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The Secretor Status

The ABO blood group and secretor status of individuals is inherited independently. ABO blood group antigens are inherited by A, B & H genes and gene responsible for secretor state is Se (Se/Se & Se/se) gene. If recessive gene se/se is inherited person is non secretor. These group specific substances, ABH may be detected in most body fluid as soluble form in secretors except cerebrospinal fluid (CSF). One of the richest and most available source is saliva. Secretor status of a person can be quite useful to determine certain doubtful cases of ABO blood grouping and also has clinical significance.

In simple terms, secretors are individuals which secrete their blood type antigens in their body fluids such as saliva, mucus etc and non secretors are people who does not or put a very little amount in them. Approximately 80% of the people are Secretors.

In forensic work, a persons blood type can be ascertained from very small traces of blood found at a crime scene. In some cases, no blood is found by the investigators, but there may be saliva or other mucus-containing bodily fluid that can be identified. If the person from whom the bodily fluid originates carries the dominant secretor gene, that individual will secrete the ABO antigens in mucus, and it is possible to infer the blood type from these fluids.

I conducted a research for finding out the prevalence of secretors and non-secretors in our region, where I tested the saliva of the blood donors to identify their secretor status using neutral gel cards. A questionnaire was given to all the participants for knowing their personal and medical history and the answers were documented in a tabulated form. Even weaker blood groups were identified using this method. Frequency distribution and percentage proportion method was used to analyze the results.

ABO blood group system is widely credited to have been discovered by the Austrian scientist Karl Landsteiner, who identified the O, A and B blood types in 1900[1]. Interestingly, the antigens comprising this blood group system were among the first human genetic markers identified [2, 3]. Later on, AB blood group was added to the ABO blood system by Alfred Von Decastello and Adriano Sturli in 1902 [4]. This major blood group system consists of four blood types: A, B, AB and O [5]. These antigens are genetic markers inherited as Mendelian characteristics in a co-dominant autosomal fashion. In 1930, Putkonen noted that a person could be either secretor or non-secretor with respect to his/her genetic ability to secrete ABH blood group substances in secretions [5]. Weiner in 1943 discovered that A & B substances are present in saliva of most A & B individuals (secretors) [6]. The ABO blood group and secretor status of individuals is inherited independently. ABO blood group antigens are inherited by A, B & H genes and gene responsible for secretor state is Se (Se/Se & Se/se) gene.

If recessive gene se/se is inherited person is non secretor. These group specific substances, ABH may be detected in most body fluid as soluble form except cerebrospinal fluid (CSF). One of the richest and most available sources is saliva [7]. The H, Fucosyltransferase 1 (FUT 1) gene codes for the ABO blood group. The secretor, Fucosyltransferase 2 (FUT 2) gene interacts with FUT 1 gene to determine the ability to secrete blood group antigens into body fluids and secretions. Absence of the blood group antigen in secretions is a health disadvantage, as this appears to increase the susceptibility to a number of diseases. There are certain diseases which show evidence of association with non secretor status [8].

ABH non secretors also have a higher prevalence of different varieties of auto-immune diseases including ankylosing spondylitis, Sjogren‟s syndrome, multiple sclerosis, reactive arthritis, psoriatic arthropathy and grave‟s disease. Non-secretors have high incidence of diseases of mouth, esophageal cancer, and epithelial dysplasia as compared to secretors [9]. Secretor status of a person can be quite useful to determine certain doubtful cases of ABO blood grouping by conventional method, especially the subgroups of ABO system [10].

It is a universal fact that blood is a person’s absolute and unchangeable identity [11]. Although almost 400 blood group antigens have been reported, the ABO and RhD are recognized as clinically significant and dominant blood group antigens. ABO blood group system derives its importance from the fact that A and B are strongly antigenic and anti A and anti B occur naturally in the serum of persons lacking the corresponding antigens [12]. ABO Blood group antigens (substances) are secreted by the secretors into various body fluids. Non-secretors secrete out very minor or none of their blood group antigens into different body fluids.

Increased degree of protection against bacterial and fimbrial lectins may be associated with the secretion of these antigens into saliva and mucus. However, secretors are more prone to hemolytic anemia and viral infections that have been cited by Raza MW et al 1991 [13]. Whereas, non secretors have a higher prevalence of autoimmune diseases including ankylosing spondylitis, reactive arthritis, sjogren‟s syndrome, psoriatic multiple sclerosis, grave’s disease, peptic ulcer, metabolic syndromes, oral ulcers etc[14, 15].

Secretors have an added degree of protection against the environment, particularly with respect to microorganisms and lectins. Non secretors are more prone to TTIs infections. Alcohol is useful for non secretors. Secretor status is also helpful to identify weaker variants of ABO group.

For reading the published research article authored by me regarding materials and methods and procedure done click here.

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[1]. Landsteiner K (1900). "Zur Kenntnis der antifermentativen, lytischen und agglutinierenden Wirkungen des Blutserums und der Lymphe". Zentralblatt Bakteriologie. 27: 357–62

[2]. Storry JR, Olsson ML: Will genotyping replace serology in future routine blood grouping? – opinion 4. Personalized versus universal blood transfusions – combining the efforts. Transfus Med Hemother 2009;36(3):232–233.

[3]. Koda Y, Tachida H, Pang H, Liu Y, Soejima M, Ghaderi AA, Takenaka O, Kimura H. Contrasting patterns of polymorphisms at the ABO-secretor gene (FUT2) and plasma α(1,3)fucosyltransferase gene (FUT6) in human populations. Genetics. 2001;158:747–756.

[4]. Von Decastello A, Sturli A (1902). "Ueber die Isoagglutinine im Serum gesunder und kranker Menschen". Mfinch med Wschr. 49: 1090–5.

[5]. Daniels G. ABO, Hh, and lewis systems. In; Daniels G. Human Blood Groups. 2nd ed. Oxford (UK): Blackwell Science; 2002:7–70.

[6]. Wiener, A. S., 1943. Genetic theory of the Rh blood types. Proc. Soc. Exp. Biol. Med. 54: 316–319.

[7]. Boorman KE, Dodd BE, Lincoln PJ. Blood group serology. 6th edn., Churchill Livingstone, UK. 1988;P.49.

[8]. S Akhter , GM Kibria , NR Akhter , MM Habibullah, SMK Islam , M Zakariah ABO and Lewis Blood Grouping with ABH Secretor and Non-secretor Status: A Cross Sectional Study in Dhaka, Faridpur Med. Coll. J. 2011;6(1):38-40

[9]. Campi C, Escovich L, Moren A, Racca L, Racca A, Cotoruelo C, et al. Expression of the gene encoding secretor type galactoside 2-α-L-Fucosyltransferase (FUT2) and ABH antigens in patients with oral lesions. Med Oral Patol Oral Cir Bucal. 2012;17(1):63-68.

[10]. Harmening DM. Modern blood banking & transfusion practices. 3rd edn., Jaypee Brothers, India, 1998;p.103.

[11]. Sherwani SK, Ahmad H, Ahmad T, Tanveer Hussain T, Akbar S et al. Status of Secretor and Non–Secretor with Respect to ABO Blood Group System in Young Population in Karachi-Pakistan. World Journal of Medical Sciences (2014) 10 (1): 22-25, DOI: 10.5829/idosi.wjms.2014.10.1.8210

[12]. Bauer, J.D., 1982. Clinical laboratory methods, 9th ed.Mosby Company, Missouri, pp: 353-76.

[13]. Raza, M.W., C.C. Blackwell, P. Molyneaux, et al.,1991. Association between secretor status and respiratory viral illness. BMJ, 303: 815-818.

[14]. D'Adamo, P.J. and G.S. Kelly, 2001. Metabolic and immunologic consequences of ABH secretor and Lewis subtype status, Alternative Medicine Review, 6(4): 395.

[15]. Suadicani, P., H.O. Hein and F. Gyntelberg, 1999. Genetic and life-style determinants of peptic ulcer. A study of 3387 men aged 54 to 74 years: The Copenhagen Male Study. Scand J. Gastroenterol., 34: 12-17.



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