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HAEMOGLOBIN GENOTYPE IN RIVERS STATE

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HAEMOGLOBIN GENOTYPE IN RIVERS STATE

 

TABLE OF CONTENT

Declaration

Dedication

Acknowledgement

Abstract

Chapter one

  • introduction
  • literature review

Chapter two

Materials and methods

2.1 reagents

2.2 appraratus

2.3 procedure

2.4 precaution

Chapter three

Results

Chapter four

4.1 discussion

4.2 conclusion

References

ABSTRACT

Haemoglobin genotype frequency was determined by cellulose acetate electrophoresis in 200 apparently healthy Rivers state staff and students of University of Prt Harcourt. The sample was made up of 88 females and 112 males.

Out of the total number of 200 subjects studied, 141 subjects (70.5%) has AA pattern on electrophoresis, 54 subjects (27%) were AS, 4 subjects (2%) were ss and one subject (0.5%) had sc pattern on electrophoresis.

These results are in agreement with the general pattern of distribution of haemoglobin genotype in tropical Africa.

 

 

CHAPTER ONE

  • INTRODUCTION

Haemoglobin is the red, oxygen carrying pigment in the red blood cells of vertebrates (Ganong).

There are three main types of normal haeglobins in human. They are haemoglobins A, A2 and F. Haemoglobins A is the major component (about 95 percent) of adult haemoglobin in the body. It consists of two alpha (   ) and two beta (B) chains. It’s structural formula is (   ) 2A B2A

Haemoglobin A2 forms a minor portion of adult haemoglobin, about 1.5 to 3 percent. It has alpha chains identical to that of haemoglobin A, but it also possesses delta (5) chains instead of beta of beta chains, differing only in ten amino acid residue. It’s formula is     2BA.

Haemoglobin F was discovered haemoglobin in the new born. It’s concentration then falls rapidly and assumes the normal adult level of 2 percent or less by one or two years of age. The level of haemoglobin F drops to lesstahn 0.5 percent by the end of the second year and this level persists throughout life. It has alpha chains identical to that of haemoglobin A but gomma (Y) chains instead of beta chains. It’s formula is therefore,    2A Y2F. (Eastham, 1977).

There are also abnormal haemoglobins referred to as the haemoglobinopathies. This is a group of conditions in which there are genetically determined abnormalities in the synthesis of the polypepetide chains of globin. In some of these there is an imbalance in the production of the different chains consistituting the whole haemoglobin molecule though the constitution of the chain themselves is normal. This is the abnormality in the majority of conditions classed as the thalassmias. In other cases, there are substitutions, deletions or shifts in the sequences of amino acids in the globin chains. Some of these produce no detectable defect of haemoglobin function but others cause profound effects. One aminor acid substitution may for instance interfere with oxygen transport while another may result in an unstable haemoglobin molecule which causes a severe anaemia. The best known structural hemoglobinopathy is sickle cell disease which occurs almost exclusively in Negroes.

More than 100  abnormal haemoglobins have ben described to date. The earliest and major haemoglobinopathies discovered by electrophoresis were haemoglobins S, C, D and E (Lehmann et al, 1977). The other abnormal haemoglobins like G and O occur only sporadically.

Haemoglobins S was the first abnormal haemoglobin discovered (by pauling). In 1957, Ingram showed by the finger-print technique that sickle cell haemoglobin s differed from haemoglobin A by the substituytion of one valine for glutamic acid in position six from the N terminal of the beta chain. It is called the sickling gene. According to Lehmann this gene originated the Arabian peninsula. He also postulated that the veddoids who lived in Arabia in the late Neolithic times carried the sickling gene south-east-wards into India and south-west-wards into Africa. The sickling gene occurs in approximately 7-14 percent of North American Negroes (Myerson et al, 1959; Petrakis et al, 1970) and a similar rate of occurrence is noted in the west Indies and through central and south America (Brandau, 1930; Wallace and killingsworth, 1935). In tropical Africa the gene frequency varies from 46 percent in some pigmoid groups in East Africa to as low was 0.8 percent in some of the Hamitic groups of Uganda (Raper, 1950; Lehmann and Raper, 1949). The reported incidence in Nigeria is 23 to 30 percent while in Ghana the incidence varies between 10 to 20 percent. Most often the sickling gene manigests in the form of haemoglobins ss, As and Sc. Haemoglobin AS is referred to as the sickle cell trait. Persons with haemoglobin ss are referred to as sticklers.

Haemoglobin c is another haemoglobin defect found in west Africa (Lesi). It is found in the homozygous (cc) and heterozygous (AC) states. The highest incidence of haemoglobin c is in Northern Gnana where it is 20 percent. In southern Ghana, the incidence is about 10 percent. In Yorubaland in western Nigeria, the incidence is about 5 percent, while across the Niger River among the Ibos of Eastern Nigeria, the incidence is only a fraction of 1 percent (Lehmann and Huntman, 1972).

A few haemoglobins are named after the locations of discovery instead of alphabetically, for example, ‘’Haemoglobin Barts’’ and Haemoglobin Norfolk.’’

1.2 LITERATURE REVIEW

The earliest studies on haeglobin genotype distrivution in Nigeria were carried out by Jelliffe and Humphreys (1952) and Watson willinams (1960) in some Nigerian tribes – Yoruba, Ibos, Hausas, Funajnis and the Binis. They were only interested in the incidence of the sickle cell trait was found to be 21.5 percent. They investigated 216 Hausa subjects and the incidence there was 21.0 percent. Also 239 Fulani subjects were investigated and 21 percent were AS, while among he NInis, 321 subjects were investigated, and the incidence of AS was 23 percent. According to Jelliffe, Humphreys, and Watson-williams, the incidence of sickle cell anaemia can be determined thus: in a community with a sickle cell trait rate of 23.7 percent (Yoruba) one would expect the frequency of homozygous s (ss) to be:

(23.7

(100)          2 x ¾ = 11.1

Per thousand births. Similarly, the incideince of sicle cell anaemia for the other tribes can be determined by the above formula.

Between June 1972 to June 1973, another study was done by Araba at Lagos University Teaching Hospital. He investigated 240 healthy Nigerian subjects (144 males and 96 felames). The distributiojn were as follows: 186 subjects (77.5 percent) had AS type of blood, 2 subjects (0.8 percent) had SC and one subject (0.4 percent) had SS types of blood. The haemoglobin genotype was done by cellulose acetate membranes electrophoresis.

Lesi asserted that, if 100 Nigerians are taken at random, about 65 percent would posses AA type of blood, and about 25 percent would have AS, while 6 percent would possess AC especially in the Western part of Nigeria. The rest that is 4 percent would be SS. SC, CC and other rare combinations. Out of the 4 percent 2 percent would be SS (Sicklers).

In saudi Arabia, works done by Gelpi and King with 391 apparently healthy adult Saudi males (age between 16 and 30 years) over a three week period revealed that, 38 subjects had an AS haemoglobin pattern on electrophoresis, 4 subjects had an S pattern, 2 subjects had AC, and 337 had AA pattern of haemoglobin. This showed a sickle cell trait frequency of 0.123 percent, which according to them compared very closely with that observed in two earlier studies which provided trait frequencies of 0.115 and 0,125 respectively (Gelpi; Lehmann et al.).

Work carried out by Lehman and Raper in Uganda showed the distribution of sickleanemia (sickle cell trait) in three Language groups of Uganda. The incidence of the sicle cell trait was uniformly low in the pastoral, Hanitic-tongued tribes, with single exception of the Teso, where th incidence was 17.8 percent. In the Nilotic-tongued tribe, the highest incidence of sickle cell trait was found amongst the Jaluo where it was 28 percent. In the Bantu tongued tribes, the highest incidence was amongst the Jaluo where it was 28 percent. In the Bantu tongued tribes, the highest incidence was amongst the Baamba (45 percent). The trait was least among the Bairu (2 percent).

In South Turkey, studies carried out by Aksoy, using 376 persons comprising two groups; healthy relations, and some of the inhabitants of a small village, catalkeli, near Taruss. Of the 376 persons 50 had sickle cell trait (13.3 percent). This is the highest incidence of sickle cell trait (13.3 percent). This is the highest incidence of sickle cell trait found outside Africa (Jeelliffe et al; 1954; Nell, 1957, Singer, 1951) except in some tribes of southern India (Lehmann and cutbush, cutbush, 1952 a and b). caminopetros reported a high incidence of 49.1 percent in Athens, but this has been disputed by Lehmann (1952) and choremis (1952).

Shahid and Hardar reported of three families with sickle cell haemoglobin from three different localities in Syria and Lebanon. The highest incidence of sickle cell disease and trait was seen in haemoglobin s in the blood.

In Rivers statue of Nigeria, as well as some other parts of Nigeria, the incidence of haemoglobin AS is still obscure. The aim of this research of haemoglobin AS is still obscure. The aim of this research project is to determine the frequency of haemoglobin AS in Rivers state and see if it compares with that obtained from other oarts of Nigeria and the outside world.

 

 

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