Professional Documents
Culture Documents
Faculty of Medicine
Postgraduate Medical Studies Board
Supervisor
Dr. Musa Mohammed Khier
MBBS, MD, Khartoum
Faculty of Medicine
University of Khartoum
To my family, Teachers
&
friends
Dr.
Medicine,
University
of
Khartoum
who
assisted
in
would
like
to
extend
my
thanks
to
my
colleagues,
Dr. Mohammed Khalaf Alla and Dr. Afrah Yousif, Dr. Maha, Ridwan and
Dr. Amira M. Zien for their help in data collection.
My
thanks
are
extended
to
Dr.
Intisar
Seed
Ahmed,
Dr. Amel Faris, Dr. Mohamed Salih, whom their assistance in the
library was of great help.
I am also indebted to my colleagues Dr. Sara Saeed and Dr.
Mohammed El Amin Awad for their help and advice in clarification of
several points.
My great thanks to Miss Widad A. Magsood for her patience for
the long hours she spend in typing the manuscript.
I am forever grateful to Relatives and friends who support
me stand with me with great love and real feelings, always asking God
success to me, my special respect and utmost thanks for them all.
BMI
BP
Blood pressure
CHD
CVA
Cerebrovascular accident
DCCT
DM
Diabetes mellitus
FBG
FH
Family history
HOT
HTN
Hypertension
IDDM
Insulin dependent DM
IGT
MRC
NIDDM
Non-Insulin dependent DM
2PPBG
RBS
UKPDA
WHO
Hypertension
(HNT)
and
diabetes
mellitus
(DM)
are
with
hypertension
compared
with
diabetic
without
.
( 2) 160
. (1)
41.2
%20 ) (.
.
.
%17.5
%10.2 %10
.
%10.2
.
%0.6
.
71
72
the
to
according
74
control group
75
Table 7: Prevalence of hypertension in diabetic patients
compared with non diabetic subjects
76
77
78
80
81
82
84
87
hypertension
89
Table 21: Ischaemic heart disease in both types of DM with
hypertension compared with diabetic patients
without hypertension
90
Fig. 1:
Fig. 2:
91
Fig. 3:
92
Fig. 4 :
93
Fig. 5:
94
95
Fig. 6:
Fig. 7:
95
Fig. 8:
97
hypertension
98
Fig. 9:
hypertension
99
Fig. 10:
100
Fig 11:
101
CONTENTS
Dedication ...I
Page
Acknowledgment....II
Abbreviations.IV
English abstract..V
Arabic abstract.......VI
List of tables and figures ........VII
CHAPTER ONE
INTRODUCTION & LITERATURE REVIEW .....1
OBJECTIVES........62
CHAPTER TWO
PATIENTS & METHODS ....63
CHAPTER THREE
RESULTS .66
CHAPTER FOUR
DISCUSSION...102
CONCLUSION ....113
RECOMMENDATIONS .....114
REFERENCES....116
APPENDIX
(Questionnaire)
HISTORICAL BACKGROUND
The first actual description of diabetes dates back some 1500
years before Christ. In the centuries near the beginning of Christianity,
the appearance of diabetes mellitus (DM) in succeeding generation
was described. The famous work of Susruta 400 BC of India and his
displine Charaka (6 A.D) noted many of the symptoms and even type
of diabetes. Aretaeus (2 A.D) used the general term diabetes, which is
an ionic Greek and meaning To run though siphon although the
Indian name for diabetes Madhumela or honey urine was used in
the sixth century A.D.
The Latin word mellitus honey was applied much later. Even
in the early period of history, observers noted that heredity was
important because various members of the same family were afflicted
with the sweet water disease.
The Roman physician, Galena (A.D 13-201) thought that
diabetes is a rare disease he employed alternative names to diabetes
including Diarrhea urinosa and (dipsakos). The later emphasing the
cardinal symptoms of thirst and polyuria.
During the periods of history another type of DM was
recorded, maturity onset in which addition to the usual symptoms, the
patient was both obese and without energy. The other type of DM with
onset in youth was described as Melting down the flesh and producing
sweet urine.
Thomas Wills, Dadson and Claude Bernard all give significance
to the condition and recognition of complications. The description of
DM now show similar finding.
The
Arabic
medical
texts
during
the
9th-11th
centuries
Willis
was
first
administered
in
1922
the
role
of
INTRODUCTION
Hypertension and DM are interrelated diseases and frequently
concomitant,
if
untreated
strongly
predispose
to
atherosclerotic
proteins
metabolism,
characterize
symptoms
of
DKA,
leading
to
absolute
insulin
deficiency)
and
depends
on
these
in
non
white
and
white
males.
In
both
Diabetes in Sudan:
The actual number of people with diabetes in Sudan is not
known. A small population-base study in 1993 of a sample of 1284
adults in Northern Sudan was conducted and showed that the crude
prevalence of 3.4% (men 3.5% women 3.4%) for diabetes and that
the highest crude prevalence was in the northern part of Sudan
(0.9%). New cases (2.2%) were almost twice as prevalent as
previously known cases (1.3%) family history of DM, obesity and
advanced age were associated with higher rates of diabetes.(10)
The influence of environmental factors in the cause of DM
needs to be maintained. One small study questioned the role of
Malaria falciparum (13 million cases in 1995) as a possible cause of
DM. Large scale studies in Sudan confirm its absence. One study
showed that people with DM constituted 7% of all hospital admission,
a value higher than that reported from other African countries.
Type II DM is associated with an overall age adjusted
mortality, that is about twice that of the non-diabetic population and
the life expectancy is reduced by 5-10 years currently. Diabetes in
Sudan (and most of Africa) is believed to have one of the highest
mortality rates for a non infectious disease. One study indicated that
10% of adult patient deaths were caused by DM.
pressure
(BP)
in
population,
160 mmHg,
held
>140
in
DBP
>90
the
sixth
mmHg,(14)now
report
of
replaced by
the
Joint
Category
Systolic
Diastolic
Optimal
< 120
< 80
Normal
< 130
< 85
High normal
130 - 139
85 - 98
140 - 159
90 - 99
Stage II (moderate)
160 - 179
100 - 109
180
110
Epidemiology of hypertension:
The prevalence of hypertension varies considerably among and
within population. In general societies in whom industrialization are
advanced have a higher prevalence of elevated Blood pressure than
developed society.
Black
Americans
have
an
incidence
of
hypertension
is
often
observed
in
the
first
degree
disease.
On
rare
occasions,
renal
cell
carcinoma
for
comparison
between
groups.
Allowing
for
the
association
between
hypertension
diabetes.(13)
and
recent
studies
however,
do
support
an
increase
patients
with
careful
matched
controls,
e.g.
Pell
and
higher
mortality
in
diabetics
than
in
non-diabetics
with
Gushing
syndrome
and
primary
Prevalence rates from other centers, including the USA and Asia,
showed values ranging from 26% - 36%.(20)
In Saudi Arabia a large study (house hold screening) was
carried during the National Screening Program for the study of DM,
revealed that the prevalence of hypertension in non diabetic males and
females was 4.48% and 2.8% respectively, while it was 11.44% and
15.98% in diabetic males and females. In all provinces the increase in
prevalence of hypertension in diabetic was significantly higher in the
females compared to the males.(27)
In African population as in Europe and North America, the
excess prevalence of hypertension in DM is well established, and
prevalence rate vary between 10 and 49% in most series in Africa
(Nigeria included). The bulk of DM is NIDDM variety accounting for 25
- 75%, whereas the origin clinical implication and evolution of
hypertension associated with IDDM are reasonably well established.
The hypertension associated with NIDDM is less well understood
especially in African population.(28)
A recent study (2001) obtained from Jos, Nigeria revealed
that, of 302 diabetic patients 36% were found to have hypertension.
Patients with HTN were older and more obese than normotensive and
almost one-third of them had their hypertension diagnosed prior to
their DM.(29)
of
the
hypertension
of
NIDDM.
Isolated
cause.
Possible
explanations
for
the
association
of
in
several
studies
consider
secondary
causes
of
NIDDM
Hypertension due to
diabetic nephropathy.
Essential hypertension.
Hypertension of obesity
Essential hypertension
Hypertension due to diabetic
nephropathy.
Secondary hypertension
diabetes.
Secondary
hypertension
DM
(20)
sodium
counter
transport.(15)Mechanisms
other
than
hypertension
or
positive
family
history
of
is
marker
of
the
sodium
hydrogen
exchange,
to
normalize
plasma
glucose,
this
produces
other
patients
hyperinsuhnaemia
may
persist
with
are
risk
factors
for
coronary
heart
disease
premature
death.(13,35,36,37,38)
Also it has been demonstrated that the insulin resistance of
essential hypertension is located in peripheral tissues (muscle), is
limited to non oxidative pathways of glucose disposal (glycogen
synthesis), and correlates directly with the severity of hypertension.
The reason for the association of insulin resistance and essential
hypertension can be sought in at least four general types of
mechanisms, sodium retention, sympathetic nervous system over
activity, disturb membrane ion transport and proliferation of vascular
smooth
muscle
cells.
Physiological
maneuvers,
such
as
caloric
restriction (in the over weight patient) and regular physical exercise,
can improve tissue sensitivity to insulin, good evidence indicates that
these maneuvers also can lower blood pressure in both normotensive
and hypertensive individuals.(39,40,41,42)
Insulin resistant state had also been proposed by others to be
explained by factors such as abnormalities in insulin binding to its
receptor, defect in glucose transport, change in the signal transudation
pathway within insulin sensitive cells and metabolic abnormalities in
glycolysis, glucose oxidation and or glucogon synthesis. Insulin
resistance can also be explained by direct action of insulin which
stimulates the calcium pump in insulin sensitive tissues and promotes
calcium loss from the cells and raising cytosolic calcium levels in an
adepocyte can induce insulin resistance. If a cell is resistant to insulin,
the insulin induced calcium loss from the cells would be decreased,
and in vascular smooth muscle cells the resistance increase and intracellular calcium would enhance responsiveness to vasoconstrictor and
increase blood pressure.(43,44,45)
Insulin also stimulates the proliferation of arteriolar smooth
muscle cells, augments collagen synthesis in the vascular wall,
increases the formation of and decreases the regression of lipids
plagues, and stimulates the production of a variety of growth factors.
an
altered
sensitivity
to
catecholamines.
greater
presser
responsiveness has been observed; in diabetics compared with nondiabetics as well as a greater elevation of BP in response to
exercise.(4,16,49,50) This altered vascular sensitivity appears to be
independent of age, duration of DM or type of therapy. There are two
possible mechanisms to explain the increased vascular sensitivity to
catecholamines. The first is sodium retention, as chlorthalidone may
normalize the augmented noradrenaline response in parallel with a
reduction in blood pressure and total exchangeable body sodium.
Enhanced
cardiovascular
responsiveness
to
of
these
system
causes
presser
response
retention.
In
diabetes,
however,
the
picture
is
not
in
diabetics,
and
improvement
of
metabolic
control
in
types
DM
often
relates
to
diabetic
between
severity
of
systolic blood pressure. Recent reports have also been suggested that
diabetic subjects with micro albuminuria have significantly higher
blood pressure values than matched diabetic subjects without the
condition. Renal histopathological studies in hypertension diabetic
patient are of interest. In a sample of 250 renal biopsy specimens
from diabetic subjects with hypertension, there was a high incidence of
atherosclerosis,
glomerulosclerosis,
and
pyelonephritis;
93%
of
Some
patients,
however,
were
found
to
have
albumin
exertion.
Microalbuminuria
and
rising
blood
the
pathophysiology
of
glomerulosclerosis
and
other
Possible
reasons
for
this
association
may
be
that
hypertension
and
diabetes
have a
similar
predisposing
genetic
blood
pressure.
The
pathological
mechanisms
for
these
is
possible
that
the
relation
between
obesity
and
to
patients
developed
endocrine
causes
hypertension
such
as
and
diabetes
thyrotoxicosis,
with
greater
frequency
in
diabetic
patients,
although
the
multiple risk
factors.(20,24,32)
Cerebrovascular disease:
Hypertension
predisposes
to
cerebral
disease,
as
does
whether
hypertension
causes
the
diabetes
and
is
clinically
apparent
in
the
eyes,
kidneys
associated
with
microangiopathy.(20,64,65)
Retinopathy:
The precise mechanism through which hypertension may
contribute to the evolution of retinopathy is not known, although
increased capillary leakage, provoked by systemic hypertension may
be a factor. The importance of hypertension as a risk factor for
diabetic retinopathy is still controversial and many of the earlier
reports were anecdotal.(20) The incidence of retinopathy was assessed
in Pima (India), through a six year follow up study which revealed that
in diabetic subjects not taking insulin, the incidence of exudate in
those with systolic BP of at least l45mmHg, was more than twice that
of those with pressure of less than 125 mmHg. This association
persisted when assessed within categories of subjects stratified
according to other variables.(66)
More recent studies do suggest, however, that diabetic
patients with hypertension may be at higher risk of developing
particularly
severe
retinopathy
than
comparative
normotensive
with
NIDDM.
The
assessed
in
the
elderly,
the
Heart
Attack
Primary
within
specific
groups
of
diabetics
have
been
renal
events.
The
accompanying
editorial
stated
that
targets
may
be
appropriate
for
diabetic
patients
with
benefits
hypertension
as
well
as
producing
restriction
blind
to
controlled
no
and
more
than
crossover
3gm/day.
studies
of
Drug treatment:
The Ideal drug for the hypertensive diabetic patients should:
- Lower the BP effectively.
-
contributory
factors
to
hypertension
may
produce
dangerous
arrhythmias.
Potassium
Both long term (6 years) and short term studies have reported
no deterioration in glucose tolerance with concurrent potassium
supplement and correction of K depletion.(85)
Although thizides are acceptable as first line agents in non
diabetic subjects, their adverse effects on glucose tolerance, plasma
lipids and potassium may explain their failure to reduce the incidence
of CHD, making them unsuitable for use in diabetic patients with
hypertension, particularly those with NIDDM (type II) DM. They also
increase the risk of impotence.(80)
2- Beta blockers:
Beta adrenergic blocking drugs were among the first to be
used in the treatment of the hypertension in association with diabetic
nephropathy. It is an effective class of drug in this setting. Recent
large-scale
studies
have
demonstrated
their
cardioprotective
complications.
There
are
however,
number of
potential side effects, which may either preclude their use or cause
worry in diabetic patients.(80) Beta blockers act by reducing heart rate
and myocardial contractility and thus reduce heart work. They increase
coronary blood flow by slowing heart rate and increasing diastolic time.
They may reduce platelet aggregability and stress-induced damage to
coronary plagues possible triggering factors in coronary occlusion.
They also have anti-arrhythmic effects. Beta-blockers have been used
to treat hypertension with the aim of reducing coronary events
(primary prevention) and both acutely and chronically after an infarct
to prevent recurrence. Although the Medical Research Council (MRC)
and other trials failed to show a positive overall effect in terms of
reducing the incidence of coronary events, metoprolol was shown to
produce a lower coronary mortality rate even in the hypertensive
smokers. Atenolol did not appear to have the same effects.
Although these drugs are often effective in lowering BP and
may have cardioprotective effect, beta-blockers tend to make the
drug
is
preferable
and
beta-blockers
with
intrinsic
and
have
the
added
secretion. Studied in non diabetics have shown that it does not modify
glucose tolerance or insulin secretion. In NIDDM patients, there is
suggestion that it may improve glucose tolerance without altering
insulin release.(88) It doesnt enhance the hypoglycaemic effects of
glibenclamide, but may produce higher plasma concentrations of this
drug. So verapamil in therapeutic doses does not appear to adversely
affect glucose tolerance. It may even have a beneficial effect in
patients with NIDD. Although a major pharmacokinetic interaction with
glibenclamide has been described, there is no real evidence of adverse
interactions with oral hypoglycemic.(80)
There is little data on the effect of diltiazem on glucose
homeostasis in man. Studies performed have either been short
term(89) or a rare anecodal, and more well designed long term studies
are required.
A recent study compared nicardipine with enalapril in a
randomized trial of antihypertensive treatment in patients with type
II DM and microproteinuria.(90) Both drugs significantly lowered systolic
and diastolic BP and urinary albumin excretion without altering renal
blood flow, GFR or filtration fraction. The authors concluded that both
drugs have similar renal function-preserving properties and that one is
no
better
that
the
other.
This
was,
causing
vasorelaxation
and,
thus,
lowering
the
enhance
perfusion
of
vital
organs,
cardiac
oxygen
demands
are
decreased.
Potential
currently
likely
to
be
beneficial.
Reports
of
fall
in
BP
and
reduced
deterioration
in
GFR,
has
been
of
postural
hypotension.(80,96)ACE
acceptability
as
inhibitors
they
have
no
enjoy
high
demonstrable
level
of
patient
psychological
or
vasodilators
(hydralazine,
minoxidil).
These
can
not
be
with a diuretic, but may also be used with a beta blocker. Initial first
dose severe hypotension has been reported with prazocine and some
patients with diabetes have persistent orthostatic hypotension with
this drug. The newer alpha blockers are reported to be better
tolerated. If this becomes established, then because of their potential
to improve, rather than worsen, plasma lipids, their role in the
management of the diabetic hypertensive should be reconsidered.
Direct vasodilators act on the arteriolar vessels to produce
vasodilatation and decrease peripheral vascular resistance without
decreasing venous return. Cardiac output and cardiac work are
increased. They should be used in conjunction with an agent which
decreases cardiac output (such as a beta blocker). As a lone, they may
precipitate angina or make preexisting angina worse. Minoxidil also
has a number of distressing side effects.(80,97)
In conclusion, it was, however, from reviewing the known
pharmacological profiles of the various classes of drugs, that both the
calcium antagonists and ACE inhibitors should now be considered as
first line treatment for hypertension in diabetic patients. Beta blockers
are acceptable alternatives, particularly if there are other indication
such as ischaemic heart disease. Thizide diuretics should be avoided if
possible. If single drug treatment fails
OBJECTIVES
RESULTS
Diabetic patients
Control subjects
Total No.
160
100
Males
81
55
Females
79
45
Males
47(SD 3.4)
42(SD 3.4)
Females
45(SD 3.5)
40(SD 3.2)
10 (SD 2.6)
Systolic
Diastolic
Type I
125
80
140
85
120
80
Gender frequency:
Mean age:
M + SD yrs
(IDDM)
Type II
(NIDDM)
Control
M = Mean
SD = Standard deviation
Not hypertensive
Males
26
8.3%
Females
21
13.3%
Sex
P = 0.2817
X2 = 1.16
Sex
Not hypertensive
Males
27
22
27%
Females
26
25
26%
Total
53
47
P = 0.8411
Sex
Males
Females
Total
P = 0.00000
No. of patients
Percentage
13
13%
7%
20
20%
Sex
Control group
DM
Males
32
51%
13
65%
Females
34
49%
35%
Total
66
100
20
100%
%
P = 0.8411
Hypertensive
Not hypertensive
Total
Type 1
13
47
60
21.6
Type II
53
47
100
53%
Control group
20
80
100
20%
Total
86
174
260
Status
No. of hypertensive
Total No. of
patients
patients
Type 1 + Type II DM
66
160
41.2%
Control group
20
100
20%
P = 0.062 (significant)
X2 = 0.5
Age group
Hypertensive patients
Not hypertensive
Total
20 30
10
31 40
24
28
41 50
12
16
51 60
> 60
(in years)
Total
13
47
60
Hypertensive patients
Not hypertensive
Total
20 30
31 40
41 50
55
14
19
51 60
16
17
33
> 60
30
13
43
Total
53
47
P = 0.0186
No. of patients
20 30
31 40
41 50
51 60
> 60
11
100
Total
20
Hypertensive patients
Not hypertensive
15
17
6 10
17
11 15
16 20
> 20
Total
13
47
P = 0.01
Hypertensive patients
Not hypertensive
13
20
6 10
11 15
16
16 20
13
> 20
Total
53
43
P = 0.27
Hypertensive patients
Not hypertensive
Good control
33
5%
Poor control
10
14
16.6
Total
13
47
P = 0.0021
Status
Hypertensive patients
Not hypertensive
Good control
20
34
20%
Poor control
33
13
33%
Total
53
47
100
P = 0.0176
Status
Type I
Type II DM
Total
DM
Good control
20
23
14.4%
Poor control
10
33
43
26.7%
Total
13
53
66
BMI (%)
Hypertensive patients
Not hypertensive
10 20
15
20 25
27
25 30
30 40
> 40
Total
13
47
Not hypertensive
10 20
10
20 25
13
25 30
14
19
30 40
26
> 40
Total
53
47
BMI (%)
Percentage
II
10 20
9%
20 25
21.1%
25 30
17
27%
30 40
32
46%
> 40
4.5%
Total
66
DM + HTN
DM only
Havent IHD
10
45
Total
13
47
3.3%
5%
Have IHD
Percentage
P = 0.0757
DM + HTN
DM only
Have IHD
25
Havent IHD
28
39
Total
53
47
Percentage
8%
25%
P = 0.0757
DM + HTN
DM only
Havent IHD
25
Total
28
10
17.5%
6.2%
Have IHD
Percentage
P = 0.0134
DISCUSSION
greater
than
in
approximately
matched
non
diabetic
patients.(16,18,19)
In
USA
according
to
the national
tolerance (IGT) and 19.8% for those with NIDDM. The prevalence ratio
of HTN was 1.8% for IGT and 2.6 for NIDDM compared with normal
glucose tolerance controlled for age, sex and BMI. In this study it was
noticed that, the prevalence of hypertension is associated with higher
fasting, but not 2 hours post load serum insulin concentration.
Adjusted for age, sex and BMI and plasma glucose and concentration,
the fasting serum insulin concentration was significantly related to
hypertension.(26)
Another study was carried during the National Screening
Programm for DM in five different provinces in Saudi Arabia. The study
group included a total of 14804 subjects (male 42.2% and females
58.0%) age range from 14-69 years. The total numbers of diabetic
subjects, excluding IDDM, was 1286 comprising 673 male (52.3%)
and 613 females (47.7%) and were grouped as hypertensive and
normal. The overall prevalence of hypertension in non-diabetic group
was 4.48% in males compared to 2.8% in females, while in the
diabetic group the prevalence of hypertension was 11.44% in males
and 15.98% in females. This study had revealed that the prevalence of
hypertension is significantly higher in the female and male diabetics in
comparison to non-diabetic. In male the prevalence of hypertension
increased almost 2.6 times in the diabetic group, while in the female
diabetics, the prevalence of HTN is increased almost 5.7 times. This
patients can be explained by the poor control of the DM, the obesity
and the change in life style in Sudanese population being more
inactive prefer the sedentary life and change in diet. Other factor that
explains the increased incidence of hypertension is the age factor,
specially in type II NIDDM, older age are more affected than younger
age groups, but in type I IDDM the age factor was not found to be
significant.
The observation of obesity and poor control of DM as causative
factors in the development of hypertension in DM are compatible with
reports in the literature.
Large number of patients are in a state of poor glycaemic
control, this is very important as recent studied demonstrated that,
tight glycaemic control prevents or delays the onset of long-term
diabetic complications.(65) Caring doctors and patients must be aware
of these facts. The association between obesity, DM and hypertension
was documented in several studies. The prevalence of over weight and
obesity amongst hypertensive and diabetic patients in Riyadh, Saudi
Arabia was studied by Yousif AA. A total of 3186 hypertensive and
diabetic patients were included in the study. He found that 19% of
patients were their ideal weight (BMI <25 kgm2), while 35% were
overweight (BMI 25.29 kgm2) and 5% were morbid obesity BMI >40.
relationship
by
calling
such
condition
"diabesity".
This
relationship doesn't exist between obesity and type I DM, but there is
no evidence to suggest obesity protects a patient against type I. Both
conditions have a genetic component. The non genetic component of
obesity is an imbalance between energy intake and expenditure and
the common link between obesity and type II NIDDM is insulin
resistance, i.e. inability of insulin to produce it is full physiological
effect on its target tissues in the body. To overcome this resistance
beta-cells have to produce more insulin to maintain normoglycemia
producing hyperinsulinaemia and thus hypertension.(103) In general,
obesity is more common in developing
chance
of
occurrence
of
stroke
in
diabetic
with
compatible with the study which revealed it to occur 2-6 times more in
diabetic subjects with hypertension compared with diabetics without
hypertension. This was observed by Roemboldt in his study of TIA and
stroke in a community based diabetic Cohort.(20)
Our study reveals increase incidence of retinopathy in DM with
hypertension compared with diabetic without hypertension, this also
was observed in different studies dated back many years,(20,66)which
proved the effect of hypertension in developing retinopathy and
diabetic patients as well as other complications of eye disease.(67,68)
The incidence of nephropathy is also found to be significantly
higher in DM with hypertension compared with diabetic without
hypertension, it is found to be 10%. This incidence is almost
compatible with the same results which was obtained from previous
Sudanese study conducted by El Bagir. In a total of 377 diabetic
patients 44% were discovered to have hypertension and 9% had
nephropathy.(30)Recent
data
however,
suggest
that
genetic
CONCLUSION
Hypertension
diabetics.
and
obesity
are
common
among
Sudanese
halting
the
serious
cardiovascular
and
cerebrovascular
RECOMMENDATIONS
1-
2-
3-
Control
of
hyperglycaemia
should
follow
the
new
4-
5-
6-
7-
The
goal
of
treatment
is
diastolic
blood
pressure
of
REFERENCES
1-
2-
3-
4-
5-
6-
Eugene B.
Harrison
8-
10-
13-
14-
24-
and NIDDM in Saudi population. Anna Saudi Med 2001; 21(12): 58.
28-
diabetics report from Sudan. J Hum Hyperten 1995 Nov; 9(11) 899901.
31-
32-
1985 Mar; 8: 3.
35-
Bommer
G.
Hyperinsulinaemia,
insulin
resistance
and
need of particular care and attention? Diabet Car 1999 Mar; 22(supl
2): 76-9.
38-
DeFronzo
RA.
Insulin
resistance,
hypertinsulinaemia
and
41-
and
insulinaemia:
relation
to
diabetes
but
not
essential
Shen DC, Shich SM, Fula MM, Wu DA, Chen YD, Reaven GM.
49-
insulin,
the
sysmpathetic
nervous
system
and
adaptive
50(1): 69-74.
51-
Sowers
JR,
hypertensive
Epstein
vascular
M.
Diabetes
disease
and
mellitus
and
nephropathy.
associated
An
Update
Evedence
for
an
association
of
high
blood
pressure
and
56-
DeFronzo RA, Cooke CR, Anders R, Falcona GR, Davis PJ. The
63-
David
M,
Nathern
MD.
The
pathophysiology
of
diabetic
pressure
and
kidney
function
in
normotensive
IDDM
with
71-
Mark
EC.
Renoprotection
with
antihypertensive
agents
in
Lenis EJ, Hunsicker LG, Bain RP, Rohde RD. The effect of ACE
Bertram LK, Roberto SN, Khalil MD, Jennie ZM, Minjen LM,
Richard C, East man HK. The impact of CVD on people with DM:
79-
Barrell
AH.
Dorson
PM.
Blood
pressure
control
in
the
83-
87-
Charles
S,
Ketelslegers
JM,
Buysschaert
M,
Lamberat
A.
19-
20.
88-
Sezulka
AV,
Gill
JS, Beevers
DG.
Diabetogenic
effect of
first dose of enalapril in heart failure. Br Med J 1985; 291: 1309 12.
95-
304(8): 1992.
97-
38.
Tight
blood
pressure
control
and
risk
of
UNIVERSITY OF KHARTOUM
FACULTY OF MEDICINE
POSTGRADUATE MEDICAL STUDIES BROAD
Questionnaire Based Study
Hypertension in Diabetic Patients Attending Khartoum Province
Hospitals
Name: ...................................................... Age:
...................................................
Gender:
Male
Female
Residence:
Occupation:...Tribe:........................
Known diabetic:
Yes
No
Duration of DM:
..................................................................................................
Treatment of DM:
...............................................................................................
Soluble
Sulphonylureas
Diet
Biguanide
insulin
Zinc
Oral
Mixed
Combined
Control of DM:
Symptoms:
Polyuria:
Yes
Thirst:
Yes
Wt. loss:
Yes
Lassitute:
Yes
No
No
No
No
Investigations:
Glycosuria:
Yes
Ketonuria:
Yes
No
No
FBG mg/dl
FH of DM
2HPPBG mg/dl
Hypertension:
Yes
No
Duration of hypertension
FH of hypertension:
First degree relative:
Second degree relative
No
Blood pressure:
SupinemmHg
Standing
mmHg
Smoking:
Yes
No
No of cigarettes/day..
Duration of smoking..
BP lowering drugs
Yes
No
Specify:..
Weight:kg..Height cm
BMI.
Complications:
I.H.D
chest pain:
Yes
No
ECG findings:
Ischaemic changes:
Yes
No
Evidence of long standing HTN:
Yes
No
Evidence of MI:
Yes
No
None:
CNS
TIA:
Yes
No
Stroke:
Yes
No
Eye symptoms:
Blurring of vision:
No
Yes
Cataract extraction:
Yes
No
Blindness:
Yes
No
Eye examination:
Presence of cataract:
Yes
No
Hypertensive changes:
Yes
No
Specify:
Diabetic changes:
Yes
No
Specify:
Nephropathy:
Urinalysis:
Proteinuria:
Yes
No
One cross
crosses
2 crosses
>3
Frequency of occurrence:
Once
Intermittent
Persistent
How many years from the discovery of DM did it develop?:
0-4 yr
14yr
RF:
5-9 yr
> 15 yr
B. urea: mg/dl
S. creatinine: .mg/dl
Dialysis:
No
Yes
10-