ORIGINAL  
Niger J Paed 2014; 41 (2): 110 –115  
Yarhere IE  
Ugwu RO  
Eneh AU  
Serum zinc levels in HIV infected  
children attending the University of  
Port Harcourt Teaching Hospital,  
Port Harcourt, Nigeria.  
DOI:http://dx.doi.org/10.4314/njp.v41i2,6  
Accepted: 21st December 2013  
Abstract: Background: Zinc defi-  
ciency is common in the Paediatric  
age group but the extent of this  
disorder is unknown in HIV in-  
fected children in Nigeria prompt-  
ing this study.  
Objective: To determine the preva-  
lence of zinc deficiency in HIV  
seropositive children, and compare  
this with age and sex matched con-  
trols.  
and analysed these using SPSS 20.  
Results: Sixty percent of the sub-  
jects were zinc deficient as against  
41.4% of the controls, p= 0.028.  
Subjects that were zinc deficient  
were more likely to be in higher  
HIV disease stages, p = 0.003, in  
lower socio-economic classes and  
aged less than 60 months. We con-  
clude that there is a high preva-  
lence of zinc deficiency in HIV  
sero-positive children and they  
should have zinc supplementation  
immediately they are diagnosed to  
reduce their morbidity and  
Yarhere IE (  
)
Ugwu RO, Eneh AU  
Department of Paediatrics and Child  
Health,  
University of Port Harcourt  
Teaching Hospital,  
Port Harcourt, Rivers State,  
Nigeria.  
Email: iroroy91@yahoo.com  
Tel: +2347067987148  
Methods: A case control study of  
7
0 HIV sero-positive and age and  
sex matched HIV sero-negative  
children was carried out in the Uni-  
versity of Port Harcourt Teaching  
Hospitaslt between 1st of June, 2009  
and 31 of May, 2010. We col-  
lected demographic, clinical, hae-  
matological and biochemical pa-  
rameters from cases and controls,  
mortality.  
Key words: Zinc deficiency, HIV  
sero-positive, socio-economic  
status  
Introduction  
ism. It is for this reason the World Health Organisation  
W.H.O) recommended zinc supplementation in children  
(
5
Zinc is an essential micronutrient found in every cell of  
every living organism and is necessary for cell growth,  
wound healing, mucosal epithelisation, DNA synthesis,  
with diarrhoea and pneumonia. This is known to reduce  
the severity, frequency and duration of diarrhoea and  
pneumonia in children and also those infected with Hu-  
man immunodeficiency virus. The prevalence of HIV  
infection has gradually dropped and this is especially so  
in Nigeria where it is now 3.4% from a high of 5.4%  
1
and support of a healthy immune system. Zinc is found  
in high concentration in flesh of beef, pork, poultry, fish  
and shellfish, and with lesser amounts in eggs and dairy  
products. Phytates in plants form complexes with zinc  
preventing absorption from the jejunum. Consumption  
of gruels made from maize, sorghum, or millet-  
containing phytates reduce absorption and cause defi-  
ciency of zinc. Rapid turnover of cells and consequent  
rebuilding during acute and chronic illn2e,3sses cause re-  
6
over a period of 6 years . However, HIV has been asso-  
ciated with over 2.1 million deaths and 330,000 of these  
are children as at the end of 2007. Nte et al actually  
showed a 2.1% HIV associated deaths in University of  
7
Port Harcourt Teaching Hospital Nigeria. HIV is associ-  
ated with under-nutrition as demonstrated by studies in  
Africa and Nige6r,i8a, and most of these were macronutri-  
duction in micronutrients including zinc.  
Caulfield et  
2
8
al in their analysis stated that children in developed  
countries have normal serum zinc levels, but most chil-  
dren in developing countries are deficient because they  
ent deficiencies. Steenkamp et al in South Africa re-  
ported zinc deficiency in some children with HIV and  
noticed that nutritional rehabilitation (with calorie and  
protein) alone did not improve serum zinc levels. For  
this reason, zinc supplementation programmes were  
initiated and sustained in East and South African chil-  
dren with HIV infection. The prevalence of zinc defi-  
ciency in HIV infected children is unknown in Nigeria,  
and it is for this reason we decided to carry out this  
study and make recommendations based on the results  
of the investigation.  
2
consume diets low in zinc. The estimated global preva-  
lence of zinc deficiency as at 2004 was 31%, but this is  
3
lower in Nigeria4n children where 20% are said to be  
deficient in zinc.  
Zinc deficiency manifests clinically with increased se-  
verity and duration of diarrhoea and pneumonia, poor  
wound healing, dermatitis, and in severe forms, dwarf-  
1
11  
Objectives  
Serum Zinc Analysis  
To determine the prevalence of zinc deficiency in HIV  
sero positive children and age and sex matched controls  
The serum zinc was analysed at the Obafemi Awolowo  
University Central Science Laboratory, Ile Ife, using  
flame atomic absorption spectrophotometer Model 210,  
manufactured by Buck Scientific Corporation, Connecti-  
cut, USA and the laboratory reference range of normal  
was 80 - 120µg/dL. Each sample was done in duplicate  
and the mean recorded. For this study, zinc deficiency  
was defined as serum zinc level less than 80 µg/dL.  
Samples were sent in batches of 20, transported frozen,  
in vaccine rush containers with ice gel packs by courier  
to OAUTH, Ile Ife and received by the Chief scientist or  
his assistants at the CSL, where they were analysed.  
(
HIV sero-negative children) attending the University of  
Port Harcourt Teaching Hospital.  
To compare serum zinc levels between the subjects and  
the controls  
Materials and Methods  
This case-control study was carried out in the Paediat-  
rics department of the University of Port Harcourt  
st  
st  
Teaching Hospital between 1 of June, 2009 and 31 of  
May, 2010, over a one year period. Ethical approval was  
obtained from the UPTH research and ethics committee  
prior to the commencement of the study. Included in the  
study, were newly diagnosed and HAART naive HIV  
infected children between ages 18 months and 16 years,  
and age and sex matched HIV negative controls. Sub-  
jects were recruited serially as they presented to the de-  
partment. When a sero-positive subject who met the  
inclusion criteria was recruited, an age and sex matched  
HIV sero-negative control who met the inclusion criteria  
was recruited as control from the Children Outpatient  
clinics (CHOP), Children Emergency Ward or DTU  
within 72 hours. Excluded from the study were children  
on zinc or multivitamin supplementation. Informed con-  
sent was obtained from the parents/guardians of all eligi-  
ble children. The minimum sample size (n) of 53 was  
calculated using the prevalence of HIV infection and  
Measurements of total WBC, AND CD4+ COUNTS  
Blood in the EDTA bottle was used for White Blood  
Cell (WBC) count and differentials as well as the CD 4  
+
cell count. Total WBC count and differentials were de-  
termined using Full Automatic Blood cell counter  
®
(ERMA INCORPORATED Tokyo). The machine was  
recalibrated daily using standard solution and diluents  
®
(ERMA INCORPORATED Control M-6) according to  
manufacturer’s specification. The white cell count and  
differential counts were crosschecked with manual dif-  
ferential cell counter after every tenth specimen and  
whenever a superfluous result was obtained with  
autoanalyser. Lymphocyte count was calculated using  
total white blood cell count and lymphocyte percentage  
with the formula:  
Lymphocyte count = Lymphocyte pe3rcent x total WBC  
4
zinc deficiency in children in Nigeria. All children had  
count (mm )  
detailed clinical history and examination performed be-  
fore blood samples were collected for HIV screening  
and serum zinc analyses. Information obtained were  
demography, risk factors for HIV and zinc deficiency,  
and the socioeconomic status of parent9s/ guardians using  
the method recommended by Oyedeji.  
100  
CD4 cell count was measured in all newly diagnosed  
HIV sero-positive subjects, and controls. The CD4 cell  
+
+
count was measured in the Haematology laboratory of  
UPTH using Partec® Cyflow Counter 05-8401 manu-  
+
factured in Germany. The CD4 % were calculated, after  
getting the total lymphocyte count for each patient using  
the formula:  
HIV Screening  
+
+
Subjects that were already in care (i.e. receiving other  
management except antiretroviral drugs) for HIV/AIDS  
were not retested for HIV and were recruited after their  
parents gave informed consent for the study. Testing of  
new subjects and controls using rapid test kits  
CD4 % = CD4 cell count x 100  
Lymphocyte count  
+
+
CD4 count and CD4 % were used to classify HIV sero  
-positive subjects and controls according to immu-  
nological status.  
(
Determine® and Stat pak was done following the  
guidelines of0the Provider Initiated Testing and Counsel-  
1
ling (PITC). Needle pricks (from the heel of a foot, or  
Data analysis  
the thumb) were used to collect one drop of blood into  
the tes®t kit. Initial tests used were Determine HIV 1 and  
The data collation and analysis were done by the investi-  
gator, with the help of statisticians. The raw data was  
collated into a Microsoft Excel sheet in a personal com-  
puter. The data was analyzed using SPSS version 20.  
HIV disease was classified using WHO clinical staging  
for infants and children and immune statu0 s was classi-  
2
kits (Abbot, Japan), and positive samples were re-  
®
tested using the Chembio HIV 1 and 2 Stat- pak kits  
Medford, NY, USA). If there was disparity between  
(
the two test kit results, a third kit, Gold check® was  
used as “tie-breaker”. Information and post-test counsel-  
ling were offered to all patients by the investigator or the  
trained assistants. All samples were tested free by the  
investigator and/ or trained assistants at no cost to the  
study groups.  
1
fied using WHO staging classification. Serum zinc  
deficiency was defined as serum zinc level less than  
4
80µg/dL. Frequencies were measured using percent-  
ages, while arithmetic means were used for continuous  
variables. Test of statistical significance included  
1
12  
Student‘s t test, Chi square test, Yates correction test  
and Fisher’s exact tests. Test of significance was as-  
sessed with 95% confidence interval and p value < 0.05  
was accepted as significant.  
Serum zinc status and study groups  
Forty-two (60%) of the subjects and 29 (41.4%) of the  
controls were zinc deficient and this difference was sig-  
2
nificant, χ = 4.830, p = 0.028.  
Serum zinc levels and age groups of subjects and  
controls  
Results  
A total of 268 HIV sero-positive children were seen  
during the study period and of these, 102 (38%) were  
aged eighteen months and above. Ten (10) were ex-  
cluded because they had already been started on antiret-  
roviral therapy. Fifteen sero-positive patients who were  
eligible were critically ill and died in the CHEW before  
their parents could be counselled for inclusion into the  
study, while seven (7) did not give consent to participate  
in the study. A total number of 140 children (70 HIV  
sero-positive subjects and 70 age and sex matched HIV  
sero-negative controls) were recruited into the study.  
There were 40 (57.1%) males and 30 (42.9%) females in  
each study group, giving a male: female ratio of 1.3:1.  
For each age group, controls had higher serum zinc lev-  
els than the subjects, though this was only significant for  
the 18-59 months age group. Table 3 shows age-related  
prevalence of zinc deficiency in subjects and controls.  
Of the 47 subjects aged 18-59 months, 28(59.6%) were  
zinc deficient as against 17 (36.1%) in the control group.  
Table 3: Age-related prevalence of zinc deficiency in subjects  
and controls  
2
Age groups  
(Months)  
Subjects  
Deficient  
(%)  
Controls  
Deficient  
(%)  
χ
p
N
n
N
n
1
8 – 59  
47 28 (59.6)  
20 14 (70.0)  
47 17 (36.1)  
20 11(55.0)  
5.16 0.02  
0.96 0.33  
0.99*  
6
1
0 – 119  
20 – 192  
3
0 (0.0)  
3
1 (33.3)  
Clinical staging of HIV sero-positive children  
Total  
70 42 (60)  
70 29 (41.4)  
Fishers exact test  
Sixty two (88.6%) of the subjects presented in advanced  
to severe stages of diseases (stages 3 and 4). There was  
no child aged 60 months and above in the asymptomatic  
and mild HIV disease stages (Table 1).  
Serum zinc Levels and HIV disease  
The mean serum zinc levels decreased as the WHO HIV  
clinical staging worsened. Subjects in stages 1 and 2 had  
normal mean serum zinc levels while those with ad-  
vanced disease, had mean serum zinc levels lower than  
normal (Table 4). There was significant difference in  
mean serum zinc levels between subjects in stages one  
and two (95.319 ± 24.01 ug/dL) and those in stages  
three and four (62.04 ± 28.80 ug/dL), with the latter  
having a lower mean, t = 3.1, p = 0.003.  
Table 1: WHO clinical staging of subjects by age group  
WHO Clini-  
cal staging  
1 n  
(%)  
2 n  
(%)  
3 n (%) 4 n (%) Total n  
(%)  
Age group  
months)  
(
1
6
1
8-59  
3(4.3)  
0 (0)  
0 (0)  
5 (7.1) 15  
21.4)  
24  
(34.3)  
47  
(67.1)  
20  
(
3 (4.3)  
(
0-119  
20-192  
0 (0)  
14 (20) 6 (8.6)  
28.6)  
Table 4: Mean serum zinc levels according to WHO clinical  
staging  
0 (0)  
1 (1.5)  
2 (2.8)  
Total  
3 (4.3) 5 (7.1) 30  
(42.9)  
32  
(45.7)  
70  
(100)  
WHO Stage n (%)  
Mean zinc levels  
ug/dL ±SD  
1
3 (4.3)  
113.9 ±34.1  
Age related immunological status of HIV sero-positive  
children.  
2
3
4
Total  
5 (7.1)  
84.2 ±2.9  
73.8 ±23.5  
51.0 ±30.1  
65.8 ±33.3  
30 (42.9)  
32 (45.7)  
70 (100)  
Only 6(8.6%) subjects had normal immunity and 46  
(
65.7%) of subjects had advanced to severe immune  
suppression.  
In subjects, the mean serum zinc level in those with nor-  
mal immune status was within normal levels, but it was  
low in those who had evidence of immune suppression.  
The mean serum zinc levels were higher in the controls  
than in the subjects across various immune categories  
except in those with normal immune status. The  
Table 2: Immunological status of subjects by age  
groups  
Immunologi-  
cal status  
Normal Mild  
Ad-  
vanced  
n (%)  
Se-  
vere  
n (%)  
Total  
n (%)  
n (%)  
n (%)  
differences were significant in the mild and severe  
immune suppression categories. Table 5  
Age group  
months)  
(
1
8-59  
2(2.9)  
8(11.4)  
12(17.1)  
25  
47 (67.1)  
(35.7)  
6
1
0-119  
20-192  
3 (4.3)  
1 (1.4)  
8(11.4)  
2 (2.9)  
8 (11.4)  
0 (0.0)  
1(1.4)  
0
20 (28.6)  
3 (4.3)  
(
0.0)  
26  
37.1)  
Total  
6 (8.6)  
18 (25.7) 20(28.6)  
70 (100)  
(
1
13  
2
Table 5: Mean Serum zinc level and immune status of  
subjects and controls  
prevalence of 31%. The higher prevalence in this study  
can be accounted for by the fact that the study popula-  
tion were ill children as against the study by Maziya-  
Immune  
Status  
Subjects  
Mean zinc  
Controls  
Mean zinc  
µg/dL (±SD)  
4
Dixon et al where apparently healthy household chil-  
n (%)  
µg/dL (±SD)  
n
(%)  
t
p
dren (children living in a household i.e. with a family as  
against street children were investigated. Serum zinc  
levels are reduced during acute and chronic infection as  
there is reduced intake, and increased utilization for  
Normal  
Mild  
6 (8.6)  
110.4(±27.6)  
22 (31.4) 92.5(±27.4) 1.4 0.168  
27 (38.6) 84.8(±25.5) -2.1 0.046*  
15 (21.4) 79.0(±14.6) -1.2 0.235  
18 (25.7) 69.3 (±23.7)  
Advanced  
Severe  
20 (28.6) 70.8 (±22.5)  
26 (37.1) 49.3(±28.1)  
1
6
(8.6) 86.6(±18.7) -3.9 0.002*  
healing. Another reason for the higher prevalence was  
Total  
70 (100)  
65.8(±33.3)  
70 (100) 86.1(±23.8)  
the relatively small sample used in the study compared  
*
p ,< 0.05  
4
to the larger population by Maziya-Dixon et al. In the  
In the control group, majority 49 (70%) had normal or  
mild immune suppression whereas majority of the  
subjects 46 (66%) had advanced or severe immune  
suppression. One of the controls with advanced immune  
suppression had a very low serum zinc level of 56 µg/dL  
which reduced the mean serum zinc in the group to  
below normal (Table 6).  
study, only serum zinc level was used to determine zinc  
deficiency state, whereas the estimated global preva-  
lence pooled results from various populations (affluent  
and impoverished) with diverse cultures and feeding  
practices, used degree of stunting in areas where serum  
zinc levels were not available and zinc contents in vari-  
ous diets to arrive at their result. Th3e HIV status of the  
children investigated by Hotz et al and Maziya-Dixon  
4
Table 6: Immune Status of Zinc Deficient Subjects and  
Controls  
et al was not ascertained and this methodological differ-  
ence could have also accounted for the higher preva-  
lence in the study.  
2
Immune  
Categories  
Subject  
Deficient  
Controls  
Deficient  
n(%)  
χ
P
N
n(%)  
N
In the HIV sero-positive children, the prevalence of zinc  
deficiency was 60%. This was higher 1than the preva-  
Normal  
Mild  
Advanced 20 14(70)  
Severe  
Total  
6
18 8(44.4)  
0(0)  
22 8(36.4)  
27 12(44.4)  
15 7(46.7)  
1.53* 0.216  
1
0.00  
1.94  
2.52*  
1.00  
0.163  
0.112  
lence of 54.3% reported by Ndeezi et al in Uganda and  
1
2
the 20% by Eley et al in South Africa. The study inves-  
tigated only HAART naïve HIV sero-positive children  
while Ndeezi et al combined children on HAART and  
those that were HAART naïve. Studies have shown that  
HAART improves serum zinc levels probably by reduc-  
ing viral load, improving general well being, immune  
status, and invariably, overall nutrition in HIV patients,  
thus reducing the number 1o3f,14HIV sero-positive children  
26 20(76.9)  
70 42(60)  
6
2(33.3)  
70 29(41.4)  
Yates correction test  
Serum zinc and Socioeconomic Status of study group  
In subjects, only those in class 1 had normal mean  
serum zinc level, and though there were fluctuations, the  
lower the classes, the lower the mean serum zinc levels.  
The fluctuation was also noted in the control group, but  
mean serum zinc level was normal in classes 1, 2, and 3.  
It was also noticed that the mean serum zinc was lower  
in subjects than controls within the same socio economic  
class, but the differences were not significant as shown  
in Table 7.  
that will be zinc deficient.  
HAART also reduces op-  
portunistic infections, and thus reduces the frequency of  
repeated infections and excessive utilization of zinc. The  
higher prevalence of zinc deficiency in HIV sero-  
positive children in this study as against that by Eley et  
al, can be explained by the fact that the children investi-  
gated by Eley et al were clinically stable, and received  
nutritional rehabilitation, thus improving their macro-  
and micro- nutrient status. In the present study, no at-  
tempt was made at nutritional rehabilitation before they  
were recruited.  
Table 7: Mean serum zinc levels and socioeconomic status of  
subjects and control  
Socioeco-  
nomic Status  
n (%)  
Subjects  
Mean zinc  
µg/dL (±SD)  
Controls  
Mean zinc  
(%) µg/dL (±SD)  
The prevalence of zinc deficiency in the control group  
was 41.4% and this was lower than the 47.5% from Bil-  
n
3
t
p
1
5
1
2
3
4
5
4 (5.7)  
14 (20)  
88.6 (±20.2)  
71.4 (±34.3)  
79.8 (±24.1)  
58.5 (±26.5)  
37.1 (±31.0)  
(4.3) 124.7 (±32.3) -2.1 0.091  
bis et al in S1 okoto, North West Nigeria, and 72% by  
6
18 (25.7) 86.7 (±26.1) -1.4 0.163  
35 (50) 89.6 (±19.3) -1.6 0.119  
11 (15.7) 66.7 (±13.4) -1.0 0.339  
Muller et al in rural Burkina Faso, but higher than  
1
7
17 (24.3)  
28 (40.0)  
7 (10)  
11% by Takyi et al in Ghana. While the present study  
inves1t5igated children between 18 and 192 months, Bilbis  
et al, studied only children less than 60 months. Chil-  
dren less than 60 months have lower zinc levels than  
older children because of the higher demand for growth  
3
(4.3) 75.5 (±25.8) -1.8 0.098  
Total 70 (100)  
65.8 (±33.3) 70 (100) 86.1(±23.8)  
2
and reduced intake from diet. The higher prevalence in  
the study by Muller et al can be attributed to the fact that  
a sub-sample of a population rather than the whole  
population was used. The method of recruitment of this  
sub sample was not stated and it may have caused some  
bias in favour of zinc deficiency. Another reason for the  
higher prevalence in the study by Muller et al, was that  
Discussion  
Zinc deficiency was seen in 50.7% of the study popula-  
tion and this was higher than the 20% previously re-  
ported by Maziya-Dixon et al and the estimated global  
4
1
14  
the children investigated were said to have consumed  
mainly cereals with little protein in their diet and this  
can account for the reduction of zinc in2,3that populatio1n7  
are very susceptible to the HIV and they get depleted  
1, 2,  
fast in the course of the disease. This finding of re-  
+
duced CD4 count with advanced disease was similar to  
as zinc is known to be low in cereals.  
Takyi et al  
reports fro6,m8,13other parts of Nigeria and other developing  
had a much lower prevalence possibly because they used  
hair zinc levels for their study which reflects chronic  
zinc nutrition rather than acute as serum zinc levels  
determines.  
countries.  
Zinc is required for the enzymes (protease  
and integrase) activities in HIV and as the virus prolifer-  
ates and disease progresses, the zinc levels in serum  
decrease. The proliferation also causes release of oxygen  
free radicals and superoxide dismutase is used to mop  
up these free radicals to prevent their accumulation to  
toxic levels.  
The mean serum zinc level in subjects was significantly  
lower than that found in controls. This wa16s comparable  
1
5
to other studies in Nigeria, and Kenya. Though the  
other studies investigated adults, the difference between  
subjects and controls may be attributed to the fact that  
HIV, being a chronic infection, predisposes infected  
individuals to under-nutrition and other opportunistic  
infections, putting excessive stress on the immune sys-  
tem and lowering the zinc levels in serum. The low se-  
rum zinc levels in some of the controls may be attribut-  
able to their ill-health poor appetite, reduced dietary zinc  
intake and the high zinc turnover rate during illness, and  
since there are no readily available stores in the body,  
that which is available for assay will be low.  
Another significant finding in the present study was that  
the lower the socioeconomic status of the guardians, the  
lower the serum zinc levels of study groups though there  
were fluctuatio4,n1s7 in some classes, and this was seen in  
other studies. Subjects in the same socioeconomic  
class with controls had lower mean serum zinc levels.  
The association has not been looked at in other studies,  
and though there were more subjects in lower socioeco-  
nomic classes, the finding shows that there is reduced  
serum7 zinc levels in children of low socioeconomic  
1
class. Children of lower socioeconomic status have  
low access to food rich in zinc, and consume diets rich  
in phytate, thereby decreasing their serum zinc levels.  
These children are also prone to recurrent infections, and  
as their immune system attempts to fight these infec-  
Mean serum zinc level in subjects was noticed to be  
lower, though not significantly, in the younger 12age  
groups than in the older age groups. Bilbis et al, in  
Northern Nigeria also noted similar findings in their  
study. Within the same age group, mean serum zinc lev-  
els were lower in subjects than in the controls. This may  
be a reflection of the HIV disease burden on the sub-  
jects. Lower serum zinc levels in younger children may  
be a consequence of higher turnover of zinc as it is  
needed for growth, metabolism and to fight infection,  
thereby reducing that which is available in serum for  
2
,3,19  
Those  
tions, there is reduction in serum zinc levels.  
parents in lower socioeconomic classes whose children  
presented in advanced disease stages may have poor  
health seeking behaviour and thus not present until the  
illness was advanced. Poverty may18also be a contribut-  
ing factor to their late presentation.  
2
analysis. Again, younger children who are being  
weaned off milk onto other diets are usually given cere-  
als that are poor sources of zinc and these contain high  
levels of2 phytate that reduce the absorption of zinc from  
the diet.  
Conclusion and Recommendation  
Our study showed a high prevalence of zinc deficiency  
in HIV infected children (60%), and also in controls  
(
40%). Most of the zinc deficient children were in low  
Advanced HIV disease stage was associated with low  
mean serum zinc levels. This signif1i1cant differen1c6e was  
also seen in Uganda, South Africa, and Kenya, even  
socioeconomic class, ages less than 60 months and in  
advanced HIV disease stage. The mean serum zinc lev-  
els were also low in HIV sero-positive. It is therefore  
our recommendation that all HIV infected children  
should be supplemented with zinc immediately after  
being diagnosed to reduce the co-morbidities associated  
with the infection and improves their immunity.  
1
6
though adult population was used in the Kenyan study.  
Advanced HIV disease stage is more likely to be associ-  
ated with recurrent and chronic infections thus reducing  
intake and increasing zinc turnover. There were also  
significantly lower serum zinc levels in subjects who  
had evidence of immune suppression than those who did  
not have evidence of immune suppression. This was also  
Limitation of the study  
11  
reported by Eley et al in South Africa. It is worth not-  
ing here, that immune categorization is bett1e0r made with  
CD4% and not absolute count in children, as the total  
white blood cell count is relatively low in children and  
following HAART administration, CD4+ counts recover  
slowly and may eventually reach optimal levels.  
The trend or change of serum zinc levels could not be  
ascertained as this was a case- control study. A longitu-  
dinal study might have assessed this change over time.  
Dietary intakes of nutrients were not assessed, as this is  
one of the main ways of assessing zinc levels. The cost  
of the study was high.  
+
CD4 count and percentage were significantly lower in  
Conflict of interest: None  
Funding: None  
+
subjects than controls. The low CD4 count and percent-  
age in HIV is a well known phenomenon, as these cells  
1
15  
Acknowledgements  
residents and the laboratory personnel, who participated  
in the study.  
We thank the children, their parents/caretakers, the  
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