Neonatal and maternal platelet function in pregnancy-induced hypertension: a comprehensive statistical analysis [regarding: platelet function in newborns and the women affected by pregnancy-induced hypertension]

We read with great interest the study by Terai et al. [1] The authors demonstrate the effect of pregnancy-induced hypertension (PIH) on platelet function in mothers and their new-borns, with emphasis on platelet count (PLT) and mean platelet volume (MPV) measurement. The authors discuss two important conclusions with significant clinical implications. Firstly, PIH causes maternal thrombocytopenia, leading to an increased MPV signifying increased platelet activation. It is important to note that an increased MPV has been known to play a vital role as a diagnostic and prognostic indicator in a wide range of acute and chronic inflammatory pathologies, such as sepsis and diabetes mellitus respectively [2, 3]. Secondly, the authors report that maternal PIH has no significant effect on neonatal platelet count or MPV. The authors correctly state that several conflicting reports exist pertaining to platelet function in PIH, and have fittingly shone light upon the role of MPV and PLT in this context. However, a comprehensive examination of all platelet indices in PIH, including the plateletcrit (PCT), platelet distribution width (PDW), and platelet-large cell ratio (PLCR) would have allowed for a more complete analysis of platelet function, as reported elsewhere [4]. Additionally, while some individual platelet parameters may fail to assume statistical significance, an analysis of their ratios, such as the MPV/PLT ratio, may have been a worthwhile addition to the manuscript. The authors have utilized accurate exclusion criteria for the study, comprising of conditions leading to thrombocytopenia and an increased MPV. However, the effect of gestational diabetes mellitus (GDM) on platelet function has not been taken into account. As previous studies have demonstrated, GDM, described as an inflammatory condition characterized by increased insulin resistance leading to platelet activation, can cause an increase in MPV [5]. Accordingly, exclusion or statistical adjustment of patients with GDM may have been warranted. The authors have employed univariate statistical methods to compare the findings in the diseased and control groups. They have additionally reported that the age and body mass index (BMI) of mothers in the disease arm was significantly higher than the controls. While the authors state that age and BMI may not have had a confounding effect on platelet function, binary logistic regression analysis could have been an effective solution to this problem. In addition, multivariate logistic regression would have conclusively adjusted for the confounding factors affecting the result of the study, including age, BMI, and underlying conditions like GDM. Notably, the authors have used a laboratory cutoff value of 11.1 fL to define an increased MPV. As the value of MPV may vary in different settings, it would have been beneficial to specify if this value was derived from a standard population nomogram, following CLSI guidelines. Within the study population, a receiver operating characteristic (ROC) curve could have been utilized to determine the precise cutoff value for the MPV, to accurately discriminate between patients with and without PIH. In conclusion, further studies are necessitated to describe the effect of PIH on maternal and neonatal platelet indices and function.

To the Editor, We read with great interest the study by Terai et al. [1] The authors demonstrate the effect of pregnancy-induced hypertension (PIH) on platelet function in mothers and their new-borns, with emphasis on platelet count (PLT) and mean platelet volume (MPV) measurement. The authors discuss two important conclusions with significant clinical implications. Firstly, PIH causes maternal thrombocytopenia, leading to an increased MPV signifying increased platelet activation. It is important to note that an increased MPV has been known to play a vital role as a diagnostic and prognostic indicator in a wide range of acute and chronic inflammatory pathologies, such as sepsis and diabetes mellitus respectively [2,3]. Secondly, the authors report that maternal PIH has no significant effect on neonatal platelet count or MPV.
The authors correctly state that several conflicting reports exist pertaining to platelet function in PIH, and have fittingly shone light upon the role of MPV and PLT in this context. However, a comprehensive examination of all platelet indices in PIH, including the plateletcrit (PCT), platelet distribution width (PDW), and platelet-large cell ratio (PLCR) would have allowed for a more complete analysis of platelet function, as reported elsewhere [4]. Additionally, while some individual platelet parameters may fail to assume statistical significance, an analysis of their ratios, such as the MPV/PLT ratio, may have been a worthwhile addition to the manuscript.
The authors have utilized accurate exclusion criteria for the study, comprising of conditions leading to thrombocytopenia and an increased MPV. However, the effect of gestational diabetes mellitus (GDM) on platelet function has not been taken into account. As previous studies have demonstrated, GDM, described as an inflammatory condition characterized by increased insulin resistance leading to platelet activation, can cause an increase in MPV [5]. Accordingly, exclusion or statistical adjustment of patients with GDM may have been warranted.
The authors have employed univariate statistical methods to compare the findings in the diseased and control groups. They have additionally reported that the age and body mass index (BMI) of mothers in the disease arm was significantly higher than the controls. While the authors state that age and BMI may not have had a confounding effect on platelet function, binary logistic regression analysis could have been an effective solution to this problem. In addition, multivariate logistic regression would have conclusively adjusted for the confounding factors affecting the result of the study, including age, BMI, and underlying conditions like GDM.
Notably, the authors have used a laboratory cutoff value of 11.1 fL to define an increased MPV. As the value of MPV may vary in different settings, it would have been beneficial to specify if this value was derived from a standard population nomogram, following CLSI guidelines. Within the study population, a receiver operating characteristic (ROC) curve could have been utilized to determine the precise cutoff value for the MPV, to accurately discriminate between patients with and without PIH.
In conclusion, further studies are necessitated to describe the effect of PIH on maternal and neonatal platelet indices and function.

Disclosure statement
No potential conflict of interest was reported by the author(s).

Funding
The author(s) reported there is no funding associated with the work featured in this article. Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.