Abstract:Summary. To verify pathophysiological mechanisms underlying thrombocytosis in low-birth-weight (LBW) preterm babies, we evaluated kinetic changes in platelet counts and thrombopoietic cytokines including thrombopoietin (TPO), interleukin 6 (IL-6) and IL-11 in 24 uncomplicated preterm infants. Platelet counts in cord blood (CB) (265^64 Â 10 9 /l) were similar to adult levels, increased by d 14 (473^140 Â 10 9 /l), and then remained fairly constant. Thrombocytosis (. 500 Â 10 9 /l) was observed in 9/24 (38%) sub… Show more
“…We and other investigators recently documented that TPO contributes to thrombocytosis, together with IL-6, in patients with certain infections [17], Kawasaki disease [18], and in those having undergone surgery [19]. Furthermore, we found a link between early elevation of TPO and subsequent thrombocytosis in preterm infants [20]. Kapsoritakis et al [21]also indicated a significant elevation of serum TPO levels in patients with inflammatory bowel disease.…”
To determine the incidence and etiology of childhood thrombocytosis, over 15,000 platelet counts in 7,539 patients performed at a single regional hospital were reviewed. When thrombocytosis was defined as ≧500 × 109/l of platelet counts, the condition could be diagnosed in 6.0% (456 cases) of the patients. All patients were classified as having secondary thrombocytosis. The incidence of thrombocytosis dramatically changed throughout child development; it was 12.5% in neonates, peaked to 35.8% in 1-month-old infants and then returned to 12.9% in 6- to 11-month-old infants. Thereafter, it gradually decreased with age to only 0.6% in 11- to 15-year-old children. Frequent causes of thrombocytosis included infection (67.5%), Kawasaki disease (9.4%), prematurity (7.7%) and iron deficiency anemia (6.4%). Thrombocytosis was an incidental finding in a substantial population of early infants. Thrombocytosis as a reaction to several types of infection and Kawasaki disease was more common in children under 7 years old, while autoimmune disease and tissue damage were major causes in children aged 11–15 years. No child had thromboembolic complications. These findings indicate that childhood thrombocytosis is a benign condition and its incidence and etiology seem to depend on age.
“…We and other investigators recently documented that TPO contributes to thrombocytosis, together with IL-6, in patients with certain infections [17], Kawasaki disease [18], and in those having undergone surgery [19]. Furthermore, we found a link between early elevation of TPO and subsequent thrombocytosis in preterm infants [20]. Kapsoritakis et al [21]also indicated a significant elevation of serum TPO levels in patients with inflammatory bowel disease.…”
To determine the incidence and etiology of childhood thrombocytosis, over 15,000 platelet counts in 7,539 patients performed at a single regional hospital were reviewed. When thrombocytosis was defined as ≧500 × 109/l of platelet counts, the condition could be diagnosed in 6.0% (456 cases) of the patients. All patients were classified as having secondary thrombocytosis. The incidence of thrombocytosis dramatically changed throughout child development; it was 12.5% in neonates, peaked to 35.8% in 1-month-old infants and then returned to 12.9% in 6- to 11-month-old infants. Thereafter, it gradually decreased with age to only 0.6% in 11- to 15-year-old children. Frequent causes of thrombocytosis included infection (67.5%), Kawasaki disease (9.4%), prematurity (7.7%) and iron deficiency anemia (6.4%). Thrombocytosis was an incidental finding in a substantial population of early infants. Thrombocytosis as a reaction to several types of infection and Kawasaki disease was more common in children under 7 years old, while autoimmune disease and tissue damage were major causes in children aged 11–15 years. No child had thromboembolic complications. These findings indicate that childhood thrombocytosis is a benign condition and its incidence and etiology seem to depend on age.
“…2,22,[24][25][26][27] Sasanakul et al 25 noted a steady rise in the platelet counts of term infants during the first 7 to 14 postnatal days with subsequent counts remaining fairly constant over the next 2 weeks. Aballi et al 22 evaluated platelet counts of premature infants whose birth weights ranged from 750 to 2250 g and observed a steady rise in counts during the first 24 days.…”
Section: Discussionmentioning
confidence: 99%
“…Other studies have shown that the mean platelet counts of premature infants with birth weights <2500 g increase steadily during the first 10 to 14 days of life then remain constant over the remainder of the neonatal period. 26,27 Obladen et al 24 determined that the platelet counts of 562 very low birth weight infants increased steadily during the first 6 weeks of life, with the most significant increase noted during the first 2 weeks. Saxonhouse et al 28 reported that reticulated platelet counts increase during the first 5 days following delivery.…”
Section: Discussionmentioning
confidence: 99%
“…[30][31][32] Both preterm and term infants show similar Tpo concentrations during the first weeks of life; concentrations increase after birth with a peak on the 2nd day and then gradually decrease to levels seen in the cord blood by the end of the first month of life. 27,32 Previous reports demonstrated that the platelet counts of neonatal rhesus monkeys began to increase 4 to 6 days after the administration of pegylated recombinant human megakaryocyte growth and development factor with counts peaking after approximately 2 weeks. 33 Collectively, these results suggest that the increase in platelet counts noted between the second and third postnatal week may be the result of a neonatal surge in Tpo and possibly other thrombopoietic factors.…”
Objective: Identifying a platelet count as abnormal (thrombocytopenia or thrombocytosis) can facilitate recognizing various disease states. However, the published reference ranges for platelet counts in neonates may be imprecise, as they were generated from relatively small sample sizes and compiled before modern platelet enumeration methods.
Study design:We derived new neonatal reference ranges for platelet counts and mean platelet volume (MPV) measurements using electronic data accumulated during a recent 6-year period from a multihospital healthcare system.Result: Platelet counts were obtained between the first and the 90th day after birth, from 47 291 neonates delivered at 22 to 42 weeks gestation. The first platelet counts obtained in the first 3 days of life, increased over the range of 22 to 42 weeks gestation. In those born p32 weeks gestation, the lower reference range (5th percentile) was 104 200 ml À1 , but it was 123 100 ml À1 in late-preterm and -term neonates. Advancing postnatal age had a significant effect on platelet counts; during the first 9 weeks, the counts fit a sinusoidal pattern with two peaks; one at 2 to 3 weeks and a second at 6 to 7 weeks. The upper limit of expected counts (95th percentile) during these peaks were as high as 750 000 ml À1 .
Conclusion:The figures herein describe reference ranges for platelet counts and MPV determinations of neonates at various gestational ages during their first 90 days. Expected values differ substantially from the 150 000 ml À1 to 450 000 ml À1 range previously used to define neonatal thrombocytopenia and thrombocytosis. The new definitions will render the diagnoses of neonatal thrombocytopenia and thrombocytosis less commonly than when the old definitions were used, because the new ranges are wider than 150 000 ml À1 to 450 000 ml À1 .
“…4 Recently, several studies have clarified the relationship between blood TPO level and platelet count in thrombocytopenic and non-thrombocytopenic non-DS neonates. [5][6][7][8][9][10][11][12] Accumulating evidence has shown that although neonates of all gestational ages produce endogenous TPO, their TPO response to thrombocytopenia may be suboptimal. 5,6 In contrast with extensive studies about thrombocytopenia in non-DS neonates, [5][6][7][8][9][10][11][12] little is known about underlying mechanisms including TPO contribution responsible for thrombocytopenia in DS newborns.…”
Background: The pathogenesis of thrombocytopenia during the neonatal period in Down's syndrome (DS) infants remains unclear.Objective: To elucidate kinetic changes of serum thrombopoietin (TPO) level and platelet count, and their correlation in DS neonates.Study Design: Twelve DS infants (male/female: 7/5, term/late preterm: 10/2) born between 1997 and 2007 were included. Blood samples were serially collected during the neonatal period and serum TPO levels were determined in 44 sera using an enzyme-linked immunosorbent assay.Results: Thrombocytopenia <150 Â 10 9 per liter was observed in seven (58%) patients. In 12 DS patients, the median TPO value showed 2.86 fmol ml -1 on day 0, rose to 4.64 fmol ml -1 on day 2, and thereafter decreased to 4.30 fmol ml -1 on day 5, 2.40 fmol ml -1 on days 11-15, and 1.75 fmol ml -1 on days 28-30. This kinetics parallels that in historical non-DS controls. In 35 pair sample analysis from 11 patients without transient myeloproliferative disease, TPO level inversely correlated with platelet count (r ¼ À0.38, P ¼ 0.023). However, there was no significant difference in TPO concentrations between thrombocytopenic and non-thrombocytopenic DS individuals.Conclusions: This is the first study to describe the relationship between TPO level and platelet count in neonates with DS. Median TPO levels and their kinetic changes in DS neonates are comparable to those in non-DS controls. In contrast to earlier findings in several studies showing higher TPO concentrations in thrombocytopenic non-DS newborns than those in non-thrombocytopenic counterparts, the response of the TPO system to thrombocytopenia in DS during the neonatal period seems suboptimal.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.