A Case of Neonatal Alloimmune Thrombocytopenia due to Anti-HLA-B35

Neonatal alloimmune thrombocytopenia (NAIT) is induced by maternal antibodies to fetal platelet alloantigens. Because the main cause of NAIT is incompatibility to platelet specific antibodies, NAIT due to HLA antibodies are relatively rare. We managed a case of NAIT induced by maternal anti-HLA-B35 antibodies. The patient was a second born male. He had no petechiae or purpura at birth. He was admitted to the hospital due to fever for 5 days and a platelet count of 106x10(9)/L. The fever subsided after admission but on the 2nd day of admission, petechiae developed on the chest wall and the platelet count decreased to 25x10(9)/L. Other laboratory findings included C-reactive protein, prothrombin time, and partial thromboplastin time were normal. His mother's platelet count was normal and she had no history of bleeding. Anti-HLA-B35, B52, B56, C3, and C14 were identified in the mother's serum by a panel reactive antibody test and HLA-B35 antigen was identified in the father's and patient's sera. These finding suggested that maternal Anti-HLA-B35 antibody was a response to neonatal HLA-B35 antigen inherited from the father. The patient received concentrated platelet and intravenous immunoglobulin. The platelet count rose to 248x10(9)/L and was maintained thereafter.

Associations of HLA Alleles with Chronic Infection and Prophylaxis in Vertical Transmission of Hepatitis B Virus

Perinatal transmission and infection of hepatitis B virus (HBV) in early childhood were observed in the offsprings of hepatitis B surface antigen (HBsAg)-positive mothers who had been vaccinated against HBV immediately after giving birth. This prophylaxis failure of perinatal HBV infection is likely due to the interplay of the virus and host immune response. To investigate whether the HLA polymorphism affected the outcome of the perinatal prophylaxis, HLA class I (HLA-A, B and Cw) and class II (HLA-DRB1, DQA1, DQB1 and DPB1) were typed using serology, PCR-SSOP (polymerase chain reaction-sequence specific oligonucleotide probe), and PCR-ARMS (amplification refractory modification system) methods in 22 HBeAg-positive mothers and their 10 prophylaxis-succeeded and 12 prophylaxis- failed children. The HLA types of the mothers and their children were compared with 198 HBsAg-negative healthy controls in a Korean population. HLA-B35 (relative risk=4.2, p<0.01), B51 (relative risk=3.2, p<0.02), DRB1*07 (relative risk=3.8, p<0.03), and DQA1*02 (relative risk=3.8, p<0.03) alleles were more frequent in HBeAg-positive mothers than in the controls. Also, HLA-DRB1*13 (relative risk=0.1, p<0.02) and DPB1*0401 (relative risk=0.1, p<0.02) alleles were less frequent in HBeAg-positive mothers. However, HLA alleles did not affect the outcome of the perinatal prophylaxis against HBV. These results suggest that the reported influences of some HLA alleles on the natural chronic HBV infections may not operate in the HBV infections in children received perinatal prophylaxis.

Evidence to show MHC-linked factors other than HLA-B27 governing susceptibility to spondylo-arthropathies in Asian Indians.

The HLA antigen profile of 129 North Indian patients with ankylosing spondylitis, 66 patients with Reiter's syndrome and 57 patients with 'unclassifiable' arthritis was compared with 380 normal, healthy controls. Besides B27 which appeared with a significantly increased frequency in the three patient groups, other HLA antigens, viz. A2 and B35, showed deviated frequencies. The HLA supratype A2, B27 was found to be at an elevated frequency in patients with ankylosing spondylitis and unclassifiable arthritis whereas the B35, B27 combination showed a decreased frequency in our Reiter's syndrome sample. These data suggest that besides B27, other HLA-linked factors influence susceptibility to spondylitic disorders and might act as 'modifier' genes for the type and severity of spondylo-arthropathy in a B27-positive individual.