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 Table of Contents  
CASE REPORT
Year : 2019  |  Volume : 4  |  Issue : 2  |  Page : 234-236

A case report of neonatal alloimmune thrombocytopenia: The utility of platelet crossmatch studies in the diagnosis and management


1 Department of Neonatology, Manipal Hospital, Bengaluru, Karnataka, India
2 Department of Transfusion Medicine, Manipal Hospital, Bengaluru, Karnataka, India

Date of Submission13-Aug-2019
Date of Acceptance23-Sep-2019
Date of Web Publication17-Oct-2019

Correspondence Address:
Dr. H A Venkatesh
Department of Neonatology, Manipal Hospital, Bengaluru, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/GJTM.GJTM_50_19

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  Abstract 


Alloimmune thrombocytopenia is the most common cause of severe thrombocytopenia and intracranial bleed in the perinatal period, resulting from placental transfer of maternal platelet antibodies directed against the paternal-derived fetal platelet antigens. It is estimated to occur in 1 in 2500 births but continues to be an underdiagnosed and underreported condition in our country. Detection of human platelet antigen-specific antibody in the maternal serum and platelet genotyping are the gold standards in the diagnosis. This case report highlights the utility of platelet crossmatch studies in the diagnosis and management of neonatal alloimmune thrombocytopenia.

Keywords: Alloimmune thrombocytopenia, neonate, platelet crossmatch


How to cite this article:
Venkatesh H A, Paul A, Kantharaj A, Chandrashekar S. A case report of neonatal alloimmune thrombocytopenia: The utility of platelet crossmatch studies in the diagnosis and management. Glob J Transfus Med 2019;4:234-6

How to cite this URL:
Venkatesh H A, Paul A, Kantharaj A, Chandrashekar S. A case report of neonatal alloimmune thrombocytopenia: The utility of platelet crossmatch studies in the diagnosis and management. Glob J Transfus Med [serial online] 2019 [cited 2019 Nov 12];4:234-6. Available from: http://www.gjtmonline.com/text.asp?2019/4/2/234/269394




  Introduction Top


Neonatal Alloimmune Thrombocytopenia should be considered in any neonate who presents with severe thrombocytopenia at birth or shortly thereafter, particularly in the absence of other risk factors, clinical signs, or abnormalities in the physical examination. Diagnosis is mostly based on clinical suspicion. In resource limited settings platelet crossmatch studies help as a pointer to diagnosis and in providing compatible platelets.


  Case Report Top


A 13-day-old male baby was born to a primi mother at 35 weeks of gestation by Cesarean section for breech presentation. His birth weight was 2800 g. The perinatal period was uneventful, and his Apgar score was 6 and 9 at 1 and 5 min, respectively. On day 3 of life, he developed respiratory distress requiring newborn intensive care unit. He was ventilated for the respiratory distress for 3 days and weaned off to room air. The complete blood count revealed thrombocytopenia (platelet count: 21000/μl) with normal white cell count and hemoglobin. His coagulation parameters were within normal limits. The direct antiglobulin test was positive. He received multiple platelet transfusions with both random-donor platelets and single-donor platelets (SDPs) with no improvement in platelet count.

Platelet crossmatch studies were done using Capture-P, Ready-Screen platelet crossmatch kit for detection of immunoglobulin G antibodies to platelets (anti-human platelet antigen-1 [HPA-1] and anti-HPA-2) on NEO solid-phase automated system (Immucor, USA), and compatible platelets were chosen for transfusion. Transfusion with crossmatch compatible platelets yielded an increment of platelet count from 39000/μl to 75000/μl which raised the suspicion of neonatal alloimmune thrombocytopenia (NAIT). Further, the mother's plasma suspected to contain antiplatelet antibodies was crossmatched with the baby's platelets and the father's (husband's) platelets. The results of crossmatch are enumerated in [Table 1]. The patient was treated with intravenous immunoglobulin (IVIg) in a dose of 1 g/kg once daily for 2 days. Gradually, the platelet count improved. He was discharged home well on full feeds.
Table 1: Demonstration of platelet crossmatch results

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  Discussion Top


NAIT is the most common underlying cause of early-onset severe thrombocytopenia, with an incidence among live-born neonates of 0.5–1.5/1000 births.[1],[2]

The true incidence of the disease is likely higher, however, since milder cases might go undetected and the most severe cases lead to intrauterine death. Intrauterine death or intracranial hemorrhage (ICH) may occur as early as at 14–16-week gestation, resulting in a relatively high incidence of intrauterine ICH (>10%). The overall incidence of ICH (prenatal and postnatal) is particularly high in this population, affecting up to 20% of infants with NAIT.[3],[4],[5],[6]

NAIT should be considered in any neonate who presents with severe thrombocytopenia at birth or shortly thereafter, particularly in the absence of other risk factors, clinical signs, or abnormalities in the physical examination.

In the present case, a diagnosis of NAIT was arrived based on the results of platelet crossmatch and after excluding other causes of respiratory distress and thrombocytopenia such as infections and septicemia. This was an otherwise healthy baby except for the sudden onset of thrombocytopenia. Posttransfusion purpura as the cause of thrombocytopenia was unlikely because the baby had thrombocytopenia even before the platelet transfusions were given. Platelet crossmatch results showed incompatibility between the mother's plasma and the baby's platelets and the husband's/father's platelets suggesting alloimmune thrombocytopenia. In the absence of platelet antigen typing, compatible platelets for transfusion were chosen by crossmatching SDP with maternal serum. Maternal platelets were not considered for transfusion, and crossmatching between the baby's plasma and the mother's platelets was not done.

Platelet antigen studies would have helped to pinpoint the nature of the platelet antibody but could not be performed due to the absence of platelet-specific laboratories in India.

Direct antiglobulin test positivity in the absence of clinical hemolysis was attributed to intravenous immunoglobulin administration.

The most common antibody implicated in NAIT is anti-HPA-1a;[7] HPA-1a (PLA1)-negative phenotypes constitute 2% of North American population and 1% in Asians; therefore, theoretically, 1 in 50 live births (American) or 1 in 100 (Asian) population should have NAIT. However, the incidence is far less, estimated to occur in 1 in 1000–2000 births.[8] Maternal immunization to HPA-1a shows human-leukocyte antigen (HLA) restriction. HPA-1a-negative women who produce alloantibodies are almost exclusively HLADRB3*0101 or DQB1*0201. Most cases of NAIT are caused by alloantibodies to HPA-1a, HPA5b (Bra), and HPA-15b (Gova). Other alloantigens implicated in NAIT are HPA-1b (PLA2), HPA-3a (Baka), HPA-3b (Bakb), HPA-4a (Pena), HPA-4b (Penb), HPA-5a (Brb), and HPA-15a (Govb).[9]

In resource-limited settings, platelet crossmatch studies of newborns and mothers help as a pointer toward a diagnosis of NAIT. However, platelet antigen studies help in establishing a diagnosis. Transfusion of platelets crossmatched and compatible with the mother's plasma may help in better management and better clinical outcomes.


  Conclusion Top


The first suspicion of NAIT usually arises when an otherwise normal newborn presents with thrombocytopenia with or without bleeding manifestations such as petechial hemorrhages, ecchymoses, or other bleeding symptoms. NAIT can be diagnosed clinically in most cases by exclusion of other causes of thrombocytopenia. Demonstrating incompatibility between the baby's serum and paternal platelets clinches the diagnosis even in the absence of HLA antigen studies. A normal platelet count in the mother ruled out immune thrombocytopenia.

Early diagnosis and treatment with IVIg or transfusion with crossmatched platelets is the key for better management of NAIT.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ferrer-Marin F, Liu ZJ, Gutti R, Sola-Visner M. Neonatal thrombocytopenia and megakaryocytopoiesis. Semin Hematol 2010;47:281-8.  Back to cited text no. 1
    
2.
Bertrand G, Jallu V, Gouet M, Kjaer KM, Lambin P, Husebekk A, et al. Quantification of human platelet antigen-1a antibodies with the monoclonal antibody immobilization of platelet antigens procedure. Transfusion 2005;45:1319-23.  Back to cited text no. 2
    
3.
Caraciolo Fernandes J. Neonatal Thrombocytopenia. Avilable from: https://www.uptodate.com/contents/neonatal-thrombocytopenia-etiology. [Last accessed on 2019 Sep 21].  Back to cited text no. 3
    
4.
Blanchette VS, Johnson J, Rand M. The management of alloimmune neonatal thrombocytopenia. Baillieres Best Pract Res Clin Haematol 2000;13:365-90.  Back to cited text no. 4
    
5.
Berkowitz RL, Bussel JB, McFarland JG. Alloimmune thrombocytopenia: State of the art 2006. Am J Obstet Gynecol 2006;195:907-13.  Back to cited text no. 5
    
6.
Arnold DM, Smith JW, Kelton JG. Diagnosis and management of neonatal alloimmune thrombocytopenia. Transfus Med Rev 2008;22:255-67.  Back to cited text no. 6
    
7.
Davoren A, Curtis BR, Aster RH, McFarland JG. Human platelet antigen-specific alloantibodies implicated in 1162 cases of neonatal alloimmune thrombocytopenia. Transfusion 2004;44:1220-5.  Back to cited text no. 7
    
8.
Brojer E, Husebekk A, Dębska M, Uhrynowska M, Guz K, Orzińska A, et al. Fetal/Neonatal alloimmune thrombocytopenia: Pathogenesis, diagnostics and prevention. Arch Immunol Ther Exp (Warsz) 2016;64:279-90.  Back to cited text no. 8
    
9.
Greer JP, Foster JF, Rodgers GM, Paraskavas F, Glader B, Arber DA, et al. Wintrobe's Clinical Haematology. Philadelphia: Lippincott Williams & Wilkins; 2009.  Back to cited text no. 9
    



 
 
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