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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Thrombocytosis in preterm infants: a possible involvement of thrombopoietin receptor gene expression.

Transient thrombocytosis is commonly observed in preterm infants after birth, but its physiological mechanism is still unknown. To understand the mechanism of the transient thrombocytosis in preterm infants we firstly evaluated a correlation between platelet counts and thrombopoietin (TPO) levels in preterm infants and next c-mpl mRNA levels on platelets in healthy preterm infants longitudinally during a half-year of life. The mean platelet counts in 45 very low birth weight infants (mean gestational age 27.4+/-1.8 weeks, mean birth weight 1047+/-249 g) was 230+/-71x10(9)/l just after birth and thereafter gradually increased to 579+/-178x10(9)/l by 5 weeks of age. The platelet counts continued this level for about next 8 weeks. Serum TPO levels soon after birth and at 1 month of age were significantly higher than those at the age of 2-6 months. There was a significant negative correlation between platelet counts and serum TPO values. The c-mpl expression levels on platelets at birth and at 1 month of age tended to be lower than those on platelets from adults, and the c-mpl levels gradually increased through 6 months of age, although they were still lower than those of adults. Our results suggest that low expression of TPO receptor on platelets until 1 month after birth cause a decreased TPO clearance and keep a high level of free TPO in blood, thereby promoting platelet production from megakaryocytes or their progenitors in bone marrow, resulting in the subsequent thrombocytosis in preterm infants.[1]

References

  1. Thrombocytosis in preterm infants: a possible involvement of thrombopoietin receptor gene expression. Nakayama, H., Ihara, K., Hikino, S., Yamamoto, J., Nagatomo, T., Takemoto, M., Hara, T. J. Mol. Med. (2005) [Pubmed]
 
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