Antwi-Baffour et al.

Lipids in Health and Disease (2018) 17:283

https://doi.org/10.1186/s12944-018-0926-y

RESEARCH Open Access

Haematological parameters and lipid

profile abnormalities among patients with
Type-2 diabetes mellitus in Ghana
Samuel Antwi-Baffour1,2* , Ransford Kyeremeh1, Samuel Owusu Boateng2, Lawrence Annison2 and
Mahmood Abdulai Seidu1

Abstract
Background: Diabetes mellitus is a non-infectious disease that has a high prevalence worldwide. Altered level of
many haematological parameters have been observed in patients with diabetes. The levels of lipids are also
affected in diabetes by many factors since carbohydrate metabolism affect lipid metabolism. So far, very little work
has been done linking haematological parameters and lipid profile in diabetics. The purpose of this study was
therefore to evaluate the haematological parameters and lipid profiles of patients with type-2 diabetes and to
correlate the results.
Method: Three hundred and four (304) patients with type-2 diabetes with an age range of 28 to 70 years (171
males and 133 females) were recruited. About 5 ml of venous blood samples were collected from each participant
after an overnight fast. A part of the blood samples was used to determine the lipid profile parameters and the
other parts for the haematological parameters. The Statistical Package for Social Science (SPSS) version 21.0 and
Microsoft office excel (2010) for windows were used for the statistical analysis of the data. Pearson’s correlation
were performed between haematological and lipid parameters. Significance was set at p < 0.05.
Results: The means and standard deviation of all the lipid parameters except TC showed significant difference in
both males and females. There was also proportional increment in LDL-C (in males), LDL-C and Triglycerides (in
females) as the age of participants increased and the ratio of TC/HDL was higher in males. There was also
significant difference in all of the haematological parameters between the male and female populations. Further, a
strong, significant positive correlation between RBC and lymphocytes and lipid parameters was observed. However,
the correlation between platelets, haematocrit and haemoglobin and the lipid parameters was negatively
significant.
Conclusion: From the results obtained, it can be concluded that there is significant difference in lipid parameters
between male and female diabetic patients. Levels of LDL-C and Triglycerides increased as the age of participants
increased and the male population showed increased risk for coronary disease. Almost all of the haematological
parameters examined differed significantly between the sexes. There was also, both strong positive and negative
correlations between the haematological parameters and the lipid profiles.

* Correspondence: [email protected]
1
Department of Medical Laboratory Sciences, School of Biomedical and
Allied Health Sciences, College of Health Sciences, University of Ghana, P. O.
Box KB 143, Korle-Bu, Accra, Ghana
2
Department of Medical Laboratory Sciences, School of Allied Health
Sciences, Narh-Bita College, Tema, Ghana

© The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
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Introduction and the coagulation factors are shown to be directly as-

Diabetes mellitus (DM) is a non-communicable disease sociated with DM [15, 16]. Systematic review and
or carbohydrate metabolism disorder which results in in- meta-analysis of cross-sectional and prospective studies
crease in blood glucose level (hyperglycaemia) [1]. It is have shown that the number of peripheral WBCs such
caused by the absence of insulin secretion due to either as basophils, eosinophils and neutrophils increased with
the progressive or marked inability of the β-Langerhans no change in the number of monocytes in patients with
islet cells of the pancreas to produce insulin or due to type-2 DM [16]. Furthermore, a study suggested that
defects in insulin uptake in the peripheral tissue (insulin high platelet activity enhances vascular complications in
resistance) [2]. DM is broadly classified under two cat- DM patients and altered platelet morphology and func-
egories - type 1 and type 2 diabetes [2]. Type 1 diabetes tion can be reflected as a factor for risk of microvascular
occurs most commonly in children, but it can sometimes and macrovascular diseases [17, 18]. Several studies have
also appear in adult age groups, particularly those in reported that increased platelet reactivation in patients
their late thirties and early forties [3]. The major factor with diabetes may confer less cardiovascular protection
in the pathophysiology of type 1 diabetes is considered with antiplatelet therapy, particularly aspirin [19, 20]. In
to be autoimmunity [4]. Type 2 diabetes on the other fact, it has already been demonstrated that insulin resist-
hand has a different pathophysiology and etiology as ance and hyperinsulinemia are associated with the
compared to type 1 diabetes. Type 2 diabetes is de- stimulation of erythroid progenitors and increased levels
scribed as a combination of low amounts of insulin pro- of inflammatory markers [21].
duction from pancreatic β-cells and peripheral insulin Other epidemiological studies have indicated a close
resistance [5]. Insulin resistance leads to elevated fatty relationship between the WBC count and components
acids in the plasma, causing decreased glucose transport of metabolic syndrome [22]. These abnormalities have
into the muscle cells as well as increased fat breakdown, been shown to markedly increase blood viscosity that
subsequently leading to elevated hepatic glucose produc- unfavourably affects the microcirculation, leading to mi-
tion [5, 6]. Insulin resistance and pancreatic β-cell dys- croangiopathy [23]. It was revealed that higher WBC
function must occur simultaneously for type 2 diabetes count, is one of the major components of inflammatory
to develop [6]. process that contributes to atherosclerotic progression
Diabetes mellitus has increasing prevalence worldwide and CVD [22, 24]. Haematological indices are therefore im-
with certain ethnic and racial groups of Asia and Africa at portant indicators for the evaluation of variations in size,
a greater risk [7]. Poorly controlled diabetes leads to vari- number and maturity of different blood cells and for the as-
ous complications such as nephropathy, retinopathy, neur- sessment and management of patients with DM [24, 25].
opathy and oxidative stress causing oxidative damage to Therefore, this study which is aimed at determining haem-
tissues and cells [8, 9]. The overall temporal burden of atological indices among type-2 DM patients will go a long
hyperglycemia is responsible for DM complications and way in assisting in their management.
adverse outcomes [10]. Patients with type 2 DM have in- It is known that many factors affect lipid levels in diabetes
creased risk of cardiovascular disease (CVD) related with because carbohydrate metabolism directly affect lipid me-
atherogenic dyslipidemia, coronary artery disease, and tabolism [26, 27]. Also insulin deficiency causes higher
myocardial infarction [9, 10]. The persistent hypergly- metabolization of free fatty acid and can cause disorder in
cemia in DM results in disturbances in cellular metabol- lipid metabolism [28]. Lipid abnormalities have also been
ism due to increased production of reactive oxygen seen to play an important role in the increased vascular risk
species (ROS) and non-enzymatic glycation of many mac- associated with type-2 DM [26, 27]. It is based on these
romolecules, which lead to changes in cellular structure facts that it was deemed fit to conduct this study to evalu-
and function and formation of advanced glycation end ate the lipid profile of patients with type-2 DM. A lipid pro-
products [11]. The formation of advanced glycation end file is a direct measure of three blood components namely;
products enhances metabolic disturbances and also in- total cholesterol (TC), triglycerides and high density lipo-
creases reactive oxygen species production via interaction proteins cholesterol (HDL-C) [29]. There are components
with the specific receptor for the advanced glycation end such as low density lipoprotein cholesterol (LDL-C) and
product [12]. This causes changes in structure and bio- very low density lipoprotein cholesterol (VLDL-C) that can
physical properties of the basement membrane which fur- also be derived from the direct measurements [29]. The
ther causes changes in permeability and vasodilatation of burden of cardiovascular disease or coronary heart diseases
blood vessels [13]. in the world is enormous and growing and the majority of
Patients with diabetes mellitus show a significant de- those affected are in developing countries [30]. Certain as-
rangement in various haematological parameters [14]. In pects of a person’s lifestyle including diet, level of physical
fact, several haematological changes affecting the red activity, level of diabetes control and smoking status may
blood cells (RBCs), white blood cells (WBCs), platelet affect lipid profile [31, 32].

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The high incidence of atherosclerosis in elderly people participant‘s name, age, sex, diabetes status, the intake of
suggests that age may be among the factors that affect lipid lowering drugs and haematinics.
lipid metabolism; hence putting elderly subjects at risk
of developing cardiovascular or coronary heart diseases
Biochemical measurements (lipid profile)
[33]. It was estimated in 2002 that, 29% of death world-
The biochemical measurements made were triglycerides,
wide (16.7 million deaths) were due to CVD [34]. Un-
total cholesterol (TC), high density lipoprotein choles-
controlled dyslipidemia also leads to various medical
terol (HDL-C) and low density lipoprotein cholesterol
complications [35]. An increase in the incidence of cor-
(LDL-C) levels in blood. About 5 ml of venous blood
onary heart disease risk has commonly been reported in
samples were collected from each participant after an
postmenopausal women [33]. The incidence of chronic
overnight fast. A part of the venous blood samples col-
heart disease (CHD) is much lower in young women
lected were dispensed into serum separating tubes and
than in men of the same age, up to the age of 65 years
allowed to clot. They were then centrifuged at 3000 rpm
[36]. However, after the age 65, the risk equalizes for
for 10 min at room temperature. Using standard labora-
both sexes [36]. This has led to the popular misconcep-
tory practice, Triglycerides, TC, HDL-C and LDL-C were
tion that cardiovascular disease is a disease of men, and
determined directly or samples were stored for analyses
is relatively rare in women but cholesterol levels tend to
later.
rise with age in both males and females [37]. There are a
lot of studies comparing haematological parameters in
patients with diabetes and others looking at lipids in dia- Biochemical measurements procedure
betics but there is paucity in studies comparing both pa- The lipid profile parameters were determined using ELI-
rameters in patients with diabetes. The aim of this study Tech chemistry reagents kit from ELITech Group Clinical
was therefore to evaluate the haematological parameters Systems (Paris, France). The cholesterol reagent kit with
and lipid profiles of patients with type-2 diabetes and to product code (SL) was used for cholesterol determination,
correlate the results. It is believed this study will uplift the HDL-C reagent kit with product code (HDL SL 2G)
awareness for the need of both haematological and lipid was used for HDL-C determination and LDL-C precipita-
analysis in patients with diabetes so the necessary steps tion and triglycerides reagent kit product code (MONO
can be taken to optimize their management. SL NEW) was used to determine LDL-C and triglycerides.
The instrument used was the Mindray B-300 chemistry
Methods analyzer manufactured by Shenzhen Mindray Bio-Medical
Study design Electronics Company, Limited. The procedures of work
The study was a cross sectional study which was con- and preparation of the working reagents were done as de-
ducted between January and December 2017. scribed by the manufacturer.

Study setting
Diagnostic criteria
The study was conducted at the Korle-bu Teaching Hos-
Dyslipidemia was considered in adult when total choles-
pital, Accra, Ghana.
terol level was ≥5.2 mmol/L, triglyceride level was ≥1.58
mmol/L, LDL-cholesterol level was ≥3.8 mmol/L and if
Characteristics of study participants
HDL-cholesterol level was < 0.9 mmol/L according to
The study population was made up of three hundred and
established reference interval by the korle-bu Teaching
four (304) patients with type-2 diabetes with an age range of
Hospital central laboratory [38].
28 to 70 years. There were 171 males and 133 females. All
the participants said they practiced healthy eating which in-
clude the type of food they ate, how much they ate and the Haematological (FBC) analysis
combinations of food types they ate. They also exercised Full blood count comprising red cell count, Hb, white
regularly where possible and were not smoking or drinking cell count and differentials, platelets as well as Hb indi-
alcoholic beverages. Finally they had regular check-ups by ces were determined from the remaining whole blood
attending the diabetic clinic regularly. The population was that was placed in EDTA test tubes using ABX Micros
stratified by age and gender into five (5) strata; 28–34 years, 60 Haematology Analyzer (Horiba-ABX, Montpellier,
35–40 years, 41–50 years, 51–60 years, 61–70 years. France). Thin blood film was prepared and stained using
Leishman stain for morphologic assessment of the red
Sampling procedure blood cells. The stained films were examined under the
Questionnaire-based data collection light microscope using × 40 objectives to select a good
Data were collected through the use of a structured area for examination and then a drop of oil placed on
questionnaire. The information collected included the the film and examined with the × 100 objective [39].

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Table 1 A table of means and standard deviations of serum increased. Also, the TC among age group 28–34 years in
lipids measurements in both male and the female participants females was the lowest as compared to the other studied
Parameters Males Females P-value age groups. However, age group 61–70 years had the high-
N = 171 N = 133 est value of HDL-C and LDL-C (Table 3).
Mean ± SD Mean ± SD
Furthermore, the percentage distribution of the lipid
Age (years) 45.8 ± 14.2 46.0 ± 14.3 0.000
parameters into high, normal and low level categories
Total Cholesterol (mmol/L) 5.00 ± 1.1 5.2 ± 1.2 0.843 was carried out among the participants. The average
HDL Cholesterol (mmol/L) 1.5 ± 0.5 1.8 ± 0.7 0.000 percentage of the participants that fell into each category
LDL Cholesterol (mmol/L) 3.2 ± 1.1 3.2 ± 1.2 0.000 was presented using a histogram. The outcome indicated
Triglycerides (mmol/L) 1.2 ± 0.6 1.1 ± 0.6 0.000 that majority of the participants fell into the normal
level category with all the parameters followed by high
level category and then low level category for the female
Data analysis participants (Fig. 1). The analysis for the male partici-
Data was collected using notebooks and transferred to a pants followed similar pattern except that here the num-
computer and kept confidential. They were later entered bers that fell into the low level category were quiet low
into Microsoft Word and analysed using Statistical Package and the difference between normal and high levels of the
for Social Sciences (SPSS, Version 21.0) and Microsoft of- parameters were significant (Fig. 2).
fice excel (2010) for windows. Normally distributed data The ratio of TC/HDL cholesterol as an indicator of
were analyzed using independent sample t-test and coronary risk factor was also calculated for both male
expressed as Mean ± SD. Pearson’s correlation was used to and female participants and their mean was found to be
determine the correlation between the obtained haemato- 3.7 ± 1.7 mmol/L in males and 3.3 ± 1.5 mmol/L in fe-
logical parameters and lipid parameters. A p-value of < 0.05 males. The ratio was therefore high in males than fe-
was considered statistically significant. males and subsequently showed a significant difference
as far as both sexes are concerned (P = 0.000) (Table 4).
Results From the table, it can be seen that the level of TC/
The total number of individuals recruited into the study HDL cholesterol ratio was high in males of age group
was 304 comprising of 171 (56%) males and 133 (44%) 20–30 years and 31–40 years as compared to females of
females. The average age of males was 45.8 ± 14.2 years the same age group. The ratio (3.5 ± 1.5; 3.5 ± 1.3) for
and that of females was 46.0 ± 14.3 years. The means and 41–50 years group of both sexes was almost the same.
standard deviation of all the lipid profile parameters of There was however a significant difference in TC/HDL
the participants were analyzed and it turned out that all ratio between the age groups of 51–60 years and 61–70
the parameters except total cholesterol showed signifi- years in males and females (P = 0.000).
cant difference in both males and females (Table 1). An independent sample t-test was conducted to investigate
The various lipid parameters were analyzed against the dif- the haematological parameters of the participants across gen-
ferent age groups among the male participants. It was real- der and there was significant difference in almost all of the
ized that age group 61–70 had the highest TC (5.5 ± 1.3 parameters between the males and females (Table 5).
mmol/L) and LDL-C (3.7 ± 1.4 mmol/L) level compared to The Pearson-Moment-r correlation test was employed
the other age groups. Also, there was proportional increment to investigate the existence of any significant relationship
in LDL-C as the age of the participants increased - a pattern between haematological parameters and the different
that was however not seen in the other parameters (Table 2). lipid profile parameters among the participants. There
Again, the individual lipid parameters were analyzed for was a strong, positive correlation between RBC and lym-
the female participants. Here it was seen that the LDL-C phocytes and the different lipid parameters, which was
and triglycerides levels increased as the participant age also significant [p = 0.003 and p = 0.002 respectively].

Table 2 A table of means and standard deviations of serum lipid measurements in studied age groups among the male participants
Age group TC(mmol/L) HDL-C(mmol/L) LDL-C(mmol/L) TG(mmol/L)
Mean ± SD Mean ± SD Mean ± SD Mean ± SD
28–34 Years 4.6 ± 0.6 1.6 ± 0.5 2.8 ± 0.9 0.9 ± 0.2
35–40 Years 4.7 ± 0.7 1.4 ± 0.5 3.1 ± 0.8 1.1 ± 0.6
41–50 Years 5.2 ± 1.2 1.7 ± 0.6 3.2 ± 1.1 1.4 ± 0.8
51–60 Years 5.0 ± 1.3 1.4 ± 0.5 3.3 ± 1.2 1.3 ± 0.5
61–70 Years 5.5 ± 1.3 1.5 ± 0.5 3.7 ± 1.4 1.2 ± 0.5

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Table 3 A table of means and standard deviations of serum lipids measurements in studied age groups among the female participants
Age group TC(mmol/L) HDL-C(mmol/L) LDL-C(mmol/L) TG(mmol/L)
Mean ± SD Mean ± SD Mean ± SD Mean ± SD
28–34 Years 4.8 ± 0.8 2.0 ± 0.4 2.2 ± 0.8 0.8 ± 0.3
35–40 Years 5.0 ± 0.9 1.6 ± 0.4 2.9 ± 0.9 0.9 ± 0.4
41–50 Years 4.9 ± 0.8 1.6 ± 0.5 3.0 ± 0.8 1.2 ± 0.5
51–60 Years 5.8 ± 0.9 1.6 ± 0.5 3.8 ± 1.0 1.3 ± 0.6
61–70 Years 5.3 ± 1.9 2.3 ± 1.2 3.9 ± 1.4 1.4 ± 0.6

Also, there was a strong negative correlation between elderly people again demonstrated significantly higher total
platelets, WBC, HCT, Haemoglobin, MCV and Neutro- cholesterol in women compared to men [42]. The finding
phils. Whilst with Platelets, Haemoglobin and HCT the of high cholesterol in females than males was however con-
correlation was statically significant [p = 0.003, p = 0.003 trary to a finding made in a study by Adediran and col-
and p = 0.020 respectively], the correlation of WBC, leagues (2012), where 39.7% of males and 54.5% of the
MCV and Neutrophils did not show significance [P = females had low cholesterol values [43].
287, p = 0.720 and p = 0.745 respectively] (Table 6). With regards to HDL-C, it was seen that the females
had higher mean value than the males and this was so
Discussion because from puberty on, women tend to have higher
From the data obtained, the means and standard devi- HDL-C levels than men due to the production of estro-
ation of all the lipid parameters except total cholesterol gen [44]. Again, looking at the LDL-C results, the mean
(TC) showed significant difference in both males and fe- values were almost the same between both sexes. This
males. In fact, the mean total cholesterol was high in fe- was expected based on the average age of both sexes in
males than males (Table 1). The higher TC in women the study for even though young women tend to have
may be due to higher sex hormone, particularly E2 in fe- lower LDL-C levels than young men this changes after
males and its effect on lipid metabolism [40]. This find- menopause. After menopause, the level of LDL-C in
ing was similar to a study presented on the distributions women tends to increase in equal measure to men as a
of blood lipids profile for a geographically defined cohort result of lack of estrogen. Estrogen increases hepatic cell
of rural elderly Iowans which demonstrated a higher surface LDL-C receptors and consequently rapid clear-
level of TC in women compared to men [41]. Another re- ance of LDL-C particles in premenopausal women.
search code named “the Bronx Aging Study” that was done However, in menopausal state this clearance is reduced
in the same year to assess risk factors for the development due to limited estrogen production [40, 45]. Now, look-
of dementia, coronary and cerebrovascular diseases in ing at the values obtained for triglycerides, the males

Fig. 1 Percentage Distribution of Lipids among Female Participants

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Fig. 2 Percentage Distribution of Lipids among Male Participants

had higher value than the females and this follows the similar pattern up to the age group of 51- 60 yrs. and
assertion that men tend to have higher triglycerides than dropped slightly within the age group of 61 – 70 yrs.
women [46]. Now from the female population (Table 3), total choles-
Also, the various lipid parameters were analyzed terol was normal for the age group of 28 – 34 yrs., it then
against the different age groups and gender among the rose slightly within the next age group of 35 – 40 yrs. and
participants. From the male population (Table 2), it was from there it dropped slightly within age 41 – 50 yrs., in-
seen that there was a rise in total cholesterol values from creased again within age 51 – 60 yrs. and finally declined mi-
age group 28 – 34 yrs. up to the 41 – 50 yrs. group. Then nutely within age 61 – 70 yrs. For HDL – C, a normal value
the value dropped a bit within the age group of 51 – 60 was seen for age group 28 – 34 yrs. and then it reduced
yrs. and thereafter was raised in the last age group of 61- slightly and maintained the level for age group 35 – 40 yrs.
70 yrs. Still with the HDL-C values for the male popula- up to 51 – 60 yrs. after which it increased slightly in the last
tion, the age group of 35 – 40 yrs. had a slightly lower age group. With LDL-C, there was exponential increase as
value against the first age group. Then the value picked up the age increased and the same pattern was seen with the
in the following age group (41 – 50 yrs) and then dropped triglyceride results. This finding is in line with a study by
again within the age group of 51 – 60 yrs. and subse- Schaefer and colleagues in 1994 which postulated that, in-
quently increased slightly within the last age group. When creased age was associated with higher plasma LDL-C,
it came to LDL-C, a marginal but exponential increase in especially in women and was significantly higher in post-
values from the lower age group (28 – 30 yrs) to the high- menopausal than in premenopausal women [47].
est (61 – 70 yrs) was seen. The triglycerides also showed a Again, the percentage distribution of the lipid parame-
ters into high, normal and low level category was carried
Table 4 A table of means and standard deviations of TC/HDL out among the participants. The outcome indicated that
ratio in the studied age groups for both males and females majority of the participants fell into the normal level cat-
Age groups Males Females P-value egory with all the parameters followed by the high level
TC/HDL ratio (mmol/L) TC/HDL ratio (mmol/L) and then low level category for the female participants
Mean ± SD Mean ± SD (Fig. 1). The analysis for the male participants follow
20–30 years 3.3 ± 1.5 2.5 ± 0.5 0.061 similar pattern except that in their case the numbers
31–40 years 3.8 ± 2.0 3.3 ± 1.2 0.314 that fell into the low level category were quiet low and
41–50 years 3.5 ± 1.5 3.5 ± 1.3 0.521 the difference between normal and high levels of the pa-
51–60 years 3.9 ± 1.3 4.0 ± 1.9 0.000
rameters were significant (Fig. 2).
Furthermore, the ratio of TC/HDL cholesterol as an
61–70 years 4.3 ± 1.9 3.2 ± 1.8 0.000
indicator of coronary risk factor was calculated for both

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Table 5 A table highlighting the haematological indices of parameters between the males and females. Also, when
study population Pearson-Moment-r correlation test was employed to in-
Parameter Females Males t P-value vestigate the existence of any significant relationship be-
WBC 5.73 ± 0.21 8.19 ± 5.87 −2.405 0.022* tween haematological parameters and the different lipid
RBC 3.98 ± 0.61 4.57 ± 0.61 −4.567 0.000* parameters among the participants, there was a strong,
positive correlation between RBC and lymphocytes and
Haemoglobin 10.63 ± 0.79 11.80 ± 1.10 −9.328 0.000*
the different lipid parameters which was also significant
HCT 31.96 ± 2.36 35.44 ± 3.28 −9.631 0.000*
[p = 0.003 and p = 0.002 respectively]. Again, there was a
MCV 75.59 ± 5.57 85.35 ± 3.94 −4.928 0.000* strong negative correlation between platelets, WBC,
Platelets 224.56 ± 18.71 275.85 ± 28.53 −8.767 0.000* HCT, Haemoglobin, MCV and Neutrophils. However,
Lymphocyte 1.49 ± 0.15 1.63 ± 0.11 4.280 0.000* only Platelets, Haemoglobin and HCT showed statically
Neutrophils 4.11 ± 0.54 5.80 ± 0.41 11.325 0.000* significant correlation [p = 0.003, p = 0.003 and p = 0.020
WBC white blood cell, RBC red blood cell, HCT haematocrit, MCV mean cell
respectively] whilst WBC, MCV and Neutrophils did not
volume. Values are presented as mean ± standard deviation. P < 0.05 is show significance [p = 287, p = 0.720 and p = 0.745 re-
considered significant. *mean difference is statistically significant, spectively] as seen from Table 6. The findings of this
study is believed to be novel and we hope it will go a
male and female participants. It could be seen that the long way to assist in the management of patients with
level of TC/HDL cholesterol ratio was high in males of type-2 diabetes.
age group 20–30 years and 31–40 years as compared to A limitation worthy of mention was the inability to re-
females of the same age group. The ratio (3.5 ± 1.5 and peat the tests for all the subjects at different time points,
3.5 ± 1.3) for 41–50 years group of both sexes was almost due to limited resources and time constraints.
the same. There was however a significant difference in
TC/HDL cholesterol ratio as far as males and females Conclusion
are concern in age group 51–60 years and 61–70 years The outcome of the study indicates that there is signifi-
(P = 0.000). According to American Heart Association, cant difference in lipid parameters between males and
TC/HDL cholesterol ratio should ideally be ≤3.5 mmol/L females. Again, we saw proportional increment in
and even though both males and females are at risk of LDL-C in males and LDL-C and Triglycerides in females
developing CVD especially elderly ones, it is not the as the age of participants increased. Furthermore, the
same in both subjects [48]. According to Maas and coronary risk factor was higher in males than females
Appleman (2010), although women and men share most and the difference was significant. With regards to
classic risk factors, the significance and the relative haematological parameters, we saw significant difference
weighting of the factors are different and cardiovascular in almost all of the haematological parameters between
disease develops earlier in men than women [49]. the male and female participants. There was also, both
The other part of the study looked at haematological strong positive and negative correlations between the
parameters and an independent sample t-test was con- haematological parameters and the different lipid param-
ducted to investigate the parameters across gender eters. This study presents some interesting and novel
among the participants. It was seen that there was sig- findings which may be very important in the care and
nificant difference in almost all of the haematological management of patients with type-2 diabetes.

Table 6 A table showing the correlation between haematological parameters and serum lipids measurements using Pearson
moment-r correlation
Parameter Total cholesterol HDL LDL Triglyceride
r P-value r P-value r P-value r P-value
Platelets − 0.496 0.003* − 0.478 0.004* − 0.522 0.002* −0.488 0.003*
WBC −0.177 0.318 −0.165 0.296 −0.169 0.321 −0.178 0.287
RBC 0.526 0.001* 0.498 0.021* 0.532 0.002* 0.518 0.003*
Haemoglobin −0.514 0.002* −0.510 0.010* −0.518 0.004* −0.499 0.003*
HCT −0.525 0.001* −0.521 0.002* −0.530 0.010* −0.518 0.020*
MCV −0.043 0.808 −0.039 0.718 −0.041 0.691 −0.050 0.720
Lymphocyte 0.432 0.005* 0.442 0.005* 0.401 0.003* 0.512 0.002*
Neutrophils −0.028 0.873 − 0.018 0.773 − 0.030 0.678 − 0.029 0.745
WBC white blood cell, RBC red blood cell, HCT haematocrit, MCV mean cell volume. *mean difference is statistically significant where P < 0.05 is
considered significant

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Abbreviations 7. Whiting DR, Guariguata L, Weil C, Shaw J. IDF diabetes atlas: global
CHD: Chronic Heart Disease; CVD: Cardiovascular Disease; DM : Diabetes estimates of the prevalence of diabetes for 2011 and 2030. Diabetes Res
Mellitus; EDTA: Ethylene Diamine-Tetra-Acetic Acid; Hb: Haemoglobin; Clin Pract. 2011;94(3):311–21.
HCT: Haematocrit; HDL-C: High Density Lipoprotein Cholesterol; LDL-C: Low 8. Comazzi S, Spagnolo V, Bonfanti U. Erythrocyte changes in canine diabetes
Density Lipoprotein Cholesterol; MCV: Mean Cell Volume; RBC: Red Blood mellitus: in vitro effects of hyperglycaemia and ketoacidosis. J Comp Clin
Cell; ROS: Reactive Oxygen Species; SD: Standard Deviation; SPSS: Statistical Path. 2004;12(4):199–205.
Package for Social Science; TC: Total Cholesterol; VLDL-C: Very Low Density 9. Elalamy I, Chakroun T, Gerotziafas GT, Petropoulou A, Robert F, Karroum A,
Lipoprotein Cholesterol; WBC: White Blood Cells; WHO: World Health et al. Circulating platelet-leukocyte aggregates: a marker of microvascular
Organization injury in diabetic patients. Thromb Res. 2008;121(6):843–8.
10. Roberto T, Dodesini AR, Lepore G. Lipid and renal disease. J Am Soc
Acknowledgements Nephrol. 2006;17:S145–7.
We are grateful to the directors and laboratory managers of the Korle-bu 11. Bergmann K, Sypniewska G. Diabetes as a complication of adipose tissue
Teaching Hospital for their assistance in carrying out this study. dysfunction. Is there a role for potential new biomarkers? Clin Chem Lab
Med. 2013;51:177–85.
Funding 12. Gerner RR, Wieser V, Moschen AR, Tilg H. Metabolic inflammation: role of
The study was funded using the University of Ghana book and research cytokines in the crosstalk between adipose tissue and liver. Can J Physiol
allowances of the research team members as well as from the PI’s personnel Pharmacol. 2013;91:867–72.
resources. 13. Letícia AS, Deoliveira MS, Paula Salles AMF, Das Graças MC. Hemostatic
changes in patients with type 2 diabetes mellitus. Rev Bras Hematol
Availability of data and materials Hemoter. 2010;32(6):482–8.
The datasets used and/or analysed during the current study are available 14. Mbata CA, Adegoke A, Nwagu C, Nyeso WA. Some Haematological
from the corresponding author on reasonable request. parameters in diabetic patients in Port Harcourt Nigeria. AJMS. 2015;3(2):
2348–7186.
Authors’ contributions 15. Mirza S, Hossain M, Mathews C, Martinez P, Pino P, Gay JL, et al. Type 2-
SAB is the PI of the study and he participated in the design, co-supervised diabetes is associated with elevated levels of TNF-alpha, IL-6 and
the research and drafted the manuscript. RK, SOB and LA participated in the adiponectin and low levels of leptin in a population of Mexican American: a
design of the study and carried out the experimental work. MAS participated cross-sectional study. Cytokine. 2012;57(1):136–42.
in the supervision of the work and proof reading of the manuscript. All 16. Gkrania-Klotsas E, Ye Z, Cooper AJ, Sharp SJ, Luben R, Biggs ML, et al.
authors read and approved the final manuscript. Differential white blood cell count and type 2 diabetes: systematic review
and meta-analysis of cross-sectional and prospective studies. PLoS One.
Ethics approval and consent to participate 2010;5(10):e13405.
Ethical approval was sought from the ethics and protocol review committee 17. Kakouros N, Rade JJ, Kourliouros A, Resar JR. Platelet function in patients
of the School of Biomedical and Allied Health Sciences, College of Health with diabetes mellitus: from a theoretical to a practical perspective. Int J
Sciences, University of Ghana as well as the management of the Korle-bu Endocrinol. 2011;2011:742719.
Teaching Hospital. Also, written informed consent was obtained from the 18. Zuberi BF, Akhtar N, Afsar S. Comparison of mean platelet volume in patients
participants who passed the selection criteria. The records obtained from the with diabetes mellitus, impaired fast. Singap Med J. 2008;49(2):114–6.
participants were coded to avoid the use of names. Again, participation of 19. Mortensen SB, Larsen SB, Grove EL, Kristensen SD, Hvas AM. Reduced
the study was made voluntary and participants were allowed to withdraw platelet response to aspirin in patients with coronary artery disease and
freely at any stage if they encountered any problem that could not be ad- type 2 diabetes mellitus. Thromb Res. 2010;126(4):e318–22.
dressed during the course of the study. 20. Christensen KH, Grove EL, Würtz M, Kristensen SD, Hvas AM. Reduced
antiplatelet effect of aspirin during 24 hours in patients with coronary artery
Consent for publication disease and type 2 diabetes. Platelets. 2015;26(3):230–5.
Not applicable. 21. Ellinger VC, Carlini LT, Moreira RO, Meirelles RM. Relation between insulin
resistance and hematological parameters in a Brazilian sample. Arq Bras
Competing interests Endocrinol Metabol. 2006;50(1):114–7.
The authors declare that they have no competing interests. 22. Chen LK, Ming-Hsien L, Zhi-Jun C, Shinn-Jang H, Chiou ST. Association of
insulin resistance and hematologic parameters: study of a middle-aged and
elderly Chinese population in Taiwan. Chin Med Assoc. 2006;69(6):248–53.
Publisher’s Note 23. Cho YI, Mooney MP, Cho DJ. Hemorheological disorders in diabetes
Springer Nature remains neutral with regard to jurisdictional claims in mellitus. J Diabetes Sci Technol. 2008;2(6):1130–8.
published maps and institutional affiliations. 24. Nakanishi N, Yoshida H, Matsuo Y, Suzuki K, Tatara K. White blood-cell count
and the risk of impaired fasting glucose or type II diabetes in middle-aged
Received: 24 September 2018 Accepted: 26 November 2018 Japanese men. Diabetologia. 2002;45:42–8.
25. Alam J, Chandra SM, Mokarrama MN, Hoque M, Hasan M, Islam S, et al. A
comparative analysis of biochemical and hematological parameters in
References diabetic and non-diabetic adults. AMS. 2015;2(1):1–9.
1. Hsu HY, Chiu HY, Lin HT, Su FC, Lu CH, Kuo LC. Impacts of elevated 26. Mullugeta Y, Chawla R, Kebede T, Worku Y. Dyslipidemia associated with
glycemic hemoglobin and disease duration on the sensorimotor control of poor glycemic control in type 2 diabetes mellitus and the protective effect
hands in diabetes patients. Diabetes Metab Res Rev. 2015;31:385–94. of metformin supplementation. Ind J ClinBiochem. 2012;27(4):363–9.
2. Scheen AJ. Pathophysiology of type 2 diabetes. Acta Clin Belg. 2003;58(6): 27. Gundogan K, Bayram F, Capak M, Tanriverdi F, Karaman A, Ozturk A, et al.
335–41. Prevalence of metabolic syndrome in the Mediterranean region of Turkey:
3. American Diabetes Association Diagnosis and classification of diabetes evaluation of hypertension, diabetes mellitus, obesity, and dyslipidemia.
mellitus. Diabetes Care. 2007; 30(Suppl 1):S42–S47. Metab Syndr Relat Disord. 2009;7:427–34.
4. Mathieu C, Badenhoop K. Vitamin D and type 1 diabetes mellitus: state of 28. Barbieri M, Ragno E, Benvenuti E, Zito GA, Corsi A, Ferrucci L, et al. New
the art. Trends Endocrinol Metab. 2005;16(6):261–6. aspects of the insulin resistance syndrome: impact in haematological
5. Kasuga M. Insulin resistance and pancreatic β cell failure. J Clin Invest. 2006; parameters. Diabetologia. 2001;44:1232–7.
116(7):1756–60. 29. Dinsmoor RS. Lipid profile. 2006. http://www.diabetesmanagement.com.
6. Røder ME, Porte D, Schwartz RS, Kahn SE. Disproportionately elevated Accessed 23 Feb 2017.
proinsulin levels reflect the degree of impaired B cell secretory capacity in 30. Beaglehole R, Yach D. Globalisation and the prevention and control of non-
patients with noninsulin-dependent diabetes mellitus. J Clin Endocrinol communicable disease. The neglected chronic disease of adult. Lancet.
Metab. 1998;83(2):604–8. 2003;362:903–8.

Content courtesy of Springer Nature, terms of use apply. Rights reserved.

Antwi-Baffour et al. Lipids in Health and Disease (2018) 17:283 Page 9 of 9

31. Attia YA, Al-Harthi MA, Korish MM, Shiboob MM. Fatty acid and cholesterol
profiles and hypocholesterolemic, atherogenic, and thrombogenic indices
of table eggs in the retail market. Lipids Health Dis. 2015;14:136. https://doi.
org/10.1186/s12944-015-0133-z.
32. Attia YA, Al-Harthi MA, Korish MM, Shiboob MM. Fatty acid and cholesterol
profiles, hypocholesterolemic, atherogenic, and thrombogenic indices of
broiler meat in the retail market. Lipids Health Dis. 2017;16(40):1–11.
33. Marhoum TA, Abdrabo AA, Lutfi FM. Effects of age and gender on serum
lipid profile in over 55 years-old apparently healthy Sudanese individuals.
Asian J Biomed Pharmaceut Sci. 2013;3(19):10–4.
34. World Health Organisation (WHO). The world health report. Reducing risk,
promoting healthy life. Geneva: World Health Organisation (WHO); 2011.
35. LaPierre D. Dyslipidaemia. 2011. Htttp: //www. Sharinginhealth.Ca/
conditions_and_diseases/dyslipidemia.Html. Accessed 23 Apr 2017.
36. Syed SH, Muhammad A, Waqas H. Gender differences in lipids and
lipoprotein (a) profile sin healthy individuals and patients with type 2
diabetes mellitus. Pak J Physiol. 2005;1:1–2.
37. Goldman R. The recommended cholesterol levels by age? 2017. http://
www.healthline.com/health/high-cholesterol/levels-by-age. Accessed 10
May 2017.
38. Ge P, Dong C, Ren X, Weiderpass E, Zhang C, Fan H, et al. The high
prevalence of low HDL-cholesterol levels and dyslipidemia in rural
populations in northwestern China. PLoS One. 2015;10(12):e0144104.
39. Adewoyin AS, Nwogoh B. Peripheral blood film – a review. Ann Ib Postgrad
Med. 2014;12(2):71–9.
40. Russo G, Pintaudi B, Giorda C, Lucisano G, Nicolucci A, Cristofaro MR, et al.
Age- and gender-related differences in LDL-cholesterol Management in
Outpatients with type 2 diabetes mellitus. Int J Endocrinol. 2015;2015:
957105.
41. Wallace RB, Colsher PL. Blood lipid distributions in older persons. Prevalence
and correlates of hyperlipidemia. Ann Epidemiol. 1992;2(1–2):15–21.
42. Frishman WH, Ooi WL, Derman MP, Eder HA, Gidez LI, Ben-Zeev D, et al.
Serum lipids and lipoproteins in advanced age: intraindividual differences.
Ann Epidemiol. 1992;2:43–50.
43. Adediran O, Akintunde AA, Edo AE, Opadijo OG, Araoye AM. Impact of
urbanization and gender on frequency of metabolic syndrome among
native Abuja settlers in Nigeria. J Cardiovasc Dis Res. 2012;3:191–6.
44. Eapen DJ, Kalra GL, Rifai L, Eapen CA, Merchant N, Khan BV. Raising HDL
cholesterol in women. Int J Womens Health. 2010;1:181–91.
45. Kannel WB. Metabolic risk factors for coronary heart disease in women:
perspective from Framingham study. Ann Heart J. 1987;114:413–9.
46. Carroll MD, Lacher DA, Sorlie PD, Cleeman JI, Gordon DJ, Wolz M, et al.
Trends in serum lipids and lipoproteins of adults, 1960-2002. JAMA. 2005;
294:1773–81.
47. Schaefer EJ, Lamon-Fava S, Cohn SD, Schaefer MM, Ordovas JM, Castelli W,
et al. Effects of age, gender, and menopausal status on plasma low density
lipoprotein cholesterol and apolipoprotein B levels in the Framingham
offspring study. J Lipid Res. 1994;35(5):779–92.
48. American Heart Association (AHA). What cholesterol levels mean-
triglyceride? 2012. https://www.medscape.com/viewcollection/32669.
Accessed 10 Jun 2017.
49. Maas AHM, Appelman YEA. Gender differences in coronary heart disease.
Neth Heart J. 2010;18(12):598–602.

Content courtesy of Springer Nature, terms of use apply. Rights reserved.

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