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Year : 2018  |  Volume : 5  |  Issue : 4  |  Page : 117-122

Platelet indices in healthy pregnant and nonpregnant Nigerian women

1 Department of Obstetrics & Gynaecology, Faculty of Clinical Sciences, College of Medicine, University of Lagos/Lagos University Teaching Hospital, Lagos, Nigeria
2 Department of Haematology, Lagos University Teaching Hospital, Lagos, Nigeria

Date of Web Publication20-Sep-2019

Correspondence Address:
Ochuwa Adiketu Babah
Department of Obstetrics & Gynaecology, Faculty of Clinical Sciences, College of Medicine, University of Lagos/ Lagos University Teaching Hospital, Lagos
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DOI: 10.4103/ssajm.ssajm_16_18

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Background: Though hematological changes occur in pregnancy, changes in platelet indices have not been widely studied, and we do not have reference ranges for use in pregnancy. Objective: To assess effect of pregnancy on platelet indices and establish reference values for these parameters in pregnancy. Methodology: A prospective descriptive study involving 161 consenting healthy HIV seronegative women: 80 pregnant and 81 nonpregnant. Information on their sociodemographic characteristics, obstetric, and past medical histories were obtained. Full blood count was determined by Mindray BC3200-automated hematological analyzer, and their platelet count (PLT), mean platelet volume, plateletcrit, and platelet distribution width (PDW) were retrieved. Data were analyzed using Epi Info version 3.5.1. Results: Platelet count that is most commonly used in clinical practice has a mean (±SD) value of 217.32 × 109 (± 64,990) cells/L in nonpregnant women and 205.48 × 109 (±57,226) cells/L in pregnant women. Only PDW showed statistically significant increase across the three trimesters as pregnancy advances (p = 0.02). The population reference ranges for PLT was 85.74–348.90 × 109 cells/L in nonpregnant women and 90.31–320.65 × 109 cells/L in pregnant women. Conclusion: Platelet indices are affected by pregnancy, and there is a need to redefine thrombocytopenia in pregnancy in our setting in order to minimize the risk of unnecessary interventions or denial of necessary treatment.

Keywords: Platelet indices, pregnancy, nonpregnant, thrombocytopenia, reference values

How to cite this article:
Babah OA, Oluwole AA, Amaeshi LC. Platelet indices in healthy pregnant and nonpregnant Nigerian women. Sub-Saharan Afr J Med 2018;5:117-22

How to cite this URL:
Babah OA, Oluwole AA, Amaeshi LC. Platelet indices in healthy pregnant and nonpregnant Nigerian women. Sub-Saharan Afr J Med [serial online] 2018 [cited 2020 Jan 24];5:117-22. Available from: http://www.ssajm.org/text.asp?2018/5/4/117/267124

  Introduction Top

Platelets play an important role in the body’s hemostatic mechanism. They initiate hemostasis by aggregating at the site of injury and plug endothelial defects that usually are a consequence of injuries sustained, in order to prevent further blood loss while other pathways of the coagulation system are being activated. Platelets are derived from megakaryocytes in the bone marrow. Compared to red blood cells, they have a shorter half-life of about 10 days.[1]

It is a well-known fact that pregnancy causes a lot of physiological alteration in most of the body systems, the hematological system inclusive. Although a lot has been documented on the effects of pregnancy on blood volume, packed cell volume, and white blood cell counts, not much has been documented about the physiological changes in platelet and platelet indices in pregnancy. The reference range for platelet count in the nonpregnant is generally accepted to be 150,000 to 400,000 cells/mL. However, considering the physiological changes that occur in pregnancy, there is a need to establish specific reference ranges in pregnancy.

Thrombocytopenia is defined as platelet count below 150 × 109/L or platelet count below 2.5th percentile for the population.[1],[2] It is said to be mild when platelet count is between 100 × 109/L and 150 × 109/L, moderate when the absolute count is between 50 × 109/L and 100 × 109/L, and severe when it is below 50 × 109/L. Thrombocytopenia found in otherwise healthy pregnant women is referred to as pregnancy-induced thrombocytopenia or gestational thrombocytopenia. The incidence of thrombocytopenia has been reported to be ∼7 to 10% of all pregnancies, of which 75% are gestational thrombocytopenia.[2],[3],[4]

The etiology of gestational thrombocytopenia is unknown; however, postulations regarding possible causes include hemodilutional effect of pregnancy, increased platelet consumption in pregnancy, and increased platelet aggregation driven by increased levels of thromboxane A2.[1] Yet quite a number of pathological conditions in pregnancy such as pre-eclampsia and eclampsia, HELLP syndrome (characterized by hemolysis, elevated liver enzymes, and low platelet count), systemic lupus erythematosus (SLE), antiphospholipid syndrome (APS), acute fatty liver of pregnancy, and immune thrombocytopenic purpura (ITP)[5] have significant effect on platelet counts with resultant adverse effects on the mother. In addition, certain drugs such as alpha methyl dopa, sulfonamides, aspirin, zidovudine, ranitidine, cimetidine, and penicillins are less common causes of thrombocytopenia in pregnancy.[6],[7] Human immunodeficiency virus (HIV) infection has also been reported to be a cause of thrombocytopenia.[8]

Some researchers have reported a decrease in platelet count in pregnancy compared to nonpregnant values.[9],[10] In a study by Boehlen et al., it was found that mean platelet count in nonpregnant women was 248 × 109/L, while in pregnancy it was 213 × 109/L, and there was no statistically significant difference between these values.[10] However, another study by Akingbola et al. found that mean value of platelet count in nonpregnant women was 330.87 × 109/L, while in pregnancy there was a significant difference in the mean platelet count between the three trimesters of pregnancy: 222.56 × 109/L in the first trimester, 229.56 × 109/L in the second trimester, and 186 × 109/L in the third trimester.[9] Amah-Tariah et al., however, did not find any significant difference in the mean values of platelet count, platelet volume, platelet distribution width (PDW), and plateletcrit (PCT) in different trimesters of pregnancy.[11]

Higher rates of induction of labor, preterm deliveries, placental abruption, lower APGAR scores of <7 at 5 minutes, and increased incidence of intrauterine growth restriction and stillbirth rates were found to be associated with maternal thrombocytopenia by Parnas et al.[12] But the adverse perinatal outcome were found in those with pathological causes of thrombocytopenia such as disseminated intravascular coagulopathy (DIC), ITP, APS, and myeloproliferative disorders, and not in those with gestational thrombocytopenia.[12] On the contrary, Boehlen et al. did not find any association between maternal complications and thrombocytopenia and none of the newborns of the women they studied had severe thrombocytopenia.[10]

Assessing platelet count in pregnancy is of clinical importance. It is useful in making diagnosis of HELLP syndrome, which often can be a complication of pre-eclampsia and eclampsia, determining the severity of these clinical disorders and assessing progress of treatment in HELLP syndrome, taking decision on the type of intervention to offer, for instance, type of anesthesia, mode of delivery and form of medical treatment to employ, timing of intervention, that is, when to institute certain medical treatment, and evaluating drug toxicity.

This study sought out to ascertain the effects of pregnancy on platelet count and platelet indices in the various trimesters of pregnancy, determine the incidence of thrombocytopenia in normal pregnancy, and derive a population reference range for platelet indices in pregnancy.

  Materials and Method Top

This was a cross-sectional analytical study conducted at the Lagos University Teaching Hospital (LUTH), the largest tertiary health institution in Lagos State, Nigeria. Ethical approval was obtained from the hospital’s Health Research and Ethics Committee with approval number ADM/DCST/HREC/282, and apparently normal women were enrolled from the hospital’s antenatal clinic and the hospital’s family planning clinics after obtaining their individual written consent. Eighty HIV seronegative pregnant women who met our selection criteria across the three trimesters of pregnancy were enrolled (cases) and 81 HIV seronegative nonpregnant women were matched for age and enrolled as controls. Gestational ages were calculated using the last menstrual period where applicable. Where a subject was unsure of her last menstrual period or there was discrepancy with the scan date, the earliest scan date was used. Those included in the study were apparently healthy women who are HIV seronegative on screening and who gave an informed written consent. Excluded from this study were women with a history of clinical illness such as recent malaria, tuberculosis, renal disease, diabetes mellitus, sickle cell disease, asthma, rheumatoid arthritis, autoimmune disorders, and so on, and those with a history of blood transfusion in the last 1 month. Also excluded were pregnant women with multiple gestations.

Information was collected using a proforma designed for this study and included the bio-demographic data of the participants, last menstrual period, estimated gestational age, and medical, social, and drug histories.

Five milliliters (5 mL) of blood was collected by venepuncture into a Vacutainer containing the anticoagulant EDTA, after the patients had rested for at least 15 minutes. All specimens were transported to the laboratory immediately or not later than 2 hours of collection and screened for HIV and subsequently analyzed for complete blood count using Mindray BC3200-automated hematological analyzer.

Data Management: The data obtained were analyzed using the Epi Info statistical software version 3.5.1. The mean values of the absolute platelet counts, mean platelet volumes (MPV), PDWs, and PCTs of each group and their standard deviations were determined. Chi-squared test, student t-test, and analysis of variance (ANOVA) were used where applicable in comparing values between groups. P-value <0.05 was considered to be statistically significant. The population reference ranges[13],[14] was established using the 95% prediction interval.

  Results Top

The mean age ± SD of all subjects was 32.3 ± 4.59 years, with a range of 22 to 45 years. There was no significant difference in the mean age of the pregnant women, 31.7 ± 4.16 years, and the nonpregnant women, 32.9 ± 4.94 years (P = 0.1042). The pregnant women were predominantly of low parity [Table 1].
Table 1 Age and Parity of Study Population

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The mean ± SD values of platelet count in this study was 217.32 ± 64.99 × 109/L in nonpregnant women and 205.48 ± 57.23 × 109/L in pregnant women. There is a decrease in mean platelet count (PLT), MPV, and PCT in pregnancy and a slight increase in PDW in pregnancy from nonpregnant values. These changes are, however, not statistically significant [Table 2].
Table 2 Mean of Platelet Count and Platelet Indices in Healthy Nonpregnant and Pregnant Women

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The reference ranges established for the population in this study for the various platelet indices using the 95% prediction interval was 85.74–348.90 × 109 cells/L and 90.31–320.68 × 109 cells/L for platelet count in nonpregnant and pregnant women, respectively. This shows a significantly lower limit in the reference range for platelet count in women. The population reference range for PDW was 14.80–16.28 in the nonpregnant women and 14.86–16.30 in pregnant women.

This study showed that while there is no statistically significant difference in the pregnant and nonpregnant mean platelet count values, there is a progressive fall as pregnancy advances toward the third trimester. The MPV and PDW fall initially in the first trimester of pregnancy from nonpregnant levels and thereafter rise progressively to reach values above the nonpregnant value in the third trimester of pregnancy [Table 3].
Table 3 Changes in Platelet Indices in Various Trimesters of Pregnancy

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The prevalence of thrombocytopenia among healthy pregnant women in this study using a cutoff of 150 × 109 cells/L originally derived for the general population was 15.1%, of which 13.8% of pregnant women had mild thrombocytopenia and 1.3% had moderate thrombocytopenia; none of the participants in this study had severe thrombocytopenia [Table 4] and [Table 5].
Table 4 Incidence and Severity of Thrombocytopenia in Pregnant and Nonpregnant Population at a Cutoff Value of 150 × 109 Cells/L

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Table 5 Prevalence of Genuine Thrombocytopenia and Thrombocytosis in Healthy Pregnant and Nonpregnant Nigerian Women Using the Reference Range Derived from This Study Based on 95% Prediction Interval

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However, using a cutoff value of 90 × 109 cells/L as derived from the reference values for pregnant women in this study, it was noted that 3 out of the 80 pregnant women studied had platelet count below 90,000 × 109 cells/L and thus the prevalence of genuine thrombocytopenia in pregnancy as defined in this study is 3.75%.

  Discussion Top

This study showed that there are changes in the platelet indices in pregnancy and mean values of these parameters differ from those in the nonpregnant women. The absolute platelet count (PLT) decreases by 5.45% in pregnancy. Similar trend was observed in other studies.[10],[15] The MPV and PCT also decrease in pregnancy; however, the PDW increases by 0.26% in pregnancy. These changes might be related to the blood volume expansion and hemodilution that occurs during pregnancy. An increase in PDW has also been associated with an increase in platelet activation.[16] This increase in PDW in pregnancy might contribute slightly to the hypercoagulability associated with pregnancy.[17] Of the platelet indices studied, the PDW showed the least alteration in pregnancy from nonpregnant values.

There is a significant increase in the PDW as pregnancy advances. There is also an increase in MPV with advancing gestation reaching values above the nonpregnant levels by the third trimester. This suggests that there is an increase in platelet production by the bone marrow during pregnancy, which does not reflect in the absolute platelet count as a result of the increase in plasma volume that occurs in pregnancy. This is probably a protective mechanism toward control of hemorrhage that occurs during delivery. The platelet count and PCT however show progressive decrease as gestational age increases. Akingbola et al.[9] also found statistically significant difference between the platelet counts in the three trimesters of pregnancy, with lowest values recorded in the third trimester. However, this study, just like a few others,[11],[18] did not show any significant differences in PLT, MPV, and PCT at different trimesters of pregnancy (p < 0.05). There is however a statistically significant difference in the PDW only (p = 0.02) and this finding is similar to that obtained in a study by Vera.[1]

An association between iron deficiency anemia and platelet indices has been found in some studies. Park et al.[19] reported a higher PLT, PCT, and PDW in severe hypochromic anemia and Cho et al.[20] found an increase in MPV and PLT in those iron deficiency anemia. This might be some form of protective mechanism in combating hemorrhage, the effect of which might be worsened by anemia.

The population reference range derived for platelet indices in this study showed wide variations in pregnant and nonpregnant women. The absolute platelet count, which showed the widest variation, is the most commonly used platelet index in clinical practice despite the availability of other platelet indices. PDW, which shows minimal change in pregnancy and is a reflection of the degree of platelet activation, may be considered a suitable alternative for use in measuring platelets in pregnancy.

Although there was no incidence of thrombocytosis (defined as PLT above 450 × 109 cells/L) in the women studied, thrombocytosis is a possible occurrence in pregnancy and has been found to be associated with adverse fetal and maternal outcomes such as increased incidence of spontaneous abortions, especially in the first trimester, fetal growth restriction, stillbirths, abruptio placentae, thrombosis, and maternal hemorrhage.[21],[22] This study revealed a prevalence of 15.1% for thrombocytopenia in pregnancy at a cutoff value of 150 × 109 cells/L. This value is similar to that obtained in a recent study in Ghana.[14] Much lower incidence of 11.6% was reported in a study by Ajzenberg et al.[3] Most of the pregnant women (13.8%) with thrombocytopenia have mild thrombocytopenia and this translates to 91.4% of thrombocytopenic women in pregnancy having platelet counts between 100 × 109 cells/L and <150 × 109 cells/L. It is thus important to always bear in mind the possibility of gestational thrombocytopenia in any apparently healthy pregnant woman with mild thrombocytopenia and no identifiable pathological factor. This was further buttressed by the discovery that the lower limit of the reference range derived in pregnancy was 90 × 109 cells/L, which means there is a need to redefine thrombocytopenia, especially in pregnancy in order to avoid unnecessary interventions or denial of necessary treatment in pregnant women with otherwise normal platelet counts. The prevalence of true gestational thrombocytopenia in this study using a cutoff value of 90 × 109 cells/L is therefore 3.75%.

It can be concluded that, like any other hematological parameter in pregnancy, platelet indices are affected by pregnancy. The lower limit of the reference range in pregnancy derived from this study is 90 × 109 cells/L, which is significantly lower than the value of 150 × 109 cells/L that is generally used in defining thrombocytopenia. There is thus a need to redefine thrombocytopenia in pregnancy in our setting in order to minimize the risk of unnecessary interventions or denial of necessary treatment.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Vera EV. Thrombocytopenia in pregnancy. Medscape Reference. Updated March 20, 2012. http:/emedicine.medscape.com/article/272867-overview.  Back to cited text no. 1
Parnas M, Sheiner E, Shoham-Vardi I, Burstein E, Yermiahu T, Levi I et al. Moderate to severe thrombocytopenia during pregnancy. Eur J Obstet Gynecol Reprod Biol 2006;128:163-8.  Back to cited text no. 2
Ajzenberg N, Dreyfus M, Kaplan C, Yvart J, Weill B, Tchernia G. Pregnancy-associated thrombocytopenia revisited: Assessment and follow-up of 50 cases. Blood 1998;92:4573-80.  Back to cited text no. 3
Shamoon RP, Muhammed NS, Jaff MS. Prevalence and etiological classification of thrombocytopenia among a group of pregnant women in Erbil City, Iraq. Turk J Haematol 2009; 26:123-8.  Back to cited text no. 4
McCrae KR. Thrombocytopenia in pregnancy: A differential diagnosis, pathogenesis and management. Blood Rev 2003;17:7-14.  Back to cited text no. 5
Aster RH, Bougie DW. Drug-induced immune thrombocytopenia. N Engl J Med 2007;357:580-7.  Back to cited text no. 6
Aster RH, Curtis BR, McFarland JG, Bougie DW. Drug-induced thrombocytopenia: Pathogenesis, diagnosis and management. J Thromb Haemost 2009;7:911-8.  Back to cited text no. 7
Khorvash F, Naeini AE, Behjati M, Jalali M. HIV associated thrombocytopenia, misdiagnosed as thrombotic thrombocytopenic purpura: A case report. Cases J 2009;2:175.  Back to cited text no. 8
Akingbola TS, Adewole IF, Adesina OA, Afolabi KA, Fehintola FA, Bamgboye EA et al. Haematological profile of healthy pregnant women in Ibadan, South-western Nigeria. J Obstet Gynaecol 2006;26:763-9.  Back to cited text no. 9
Boehlen F, Hohlfeld P, Extermann P, Perneger TV, de Moerloose P. Platelet count at term pregnancy: A reappraisal of the threshold. Obstet Gynecol 2000;95:29-33.  Back to cited text no. 10
Amah-Tariah FS, Ojeka SO, Dapper DV. Haematological values in pregnant women in Port-Harcourt, Nigeria II: Serum iron and transferrin, total and unsaturated iron binding capacity and some red cell and platelet indices. Niger J Physiol Sci 2011;26:173-8.  Back to cited text no. 11
Parnas M, Sheiner E, Shoham-Vardi I, Burstein E, Yermiahu T, Levi I et al. Moderate to severe thrombocytopenia during pregnancy. Eur J Obstet Gynecol Reprod Biol 2006;128:163-8.  Back to cited text no. 12
Marshal WJ. The interpretation of biochemical data. In: Marshall WJ, Bangert SK, editors. Clinical Biochemistry: Metabolic and Clinical Aspects. Philadelphia, PA: Churchill Livingstone/ Elsevier 2008. p. 19.  Back to cited text no. 13
Sterne JAC, Kirkwood BR, editors. The normal distribution. Essential Medical Statistics. 2nd ed. Malden, MA: Blackwell Science; 2003. p. 48.  Back to cited text no. 14
Chandra S, Tripathi AK, Mishra S, Amzarul M, Vaish AK. Physiological changes in hematological parameters during pregnancy. Indian J Hematol Blood Transfus 2012;28:144-146.  Back to cited text no. 15
Jaremo TL, Lindahl C, Forsgren H. The use of platelet density and volume measurements to estimate the severity of pre-eclampsia. Eur J Clin Inv 2000;30:1113-8.  Back to cited text no. 16
Vagdatli E, Gounari E, Lazaridou E, Katsibourlia E, Tsikopoulou F, Labrianou I. Platelet distribution width: A simple, practical and specific marker of activation of coagulation. Hippokratia 2010;14:28-32.  Back to cited text no. 17
Tygart SG, McRoyan DK, Spinnato JA, McRoyan CJ, Kitay DZ. Longitudinal study of platelet indices during normal pregnancy. Am J Obstet Gynecol 1986;154:883-7.  Back to cited text no. 18
Park MJ, Park PW, Seo YH, Kim KH, Park SH, Jeong JH et al. The relationship between iron parameters and platelet parameters in women with iron deficiency anemia and thrombocytosis. Platelets 2013;24:348-51.  Back to cited text no. 19
Cho SY, Yang JJ, Suh J, Lee W, Lee HJ, Park TS. Mean platelet volume/platelet count ratio in anemia. Platelets 2013;24:244-5.  Back to cited text no. 20
Valera M, Parant O, Vayssiere C, Arna J, Payrastre B. Essential thrombocythemia and pregnancy. Eur J Obstet Gynecol Reprod Biol 2011;158:141-7.  Back to cited text no. 21
Jønsson V, Bock JE, Mortensen TH, Staun M, Thorsen S. Pregnancy-related thrombocytosis. Ugeskr Laeger 2002;164:3946-9.  Back to cited text no. 22


  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


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