ABSTRACT
Stroke has been a global burden, with increasing
morbidity and mortality. Several risk factors have been identified, which
include: hyperhomocysteinaemia, hypovitaminosis B12,
and low zinc levels, which are the now target of preventive strategies. Limited
studies have been done on the risk factors (analytes) in our environment hence
the current study was undertaken to evaluate the serum levels of homocysteine,
vitamin B12
and zinc in patients with acute ischaemic stroke in Zaria and healthy controls.
One hundred ischaemic stroke patients on admission confirmed by brain CT-scan
or Siri-raj stroke score of less than minus one.(-1) and equal number of
apparently healthy age and sex-matched were recruited. Their serum
homocysteine, and vitamin B12 were measured using enzyme linked Immunosorbent
assay,and zinc was measured using direct colorimetric method. Stroke severity
was determined using National Institute of Health Stroke Score (NIHSS). Mean
serum homocysteine for patients was significantly higher than that of controls
(p<0.05) and mean serum vitamin B12and zinc were significantly lower compared to that of
controls (p<0.05), with an odds ratio of 0.04, 0.19 and 0.54 respectively.
The reference intervals obtained from the healthy controls were found to be
0.90 -1.70µmol/l, 199.72-685.48pg/ml and 52.26-111.86µg/dl for homocysteine,
vitamin B12
and zinc respectively. Hyperhomocysteinaemia was seen in 34%, hypovitaminosis B12
was seen in 81% and low zinc was seen in 46%. Patients
with hyperhomocysteinaemia, hypovitaminosis B12 and low zinc presented
with more severe neurologic deficits even though the difference was not
statistically significant with p-values of 0.946, 0.735, and 0.566
respectively. Elevated serum homocysteine, low vitamin B12 and zinc were found to be associated with ischaemic stroke. There was
negative correlation between homocysteine and vitamin B12 and stroke severity and therefore early management of those
conditions may be an effective way of decreasing the incidence of stroke in our
environment. Vitamin B12
and zinc supplements may be beneficial to patients at risk.
TABLE OF CONTENTS
Title page
Abstract
Table of Contents
Abbreviation/Symbols used
CHAPTER ONE
1.0 INTRODUCTION
1.1 Background
1.2 Statement of
problems
1.3 Justification
1.4 Aim and
objectives of the study
1.4.1 Aim
1.4.2 Objectives
1.5 Research question/hypothesis
CHAPTER TWO
2.0 LITERATURE
REVIEW
2.1 Stroke
2.1.1 Brief History
2.1.2 Epidemiology
2.1.3 Anatomy of the
brain
2.1.3.1 Gross
2.1.3.2 Arterial
distribution
2.1.4 Aetiology and
classification of stroke
2.1.5 Risk factors
for stroke
2.1.6 Pathophysiology
of stroke
2.1.6.1 Molecular pathophysiology of stroke
2.1.6.2 Pathology of stroke
2.1.7 Clinical
features
2.1.8 Investigation
of patient with stroke
2.1.8.1 Haematological
2.1.8.2 Radiological
2.1.8.3 Microbiological/Immunological
2.1.8.4 Biochemical
2.2 Some
Biomedical Markers of Stroke
2.2.1 Homocysteine
2.2.2 Vitamin B12
2.2.3 Zinc
2.3.4 Homocysteine in
acute ischaemic stroke
2.3.5 Vitamin B12 in
acute ischaemic stroke
2.3.6 Zinc in acute
ischaemic stroke
CHAPTER THREE
3.0 MATERIALS AND
METHODS
3.1 Background of
study area
3.2 Study
population
3.2.1 Subjects
3.2.2 Inclusion
criteria for patients
3.2.3 Exclusion
criteria for patients
3.2.4 Inclusion
criteria for controls
3.2.5 Exclusion
criteria for controls
3.2.6 Informed
consent
3.2.7 Sample size
determination
3.2.8 Ethical
approval
3.3 Study protocol
3.3.1 Siri raj stroke
score
3.4 Specimen
collections and processing
3.5 Chemicals
3.6 Equipment
3.7 Analytical
methods
3.7.1 Measurement of
serum Homocysteine
3.7.1.1 Principle
3.7.1.2 Procedure
3.7.1.3 Calculation
3.7.2 Measurement of serum vitamin B12
3.7.2.1Principle
3.7.2.2 Procedure
3.7.2.3 Calculation
3.7.3 Measurement of
serum Zinc
3.7.3.1Principle
3.7.3.2 Procedure
3.7.3.3 Calculation
3.8 Quality
Control
3.9 Statistical analysis
of the result
CHAPTER FOUR
4.0 RESULTS
4.1 Clinical and
demographic characteristics of study population
4.2 Admission
homocysteine, vitamin B12 and Zinc (mean±SD) in stroke cases and controls
4.3 Reference
intervals of serum homocysteine, Vitamin B12 and Zinc using healthy controls
4.4 Serum
levels of homocysteine vitamin B12 and Zinc of ischaemic stroke patients based
on different modifying risk factors
4.5:
Frequency of elevated homocysteine, low vitamin B12 and low zinc among controls
and patients with ischaemic stroke
4.6: Serum level of
homocysteine vitamin B12 and Zinc of stroke patients based on severity
4.7 Relationship
between stroke severity and analytes abnormalities
4.8 Correlation
between serum homocysteine and vitamin B12 among stroke patients
CHAPTER FIVE
5.0 DISCUSSION
CHAPTER SIX
6.0 CONCLUSION AND
RECOMMENDATIONS
6.1 Summary
6.2 Conclusion
6.3 Recommendations
References
Appendices
CHAPTER ONE
1.0 INTRODUCTION
1.1 BACKGROUND
Stroke is defined as a clinical syndrome of sudden onset of
rapidly developing symptoms or signs of focal and at times global loss of
cerebral function, with symptoms lasting more than 24 hours or leading to
death, with no apparent cause other than that of vascular origin (Kameshwaret
al, 2012).
The World Health Organization estimates that cardiovascular
disease and stroke will be the leading cause of death and disability world wide
by 2020 (Lynn,2000). Stroke is one of the
leading causes of death in any population, and its prevention is a key strategy
in reducing the rate of mortality and morbidity (Hoseinaliet al, 2011).
It is the third commonest cause of death in Western industrialised countries (James et al,2000). Stroke is presently the leading cause of
disability and the third leading cause of death in United States (US centers,
2007). In the United States, blacks have an age-adjusted risk of death from
stroke that is 1.49 times that of whites (Schneider
et al, 2004). More than 700,000 persons
per year suffer a first time stroke in the United States with 20% of these individuals dying within
the first year after stroke (American Heart Association,
2002).If current trend continues, this number
is projected to reach one million per year by the year 2020(Ralph et al, 1997). In low income and middle income
countries, the burden of stroke and other vascular diseases is likely to
increase substantially over time in the next few decades because of their
expected health and demographic transition (Ralphet al, 1997).
Globally in 2005, it was estimated that stroke caused 5.7
million deaths, and 87% of these occurred in low income and middle-income
countries of the world (Strong et al, 2007)
Several risk factors for stroke have been identified, which
are the target of both primary and secondary preventive strategies (Hoseinaliet
al, 2011), these risk factors include hypertension, diabetes mellitus,
cardiac diseases, sickle cell anaemia, cigarette smoking, other immerging or
noble risk factors include hyperhomocysteinaemia, hypovitaminosis B12,and
low zinc levels etc. The role of hyperhomocysteinaemia as it relates to stroke
in Africans is still uncertain. It was hypothesized that homocysteine levels
are significantly higher in stroke patients than in normal controls and worsen
stroke severity, and increase short-term case fatality rates following acute
ischaemic stroke(Okubadejoet al,2008)
Homocysteine is an amino
acid. It is a homologue
of the amino acid cysteine,
differing by an additional methylene
bridge (-CH2-).
It is biosynthesized from methionine
by the removal of its terminal C methyl
group. Homocysteine can be recycled into methionine
or converted into cysteine with the aid of B-vitamins
(Wikipedia, 2013).
Hyperhomocysteinaemia is a potentially modifiable risk
factor for stroke, and may have a negative impact on the course of ischaemic
stroke (Okubadejoet al, 2008).
The accumulation of homocysteine and its metabolites is
caused by disruption of any of the 3 interrelated pathways of methionine metabolism
deficiency in the cystathionine B-synthase (CBS) enzyme, defective
methylcobalamin synthesis, or abnormality in methylene tetrahydrofolate
reductase (MTHFR) (Pitchaiah, 2013)
Hyperhomocysteinaemia may cause endothelial dysfunction
through oxidative stress, resulting in local thrombosis and subsequent
ischemia. Another possible mechanism is the direct toxicity of homocysteine to
blood vessels but there is no definite evidence to support either of these
mechanisms(Hoseinaliet al, 2011).
For more Chemical Pathology Projects click here
================================================================
Item Type: Project Material | Attribute: 83 pages | Chapters: 1-5
Format: MS Word | Price: N3,000 | Delivery: Within 2hrs
================================================================
No comments:
Post a Comment