERDC Category C1 - Journal Article (DEST)
Abstract Background. The mechanisms underlying lung injury in vivax malaria are not well understood. Inflammatory responses to Plasmodium falciparum and P. vivax, to our knowledge, have not previously been compared at an organ level. Methods. Respiratory symptoms and physiological aspects were measured longitudinally in Indonesian adults with uncomplicated vivax (n = 50) and falciparum (n = 50) malaria. Normal values were derived from 109 control subjects. Gas transfer was partitioned into its alveolar-capillary membrane (D-M) and pulmonary capillary vascular (V-C) components, to characterize the site and timing of impaired gas transfer. Results. Mean baseline V-C volume was significantly reduced in vivax and falciparum malaria, improving with treatment in each species. Baseline D-M function was not impaired in either species. The progressive deterioration in D-M function after treatment was statistically significant in vivax malaria but not in uncomplicated falciparum malaria. Oxygen saturation deteriorated after treatment in vivax but improved in falciparum malaria. Conclusions. The baseline reduction in V-C volume but not in D-M function suggests encroachment on V-C volume by parasitized erythrocytes and suggests that P. vivax -infected erythrocytes may sequester within the pulmonary microvasculature. Progressive alveolar-capillary dysfunction after treatment of vivax malaria is consistent with a greater inflammatory response to a given parasite burden in P. vivax relative to that in P. falciparum.
Keywords RESPIRATORY-DISTRESS-SYNDROME
BENIGN TERTIAN MALARIA
PLASMODIUM-VIVAX
FALCIPARUM-MALARIA
DIFFUSING-CAPACITY
ENDOTHELIAL-CELLS
GAS TRANSFER
MEMBRANE
VOLUME
EDEMA
DOI http://dx.doi.org/10.1086/510756   (check subscription with CDU E-Gateway service for CDU Staff and Students  check subscription with CDU E-Gateway in new window)
 
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