case-report | 30-November-2020
used in both phases of reverse typing. However, the strength of reactivity with group O and group A RBCs was enhanced when incubated at 4°C for 1 hour (Fig. 1B and C). The autologous control at 4°C and at RT was negative (not shown in Fig. 1). Hence, based on the results summarized in Table 1, forward typing showed a picture of Bombay/para-Bombay phenotype, and reverse typing suggested the presence of anti-B, along with the possibility of anti-H, anti-IH, or other cold-reacting antibodies in the
M.S. Bhagavathi,
N. Das,
S. Prakash,
A. Sahu,
S. Routray,
S. Mukherjee
Immunohematology, Volume 37 , ISSUE 4, 160–164
Article | 01-April-2020
The galactophilic lectins Aplysia gonad lectin (AGL) and Pseudomonas aeruginosa lectin (PA-IL),which detect human I and P1 RBC antigens, were examined for hemagglutination of H+ (group O and B) and H-deficient (Bombay and para-Bombay phenotype) RBCs. The results were compared with those obtained using two other galactophilic lectins, Maclura pomifera lectin (MPL) and Arachis hypogaea (peanut) agglutinin (PNA), which share T-antigen affinity, and two fucose-binding H-specific lectins, Ulex
Nechama Gilboa-Garber,
Dvora Sudakevitz,
Cyril Levene,
Naomi Rahimi-Levene,
Vered Yahalom
Immunohematology, Volume 22 , ISSUE 1, 15–22
case-report | 25-June-2021
The Bombay phenotype was identified in 1952 by Bhende and colleagues.1 The Bombay phenotype results from a homozygous deficiency of the FUT1 gene along with a silenced mutation of the FUT2 gene. The incidence of the Bombay phenotype in the Indian population is approximately 1 in 10,000 and is most often due to a T725G mutation in the FUT1 gene and a 10-kb deletion in the FUT2 gene.2 The para-Bombay phenotype is either due to a point mutation or a silence mutation on the FUT1 gene with a normal
G. Mohan,
A. Vaidya,
S. Shastry
Immunohematology, Volume 37 , ISSUE 2, 59–63