Thrombocytopenia In Newborns Research Articles

THROMBOCYTOPENIA IN NEONATES: INCIDENCE, PRESENTATION, AND STUDY OF CORRELATED FACTORS AT A LAHORE TEACHING HOSPITAL

Background: Patients with thrombocytopenia have been observed to experience changes in their coagulation profile and severity of disease. This study aims to see the incidence, presentation, and correlating factors of thrombocytopenia in newborns. Methods: From Jan 2023 to Jan 2024, 200 newborns in the Paediatric and Pathology Departments of Chaudhry Muhammad Akram Teaching and Research Hospital participated in a cross-sectional study. Utilizing SPSS-23, overall data was analysed. Results: In this study 138 (69%) of the 200 newborns were female, and 62 (31%), were male. Seventy-six (38%) neonates had thrombocytopenia, whereas 124 (62%), neonates had normal platelet counts. Of the 76 newborns, 42 (21%) had mild thrombocytopenia, 25 (12.5%) had moderate thrombocytopenia, and 9 (4.5%) had severe thrombocytopenia. Thirty-five percent early-onset neonatal thrombocytopenia (EOT) had early onset thrombocytopenia, while 46 (23%) had thrombocytopenia in the late onset (LOT) phase. There was a strong correlation discovered between thrombocytopenia and anaemia, jaundice asphyxia, low birth weight, preterm and full-term neonatal birth, and neonatal jaundice. The correlation of bleeding in neonates with thrombocytopenia was significant (p>0.05). Conclusion: Moderate to severe thrombocytopenia in newborns often follows mild thrombocytopenia. Thrombocytopenia is highly correlated with bleeding, preterm birth, full-term birth (extensive monitoring during childbirth), anaemia, hypoxia, and sepsis. In sick newborns, severe thrombocytopenia is considered as a prognostic marker. Pak J Physiol 2024;20(3):37–9, DOI: https://doi.org/10.69656/pjp.v20i3.1703

Incidence of Thrombocytopenia in NICU and Its Association with Immature Platelet Fraction and Absolute Immature Platelet Count: A Cross-sectional Study

Introduction: Neonatal Thrombocytopenia (TCP) is frequently encountered in the Neonatal Intensive Care Unit (NICU), occurring either due to decreased production or increased destruction of platelets. This condition often leads to increased platelet transfusions in a NICU setting. Immature Platelet Fraction (IPF) and Absolute Immature Platelet Count (AIPC) are hypothesised to be surrogate markers of bone marrow activity and can help in differentiating between TCP caused by decreased production or increased destruction. Aim: To estimate the incidence of neonatal TCP in newborns admitted to a tertiary care NICU and to investigate the association of IPF percentage and AIPC values with the cause of TCP. Materials and Methods: This cross-sectional study was conducted in the Department of Paediatrics and Neonatology at Dr. D.Y. Patil Medical College, Navi Mumbai, Maharashtra, India, from April 2021 to May 2022. All 46 newborns admitted to the NICU with TCP were enrolled in the study. The total number of NICU admissions during the study period was used to calculate the incidence. The Complete Blood Count (CBC) with reticulocyte count and peripheral smear was examined using the impedance technique. The IPF and AIPC values were determined using an automated CBC counter based on flow cytometry principles. Statistical analysis was performed using the Chi-square test. Results: The study included a total of 46 neonates with TCP, with an incidence rate of 6.14%. Among the patients with TCP, 18 (39.13%) had mild, 17 (36.95%) had moderate, and 11 (23.91%) had severe TCP. The majority of neonates (21.7%) had a significant maternal history of Pregnancy Induced Hypertension (PIH). Of the neonates with TCP, 42 (91.3%) had high IPF and 4 (8.6%) had normal IPF. Regarding AIPC, 29 (63.04%) had normal values, 11 (23.91%) had high values, and 6 (13%) had low values. No significant association was found between IPF and AIPC values and the diagnosis of TCP in this study. Conclusion: The present study concludes that IPF and AIPC investigations cannot be recommended as markers to confirm the cause of TCP.

Heparin-induced thrombocytopenia in newborns: experience at a pediatric hospital and a literature review

Heparin-induced thrombocytopenia in newborns: experience at a pediatric hospital and a literature review

A rare combination of immune thrombocytopenia and disaggregation thrombocytopathy: course and termination of pregnancy complicated by COVID-19 (Clinical case)

Immune thrombocytopenia (ITP) is an autoimmune disease which is characterized by antibody-mediated destruction of platelets by the reticuloendothelial system. The rate of ITP is 3.3 per 100,000 adults per year with a prevalence of 9.5 per 100,000 adults. Pregnancy does not increase the frequency or severity of ITP, but ITP can significantly affect pregnancy and cause bleeding in women.Pregnancy requires regular control of the number of platelets: monthly in the I and II trimesters, every 2 weeks – in the III trimester, and weekly control near the delivery date. Indications for treatment are determined by the pregnant woman condition, not the fetus, since it has not been proven that the treatment reduces the risks of thrombocytopenia in newborns with the development of cerebral hemorrhage.The drug of the first line of treatment of such pathology is prednisolone at a dose of 1 mg/kg orally once a day. An increase in the number of platelets is usually observed within 3-7 days, the maximum response is determined after 2-3 weeks. If necessary, the dose can be increased. When the required level of platelets is reached, the dose can be gradually reduced by 10-20 % to the minimum dose necessary to maintain the number of platelets at an acceptable level.Thrombocytopathy can be the cause of primary hemostasis disorders, even if the number of platelets in the blood is normal. For diagnosis, tests are carried out to detect the aggregation ability of platelets. In addition, flow cytometry can be used, which makes it possible to detect the defects of surface membrane receptors, as well as defects of the end point of secretion.ITP is a common cause of thrombocytopenia after viral infections. The onset of this pathology is more often detected in the second and third weeks after the onset of COVID-19. The treatment aim is to prevent the significant bleeding in patients with COVID-19.The article presents a clinical case of a pregnant woman with ITP and thrombocytopathy, whose pregnancy was complicated by COVID-19. The patient complained on bleeding gums, the appearance of hematomas on the skin. Medical treatment of the main disease included prednisolone, eltrombopag, intravenous human immunoglobulin, transfusion of platelet concentrate. At 34–35 weeks of pregnancy alive boy was born with a body weight of 2800 g, length of 49 cm, 7–8 points on the Apgar scale.

Immune neonatal thrombocytopenia - review

Introduction: Thrombocytopenia is the most frequent hematological change in the neonatal period, with immune thrombocytopenia as the main cause of moderate-to-severe thrombocytopenia in apparently healthy newborns. Immune thrombocytopenia in the fetus or newborn may result from platelet alloantibodies against paternal antigens inherited by the fetus (alloimmune thrombocytopenia) or platelet autoantibodies due to maternal autoimmune disease (autoimmune thrombocytopenia).Objetives: To review published literature about immune thrombocytopenia in newborns, including the latest advances in pathogenesis, diagnosis, treatment, and prevention.Results: Neonatal alloimmune thrombocytopenia is the most common cause of severe thrombocytopenia and intracranial hemorrhage in term neonates. Clinical presentation varies from mild thrombocytopenia to life-threatening bleeding and death. As maternal screening is not routinely performed, most cases are diagnosed in the first child. Despite intensive research, a consensus strategy for prevention and treatment of the condition is lacking. Diagnosis of neonatal autoimmune thrombocytopenia is usually apparent from maternal medical history and thrombocytopenia. Although maternal immune thrombocytopenic purpura does not carry a high risk of perinatal hemorrhage, it may lead to thrombocytopenia in the newborn, mostly mild-to-moderate. Clinical presentation varies from no symptoms to mucocutaneous signs of thrombocytopenia and may persist for weeks to months requiring long-term monitoring. Conclusions: Fetal and Neonatal alloimmune thrombocytopenia can cause severe disease in the affected fetus or newborn. Facing the lack of routine antenatal screening, the strategies currently proposed for pregnancies at risk. We also discussed the latest research and therapies in development, aiming at potential improvements in diagnosis, treatment, and prevention of this disease. Neonatal autoimmune thrombocytopenia may cause long-lasting low platelet count, that need regular checking.

5 Years' Experience of a Tertiary Center with Thrombocytopenic Pregnancies: Gestational Thrombocytopenia, Idiopathic Thrombocytopenic Purpura and Hypertensive Disorders of Pregnancy.

Aim To evaluate thrombocytopenic pregnancies including gestational thrombocytopenia (GT), idiopathic thrombocytopenic purpura (ITP), and hypertensive disorders of pregnancy (HDP). Materials and Methods We evaluated the pregnancy outcomes and laboratory findings of 385 patients diagnosed with GT, ITP, or HDP whose thrombocyte levels were < 150 000/µL. Results GT, ITP, and HDP were the final diagnoses in 315 (81.8%), 35 (9.1%), and 35 (9.1%) cases, respectively. Patients diagnosed during the 1st trimester and diagnosed with ITP had significantly lower minimal platelet counts during the antenatal period and prior to delivery (p < 0.001; p < 0.001; p < 0.001; p < 0.001). Transfusion of any kind of blood product was given in 9.9% (n = 38) of all cases. Twelve patients had methylprednisolone and/or intravenous immunoglobulin treatments during the antenatal period. All patients who had undergone medical treatment were also found to have ITP. Four out of 385 patients underwent hysterectomy post partum due to refractory hemorrhage. Analysis of newborn platelet levels showed no statistical differences between any of the groups. Despite the lack of statistical significance, the rate of thrombocytopenia in newborns was 50% in patients with severe thrombocytopenia, while rates were 25.6 and 18.1% in patients with moderate and mild thrombocytopenia, respectively. Conclusion Thrombocytopenic pregnancies must be carefully evaluated with regard to the severity of thrombocytopenia, gestational period at initial diagnosis, and etiology. In particular, patients with ITP must be evaluated carefully as these patients are more likely to require transfusions and have platelet counts < 50 × 10 3 /µl.

Plasma thrombopoietin levels as additional tool in clinical management of thrombocytopenic neonates

Plasma thrombopoietin (Tpo) levels distinguish thrombocytopenia resulting from increased platelet destruction or decreased platelet production. We investigated whether measuring plasma Tpo levels in thrombocytopenic newborns is of diagnostic value to establish the underlying mechanism of thrombocytopenia.Tpo levels were measured with in-house developed ELISA in samples referred to our center because of thrombocytopenia noticed in the first 10 days of life. Clinical data were collected.Plasma Tpo levels <128 AU/ml were found in the majority (92%) of 121 newborns with immune-mediated thrombocytopenia (n = 104) and thrombocytopenia due to bacterial infections (n = 7); increased plasma Tpo levels (≥128 AU/ml) were found in thrombocytopenic newborns with severe asphyxia (n = 24). Highly increased plasma Tpo levels (>200 AU/ml) were found in thrombocytopenic neonates with congenital viral infections (n = 22) or amegakaryocytosis (n = 6). A plasma Tpo level <128 AU/ml excludes (negative predictive value 96%, 95% CI 90–99) severe asphyxia, congenital viral infections and amegakaryocytosis as the cause for thrombocytopenia in newborns.Increased plasma Tpo levels indicate that thrombocytopenia in newborns, as a result of various nonimmune disorders, is often caused by (temporary) bone marrow suppression/failure. Measurement of plasma Tpo levels provides the clinician with an additional tool to decide on the differential diagnosis, the necessity for subsequent diagnostics and treatment in neonates with thrombocytopenia.

Trombocitopenija kao jedan od razloga produžene hospitalizacije na Odeljenju neonatalne intenzivne nege

The aim of this paper was to present the occurrence and severity of thrombocytopenia, with intracranial and another bleeding in neonates with sepsis, analyze the risk factors for the development of thrombocytopenia and compare it with the length of hospitalization in the Neonatal Intensive Care Unit (NICU). Thrombocytopenia is a platelet count &lt;150 x 109/L and is common in newborns during hospitalization in the NICU. In the early days of life, the most common causes of thrombocytopenia in newborns are conditions that lead to fetal hypoxia, intrauterine growth failure, maternal hypertension, and sepsis. In this study were included all newborns with thrombocytopenia, who were hospitalized in NICU, Children's Disease Clinic, University Clinical Centre in Tuzla, from 01. 01. 2014 to 01. 01. 2019. In our results, 379 newborns had severe, 337 moderate, and 127 milder forms of thrombocytopenia, without a statistically significant difference in the incidence of thrombocytopenia between groups of neonates born &lt; 37 GW and 37 GW. Sepsis was the most common cause of thrombocytopenia, 300 children had early sepsis and 190 late. We found the statistically significant difference in intracranial hemorrhage of the second degree and pulmonary hemorrhage among neonates born &lt; 37 GW in relation to newborns born 37 GW. A statistically significant effect of length of stay of our neonates in the Department of Neonatal Intensive Therapy and morbidity was shown in relation to the lower gestational age and lower platelet counts. Conclusion: Timely diagnosis of the cause and development of thrombocytopenia with adequate and effective treatment can reduce the mortality and morbidity of newborns with perinatal risk for neonatal thrombocytopenia.

PP-18 Ranitidine-induced thrombocytopenia in a neonate-a case report and review of literature

Background Thrombocytopenia is defined as a plate-let count 72 hours)-onset thrombocy-topenia are caused by different categories of underlying conditions. Chronic fetal hypoxia and sepsis or necrotiz-ing enterocolitis are by far the most frequent causes of, respectively, early-and late-onset neonatal thrombocy-topenia.1,3 Methods We describe the clinical case of a SGA (small for gestational age) neonate who experienced a severe ranitidine-induced thrombocytopenia. An extensive lit-erature search was performed to document other cases of ranitidine-and H2-antagonist-induced thrombocyto-penia. Furthermore, other case reports of drug-induced thrombocytopenia in newborns were explored. Results We report on a late preterm male infant, who showed an unexpected, severe thrombocytopenia (8 × 109/L) at day 5 of life. He was born SGA and had also showed a mild early-onset thrombocytopenia with a low-est platelet count of 87 × 109/L on day 1, spontaneously normalising by day 3 (169 × 109/L). The low platelet count on day 5 only minimally responded to platelet transfu-sion. It did however recover completely within 5 days after cessation of ranitidine (4 × 0.5 mg/kg/day), which was started on day 3 of life in a context of feeding diffi-culties. Other causes of neonatal thrombocytopenia were explored and ruled out. The likelihood of an adverse drug reaction in this case was indicated as ‘probable’ on the Naranjo scale.4 Besides a brief report on a cimetidine-in-duced thrombocytopenia over 25 years ago,5 no other neonatal or paediatric cases of H2-antagonist-induced thrombocytopenia have been reported to date. Several adult cases have been published nevertheless.6 It seems that neonatalthrombocytopenia, although one of the most frequent haematological conditions in newborns, is only rarely attributed to an adverse drug reaction. Conclusion Neonatal thrombocytopenia is a frequent haematological abnormality and has a variety of causes. In rare cases, this low platelet count might be caused by an adverse drug reaction, supposedly immune-mediated. Although H2-antagonist are widely used in paediatric and neonatology departments, we describe the first case of a severe ranitidine-induced thrombocytopenia in a neo-nate. We believe that SGA infants are more at risk because of their inherent state of bone marrow depression at birth. Clinicians should be aware of the risks for (unexpected) adverse reactions, especially in routinely used drugs and in critically ill patients. Case reports may aid in expanding our knowledge of rare pharmacological complications.

Neonatal Thrombocytopenia Associated with Breast Milk

Immune-mediated thrombocytopenia in newborns can result from the placental transfer of autoantibodies, generally of the immunoglobulin-G type, from

Glanzmann's Thrombasthenia Complicating Pregnancy.

Glanzmann’s thrombasthenia is a rare autosomal recessive hemorrhagic disorder caused by abnormal platelet glycoprotein complex (GP IIb-IIIa) presenting with hemorrhagic symptoms. Pregnancy is not uncommon because fertility is not affected but an association is rare. Also delivery often results in haemorrhage. Newborn thrombocytopenia is occasionally severe, but is always transitory. We report a 21-year old primigravida, who underwent vaginal delivery at term with IUGR and Oligohydramnios. Glannzmann’s thrombasthenia was characterized by aggregation and this patient went undiagnosed till adolescence until evaluated for puberty menorrhagia which is uncommon. She received single donor platelet transfusion during the intrapartum period along with tranexemic acid. Platelet transfusion may result in alloimmunization and make successive transfusions less effective. We did not use Factor VII in the intrapartum period due to cost and suspected fetal effects. Postnatally she had hematuria settled on the 2nd day with conservative management. We present this case because of association of Glanzmann’s thrombasthenia with IUGR and oligoamnios the only reported case so far.

Glanzmann’s Thrombasthenia Complicating Pregnancy

Glanzmann’s thrombasthenia is a rare autosomal recessive hemorrhagic disorder caused by abnormal platelet glycoprotein complex (GP IIb-IIIa) presenting with hemorrhagic symptoms. Pregnancy is not uncommon because fertility is not affected but an association is rare. Also delivery often results in haemorrhage. Newborn thrombocytopenia is occasionally severe, but is always transitory. We report a 21-year old primigravida, who underwent vaginal delivery at term with IUGR and Oligohydramnios. Glannzmann’s thrombasthenia was characterized by aggregation and this patient went undiagnosed till adolescence until evaluated for puberty menorrhagia which is uncommon. She received single donor platelet transfusion during the intrapartum period along with tranexemic acid. Platelet transfusion may result in alloimmunization and make successive transfusions less effective. We did not use Factor VII in the intrapartum period due to cost and suspected fetal effects. Postnatally she had hematuria settled on the 2nd day with conservative management. We present this case because of association of Glanzmann’s thrombasthenia with IUGR and oligoamnios the only reported case so far.

Maternal Anti-HPA1a Antibody Level as Predictive Value in Neonatal Alloimmune Trombocytopenic Purpura (NAITP).

Abstract NAITP is suspected if a neonate unexpectedly presents with petecchiae and is severely trombocytopenic. The thrombocytopenia is caused by maternal alloantibodies to platelet-specific antigens, most often anti-HPA 1a. A mother who has previously given birth to an affected child is usually considered at high risk for giving birth to a trombocytopenic child also in the subsequent pregnancy. The aim of the present study was to compare to what extent quantification of anti-HPA 1a versus obstetric history can predict the severity of thrombocytopenia in new-borns. Anti-HPA 1a was repeatedly quantified in 152 immunized pregnant women who were included in a large Norwegian prospective study. Sixty-eight of the women gave birth to thrombocytopenic children of which 42 suffered severe thrombocytopenia (plt. count &lt;50x109/l). Ten women had previously given birth to children with symptomatic NAITP. Five of these did not give birth to children with severe thrombocytopenia in their subsequent pregnancy. Positive predictive values for thrombocytopenia (&lt;150x109/l) were 0.75 using obstetric history and 0.80 for anti-HPA 1a antibody level above 100 Arbitrary Units (AU). Positive predictive values for severe NAITP (&lt;50x109/l) were hence 0.50 and 0.51 for obstetric history and antibody level. However, the diagnostic sensitivity for obstetric history was only 0.12, whereas anti-HPA 1a level above 100 AU had a diagnostic sensitivity of 0.88. In addition, we found that the level of anti-HPA1a tend to increase in first pregnancy and decrease in subsequent non-compatible pregnancies. This observation is in accordance with the fact that half of the women, who gave birth to NAITP children in their first pregnancy, did not get an affected child in their next pregnancy. In conclusion, obstetric history only identifies a few of the affected cases since all first time cases of sever NAITP are missed. Both obstetric history and antibody level has comparable positive predictive values for severe NAITP. However, the level of anti-HPA 1a antibody would be the best marker to identify severe NAITP cases because of independence of parity and obstetric history.

Approach to the Newborn Who Has Thrombocytopenia

After completing this article, readers should be able to: 1. List the platelet counts that represent mild, moderate, and severe thrombocytopenia. 2. List common causes of thrombocytopenia in sick neonates, preterm infants, and infants who have other medical conditions. 3. List the conditions characterized by physical abnormalities or dysmorphic features that commonly are associated with thrombocytopenia. 4. List potential causes of thrombocytopenia in healthy-appearing neonates. 5. Describe the clinical manifestations of and treatment for neonatal alloimmune thrombocytopenia. Platelet counts in healthy fetuses (mid-second trimester) and neonates are the same as in normal children and adults. Neonatal platelet counts of 100 to 150 × 10 3/mcL (100 to 150 × 10 9/L) represent mild thrombocytopenia, platelet counts of 50 to 100 × 10 3/mcL (50 to 100 × 10 9/L) are considered moderate thrombocytopenia, and levels less than 50 × 10 3/mcL (50 × 10 9/L) are categorized as severe thrombocytopenia. Thrombocytopenia in newborns is a result of increased platelet consumption (infections, thrombosis, immune-mediated) or decreased platelet production. In many neonates, particularly sick preterm infants, both impaired megakaryopoiesis and accelerated platelet destruction may occur simultaneously. Mild asymptomatic thrombocytopenia occurs in 1% of healthy term infants. Severe thrombocytopenia in term infants, however, is rare, and most affected infants usually are recognized because of hemorrhagic manifestations (petechiae, purpura, or frank bleeding). Any term neonate whose platelet count is less than 50 × 10 3/mcL (50 × 10 9/L) should be evaluated to establish a cause. In contrast to the rarity of thrombocytopenia in healthy term neonates, low platelet counts are noted commonly in sick infants who often are preterm. Up to 25% of infants admitted to the neonatal intensive care unit (NCIU) have thrombocytopenia. Also, in contrast to term newborns who present with hemorrhagic manifestations, most cases of thrombocytopenia in …

Thrombasthénie de Glanzmann et grossesse : à propos d’un cas, revue de la littérature

Glanzmann's thrombasthenia is a thrombopathy due to a qualitative or quantitative abnormality of glycoproteins GP IIb-IIIa. Pregnancy is uncommon and dangerous. Delivery often results in important haemorrhage, which is treated with HLA compatible platelet and packed red blood cells transfusions. Platelet transfusion may produce antibody that render transfusions ineffective. Newborn thrombocytopenia is occasionally severe, but is always transitory. Caesarean section has no proven advantage. We report a case with caesarean, which was successfully managed by platelet transfusion over seven peripartum days, with no adverse event. Literature is discussed.

Development and validation of a genotyping kit for the eight principal human platelet alloantigen systems

Thrombocytopenia in newborns is often due to maternal alloimmunization against platelet alloantigens of the foetus which have been inherited from the father and are absent in the mother. Our aim was to develop a "ready-to-use" typing kit based on polymerase chain reactions, using sequence-specific primers for rapid and simultaneous genotyping of the eight principal human platelet alloantigens. The typing technique uses two specific primer pairs for each bi-allelic system and a monomorphic primer pair as amplification control, with a single temperature cycle programme and identical PCR stringency conditions for all pairs of primers. This kit allows typing of blood samples of small volume within three hours after reception. Validation criteria are essential to check the reliability and specificity of the test, and DNA controls carrying the targeted HPA alleles must be obtained from typed individuals or created in vitro by PCR.

Frequency of Immune Thrombocytopenia in Newborns: A Prospective Study

Thrombocytopenia is a common condition in distressed newborns, but little is known about thrombocytopenia in an unselected cohort of neonates. In an attempt to address this issue, a multicenter prospective study was conducted in three obstetrical wards of AP-HP in Paris. We found the frequency of neonatal thrombocytopenia (<150 x 10(9)/L) to approximate 0.9% (48 of 5,632 appropriate samples). An immune mechanism was likely to be the cause of thrombocytopenia in 10 of the 33 cases studied, implying an incidence of 0.3% of immune neonatal thrombocytopenia in the general population. The frequency of alloimmune thrombocytopenia was 1.5/1,000 liveborn neonates, and 1/1,000 when considering anti-HPA-1a allo-immunization. Because thrombocytopenia, whatever its cause, was often silent and delayed, it appears that the only way to detect neonatal thrombocytopenia in time to prevent its potential disastrous complications would be to perform a systematic neonatal blood sampling for platelet count. All cases of ascertained thrombocytopenia should then be screened for an immune mechanism to enable early detection of autoimmune diseases in mothers and careful monitoring of subsequent pregnancies and deliveries, leading to appropriate prevention of potential severe deleterious effects in the offspring.

Analysis of immunoglobulin class, IgG subclass and titre of HPA‐1a antibodies in alloimmunized mothers giving birth to babies with or without neonatal alloimmune thrombocytopenia

We analysed the titre and isotype composition of antibodies produced by mothers giving birth to babies with or without neonatal alloimmune thrombocytopenic purpura (NAITP) and patients with post-transfusion purpura (PTP). All these individuals produced an antibody specific for the HPA-1a allotype present on the platelet glycoprotein IIb-IIIa (GPIIb-IIIa). Sera from mothers who gave birth to thrombocytopenic babies (group 1, n = 36), non-thrombocytopenic babies (group 2, n = 4) or from PTP patients (group 3, n = 3) were tested by an indirect-ELISA. Results indicated no evident differences in the isotype composition or titre of the antibodies from the three groups of sera. The antibody titre ranged from 1:120 to 1:3500. Antibodies with the IgG1 subclass were present in all sera. Most sera contained IgG1 alone (24/43 sera tested) or in combination with IgG3 (10/43). IgG2 was never present and only three sera showed intermediate reactivity with anti-IgG4 MAb. Few sera (nine sera from groups 1 and 2) were weakly positive when tested with the anti-IgM antibodies. These results suggest that neither the titre nor the isotype composition can be used to predict the severity or the occurrence of thrombocytopenia in newborns.

The adverse effect on fetal hemogram by preeclampsia: marked anisocytosis with normocytic, normochromic erythrocythemia as well as thrombocytopenia

Whether preeclampsia affects the fetal hematologic system still remains a controversial issue. The purpose of this series was to examine the hypothesis that preeclampsia may or may not cause adverse effects on fetal hemogram, including erythrocytes, leukocytes, and platelets. In addition, no one, to date, has reported the effect on red cell distribution width (RDW) of fetal cord blood by preeclampsia. Therefore this series also tested the hypothesis that preeclampsia may induce elevation of RDW in fetal cord blood. From August 1, 1989 to July 31 1990, we prospectively collected cord blood samples at parturition from 21 preeclamptic pregnancies and 366 uncomplicated controls and measured their complete blood counts by computerized blood autoanalyzer. The results of the comparison with red blood cells showed significant erythrocythemia (P < 0.05), increased hematocrit (P < 0.05), elevated hemoglobin (P < 0.05), and marked anisocytosis (as reflected by RDW, P < 0.0001) in preeclamptic pregnancies than in controls. Though no significant differences were demonstrated in the white cell counts, severe thrombocytopenia (P < 0.001) was observed in the preeclamptic group than in controls. We concluded that preeclampsia may cause significant normocytic, normochromic erythrocythemia, marked anisocytosis and severe thrombocytopenia in newborns, which deserved the attention of obstetricians and neonatologists. Further studies are warranted to elucidate the underlying pathophysiological mechanisms.

Thrombocytopenia in Newborns, Infants, and Children

There are many causes of thrombocytopenia in infants and children. With experience, they can be readily identified and appropriate treatment instituted, if required. Particular attention should be paid to the well baby with unexplained thrombocytopenia, as alloimmune thrombocytopenia is the most common cause of intracranial hemorrhage due to thrombocytopenia and can be prevented if identified and treated early on. Autoimmune thrombocytopenia of childhood is generally benign, but children may require careful management until spontaneous resolution occurs. Human immunodeficiency virus infection should be looked for in these patients.