Insufficient thrombopoietin due to hepatic dysmature results in thrombocytopenia in small‐for‐gestational‐age rats

Takeshita, Sho; Kakita, Hiroki; Toriuchi, Kohki; Aoki, Hiromasa; Ueda, Hiroko; Wakatsuki, Akihiko; Yamada, Yasumasa; Aoyama, Mineyoshi

doi:10.1111/bjh.17294

Cited by 2 publications

(4 citation statements)

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“…We previously demonstrated that a decrease in TPO production due to hepatic dysmaturation resulted in thrombocytopenia in SGA model rats. 9 In the present study, SGA infants with thrombocytopenia had lower IPF and serum TPO levels than non-SGA infants with thrombocytopenia. These results suggest that IPF and TPO levels do not increase in response to thrombocytopenia in human SGA infants, similar to SGA model rats.…”

Section: Discussionsupporting

confidence: 47%

“…These results demonstrate that all SGA infants showed asymmetrical growth due to maternal/placental factors. 9 , 12 These SGA infants are at increased risk for complications, such as prematurity, asphyxia, hypothermia, hypoglycemia, hypocalcemia, polycythemia, and thrombocytopenia. 1 , 2 Chronic intrauterine hypoxia caused by maternal factors for SGA infants leads to high fetal erythropoietin and polycythemia.…”

Section: Discussionmentioning

confidence: 99%

“… 10 The cause of thrombocytopenia in SGA infants has been postulated to be a decrease in platelet production. 5 – 9 , 19 However, there are few studies on infants, and the etiology of thrombocytopenia in human SGA infants remains unclear. Wasiuk et al evaluated thrombopoiesis in SGA infants and postulated that intrauterine hypoxia is responsible for the increase of erythropoietin and impairment of thrombopoiesis in SGA infants.…”

Section: Discussionmentioning

confidence: 99%

“…We have previously reported animal studies that showed that chronic hypoxia in utero causes immaturity of liver function and a decrease in TPO expression in the liver, which in turn suppresses platelet production. 9 However, the etiology of thrombocytopenia in human SGA infants remains unclear. The present study attempted to demonstrate that thrombocytopenia in human SGA infants is due to insufficient TPO production.…”

Section: Introductionmentioning

confidence: 99%

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Thrombocytopenia and insufficient thrombopoietin production in human small-for-gestational-age infants

et al. 2022

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Background Small-for-gestational-age (SGA) infants are at increased risk for transient thrombocytopenia. The aim of this study was to determine whether thrombocytopenia in human SGA infants is due to insufficient thrombopoietin (TPO) production. Methods A prospective study of 202 infants with gestational age less than 37 weeks was conducted; 30 of them were SGA infants, and 172 were non-SGA infants. Thrombocytopenia was seen in 17 of 30 SGA infants and 40 of 172 non-SGA infants. Results Platelet counts were significantly lower in the SGA group than in the non-SGA group at the time of the lowest platelet count within 72 h of birth. The platelet count and immature platelet fraction (IPF) were negatively correlated in non-SGA infants, but not in SGA infants. In addition, the platelet count and TPO were negatively correlated in non-SGA infants. IPF and TPO were significantly lower in SGA than in non-SGA infants with thrombocytopenia. Conclusion IPF increased with thrombocytopenia to promote platelet production in non-SGA infants due to increasing TPO, but not in SGA infants. This study found an association between insufficient TPO production and thrombocytopenia in SGA infants. In addition, this study is important for understanding the etiology of thrombocytopenia in SGA infants. Impact The immature platelet fraction was low, and serum thrombopoietin was not increased in small-for-gestational-age (SGA) infants with thrombocytopenia. Thrombocytopenia in SGA infants is due to insufficient thrombopoietin production. This study is important for understanding the etiology of thrombocytopenia in SGA infants.

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Section: Discussionsupporting

confidence: 47%