September 2017 ARTICLE LIST >>
PharmaTutor (September - 2017)
ISSN: 2347 - 7881
(Volume 5, Issue 9)
Received On: 13/04/2017; Accepted On: 22/05/2017; Published On: 01/09/2017
AUTHORS:
L Reddenna1*, Dr. P. Venkatesh1, K Siva Kumar2, A Sai keshava Reddy2
1 Department of Pharmacy Practice,
Jagan’s College of Pharmacy, Nellore, Andhra Pradesh, India
2 Department of Pharmacy Practice,
Nirmala College of Pharmacy, Kadapa, Andhra Pradesh, India
* reddennapharmd@gmail.com
ABSTRACT:
The subsistence of a human H/h genetic polymorphism was first recognized by the innovation of an individual devoid of the H antigen on red cells in Bombay who had antibodies in plasma reacting with all the red cells exhibiting the normal red cell ABO phenotypes. These persons were genetically termed as homozygous hh or Bombay phenotype. H-deficient Bombay phenotype is exceptional, since it occurs in about 1 in 10,000 individuals in India and 1 per 1,000,000 individuals in Europe. After the first report of Oh phenotype from Mumbai in 1952 by Bhende, numerous other workers detected this weird phenotype in India.The complexity with the Bombay phenotype is that the individuals having blood group of Bombay phenotype (Oh) can either receive autologous donation or blood from an individual of Bombay phenotype only; no other blood will match in case of an emergency blood transfusion. The aim of present study was to communicate the information about rare blood entity and to review the previous case reports.
How to cite this article: Reddenna L, Venkatesh P, Kumar KS, Reddy ASK;Nitazoxanide: H/H Blood Group System: A Rare Blood Group; PharmaTutor; 2017; 5(9);69-71
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REFERENCES:
1. Yu LC, Yang YH, Broadberry RE, Chen YH, Lin M. Heterogeneity of the human H blood group alpha (1,2) fucosyltransferase gene among para-Bombay individuals. Vox Sang 1997; 72:36-40.
2. Fernandez-Mateos P, Cailleau A, Henry S, Costache M, Elmgren A, Svensson L, et al. Point mutations and deletion responsible for the Bombay H null and the Reunion H weak blood groups. Vox Sang 1998; 5:37-46.
3. Simmons RT, D'senna GW. Anti-H in group O blood. J Indian Med Assoc 1955; 24:325-7.
4. Roy MN, Dutta S, Mitra PC, Ghosh S. Occurrence of natural anti-H in a group of individuals. J Indian Med Assoc 1957; 29:224-6.
5. Alosia Sister Mary, Gelb AG, Fundenberg H, Hamper J, Tippett P, Race RR. The expected "Bombay" groups OhA1 and OhA2.1. Transfusion 1961; 1:212-7.
6. 12. Aust CH, Hocker ND, Keller ZG, Arbogast JL. A family of "Bombay" blood type with suppression of blood group substance A1. Am J Clin Pathol 1962; 37:579-83.
7. Levine P, Robinson E, Celano M, Briggs O, Falkinburg L. Gene interaction resulting in suppression of blood group substance B. Blood 1955;10:1100-8.
8. Lanset S, Ropartz C, Rouseau P, Guerbet Y, Salmon C. Une familie comportant les phenotypes Bombay O h AB et O h B. Transfusion (Paris) 1966; 9:255-63.
9. Bhatia HM, Solomon JM. Further observations on Ahm and Ohm phenotypes. Vox Sang 1967; 13:457-60.
10. Bhende YM, Deshpande CK, Bhatia HM, Sanger R, Race RR, Morgan WT, et al . A new blood group character related to the ABO system. Lancet 1952; 1:903-4.
11. Watkins WM, Morgan WT. Possible genetic pathways for the biosynthesis of blood group mucopolysaccharides. Vox Sang 1959; 4:97-119.
12. Gerard G, Vitrac D, Le Pendu J, Muller A, Oriol R. H-deficient blood groups (Bombay) of Reunion Island. Am J Hum Genet 1982; 34:937-47.
13. Kaneko M, Nishihara S, Shinya N, Kudo T, Iwasaki H, Seno T, et al . Wide variety of point mutations in the H gene of Bombay and para-Bombay individuals that inactivate H enzyme. Blood 1997; 90:839-49.
14. Oriol R, Candelier JJ, Mollicone R. Molecular genetics of H. Vox Sang 2000;78:105-8.
15. Le Pendu J, Gerard G, Vitrac D, Juszczak G, Liberge G, Rouger P, et al . H-deficient blood groups of Reunion Island, II: Differences between Indians (Bombay Phenotype) and White (Reunion phenotype). Am J Hum Genet 1983; 35:484-96.