The SA Journal Diabetes & Vascular Disease Vol 14 No 1 (July 2017)

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SA JOURNAL OF DIABETES & VASCULAR DISEASE RESEARCH ARTICLE
VOLUME 14 NUMBER 1 • JULY 2017 35
writing. Ethical approval was obtained from the Tshwane University
of Technology Ethics Committee (Ref: 2010/09/004). A standard
informed consent form was signed by all participants.
A questionnaire was used to obtain information on demographic
characteristics, lifestyle, eating habits, health conditions such as
surgical operations, diabetes mellitus, previous arterial thrombosis,
previous pulmonary embolism, hyperlipidaemia, kidney problems,
obesity/overweight and heart failure. Cardiovascular disease was
one of the ailments that no participants reported to be suffering
from.
Fasting blood samples were collected from participants at the
Nobody Clinic in Ga-Mothapo. Subjects who had not fasted for at
least nine hours before sample collection and could not withdraw
medication for that period were excluded from the study.
Blood was collected by professional nurses. One 4.5-ml blood
sample was collected from each participant in a sodium fluoride
tube for glucose analysis, in a plain tube for triglycerides and
cholesterol estimation, and in an EDTA-anticoagulated tube for
homocysteine level assay.
The body weight of the participants wearing light clothing
without shoes was measured using a weight scale from Omron. The
height was measured without shoes in an upright position using
the Seca telescopic height-measuring rod. The BMI was calculated
using the formula: BMI = weight in kg/(height in m)2.
Blood pressure was measured using the Omron MI-5. Blood
glucose, triglyceride and cholesterol levels were measured using
the ILab 300 Plus Chemistry System from Beckman Coulter.
Homocysteine was estimated using the Beckman Coulter Synchron
system analyser. Enzymatic methods were used for all biochemical
parameters.
The diagnostic criteria used for the parameters were set as
follows: hyperhomocysteinaemia = blood homocysteine > 15 µmol/l,
hyperglycaemia=bloodglucose>7.0mmol/l,hypercholesterolaemia
= blood cholesterol > 5.7 mmo/l, hypertriglyceridaemia = blood
triglyceride > 2.26 mmol/l, obesity = BMI > 30 kg/m2, systolic blood
pressure > 140 mmHg = hypersystolic blood pressure, and diastolic
blood pressure > 90 mmHg = hyperdiastolic.
The collected data were analysed with Statistical Package for
Social Science (SPSS) version 18. The results were expressed in
percentages of p-values for association. A p-value of 0.05 was
regarded as statistically significant.
Results
The study consisted of 382 participants. The mean age of the study
participants was 38.45 years. The mean values for the studied
parameters were as follows: homocysteine 9.44 µmol/l, glucose
5.42 mmol/l, systolic blood pressure 125.65 mmHg, diastolic blood
pressure 81.06 mmHg, cholesterol 4.18 mmol/l, triglycerides 1.22
mmol/l and BMI 26.80 kg/m2 (Table 1).
The associations of hyperhomocysteinaemia with hyper-
glycaemia (p = 0.175), hypertriglyceridaemia (p = 0.442) and
hypercholesterolaemia (p = 0.480) were statistically insignificant.
The association of hyperhomocysteinaemia with obesity was
found to be partially significant (p = 0.080). The associations
of hyperhomocysteinaemia with hypersystolic (p = 0.002) and
hyperdiastolic (p = 0.033) blood pressures were statistically
significant.
Of the 45 hyperglycaemic participants, three were also
hyperhomocysteinaemic, constituting about 6.7%. Of the 39
hypertriglyceridaemic participants, three were also hyperhomo-
cysteinaemic, constituting about 7.7%. Of the 38 hypercholes-
terolaemic participants, five were also hyperhomocysteinaemic,
constituting about 13.1%. Of the 72 participants with high systolic
blood pressure, 11 were also hyperhomocysteinaemic, constitut-
ing about 15.3%. Of the 84 participants with high diastolic blood
pressure, 16 were also hyperhomocysteinaemic, constituting about
19.0%. Of the 95 obese participants, 10 were also hyperhomo-
cysteinaemic, constituting about 10.5%.
Discussion
We estimated homocysteine levels in 45 hyperglycaemic subjects
for evaluation of association and found no statistical significance
(p = 0.175) (Table 2). Three hyperglycaemic subjects (6.7%) were
hyperhomocysteinaemic (Table 3). Different findings about the
relationship have been reported above.
Vayá et al., in their study of the relationship between
homocysteine and hyperglycaemia, found a partial association.15
Elias and Eng, and Shaikh et al. reported that homocysteine levels
can be low or elevated in diabetes mellitus.1,13 These findings and
ours are contrary to the findings of Mishra et al .2 and Akali et al.12
who found high homocysteine levels in diabetic patients. They
found high levels of homocysteine to be a strong risk factor in
diabetic patients. This was supported by the findings of Shaikh et
al. and Schalinske.1,14
Shaikh et al. found more than half of their diabetic participants
had elevated homocysteine levels. 1 The discrepancy with our results
could have been attributable to the influence on homocysteine
of insulin concentrations, therapy with insulin and medication.12
Control of these confounding factors in our study may have
improved the level of association.
Table 1. Characteristics of the participants
Variable Mean ± SD
Age (years) 38.45 ± 17.283
Homocysteine (μmol/l) 9.44 ± 4.13
Glucose (mmol/l) 5.42 ± 2.555
Systolic blood pressure (mmHg) 125.65 ± 19.164
Diastolic blood pressure (mmHg) 81.06 ± 11.351
Cholesterol (mmol/l) 4.18 ± 1.396
Triglycerides (mmol/l) 1.22 (0.83–1.68)
Body mass index (kg/m2) 26.80 ± 6.20
Table 2. P-values for significance of association
Homocysteinaemia Metabolic disorder p-value
n = 45 Hyperglycaemia (n = 45) 0.175
n = 39 Hypertriglyceridaemia (n = 39) 0.442
n = 38 Hypercholesterolaemia (n = 38) 0.480
n = 72 Systolic blood pressure (n = 72) 0.002
n = 84 Diastolic blood pressure ( n = 84) 0.033
n = 95 Obesity ( n = 95) 0.080
95% confidence interval and p = 0.05 level of significance.