89 TRANSACTIONS OF THE ROYAL SOCIETY OF TROPICAL MEDICINE AND HYGIENE.
Vol. 63.
No. 1.
1969.
VALUES FOR 14 BLOOD CONSTITUENTS IN YOUNG ADULT GHANAIANS IN ACCRA, WITH COMPARATIVE DATA FROM TROPICAL AND NON, TROPICAL COUNTRIES BELA R I N G E L H A N N , J. MAUD DAGADU AND H. S. SODHI Department of Pathology and Internal Medicine, Ghana Medical School and National Institute of Health and Medical Research (Ghana Academy of Sciences) For the proper interpretation of a laboratory report it is essential to know the range of "normal" values found in that particular laboratory. Many laboratories publish "normal" values based on an evaluation of their own data (EDOZIEN, 1958; ROBERTS, 1967; Massachusetts General HospitaL, 1967). These serve as guidelines for comparison with the actual report. The appropriateness of the word "normal" has been challenged. PICKERING(1959) using the example of blood pressure, rejects this concept. JUVANCZ(1965) recommends the word "physiological." Yet the statistical mean obtained from a group of healthy individuals~ certainly does not represent in every instance either the physiological or optimal value. The inhabitants of many developing countries are underfed, and their statistical mean of body weight is biased downward. Or, taking an example from our present study, the serum carotene level in adult healthy Ghanaians in Accra is about 3 times as high as was found with similar methods in Great Britain. This is statistically "normal" but not necessarily "physiological." Turning to the utility of these values, we have to consider that apart from the diversity of the laboratory methods in use, striking differences exist owing to age, sex, ethnic origin, diet, socio-economic status, climate, altitude and other environmental conditions. In this paper we present our "normal" values for some blood constituents obtained from young, adult, healthy Ghanaians. N o such data have been published from Ghana and very few similar reports have come from West Africa. These values might be useful for a better understanding of the effect of the tropical surroundings on the function of the human body.
Material and methods Blood was taken from individuals belonging to the groups shown in Table I. The nurses in both hospitals live communally; with rare exceptions they eat the same food and their physical health is good. The Borstal inmates also live communally, have satisfactory food and their physical condition is good. All four groups are under medical supervision. The individuals in all four came from various parts of Ghana The authors wish m express their thanks to Dr. J. E. Bowman and Dr. P. E. Carson from the University Of Chicago, for their kind co-operation and for the performance of Hb electrophoresis. The authors wish to express their thanks to Prof. S. R. Dodu for allowing them to use the laboratories in the Internal Department, to Dr, F. I. Konotey-Ahulu for his help in organizing the collection of blood, to Mrs. A. Casukas and Dr. K. Miltenyi for their advice in the statistical evaluation of the results, and to Mr. S. Q. Maddy and Mr. C. BannermanWilliams for their help in the laboratory work.
90
BLOOD CONSTITUENTS I N YOUNG ADULT GHANAIANS
and have been living for a longer or shorter period in Accra. No medical examination was carried out before taking the blood. The subject was accepted as healthy if she or he felt fit and had no complaint. Those with visible signs of disease tiave been excluded. TABLE I
Group
Sex
Number
Age range, years
Average age, years
Nurses from Korle Bu Hospital
Males Females
53
18-34
22" 9
Nurses from Military Hospital
Males Females
67 9
20-32 18-40
25 27 "8
Borstal inmates
Males Females
62
16-23
21
Medical students and technicians
Males Females
17
21-35
25"7
Total
Males Females
146 62
16-35 18-40
23 "9 23 "6
We used vacuum tubes containing E D T A and similar tubes without anticoagulant, taking blood between 8 and 10 a.m., except in a group of Korle Bu nurses where we took it between noon and 1 p.m., and in Borstal inmates, between 3 and 5 p.m. We estimated haemoglobin (DRABKIN,1949), serum iron (RAMSAY,1953, modified by RINGELHANN,1956) and total iron binding capacity (RAMSAY, 1957), total serum protein (WoLFSONet al., 1948) albumin/globulin ratio, albumin, alpha 1, alpha 2, beta and gamma globulin (BEcx~ViAN, 1960), amino acid imbalance ratio (WHITEHEAD, 1964), serum carotene and vitamin A (I~rERDEP. COM~aITTEEON NUTRITION, 1957, modified by DAGADV),folic acid (TEMFERL~Y and HORNER, 1966), vitamin BI2 (MELNA, 1965). One or more tests were carried out on the same sample, according to the available quantity of serum. All tests were performed in duplicate as soon as possible after taking the blood. The sera were kept frozen; sera used for folic acid determination were preserved by ascorbic acid. Samples with apparent haemolysis or lipaemia were discarded. Hb electrophoresis was performed and samples with homozygote haemoglobinopathy were excluded. From the results, mean, median, standard deviation and coefficient of variation were calculated.
Discussion
Our patients were not fasting and there had been no previous examination. However, in clinical practice we have to carry out tests in conditions such as these. Table I I I contains our data and some comparative results compiled from publications from both tropical and non-tropical countries. It is questionable whether we are justified in comparing results of laboratory tests performed in different parts of the world by different methods; nevertheless the comparison gives us a basis for assessing environmental influences upon biochemical values and functions of the organism.
91
BELA RINGELHANN, J. MAUD DAGADUAND H. S. SODHI
Results Table I I summarizes our data. TABLE II.
Blood constituent
Sex
No.
Mean
Median
Range
Haemoglobin, g./100 ml.
Male Female
57 37
14-8 12.7
14.9 12.6
12.0-17.1 11-1-14.9
normal normal
l ± 1.o6
Serum iron >g./100 ml.
Male Female
59 52
95.3 80.7
95 70
10 43
- 275 - 232
normal normal
i±46 ~±38
Total iron binding Male capacity btg./100 ml. Female
49 48
34O 377
340 376
183 - 611 244 - 617
normal normal
~ 74 73
Total serum protein g./100 ml.
Male Female
61 5O
7.6 7.4
6 . 0 - 8.9 5 . 9 - 9.0
normal normal
± 0.56 ± 0.45
alb./glob. ratio
Male Female
57 47
1.08 1.12
1.08 1.06
0"64-1.84 0.69-1.78
normal normal
± 0.21 :t- 0.26
Albumin g./100 ml.
Male Female
57 47
3.89 3.79
3"85 3"73
2.89-4.60 2" 84-4.65
normal normal
Alpha 1 glob. g./100 ml.
0"15-0.38 0" 14-0:42
normal normal
Alpha 2 glob. g./100 ml.
0.23-0-99 0.33-0.88
normal normal
Beta glob. g./100 ml.
0'55-1.25 0'52-1.40
normal normal
Gamma glob. g./100 ml.
1.21-3.70 1.18-3-30
lognormat lognormal
Amino acid imbalance ratio
1"2 - 8"4 1.4 - 7-5
lognormal lognormal
Carotene btg./100 ml.
102- 955 211-1154
lognormal lognormal
Vitamin A. b~g./100 ml.
1 6 ' 104 11- 101
normal normal
Folic acid ruing./100 ml.
2.1~12.4 2 . 1 - 9.5
normal normal
Vitamin B 12 b~~tg./ml.
125-1300 200-1500
normal normal
Type
i
SD ± 0"89
I - -
7-7 7.4
J ~
± 0"35 ± 0"43
92
BLOOD CONSTITUENTS' I N YOUNG ADULT GHANAIANS TABLE I I I Tropical countries
Blood constituent
Haemoglobin g. per 100 ml.
Serum kon ~g. per lOOml.
Total ironbinding capacity ~tg. per 100 ml.
Total serum proteins g. per 100 ml.
Remarks
Country
Non-tropical countries Author
African students Kampala Africans Karamoja Africans
Uganda
Holmes, 1955
Dispensary patients
Gambia
Woodruff, 1957
Bantus
South Africa
Kinnear, 1956
Students
Indonesia
Luan Engo 1962
Vinage inhabitants
Nigeria
Edozien, 1965
Civilians Soldiers
Nigeria
Nutrkion Survey 1965
Patients " with slight complaints
Gambia
Bantus Indians
Country
Gt. Britain
Author
U.S.A.
Medical Research Council, 1945 Drabkin, 1951
Gt, Britain
Pryce, 1960
Hungary
Horvatth, 1966
Gilles, 1956
Germany
Heilmeyer, 1937
Scandinavia
Rnstung, 1949
S. Africa
Wainwright, 1957
U.S.A.
Cartwright, 1948
Zuhis
S. Africa
Hathorn, 1961
U.S.A.
Christian, 1954
Labourers hospital orderlies Bo Tonga tribesmen
Rhodesia
Carr, 1961
Hungary
Ringelhama, 1957
U.S.A.
Fischer, 1964
Chinese Malays Indians
Malaya
Luan Eng, 1964
Village inhabitants
Nigeria
Edozien, 1965
Zulus
S. Africa
Hathorn, 1961
Sweden
Lanrell, 1947
Labourers hospital orderlies Bo Tonga tribesmen
Rhodesia
Cart, 1961
U.S.A. Germany
Path, 1949 Rechenberger, 1955
Village inhabitants
Nigeria
Edozien, 1965
U.S.A. Hungary U.S.A.
Peters, 1956 Ringelharm, 1964 Fischcr, 1964
African students Kampaia Africans Karamoja Africans Kigezi Africans
Netherlands Oosterhuis, 1954
Uganda Holmes, 1955
Students
India
Satoskar, 1954
Nigerians Europeans Male Nurses Cato Manor tribesmen Europeans Chinese Europeans
Nigeria
Edozien, 1957
S. Africa
Powell~ 1958
Hong Kong
Ma~ 1962
Bantus Coloured Europeans
S. Africa
v. Heerden, 1962
U.S,A. Gt. Britain Canada U.S.A.
Sunderman, 1957 MacGillivray,1957 Dunn, 1961 Pollack, 1961
93
BELA RINGELHANNj J. MAUD DAGADU AND H. S. SODHI TABLE III.--Continued Tropical countries " Blood constituent
Remarks
Total serum proteins g. per 100 nil, (confirmed)
xopical countries
Country
Author
New Guinea
Neeb, 1963
African outpatients African students Asian students Civilians Soldiers
Uganda Nigeria
Leonard, 1965 Nutrition Survey 196~
Laboratory personnel Village inhabitants
Congo
Michaux, 1966
Uganda
Holmes, 1955
Papuans, sago eaters Papuans, police recruits Papuans in Holland Europeans
Country
Author
Netherlands U.S.A.
Oosterhuis, 1954 Sunderman, 1957
Gt. Britain
MacGillivray, 1957
(*)
Albumin/ globulin ratio
India
Satoskar, 1954
Nigeria
Edozien, 1957
Canada
Dunn, 1961
S. Africa
Powell, 1958
U.S.A.
Pollack, 1961
Hong Kong
Ma~ 1962
S. Africa
v. Heerden, 1962
New Guinea
Neeb~ 1963
Uganda
Leonard, 1965
Nigeria
Nutrition Survey, 1965
Congo
Michaux, 1966
Uganda
Holmes, 1955
Netherlands U.S.A.
Oosterhuis~ 1954 Sunderman, 1957
Gt. Britain
MacGillivray, 1957
(*)
Serum albttrnin g. per 100 ml.
4-52
India
Satoskar~ 1954
Canada
Dunn~ 1961
3.25 4.05
Nigeria
Edozien, 1957
U.S.A.
Pollack, 1961
4-26 3.53 4.19
S. Africa
Powell~ I958
4-19 4.46
Hong Kong
Ma, 1962
(*) The groups are the same as in total protein.
94
BLOOD CONSTITUENTS IN YOUNG ADULT GHANA!ANS TABLE III.--Continued
Blood constitflent
Our results M
F
Serum " albumin g. per 100 ml. (continued)
I
Tropical countries Resl dts M
Remarks
I
F
Author
Results M
i
~'16 3.3 4.171
Non-tropical countries
L,
Country S. Africa
I
Remarks
Country
Author
F
v. Heerden 1962
I
3.1 4.0 3.1 4-0
New Guinea
3.15 3.39 3" 74
Uganda
3.55 3.38 3-90 --
Nigeria
4.46 4.47
Congo
4.51 4.60
(*)
0"20 0"31
Michaux, 1966
India
S. Africa
0-21
Netherlands
Oosterhuis, 1954
Edozien, 1957
0"42
U.S.A.
Sunderman, 1957
Powell, 1958 0 "24 0"22
Gt. Brkmn Canada
MacGillivray, 1957 Dunn, 1961
U.S.A.
Pollack, 1961
Netherlands
Oosterhuis, 1954
U.S.A.
Sunderman, 1957
Gt. Britain
MacGillivray~ 1957
Canada
Dunn, 1962
U.S.A.
Pollack,
q
Hong K o n g
0"29 0-29 0 '23
S. Africa
v. Heerden, 1962
New Guinea
Neeb, 1963
0"21 0'30 0'31
Uganda
L~onard, 1965
Ma, 1962
0"27 0.29 0 ' 2 7 0.25
Congo
0" 29 0"32
I i
I
I
0"32
(*)
India
.
Michaux, 1966 ,
i
I
I Satoska-------r1954i [0"41
0 "51 0'52
Nigeria
0"59 0" 73 0" 64
S. Africa
0" 64 0 "62
Hong Kong
[Ma, 1962 [10"61
0"59 0'61 0.51
S. Africa
' v. I-Ieerden I 1962
i 0' 6.7
Powell, 195810"52
I
0"61 i10"64
196i
I
i
New Guineai Neeb, 1963 i I
I
I'
0-52 0 '56 0'79 0'45 0'46
Edozien, 1957
I
0-6 0-7 0"7 0"6
10.74 0'79
.[
'i Satoskar, 1954
0'32 0"34
0"3 0'3 0'4 0"3
"Beta globulin[ g. per 100 nil.
J
Nutrition ] Survey, 1965 [
Nigeria
0"28 0:33 0"30
I
Leonard, 1965
I
Alpha 2 globulin [ g. per 100ml. 0.53 0.55
1963
iI
0.2510" 26 0.19
j Alpha 1 globulin g. per 100 ml.
i Neeb,
Uganda
Leonard, 1965
I
l
I
0"50 0"49
0' 74 0'67 0 '56 0'69
(*) • The groups are the same as in total protein.
Congo
Michatvx, 1966
I [
Uganda
0.56 Holmes, 1955 0.91 0- 93
I I Netherlands U.S.A. Gt. Britain
Oosterhuls, 1954 Sunderman, 1957 MacGfllivray, 1957
95
BELA RINGELHANN ~ J. MAUD DAGADU AND H . S. SODHI TABLE III.--Continued
Blood constituent
Results
M
M
F
Beta globulin g. per 100 mI. (continued)
Non-tropical countries
Tropical countries
Our results
Remarks
..
Country
Author
, Results
Remarks !'
Country
Author
F
0"81 0"64 0-82
India
Satoskar, 1954
Nigeria
Edozien, 1957
S. Africa
PoweI% 1958
Hong Kong
Ma, 1962
I
0-79 0"93 0"85
I
0"80 0"86
S. Africa
0-78 0 "85 0 "72
3~92
3-86 3-98
F ]
Canada
Dunn, 1961
U.S.A.
Pollack, 1961
k
!
[
i
i v. Heerden, 1962
[
i I
I
0-8 0-9 0"8 0"8
New Guinea
Neeb, 1963
0"90 0"80~ 1 "09!
Uganda
Leonard, 1965
0-63; 0-73 0"71 ! 0.69
Congo
Michaux, 1966
Uganda
Holmes, 1954
I
[ (8)
G~rnma globulin 1 '51 g. per 100ml. 2.17 1-94 2" 42 2" 95 1 "87
I 1"57 1.62 1" 22
Amino acid imbalance ratio
Carotene ~g. per 100 mL
2-37 2.57
321 511
Oosterhuis, 1954 Stmderman, 1957 MacGillivray, 1957
Satoskar 1954 1.30
Canada
Dunn, 1961
1" 13 1 "37
U.S.A.
Pollack, 1961
Gt. Britain
Neale, 1967 (pets. commun.)
Gt. Britain
Leimer, 1960
U.S.A.
Interdepartmental Committee 1963
Nigeria
Edozien, ! 1957
S. A~ica
i Powell, 1958
0-98
i i
1 "62 1 "39
H o n g K o n g [ Ma, !962
1 "37 1 "29 0 "92
S, Africa
i v. t-Ieerden, i962
I "86 1.73 1.56
Uganda
] Leonard, 1965
I
1 '57 1.88 2"16 2-13
Congo
Michaux, I 1966
I
1-5
74 426
8501 50 281 285 (8)
Netherlands U.S.A. Gt. Britain
!
India
1 "86 I 2-101 1 "20
I
1.22 1- 53
I
>2[
Children Uganda with kwashiorkor successfully treated European and African
Whitehead, 1964
Bantu males
S. Africa
Kirmear, t956
121
Healthy adult Nigerians
Nigeria
Edozien,
64
Soldiers
Ghana
Village inhabitants
Northern Ghana
Dagadu, 1963
Nigeria
Nutrition Survey, 1965
285 Civilians - - Soldiers
The groups are the same as in total protein.
!
1960
i Dagadu, 1963
131
96
BLOOD C O N S T I T U E N T S I N Y O U N G A D U L T G H A N A I A N S TABLE III.--Continued
Blood constituent
Our results
[email protected] Fi
Vitamin A
b~g. per 100 ml.
Tropical countries Results M 70:4
Remarks
Country
Non-tropical countries Author
Results
~a
F
Bantu males
S. Africa
Kinnear,
Remarks
Country
86
G t . Britain
Oxford Nutritional Survey, 1947
142
Gt. Britain
Leitner, 1960
1956 26 701 41 21 "0 43- 5 59"8 60.3
i Folic acid [5.10 5.04 m~g. per ml. li
Vitamin B12 i' 480 ~zy.g. per nil.
1
2"5 5.93
543 - -682 694
Healthy adult Nigeria
Nigerians
Soldiers Village inhabitants
Northern Ghana
Bantus
Australia
Dagadu, 1963
Leonard 1964
Nutrition Survey 1965 Davis, 1965
9 "9 6' 13 6"90 5' 1 6 1
526 472 667 105 322
1581 Vegetarians 295 Non-
vegetarians
Gt. Britain Gt. Britain
Ireland Gt. Britain
! Waters, 1961 Ball, 1964 Temperley, 1966 Girdwood, 1967
S. Africa
Brandt, 1961
1-~!
Japan
Okuda, 1954
450
Gt. Britain
Spray, 1958
S. Africa
Brandt, 1963
360
Gt. Britain
Girdwood, 1967
India
Mehta, 1964
! Township
Bantus Bantu miners • Coloured ' Indians Caucasians
820
1960
18.9 Bugandaout- Uganda patients - - Asians 56" 1 Civilians Nigeria - - Soldiers Aborigines Europeans
Edozien,
Author
F
Haemoblogin Our results do not deviate substantially from the figures found in other .parts of the world in similar groups. S e r u m iron and total iron binding capacity The values of iron in both males and females in our study are low, and we observed a fairly large number of persons with unusually low serum iron. In the males 21 of 59 (36%), and in females 27 of 52 (52%) had values less than 80 ~g. There is a large range below and above the mean; the coefficient of variation being the greatest, 51 and 56% among the tests presented here. The low serum iron could be the consequence of iron deficiency and decreased release of iron into the plasma. The infection rate with hookworm and bilharzia in Ghana is high, so iron deficiency, secondary to bleeding, could not be ruled out. Nevertheless, the haemoglobin is not decreased significantly either in males or females, and the total iron binding capacity in males is only slightly elevated. In females, however, the transferrin is higher, which suggests iron deficiency. The decreased release of iron into the plasma has a major role in reducing serum iron in both sexes. Chronic infections, malaria, schistosomiasis, subclinical chronic renal disease, hypovitaminoses (especially C avitaminosis) are the main causes of increased activity of the reticulo-endothelial system and as a result the serum iron is decreased. Finally, it is possible that during the laboratory procedure the separation of iron from the carrier transferrin is not complete, and the non-ionized fraction is not linked with the dipyridyl, so the low value might be due to a technical error. We added a mixture of ~gFe and inert iron to the plasma and after precipitation of the proteins we did not find a measurable amount of iron in the latter, so methological failure could be ruled out.
BELA RINGELHANN, J. MAUD DAGADU AND H. S. SODHI
97
Siderosis has been reported in the adult Bantu population in South Africa (WAINWRIGHT, 1957; BOTHWELLand BRADLAW, 1960) and from Rhodesia (GELFAND, 1955). HADDOCK(1965) in Tanzania found a high incidence of siderosis in liver biopsy specimens. EDINGTON (1954) examined the iron content of the livers and spleens of dead Ghanaians and concluded that haemosiderosis is apparently a common and fortuitous occurrence in Ghana. DODU (1958) has shown that haemochromatosis is not uncommon among diabetics in Ghana. We found 2 cases with serum iron values above 180 ~zg. among the males and 1 among the females. In all three the total iron binding capacky was also raised, the percentage of saturation being 52, 51 and 53, which is a picture similar to that of patients with apparent haemosiderosis. The presence of both very low and high values of serum iron is a characteristic finding in Africans living in tropical surroundings. Malaria, bilharzia, ancylostomiasis and malnutrition might provoke anaemia with the consequence of augmented iron absorption. The iron metabolism "runs in a higher gear" which might lead to increased iron stores in later years. The increased demand for iron may slow down, but absorption for some unknown reason may remain higher than appropriate.
Serum proteins The total serum protein concentration is slightly higher and the albumin/globulin ratio lower than found in non-tropical countries. The alpha 1, alpha 2 and beta globulin values are similar to those published from tropical and non-tropical countries. We found reduced serum albumin and elevated gamma globulin in conformity with other authors from tropical countries. The low albumin might be the consequence of low protein diet or of liver damage, infections or deficient diet. There is disagreement about the cause of increased gamma globulin level. RAWNSLE¥et al. (1956) examined the blood of Caucasians and Negroids in the United States and took the view that the higher gamma globulin in Negroes may be an inherited property. POLLACKet al. (1961) also found increased gamma globulin in American Negroes and think that this suggests, but does not prove, that there are hereditary differences. According to EDOZIEN (1957) and COMENS (1957) the high gamma globulin could reflect a genetically determined protein pattern. MA (1962) found high gamma globulin levels in inhabitants of Hong Kong where malaria has been eradicated as a probable cause of acquired high gamma globulin level, and his finding also supports the hereditary theory. EDOZIEN (1961) found higher gamma globulin levels in the cord blood of new-born Nigerian babies, which might signify a hereditary origin. ROTHSTEIN(1965 and personal communication) in Ghana estimated the serum protein values in cord blood of African new-born babies, pregnant women, members of the Ghana Workers' Brigade, Ghanaian schoolchildren and young Caucasians (American Peace Corps). He concluded that the Ghanaian pattern of serum proteins differs from that of Caucasians, but the values in African cord blood were similar to the latter. The data of this author are given in percentage values but a careful examination shows that the average gamma globulin level of the 130 Ghanaian cord bloods is higher than the average of the adult Caucasians, 21.4 versus 17, but lower than that of the adult Ghanaians, which is 29.8. GILLESand MCGREGOR (1959) and McGI~GOR and GILLES (1960) in Gambia followed the development of gamma globulin levels in two groups of children, one protected and one not protected against malaria. Although the "protected" African children followed the pattern of European children, the concentration of gamma globulin was higher in the African children. In the fourth, fifth and sixth years of life the malarious children had significantly higher gamma globulin levels.
98
BLOOD CONSTITUENTS I N YOUNG ADULT GHANAIANS
SCHOFIELD(1957) takes the view that the African pattern of serum proteins is due to environmental factors and is at least partly reversible if the environment can be altered. NEEB and BOLLE-DE GROOT (1963) explain the abnormal protein pattern of West Guineans by the lifelong protein-deficient diet which they consume. JOUBERT et al. (1959) try to reconcile the two divergent views by assuming that circumstances have favoured the survival of those persons in tropical countries who are born with an increased gamma globulin level or with the ability to increase the production of this fraction to a greater extent than the Europeans. However, the adult protein pattern in Africans, in part at least, is acquired. Another important question is~,which fraction of the gamma globulin is elevated, Since the introduction of immuno-electrophoresis we know that the relatively cruder technique of paper electrophoresis shows only the grosset changes in IgG globulin (ALPER et al., 1966). In a recent study MICtlAUX(1966) in the Congo found no differences in the immunoglobulins of IgA; IgM and IgD between B~r/tus and Caucasians, but the IgG concentration varied according to sex, age and region inhabited. According to TURNERand VOLLER(1966) the IgD and IgA showed no difference between Nigerians and Caucasians, but the IgM was elevated in the blood of latter. The most striking difference occurred in IgG level, which was higher in Nigerians. They found no evidence that the malarial antibody activity is bound to any particular immunoglobulin fraction. Treatment of malaria resulted in a decrease of IgG level, which never fell to the normal value (CoHENIet al., 1961). A m i n o acid i m b a l a n c e ratio
WHITEHEAD (1964) published a chromatographical method for diagnosis of subclinical kwashiorkor in children. Two groups of amino acids are estimated. Group I contains leucine, isoleucine, valine, and methionine and this group is diminished in kwashiorkor, while Group II, containing glycine, serine, glntamine and taurine, does not change. The reduction of the ratio of these two groups, the imbalance, is the first biochemical abnormality in kwashiorkor and appears before any clinical signs of protein deficiency. Children with ratios above 3.5 are classified as potential kwashiorkor cases. Our figures for apparently healthy males and females are higher than in Whitehead's successfully treated kwashiorkor patients. NEALE(personal communication) also found lower ratios in healthy male patients in England. We do not know whether the high ratio in young adult Ghanaians does indeed reflect marginal malnutrition or whether it is related to the low albumin and high gamma globulin levelS. " The fact that in most cases the blood was taken from non-fasting persons might have influenced the result. S e r u m carotene
In a previous publication one of us (DAGADU and GILLMAN, 1963) found high levels of serum carotene in pregnant women and attributed it to high intake of carotenerich food (palm oil, tomatoes, mangoes, pawpaw). Low values were reported, however, from Northern Ghana, where carotene-rich fruits and vegetables and palm oil are not abundant (DAGADU, 1963)/ Carotene is found in high concentration in the blood of mothers in southern Ghana (mean 410 ~g. per 100 ml.) but it is lowin the cord blood of new-born babies (mean: 58 ~g.) (DA~ADU, 1965). I n our cases the concentration was significantly higher in females (p < 0.01). The averages of large groups have proved the influence of sex on these values, the carotene being higher in females and the vitamin A in males (MOORE, 1957).
BI~LA RINGELHANN, J. MAUD DAGADU AND H. S. SODHI
99
Folio acid Publications on serum folic acid levels in tropical countries are limited; some of the results are not comparable because of differing methods. In a study performed in Australian Aborigines, the average serum folic acid level was half as much as the same authors found in Caucasians. This is presumably because the Aborigines consume a deficient diet (DAvis et al., 1965). EDOZlEN(1965) without giving the figures, states that among village inhabitants in Nigeria 17% had a value which fell in the deficiency range, and 36% had low values. In our study 8 males (18%) and 5 females (13%) had lower than 3 mtxg. per ml. concentration in blood, although the average is within the range found in non-tropical countries. It seems to us that folic acid deficiency, even if not common, might occur in young Ghanaians.
Vitamin BI2 The level of this vitamin is not reduced in our cases. There were only 2 males and no females in whom it was lower than 200 ~ g . per ml. Vitamin B12 deficiency is not a common finding in tropical countries. It may occur in vegetarians, as has been described in India (MEHTA et al., 1964). Summary We have examined the blood of healthy young adult Ghanaians, estimating haemoglobin, serum iron, total iron binding capacity, total proteins, albumin/globulin ratio, albumin, alpha 1, alpha 2, beta and gamma globulin, amino acid imbalance ratio, serum carotene, vitamin A, folic acid and vitamin B12. The results were compared with figures published in tropical and non-tropical countries. The haemoglobin concentration did not show any particular deviation from results published in other parts of the world. The serum iron was low in both sexes and the total iron binding capacity in females was higher. The total serum protein was slightly elevated and low albumin and high gamma globulin levels were found, in conformity with other studies performed in tropical countries. The amino acid imbalance ratio was also high. The serum carotene was very high and the vitamin A was within the range considered as normal in tropical and non-tropical countries. The average folic acid level did not differ from figures published from non-tropical countries, but in individual cases low values were found. The vitamin B12 concentration was similar to the values found in non-tropical countries. REFERENCES ALPER, C. A., ROSEN, F. S. & JENEWAY,C. A. (1966). New Engl. ft. Med., 275, 591. BALL, E. W. & GILES, C. (1964). ft. clin. Path., 17, 165. BECKMAN,H. (1960). Beckman Technical Bulletin, No. TB 6050 A. BOTHWELL,T. H. & BRADLOW,B. A. (1960). Arch. Path., 70, 279. BRANDT, V. & METZ, J. (1961). S. Aft.ft. reed. Sci., 26, 1-3. , KERRICK,J. E. & METZ, J. (1963). Ibid., 28, 125. CARR, W, R. & GELFAND,M. (1961). Trans. R. Soc. trop. Med. Hyg., 55, 452. CARTWRIGHT, G. E., HUGULEY,C. M., ASHENBRUCKER,H., FEY, J. & WINTROBE, M. M. (1948). Blood, 3, 501. CHRISTIAN,E. R. (1954), Arch. intern. Med., 94, 22. COHEN, S., MCGREGOR, I. A. & CARRINGTON,S. (1961). Nature, 192, 733. COMENS, P. (1957). Am.ft. med. Sci., 215, 275. DAGADU, J. M. & GILLMAN,J. (1963). Lancet, 1, 531.
100
BLOOD CONSTITUENTSIN YOUNGADULTGHANAIANS
(1963). Ghana reed. ft., 2, 153. (1965). Ibid., 4~ 121. Modifications of Whitehead's method for estimation of amino acid imbalance ratio. To be published. DAVIS, R. E., KELLEY,A. & BYRNE, G. (1965). Med. ff. Austr., 1, 21. DODU, S. R. (1958). Trans. R. Soc. trop. Med. Hyg., 52, 425. DRABKIN, D. L. (1949). Am. ft. reed. Sci., 217, 710. .(1951). cit. ALTMAN, P. L. & DITTMER, D. S. (1961). Blood and other Body Fluids. Fed. Amer. Soc. Exp. Biol. Washington, D.C., p. 111. DUNN, W. L. & PEARCE, R. H. (1961). Canad. med. Ass. ft., 84, 272. EDINGTON, G. M. (1954). W. Aft. reed. ft., 8, 66. EDOZIEN, J. C. (1957). 37. clin. Path., 10, 276. (1958). W. Afr. reed. 37., 7, 121. (1960). Ibid., 9, 204. (1961). 37. din. Path., 14, 644. (1965). Ghana reed. 37., 4~ 94. FISCHER, D. S. & PRICE, D. C. (1964). Clin. Chem., 10, 21. GELFAND, M. (1955). Trans. R. Soc. trop. Med. Hyg., 49, 370. GILLES, H. M. & SCOTT, J. G. (1956). Ann. trop. Med. Paras#., 50, 103. & McGREGOR, J. A. (1959). 1bid., 53, 492. GIRDWOOD, K. H., THOMPSON, A. D. & WILLIAMSON,J. (1967). Br. reed. 37., 2, 670. HADDOCK,D. R. (1965). E. Aft. reed. ft., 42, 67. HATHORN, M., CANrL~a, P. & GILLMAN, T. (1961). S. Aft. 37. lab. clin. Med., 7, 14. VAN HEERDEN,P. D. & BRINK, A. J. (1962). Ibid., 8, 118. HEILMEYER, L. & PLOTTNER, K. (1937). Das Serumeisen und die Eisenmangelkrankheit. Jena: Fischer. HOLMES, E. G., STAINER,M. W. & THOMPSON, M. D. (1955). Trans. R. Soc. trop. Med. Hyg.o 49~ 376. HORVATTH,I. & KOVACS,M. (1966). Orv. Hail., 107, 1506. INTERDEPARTMENTALCOMMITTEE ON NUTRITION FOR NATIONAL DEFENCE (1957). Manual for Nutritional Surveys. U.S. Government Printing Office, pp. 108-11 and 124-9. JOUBERT, S. M., HOOKINS, K. W. & HUNTER, W. G. (1959). S. Aft. 37. lab. din. Med., --~
5, 1. JUVANCZ,I. (1965). Indextulajdonsagok szer'epe az orvosi es biologiai kutatasban. Akademiai Kiado, Budapest, p. 52. KINNEAR, A. A. (1956). S. Aft. 37. lab. din. Med., 2, 263. LAURELL, C. B. (1947)Acta physiol, scand., Suppl. 46. LEITNER, Z. A. (1960). Br. 37. Nutr., 14, 157. LEONARD, ]'. P. (1964). E. Aft. med. 37., 41, 133. & SHAPER, A. G. (1965). Ibid., 42, 689. LUAN ENG, L. I., HOLY GIOK, P. O. & SUMARKO,J. (1962). J. trop. Med. Paras#., 65, 45. & DE WITT, G. (1964). Med. 37. Malaya, 18, 269. MA, L. (1962). Trans. R. Soc. trop. Med. Hyg., 56, 222. MAcGILLIVRAY,J. & TOWEY, J. E. (1957). J. Obst. Gyn. Brit. Emp., 64, 361. McGREGOR, J. A. & GILLES, H. M. (1960). Ann. trop. Med. Parasit., 53, 275. MASSACHUSETTSGENERALHOSPITAL CLINICALLABORATORIES(1967). New Engl. 37. Med., 276~ 267. MEDICAL RESEARCHCOUNCILREPORT ON HAEMOGLOBINVALUES(1945).
cit. PRYCE, (1960).
Lancet, 2~ 333. MEHTA, B. M., REGE, D. V. & SATOSKAR,R. S. (1964). Am. 37. din. Nutr., 15, 77. MELNA, P. F. (1965). West Indian reed. ft., 14, 230. MICHAUX, J-L. (1966). Ann. Soc. belge Mdd. trop., 46, 483. MOORE, T. (1957). Vitamin A. Amsterdam: Elsevier Publishing Co. p. 503. NEEB, H. & BOLLE-DE GROOT, S. (1963). Trop. geogr. Med., 15, 371. NIGERIA, NUTRITIONALSURVEY(1965). Report of the Nutrition Section, Bethesda, Maryland, 1967, p. 105 and 216. OKUDA, K. (1954) cit. GRASBACK,R. (1960). Advances of Clinical Chemistry, Vol. 3. New York & London: Academic Press. p. 319. OOsTERHuIS, H. K. (1954). 37. Lab. clin. Med., 44, 280. OXFORD NUTRITIONAL SURVEY, cit. DYKE, S. C. (1947). Recent Advances in Clinical Pathology. London: Blakiston.
BI~LARINGELHANN,~. MAUDDAGADUAND H. S. SODHI
IOl
PETERS, T., GIOVANNIENELLO,T: J., APT, L. & Ross, J. F. (1956). J. Lab. clin. Med., 48, 274. PICKERING, G. (1959). Ciba Foundation, Tenth Anniversary Symposium on Significant Trends in Medical Research. London: Churchill. p. 287. POLLACK,V., MANDEMA,E., DOIG, A. B. & KARK,R. M. (1961). J. lab. clin. Med., 58, 353. POWELL, S. J. (1958). S. Afr. J. lab. clin. Med., 4, 273. PRYCE, J. D. (1960). Lancet, 2, 333. RAMSAY, W. N. (1953). Biochem. J., 53, 227. (1957). Clin. chim. Acta, 2, 221. RATH, C. E. & FINCH, C. A. (1949). J. clin. Invest., 28, 79, RAWNSLEY,H. M., YONAN, V. L. & REINFOLD,J. G. (1956). Sci.ence, 123, 991. RECHENBERGER,J. (1955). Z. Altersforsch, 9, 98. RINGELHANN,B. (1956). Orv. Hetil., 97, 55. (1957). Adatok a vasforgalom korelettanahoz. Kand. Diss. Budapest. & LAUB, M. (1964) Acta reed., 20, 263. ROBERTS,L. B. (1967) Clin. chim. Acta, 16, 69. ROTHSTEIN,N. (1965). Ghana med.J., 4, 165. RUSTUNG,E. (1949). Acta derm.-vener., 29, Suppl. No. 21. SATOSKAR,R. S. & LEWIS, R. A. (1954). IndianJ. med. Sci., 8, 663. SCHOFIELD,F. D. (1957). W. Afr. J. biol. Chem., 1, 44. SPRAY, G. H. • WITTS, L. J. (1958). Br. reed. J., 1, 295. SUNDERMAN,W. F. JR. & SUNDERMAN,W. F. (1957). Am. J. clin. Path., 27, 125. TEMPERLEY, I. J. & HORNER,N. (1966). ~. clin. Path., 19, 45. TURNER, M. W,, VOLLER,A. • McFARLANE,H. (1966). J. trop. Med, Hyg., 69, 99 and 104. WAINWRIGHT, H. M. (1957). S. Aft. J. lab. din. Med., 3, 1. WATERS, A. H. 8z MALLIN,D. J. (1961). J. clin. Path., 14, 335. WHITEHEAD,R. G. (1964). Lancet, 1, 250. WOODRUFF, A. W. & SCHOFIELD,F. D. (1957). Trans. R. Soc. trop. Med. Hyg., 51, 217. WOLFSON,W. Q., COliN, C., CALVREY,E. ~¢ ICHIBA,F. (1948). Am.J. clin. Path., 18, 723.