Platelet antigens are expressed on a number of glycoproteins (GP). Interactions of the platelet glycoproteins with the extracellular environment is important to platelet function:
- GPIIb/IIIa, a heterodimeric integrin made up of α and β subunits and encoded on chromosome 17, is a fibrinogen receptor
- GPIb/IX/V, made up of 4 transmembrane components, with subunits encoded on chromosome 17 and chromosome 22, is a von Willibrand factor receptor involved in platelet adhesion
- GPIa/IIa is a collagen receptor
- CD109 may be involved in cell-cell interactions
Single amino acid substitutions in the sequences of these glycoproteins give rise to different platelet specific antigens.
The platelet antigen system is made up of 24 alloantigens which have been defined by serology. Twelve of these antigens have had the thetical and antithetical antigens defined i.e. they are biallelic antigens – HPA-1a and -1b, -2a and -2b, -3a and -3b, -4a and -4b, -5a and -5b and -15a and -15b. The remaining 12 HPA antigens have had the thetical but not the antithetical antigens observed. Altogether, the molecular basis of 22 of the 24 HPA antigens have been defined. These include the biallelic as well as HPA-6w, -7w, -8w, -9w, -10w, -11w, -12w, -13w, -14w, -16w.
The distribution of HPA antigens on glycoproteins is as follows:
| Antigen | Glycoprotein |
| HPA-1 | GPIIIa |
| HPA-2 | GPIbα |
| HPA-3 | GPIIb |
| HPA-4 | GPIIIa |
| HPA-5 | GPIa |
| HPA-6w | GPIIIa |
| HPA-7w | GPIIIa |
| HPA-8w | GPIIIa |
| HPA-9w | GPIIb |
| HPA-10w | GPIIIa |
| HPA-11w | GPIIIa |
| HPA-12w | GPIbβ |
| HPA-13w | GPIa |
| HPA-14w | GPIIIa |
| HPA-15 | CD109 |
| HPA-16w | GPIIIa |
GP to HPA Mapping
| Glycoprotein | HPA |
| GPIa | HPA-5 |
| GPIb | HPA-2 HPA-12w |
| GPIIa | |
| GPIIb | HPA-3 HPA-9w |
| GPIIIa | HPA-1 HPA-4 HPA-6w HPA-7w HPA-8w HPA-10w HPA-11w HPA-14w HPA-16w |
| CD109 | HPA-15 |
GP Complex to Common HPA Mappings:
| GP Complex | Biallelic HPA |
| GPIIIa/IIb | HPA-1 HPA-3 HPA-4 |
| GPIb/IX/V | HPA-2 |
| GPIa/IIa | HPA-5 |
| CD109 | HPA-15 |
In pregnancy, treatment of ITP involves treating the mother to minimise bleeding by regular checking of platelet counts. Treatment is not required in the absence of bleeding unless platelet counts drop below 20. First line treatment is with steroid, primarily the corticosteroid prednisone. If effective, it leads to an increase in platelet count within 3-5 days. The duration of use should be kept to a minimum as steroid use is not unharmful to the baby. IvIG is a second line treatment if patient does not respond to steroids. Anti-D can be used in Rh-D Neg mothers. Evidence for the use of other steroid sparing alternative treatments such as Rituximab and thrombopoietin in pregnancy is limited. Some experts recommend early deliver, even caesarean, to reduce the risk of intracranial haemorrhage as a result of low platelet count.
In the neonate, the major risk is intracranial bleeding due to NAIT. A platelet count at birth is required. A cranial ultrasound may be required if the platelet count < 50. Treatment involves rapid platelet transfusion, usually with HPA-1a5b Neg platelets ahead of platelet genotyping. Use of IvIG has been demonstrated to increase platelet count in some NAIT cases.