SUMMARY. Neonatal alloimmune thrombocytopenia (NAIT) is caused by platelet antigen incompatibility between the mother and fetus. NAIT is mainly due to alloimmunization; the frequency varying among ethnic groups. In Caucasians HPA‐la is the antigen most frequently implicated. In Japan, NAIT due to anti‐HPA‐4b antibody has already been described, but this is the first case to be reported in Caucasians.
Background: Incompatibilities between the mother and unborn baby can cause complications that must be identified early to initiate the appropriate treatment. For example, neonatal alloimmune thrombocytopenia (NAIT), neonatal alloimmune neutropenia (NAIN), and morbus hemolyticus neonatorum affect children worldwide. Aim: This literature review aims to depict the similarities and differences between these three disorders from a clinical and mechanistic point of view. Material and Methods: The current literature review entailed conducting a systematic search to locate articles on the three conditions. Different electronic databases, including PsycINFO, PubMed, Web of Science, and CINAHL, were searched using the search terms “neonatal alloimmune thrombocytopenia”, “neonatal alloimmune neutropenia”, “morbus hemolyticus neonatorum”, “NAIT”, “FNAIT”, “fetal”, “NAIN”, and “hemolytic disease of the newborn”. Results: This review shows that these three diseases are caused by incompatibilities between the maternal and fetal immune systems. Furthermore, these conditions can lead to severe complications that hinder fetal development and cause death if not well managed. Discussion: The current literature review shows that NAIT, NAIN, and morbus hemolyticus neonatorum are rare conditions that occur when the mother produces antibodies against the fetal immune system. Thus, there is a need for the early detection of these conditions to initiate appropriate treatment before the child experiences adverse effects. Conclusion: The development of NAIT, NAIN, and morbus hemolyticus neonatorum is linked to the production of antibodies against the fetal immune system and fetal antigens. Further studies are required to determine potential interventions to reduce the risk of developing these three conditions.
SUMMARY. Neonatal thrombocytopenia affects 20–40% of the infants in intensive care units. The frequency of neonatal alloimmune thrombocytopenia (NAIT) is estimated at 1/1500 to 1/5000 live births. The risk of morbidity is significant with 20% neurological sequelae and the death rate is estimated at 10% of affected infants. During recent years considerable efforts have been made to prevent fetal bleeding and to avoid birth trauma, which have significantly changed the natural history of NAIT.
BACKGROUND Neonatal alloimmune thrombocytopenia (NAIT) has been reported only rarely in twins and not at all, to our knowledge, in triplets. CASE REPORT Nonidentical triplets were born with severe thrombocytopenia. Nadir platelet (PLT) counts were 17 × 109, 12 × 109, and 10 × 109/L. NAIT was confirmed by an incompatibility for human PLT antigen (HPA)−1a and the presence of maternal anti‐HPA‐1a. The maternal genotype was HPA‐1bb and the paternal genotype was HPA‐1aa; thus, all children were affected. RESULTS PLT counts for each infant improved with the administration of random‐donor PLT transfusions. All three infants also received intravenous immunoglobulin. None had major bleeding. A small isolated subependymal hemorrhage was found incidentally in one infant; this remained stable on repeat imaging. CONCLUSIONS This is the first report of triplets with NAIT. Anti‐HPA‐1a is sufficiently potent to affect three infants simultaneously. Random‐donor PLTs were effective in improving PLT counts in all three infants.
BACKGROUND: Maternal antibodies that cause neonatal alloimmune thrombocytopenia are commonly identified by solid‐phase assays that detect the causative antibodies on the basis of their reactions with specific PLT glycoproteins. Two cases of severe neonatal alloimmune thrombocytopenia caused by maternal antibodies specific for human PLT antigen 3a (HPA‐3a (Baka)) that failed to give the expected reactions in some solid‐phase assays were recently encountered. STUDY DESIGN AND METHODS: PLT‐reactive antibodies were characterized by three different solid‐phase assays and by flow cytometry. RESULTS: The two maternal antibodies gave negative reactions in the antigen capture ELISA, modified antigen capture ELISA, and MoAb immobilization of PLT antigens tests but reacted strongly in flow cytometry with intact PLTs that were HPA‐3a+. Other sera samples specific for HPA‐3a reacted equally well in all assays. CONCLUSIONS: The two antibodies appear to recognize an epitope on the HPA‐3a+ form of glycoprotein IIb that is lost when PLTs are solubilized in detergent, as required for solid‐phase assays. The diagnosis was made in these cases because no HLA antibodies were present, allowing an HPA‐3a‐specific reaction to be identified with intact PLTs as targets. Such antibodies are likely to be overlooked when HLA antibodies are also present.
BACKGROUND: Clinical detection of neonatal allo‐immune thrombocytopenia (NAITP) is often less than the incidence predicted in prospective studies. The aims of this study were to calculate the observed and expected incidence of NAITP in Quebec, Canada, and to evaluate the clinical outcome of infants with anti‐HPA‐5b NAITP. STUDY DESIGN AND METHODS: Records from 1998 to 2002 of the only PLT serology laboratory for the province of Quebec were reviewed, as were hospital charts of all HPA‐5 cases. The number of expected NAITP cases was estimated with known alloantigen gene frequencies. RESULTS: Ninety cases of NAITP were identified. The clinical detection rate was 1 in 4100, with 9 to 30 percent of expected HPA‐1a and 11 to 23 percent of expected HPA‐5b NAITP cases detected. Seventy‐eight percent of cases of HPA‐5b NAITP were asymptomatic. Sixty‐three percent of all deliveries but 94 percent of HPA‐5b cases occurred in hospitals performing cord blood PLT counts. CONCLUSION: The NAITP detection rate was 25 to 50 percent of the rate reported in prospective trials. The less severe clinical presentation of NAITP owing to HPA‐5b was confirmed. The frequent routine determination of cord blood PLT counts may explain increased detection of asymptomatic NAITP involving anti‐HPA‐5b.