Prevalence of Hypertension in Sudanese Patients

UNIVERSITY OF KHARTOUM
Faculty of Medicine
Postgraduate Medical Studies Board
PREVALENCE OF HYPERTENSION IN SUDANESE PATIENTS

WITH DIABETES MELLITUS
By
Dr. Asma Mohammed Ahmed El Bellaa
M.B.B.S (University of Khartoum)
A thesis Submitted in partial fulfillment for the requirements

of the Degree of Clinical MD in Medicine,
April 2002
Supervisor
Dr. Musa Mohammed Khier
MBBS, MD, Khartoum
Faculty of Medicine
University of Khartoum
To my family, Teachers
&
friends
I am extremely grateful to my teacher and supervisor
Dr.
Musa Mohamed Khier, for his confidence in delivering this subject to

me to work on. My deepest gratitude would be expressed for him for
his advice, encouragement and meticulous supervision.
My gratitude is enormous to Prof. EL Daw Mukhtar, Prof. El
Mahdi Mohamed Ali and Mr. El Fahal, whom their valuable advice and
comments are highly appreciated.
I would like to thank Dr. Awad Mohamed Ahmed for his supply
with some papers and articles, Dr. Hamdna Alla, Department of
community
Medicine,
University
of
Khartoum
who
assisted
in
calculating the sample size of this study.

I am greatly indebted to Dr. Abdel Rahiem Mohamed Babiker
for his help in discussing the data analysis and formulation.
My deepest sincere and thanks to Dr. Azahir Yousif and
Dr. Zuhir M. Taha for their help in the questionnaire construction and
typing.
I
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
Body mass index
BP
Blood pressure
CHD
Coronary heart disease
CVA
Cerebrovascular accident
DCCT
Diabetes complication control trial
DM
Diabetes mellitus
FBG
Fasting blood glucose
FH
Family history
HOT
Hypertension optimal treatment
HTN
Hypertension
IDDM
Insulin dependent DM
IGT
Impaired glucose tolerance
MRC
Medical Research Council
NIDDM
Non-Insulin dependent DM
2PPBG
2 hours post prandial blood glucose
RBS
Random blood sugar
UKPDA
United Kingdom Prospective diabetes study
WHO
World Health organization
Hypertension
(HNT)
and
diabetes
mellitus
(DM)
are
interrelated diseases and frequently concomitant. They are worldwide
increasing problems with significant impact on patients, public health

and governments funding.
In this study 160 Sudanese diabetic patients were included.
Hundred of them were type II (NIDDM) and 60 were type I (IDDM).
Hundred non-diabetic subjects were chosen as control.
The prevalence of HTN in diabetic patients (type I and type
II) was found to be 41.2% while in the control subjects it was found to
be 20% (twice as common). No significant differences were found
among gender.
Obesity, poor glycaemic control and old age are found to be
risk factors particularly in type II DM.
The incidence of IHD (17.5%), retinopathy (16.9%) and
nephropathy (10%) were found to be significantly higher in diabetic
patients
with
hypertension
compared
with
diabetic
without
hypertension. Other neurological complications as stroke was found to

be insignificant (0.8%) on the other hand, incidence of TIA is 10.2%.

.
( 2) 160
. (1)
41.2
%20 ) (.
.

.
%17.5
%10.2 %10
.
%10.2
.
%0.6
.
LIST OF TABLES & FIGURES

Page
70
Table 1: Demographic characteristic of the two groups
71
Table 2: Hypertensive patients in type I DM according to sex
72
Table 3: Hypertensive patients in type II DM according to sex
Table 4: Hypertensive patients in control group according to sex 73

Table 5: Hypertension in both types of DM and control group
sex
the
to
according
74
Table 6: Hypertensive patients in both types of DM and
control group
75
Table 7: Prevalence of hypertension in diabetic patients
compared with non diabetic subjects
76
Table 8: Hypertensive patients in type I DM according to age
77
Table 9: Hypertensive patients in type II DM according to age
78
Table 10: Hypertensive patients in control group

according to age
79
Table 11: Hypertensive patients in type I DM in relation to
duration of DM
80
Table 12: Hypertensive patients in type II DM in relation to

duration of DM
81

control of DM
82
Table 14: Hypertensive patients in type II DM in relation to

the control of DM
83
Table 15: Hypertensive in both types of DM in relation to
the control of DM
84

the body mass index (BMI)
85
Table 17: Hypertensive patients in type II DM in relation to BMI 86
Table 18: Hypertensive patients in both types of I DM
in relation to BMI
Table 19: Ischaemic heart disease in type I DM with
87
hypertension compared with diabetic patients

without hypertension
88
Table 20: Ischaemic heart disease in type II DM with
without
hypertension
89
Table 21: Ischaemic heart disease in both types of DM with
90
Fig. 1:
Neurological complications in type I DM with

Fig. 2:
91
Neurological complications in type II DM with

Fig. 3:
92
Neurological complications in both types of DM

with hypertension compared with diabetic patients
Fig. 4 :
93
Retinopathy in both types diabetic patients with

hypertension compared with diabetic
Fig. 5:
94
Retinopathy in type II diabetic patients with

95
Fig. 6:
Retinopathy in type I diabetic patients with

Fig. 7:
95
Retinopathy in both types of diabetic patients

with hypertension compared with diabetic
Fig. 8:
97
Nephropathy in both types of diabetic patients

with
hypertension
98
Fig. 9:
Nephropathy in type II diabetic patients with

without
hypertension
99
Fig. 10:
Nephropathy in types I diabetic patients with

100
Fig 11:
Nephropathy in both types of diabetic patients

with hypertension compared with diabetic
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
emphasized the sweet taste of urine.

Thomas
Willis
(1621-1675) an English physician clearly
documented the sweet taste of urine. Mathew Dabson in 1776 showed

that the sweet urine was largely a yeast fermentable sugar. This
observation made it possible to distinguish DM from diabetes insipidus.
In 1788 Thomas Cawly in England reported that DM may
follow damage to the pancreas. Paul Langerhaus (1847-1888) working
in Berlin identified pancreatic islets without speculating to their
possible function.
Two German scientists, Von Merring and Minkowiski noted in
1889 that if the pancreas was removed, the animal developed DM.
Later scientists discovered that even if the pancreas was destroyed,
the animal did not become diabetic if the islets were preserved.
Opie in USA confirmed the fact that the small islets were
damaged in human with DM.
The Belgian, Jean de Meyer (1909) gave the name insulin to

the glucose-lowering hormone, whose existence at that time was still
hypothetical.
Using the preliminary information available in l92l plus earlier
works contributed by other scientists around the world. Banting & Best
in Ontario, Canada began an important and historical research project,
when they obtained the mixed and purified islet tissues from animals
and injected the material into an animal with DM, they found that the
blood sugar levels felt. That was the time of discovery of insulin, which
was met with great expectations. This was an important events for
many thousands of diabetic throughout the world and signaled a whole
new era in the treatment of DM. At one stroke, life was substituted for
death for the multitudey of people with DM.
Insulin
was
first
administered
in
1922
the
role
of
sulphonylureas as hypoglycemic agents was obvious by 1942 and the

biguanids were described as effective hypoglycemic agents in
1957.(1,2)
INTRODUCTION
Hypertension and DM are interrelated diseases and frequently
concomitant,
if
untreated
strongly
predispose
to
atherosclerotic
cardiovascular disease. Life style and genetic lactors are important in

the genesis of both conditions.
Since the last Canadian Conference on Hypertension and
Diabetes mellitus in 1987, new information on hypertension, insulin
resistance, hyperlipaedaemia and anti-hypertensive drugs in diabetic
patients has become available. It appears that both hypertension and
DM may be part of a group of risk factors that include impaired
glucose tolerance, NIDDM obesity and increase serum levels of
triglyceride (TG) and hypertension.(3,4)
Only recently has it been appreciated that the link between
hypertension and DM is close, understanding these links may provide
important insights into both disorders. So diabetes and hypertension
are common diseases that coexist at a greater frequency than chance
alone would predict.(5)
Definition of DM:
DM comprises a group of common disorders that share the
phenotype of hyperglycemia classically associated with symptoms of
excessive thirst increase urine volume and if severe enough weight
loss. It is difficult to produce a single binding definition because of the
different aetiologies and varying severity and manifestation of DM
caused by a complex interaction of genetics, environmental factors
and life style choices.
In the classical young onset form of disorders there is near

total insulin deficiency with inevitable spread metabolic changes.
In the older age onset form, there is diminished and or
delayed insulin secretion in response to glucose combined with varying
degrees of diminished effectiveness of circulating insulin, when there is
associated obesity insulin resistance predominates. Therefore, DM can
be defined as a state of diminished insulin action due to its decreased
availability or effectiveness in varying combination.(6,7) In other way it
is a state of hyperglycaemia due to relative or absolute deficiency of
insulin leading to metabolic disturbance of carbohydrates (CHO), lipids
and
proteins
metabolism,
characterize
symptoms
of
DKA,
microangiopathy, macroangiopthy, and peripheral nerve damage.

In the US the number of diagnosed cases of diabetes mellitus
has substantially increased in the last half of the 20th century. DM is
the forth most common reason for patient contact with a physician,
account for nearly 15% of health care costs in USA and is a major
cause of premature disability and mortality. It is
the leading cause of blindness among working age group of end stage
renal disease and of non traumatic limb amputations. It is a major
factor contributing to the neonatal morbidity and mortality. On the
bright side recent data indicate that most, if not all of the debilitating
complications of the disease can be prevented or delayed by
prospective treatment of hyperglycaemia and other cardiovascular risk

factors.
Classification of diabetes mellitus:
This is also an area of change and conflict. The only certainity
is that the age old terms juvenile onset and maturity onset DM have
out lined their usefulness. Recent advances in the understanding of
aetiology and pathogenesis of DM have led to a revised classifications:
1-
Type I diabetes mellitus: (Beta-cell destruction usually
leading
to
absolute
insulin
deficiency)
and
depends
on
exogenous insulin to prevent metabolic decompensation and

death. Commonly, but always, diabetes appears abruptly i.e.
over days or weeks in previously healthy non-obese children or
young adults. In older age groups it may have a more gradual
onset. Type I diabetes is believed to have a long asymptotic
preclinical stage often lasting years, during which pancreatic
beta-cells are gradually destroyed by autoimmune attack that is
influenced by HLA and other genetic factors as well as
environmental. In some an acute illness may speed the
transition from the preclinical to clinical staga However, a so
called honey moon period may follow and last weeks or months
during which time smaller doses of insulin are required because
of partial recovery of beta cell function and reversal of insulin
resistance caused by acute illness, therefore, insulin secretory

capacity is gradually lost. That type I DM is an autoimmune
disease is supported by its association with specific immune
response (HLA) gene and the presence of antibodies to islet cells
and their constituents. This syndrome accounts for less than
10% of diabetes in US.
2- Type II diabetes mellitus:
Type Il by far the most common form of the disease is found
over 90% of the diabetic patient population. These patients retain a
significant level of endogenous insulin secretory capacity, many ranges
from predominately insulin resistance with relative insulin deficiency to
a predominately insulin secretory defect with insulin resistance. Type
II patients are not dependent on insulin for immediate survival and
ketosis rarely develops, except under conditions of great physical
stress, nevertheless, these patients may require insulin therapy to
control hyperglycemia. Type II DM typically appears after the age of
40 years as a high rate of genetic
penetrance unrelated to HLA genes and is associated with obesity. The
clinical features of type II DM are much more insidious. The classic
symptoms of diabetes may be mild (fatigue, weakness, dizziness,
blurred vision or other non specific complaints) may dominate the
picture or may be tolerated for many years before the patient seeks
medical attention. Moreover, if the level of hyperglycaemia is

insufficient to produce symptoms, the disease may become evident
only after complications develop.
3- Other specific types of diabetes mellitus:
Including genetic defects of beta cells, defects of insulin
action, disease of exocrine pancreas and endocrinopathies, drug
induced infection and gestational DM.
Diagnosis of diabetes mellitus:
Revised criteria for diagnosing DM have been issued by
consensus panel of experts from National Diabetes Data Group and the
WHO. It reflects new epidemologic and metabolic evidence criteria for
diagnosis of DM:
* Symptoms of DM plus R.B.S coflcentration 11.l mmol/L (200mg/di)
or
* Fasting blood sugar 7.0 mmol/L (126 mg/dl)
or
* 2 hours plasma glucose 11.1 mmol/L (200 mg/dl) during oral

glucose tolerance test.(5)
Prevalence and incidence of DM:
Prevalence: type I IDDM is predominately a disease of white
or population with a substantial white genetic admixture such as
American black. It is rare in Japan, Chinese, Philippians, Asiatic Indian,
American Indian and Melanesians. In Israel children of European
parentage the prevalence of IDDM is almost 3 times in Israch children
of Asiatic or African parentage. These differences may not be entirely
racial, because they are said to be striking regional differences in
prevalence in the same country. The prevalence of type I IDDM in US
is about 260 per 100/000(0.26%) by the age of 20 years. In England
it is 220 per 100,000 (0.22%) by the age of 20 years. The equivalent
figure in Denmark at age of 19 is 240 per 100,000 (0.24%).
The incidence of type I
IDDM in the countries in which the
population is predominately white, the reported yearly appearance

rate of IDDM range from 3.7 to 20 per 100,000 in US an incidence
ranging from 10 per 100,000 per year for non white males to 16 per
100,000 per year for white males. Rates in women were intermediate
between
these
in
non
white
and
white
males.
In
both
the US and Denmark the peak age of onset is between 10 and 14

years.
In type II NIDDM the disease exist in all populations but
prevalence varies greatly e.g. 1% in Japan 34% in the Micronesians of
Nauru and greater than 40% in the Pima India of Arizona. In white
figure is probably between 1% and 2%. The high prevalence of NIDDM
among Naeruans and Pimas appear to be a relatively recent
development that followed a change in pattern of food intake from one
of caloric deprivation in which both obesity and DM were rare to one of
caloric abundance in which both abnormalities are common. A similar
phenomenon usually called urbanization has been described in other
American Indian tribes, Pacific and Australian aboriginal and Asiatic
Indian group. Presumably the change in lifestyle that accompany
urbanization results in obesity which facilitates expression of a
predisposition for
NIDDM.
Few reliable studies of the incidence of NIDDM are available.
The Pima Indian have an appearance rate of 2650 per 100,000 per
year (the highest in the world). This value is approximately 20 times
that in white 134 per 100,000 per year. In Rochester Minnesota
incidence in white is 158 per 100,000 per year in men and 113 per
100,000 per year in women.(9)
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.
The figure may be underestimated as patients who died at

home or were unable to reach hospital due to lack of transportation or
economic constraints were not included.
Many problems adversely affect the management of DM in
Sudan. These include ignorance illiteracy, lack of health education
including trained medical personnel in DM e.g. educators or dietitions
who are very few or non-existent, as are diabetologists, dominance of
wrong beliefs e.g. some patients think that taking anti-diabetic
treatment removes the need for dietary restriction for sugar and
refined carbohydrate (CHO), which is thought to be burn by insulin.
Another factor is that health care being a low priority for the
government. So the road to efficient diabetic care is to implement a
National Diabetes Programm (NDP), which ensure the multidisciplinary
cooperation of relevant national and local health staff, cooperation of
professionals of different specialties to achieve a common goal.(11)
Definition and diagnosis of hypertension:
A great effort has been devoted to search for a diving line
between normotension and hypertension, in fact there is no evidence
for any. The challenge has not been accepted because there is no such
evidence. When we study the frequency distribution curves of arterial
blood
pressure
(BP)
in
population,
there is no dividing line so is the relationship between arterial pressure

and incidence of coronary heart disease. The dividing line is in fact,
nothing more than an artifact.(12)
Since there is no dividing line between normal and high blood
pressure, arbitrary levels have been established to define person who
have an increase risk of developing a morbid cardiovascular events
and or will benefit from medical therapy. The definition should take
into account not only the level of diastolic pressure but also systolic
pressure, age, sex, race and concomitant diseases.(6)
Kaplan has proposed that the concept of hypertension be "that
level of blood at which benefits of action exceed the risk and costs of
an action.(13)
When hypertension is suspected, blood pressure should be
measured at least twice during separate examinations after the initial
screening over one week or more.
The definitions that were developed in the past National Heart,
Lung and Blood Institute; Isolated systolic hypertension
160 mmHg,
diastolic blood pressure (DBP) <9OmmH, and systolic diastolic

hypertension (SBP)
classification
held
>140
in
DBP
>90
the
sixth
mmHg,(14)now
report
of
replaced by
the
Joint
National Committee of Prevention Evaluation and Treatment of High

Blood Pressure (J.N.C VI, 1997) which state that:(6,15)
Blood pressure
Category
Systolic
Diastolic
Optimal
< 120
< 80
Normal
< 130
< 85
High normal
130 - 139
85 - 98
Stage I hypertension (mild)
140 - 159
90 - 99
Stage II (moderate)
160 - 179
100 - 109
180
110
Stage III (severe)
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
approaching 40% while the incidence among White American is

between 20-40%. Blood pressure also increases with age in highly
developed society and more than 60% of American over the age of 65
years have an increase in blood pressure. An increase frequency of
hypertension
is
often
observed
in
the
first
degree
relatives of hypertensive subjects. The familial genetic role of

hypertension has been well demonstrated. However, the mechanism of
this observation remains elusive.(14)
Paediatric hypertension:
When hypertension occurs in childhood it is often the result of
an identifiable secondary cause. The kidney is the most common organ
involved and may produce hypertension by renal vascular or renal
parenchymal
disease.
On
rare
occasions,
renal
cell
carcinoma
(hypernephroma) may present as an elevation in blood pressure

because of the production of renin by the tumor. Pheochromocytoma is
sometimes a cause of hypertension in children and may be bilateral or
malignant. An even more unusual cause of hypertension in children is
that due to primary aldosteronism, which is usually the result of
bilateral adrenal hyperplasia and often includes a familial incidence
due to dexarnethazone-suppressible hyperaldosteronism. Coarctation
of the aorta is not uncommon as a cause of hypertension in children
and should be considered. Rarely essential hypertension can be
manifest in childhood and may be suggested by a strong family history
of hypertension.(14)
Prevalence of hypertension in diabetes mellitus:

Several studies have assessed the prevalence of hypertension
in patients with DM, however, methodological problems have often
made the interpretation of these difficult. The earlier studies suffered
from experimental design or lack of appropriate controls, often
omitting in the analysis many factors that are now considered routine
in the assessment of diabetic patients. These confounding variables
include age, degree of obesity, racial group, presence or absence of
nephropathy, type of diabetes and treatment (diet, oral hypoglycaemic
drugs or insulin). Furthermore, the methods for obtaining blood
pressure measurement were not uniform among the studies; these
included appropriate cuff size for increase arm girth and uniformity of
observer
for
comparison
between
groups.
Allowing
for
the
methodological problems most studies have confirmed a greater than

chance
association
between
hypertension
diabetes.(13)
and
Hypertension is twice as prevalent in diabetic as in non diabetic in

several studies.(16,17,18) In some it is approximately 1.5-2 times greater
than in appropriately matched non diabetic population.(19)
More
recent
studies
however,
do
support
an
increase
prevalence of hypertension in diabetes. In a large study of 662

diabetic
patients
with
careful
matched
controls,
e.g.
Pell
and
DAlanzo found a 54% greater prevalence of hypertension among

diabetic compared with controls and this was independent of obesity.
The Framingham Study Group demonstrated that mean
systolic blood pressure was high in diabetics and this was more
marked in females than in male subjects. The large population studies
of Whitehall and Bedford who showed a correlation in men over the
age of 40 years between both systolic and diastolic blood pressure and
blood glucose level, which was independently of body weight.(20)
In unselected but representative diabetic population, Brylogle
and Bradley found an over hypertension prevalence of 20% increasing
to 41% in patients over 50 years. The prevalence in men and women
younger than 50 years was equal but it was greater in women above
this age, the ratio 2.6:1. Similarly high
systolic blood pressure was
noted in women diabetic. However, hypertension did not appear to

account for much of the excessive rate of macrovascular disease.(21)
On the other hand Good Kin, in a 20 year survey found a
much
higher
mortality
in
diabetics
than
in
non-diabetics
with
comparable degree of hypertension, suggesting a worse prognostic

significance of hypertension in diabetics. While both hypertension and
diabetes mellitus may be caused by such endocrine diseases as
pheochomocytoma,
Gushing
syndrome
and
primary
hyperaldosteronism, these disorders are rare and do not account for

higher prevalence of hypertension of most diabetic patients.(21)
In a population-based study in southern Wiscon (USA),
revealed that, the 10 year incidence of hypertension was greater in
older age, long duration of DM, proteinuria and higher glycosylated
haemoglobin (Hb) level with more severe retinopathy and male
gender.(22)
According to the National High Blood Pressure Education
Programrn Working Group report on hypertension, hypertension is
twice as common in people who have diabetes as in those who do not.
The problem is particularly pervasive among women and specific
ethnic groups, almost twice as many African Americans as Whites, and
three times as many Mexican Americans as non Hispanic Whites, have
co-existent DM and hypertension. Although hypertension occurs more
often in patients with type I DM than
type II, often adjustment for
age, the prevalence of hypertension in type II diabetic patients

increases with age. About 90% of patients who have a dual diagnosis
of DM and hypertension have type II DM. Consequently patient with
type II DM represent the majority of hypertensive patients.(23)
Hypertension affects over 30% of European diabetic patients
and is twice as common as in non-diabetic population. In UK it was
present in 39% of patients at diagnosis of DM, with an associated
increased age-adjusted risk of 1.8 for developing a diabetes related

death and 1.6 for a major clinical complication.(24.25)
In a study carried at Pima Indians a strong association
between hypertension and abnormal glucose tolerance was observed
regardless of age, sex or obesity. The age and sex adjusted prevalence
of hypertension was 7.l% in subjects with normal glucose tolerance,
13% in those with impaired glucose tolerance (IGT) and 19.8% in
those with diabetes. Among diabetic patients, the prevalence was 2.6
times that in those with normal glucose tolerance and 1.5 times than
in those with IGT.(26)
The most recent report from the diabetes intervention study
demonstrated a striking excess of hypertension in newly diagnosed
type II DM as well as of other well recognized risk factors. Hospital
Diabetic Clinic and community-based population studies also confirm
an excess frequency of hypertension in diabetes. Few of these studies
have differentiated between type I IDDM and type II NIDDM. Christieb
studied type I DM and found a significant high incidence of
hypertension. A further study by Moss using matched
controls showed that children with diabetes have higher systolic BP
from adolescence onwards. Between the ages of adolescence and 45
years, the prevalence of hypertension and diabetic nephropathy are
similar. In older age group (60-80 years), there is a consistent
association between hypertension and diabetes in both sexes, with

systolic hypertension being the most common.(20)
In a recent report from a District General Hospital diabetic
clinic, 40% (203/507) of diabetics under the age of 65 years were
hypertensive according to the WHO criteria. Interestingly there
appeared to be differences between the different racial groups.
Diabetic subjects of West Indian origin had a greater prevalence
(49%) of hypertension than those of either White (37%) or Asian
(35%) origin. Females showed a greater prevalence of hypertension
than males, a trend confirmed in other studies.
Geographical variation and frequency of hypertension in
diabetics have also been studied. One recent report from the WHO
multinational study of vascular disease and diabetes included 6695
diabetic men and women between ages of 35 years and 54 years from
14 centers throughout Europe. The overall proportion of diabetes with
hypertension was 36% but, within the European capital cities, values
ranged from 22% in London to 38% in Berlin.
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)
In Sudan the prevalence of hypertension in diabetic patients in

an Urban Sudanese population compared with non- diabetic group. It
was found that there was a higher prevalence of diastolic hypertension
(44%) in the NIDDM patients. The BP did not correlate with age,
duration of diabetes or nephropathy (9%) of cases, but obesity, which
was detected in 34% of NIDDM group, may possibly explain the
prevalence of hypertension in diabetic.(30)
There is, therefore, sound evidence for an increase frequency
of hypertension in diabetes. In the elderly, this is predominately
systolic hypertension and in the younger age groups, there is a less
clear relationship with diastolic hypertension. The latter finding may
reflect the difference in aetiology of hypertension between two age
groups.(20)
Classification of hypertension in diabetes mellitus:
In contrast to IDDM, where the natural history of diabetic
nephropathy and the contribution of impaired renal function to the
development of raised arterial blood pressure is well characterized, the
hypertension in NIDDM is not as well defined. Obesity common in
NIDDM, may play an important pathogenic role, elevation in BP have
been observed, however, in the absence of obesity. Advancing age, a
factor for increased BP and the development of NIDDM is another
feature
of
the
hypertension
of
NIDDM.
Isolated
systolic hypertension may be seen in the elderly and subjects with

wide spread atherosclerotic disease. The majority of subjects with
NIDDM and coexistent hypertension have diabetic hypertension or
essential hypertension as oppose to hypertension of a definable
secondary
cause.
Possible
explanations
for
the
association
of
hypertension and NIDDM are that similar genetic and or environmental

factors predispose to each condition. An inherited link has been
demonstrated
in
several
studies
consider
secondary
causes
of
hypertension may coexist with either IDDM or NIDDM. Classification of

hypertension in diabetes.(13)
IDDM
NIDDM
Hypertension due to
diabetic nephropathy.
Essential hypertension.
Hypertension of obesity
Essential hypertension
Hypertension due to diabetic
nephropathy.
Secondary hypertension
diabetes.
Secondary
hypertension
DM
Aetiology of hypertension in diabetes mellitus:

The aetiology of hypertension in diabetic people with high BP
may believe that it's caused by being tense or nervous. Some believe
it is an unavoidable part of aging, or even that older people
need higher BP to get blood to vital organs. Causes of hypertension in

the person with diabetes fall into one of two categories primary or
essential hypertension, which are generally related to genetics and life
style or 2ndary hypertension which include hypertension associated
with diabetic renal disease as well as hypertension from other
diseases.
In the primary or essential hypertension most people with DM
develop hypertension for the same reasons that people without
diabetes get it, namely genetic (race, gender, heredity and life style
factors and this is the most prevalent type of hypertension among
people with diabetes. Only 5-10% have secondary hypertension due to
other causes.(31)
It was also said that several aetiological features of non
diabetic hypertension-genetic (e.g. positive family history, advancing
age, gender and environmental factors (e.g. salt, alcohol) may also
contribute to the development of diabetic hypertension, stress is a
conventional factors in the development of sustained hypertension.(13)
No single physiological factor has linked to the development of
hypertension in diabetes. Experimental and clinical studies comparing
normotensive and hypertensive diabetic subjects, as well as non
diabetic controls, have highlighted several
factors of possible pathophysiological importance in the hypertension

of diabetes.(13)
Pathogenesis of hypertension in diabetes may differ between
the two types of diabetes, hypertension in type I DM is related to the
development of diabetic nephropathy, which is not usually the case in
type II diabetes. Evidence that in diabetic patients hypertension may
have its inception early in the course of diabetes and without an
association of renal disease and derived from the study of Mass who
evaluated blood pressure in 123 diabetic and 889 non diabetic
children. He found that systolic BP, although not at hypertensive
levels, increases significantly in diabetic children at about the age of
13 with no relation between the elevated blood pressure and the
duration of diabetes, increased glomerular filtration rates have been
observed. Both elevations of the systolic blood pressure and increase
glomerular filtration rate could be the result of increased cardiac
output.(12)
Many possible pathways in the development of hypertension in
diabetes investigated (Na+ retention, hyperinsulinaemia, obesity,
nephropathy, catcholamines, renin angiotensin system (RAS), atrial
naturetic peptides (ANP) and drugs should be all considered.
(20)
Insulin and sodium retention:

Based hyperinsulinaemia is commonly associated with type
II DM and persists in diabetics with hypertension and appears to be
independent of obesity. Insulin and sodium may have key roles in the
aetiology of hypertension in diabetes. There are reports of significant
renal sodium retention with only small increase in plasma insulin. This
suggests that a moderate increase in plasma insulin level, such as
seen in type II DM may give rise to increase total body exchangeable
sodium content. This hypothesis is supported by the finding of
impaired sodium excretion in diabetics compared with controls,
preliminary evidence of a defect in sodium pump of red cells and
consistent evidence of a 10% increase in total exchangeable sodium in
diabetes.(4,16,19,20,24)
Plasma volume may be higher than normal even in the
absence of hyperglycaemia. Hyperglycaemia Itself however results in
glomeruler hyper filtration, which is a potent stimulus of the proximal
tubular
sodium
counter
transport.(15)Mechanisms
other
than
hyperinsulinaemia may be operative in sodium retention associated

with nephropathy, there may be increased renal sodium excretion or
reduction in the intrarenal levels of prostaglandins and kinins. In
addition, factors causing a shift of fluid and sodium from intra to
extravascular compartments may occur, which may promote sodium
retention in the kidney. Diabetes may also be associated with elevation

of other hormones which may be sodium retaining such as growth
hormone.
Although other mechanisms may be responsible for the
hypertension in type I DM (such as nephropathy), there is strong
evidence favouring a pathogenic role of insulin in the hypertension
with type II DM. Supporting data have also been obtained from non
obese essential hypertensives in whom there is an association between
hypertension and both hyperinsulinaemia and insulin resistance.(20)
The proposed mechanism of insulin-mediated hypertension,
had been derived from the observed effects of insulin on several
determinants of hypertension, it was found to:
- Stimulate the sympathetic nervous system.
- Promote renal sodium retention.
- Influences cell membrane ion-exchange mechanisms.
- Enhances vascular growth.
Essential
hypertension
or
positive
family
history
of
hypertension is associated with an increased maximal rate of red cell

Na lithium counter-transport. This easily measured (in vitro) transport
system
is
marker
of
the
sodium
hydrogen
exchange,
which may be stimulated by insulin. It is a fairly weekly linked marker

for hypertension in family studies.(13,34)
The fundamental abnormality in essential hypertension is an
increase in the wall to the lumen ratio of the resistance vessels, this
gives rise to apparent hyperactivity of the vessels to stress, insulin
may act as a trophic factor predisposing vessels to hypertrophy and
therefore, setting up a pressure mechanism.(16)
There is a strong epidemiological and clinical evidence for the
close association of hypertension, impaired glucose tolerance or
NIDDM, obesity and dyslipidaemia (increased serum TG and reduced
high density lipoprotein cholesterol). While the true causal interactions
between these conditions are incompletely understood, it has been
proposed that a state of insulin resistance and or hyperinsulinaemia is
a common pathophysiological link. Bath Modan and Reaven have
described a syndrome (syndrome X) which links these metabolic
features to the development of cardiovascular disease.(13)
Insulin resistance has been classically defined as a reduced
sensitivity to insulin to produce its full physiological effect on its target
tissues in the body. This leads to a rise in plasma glucose with a
compensatory stimulation of insulin secretion in an
attempt
to
normalize
plasma
glucose,
this
produces
hyperinsulinaemia. However, some believe that hyperinsulinaemia is

the first abnormality to occur as a result of genetic or intrauterine
factors. The insulin resistance state is then a secondary defense
mechanism to prevent the excessive effect of insulin. In some
individuals B-cells can not maintain this high rate of insulin secretion
for a long period, B cell failure occur and hyperglycaemia follows.
In
other
patients
hyperinsuhnaemia
may
persist
with
normoglycaemia but hypertension may appear, It is assumed with

little evidence so far, that their genetic make up determines whether
an individual patient with insulin resistance develops hyperglycaemia
or hypertension or hyperlipidaemia or all of these conditions or a
combination of them. The importance of all these conditions is that
they
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.
Ethnic or racial differences in sympathetic nervous system

activity might explain the differences in relation of insulin resistance to
blood pressure, this had been studied in Pima India which revealed
that the relations between insulinaemia, insulin resistance and blood
pressure differ among racial groups and may be mediated by
mechanisms active in whites, but not Pima Indians or black, also in
White of European decent there is strong relationship between insulin
resistance and blood pressure.(46,47,48)
Catecholarnines:
They are involved in the pathogenesis of hypertension in
diabetes. Although basal levels of plasma catecholamines (both
noradrenaline and adrenaline) are normal in diabetics compared with
age matched controls, there is evidence that, in some diabetics there
is
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.
Second alteration of the structural autoregulation of peripheral vessels

in hypertension, due to increase in the ratio of vascular wall to lumen
may cause differing sensitivity and perhaps an altered response to
catecholamines.
Enhanced
cardiovascular
responsiveness
to
catecholamines may contribute to the hypertension in DM.(20,51)

Atrial natruretic peptide:
The major stimulus for its release is the expansion of vascular
volume. In patients with essential hypertension there may be an
exaggerated ANP response. In diabetics there is volume expanded
state and its possible that exaggerated ANP responses observed in
diabetic is secondary to this, which contribute to the development of
hypertension in DM.(20,48)
Renin-Angiotensin-aldosterone system:
Activation
of
these
system
causes
presser
response
meditated by angiotensin II combined with aldosterone-induced

sodium
retention.
In
diabetes,
however,
the
picture
is
not
straightforward. In uncomplicated diabetes mellitus, rennin (or plasma

renin activity, levels have been reported as normal, high or
low). In diabetics with target organ damage, for example, nephropathy
or autonomic neuropathy, plasma renin activity and aldosterone levels
are generally reduced. The reduction in plasma renin activity may be
due to neuroendocrine processes such as reduced sympathetic activity,
increased levels of inactive prorenin as opposed to renin, and

alterations in renal prostaglandins. Other possible causes include
sodium retention and Juxta glomerulor hyalinosis. Plasma renin
activity may however, simply represent a feed back inhibition due to
coexisting hypertension.(20)
An increase vascular sensitivity to angiotensim II has been
observed
in
diabetics,
and
improvement
of
metabolic
control
normalizes circulating angiotensin II and aldosterone levels. This later

observation may be due to a reduction in sympathetic out flow. It may
be that although plasma rennin activity is partially suppressed, the
resulting reduced levels of angiotensin II are still inappropriately high,
especially in the face of volume expansion.(20) Central nervous
system:
Central nervous mediation of blood pressure may either be
neural or neuroendocrine. Neural pathway defects are attractive as
impaired glucose tolerance and hypertension may represent a common
pathophysiological pathway. The major neurally mediated mechanisms
in hypertension may be a direct primary increase or a
baroreceptor mediated increase in sympathetic output, which may be
important in diabetes as an increase in sympathetic activity, has been
shown to be a direct effect of insulin. The principal neuroendocrine
pathways that may provide a common link are the endogenous opiate
and the central renin angiotensin system. Endogenous opiates have

profound effects on both blood pressure regulation and glucose
control, but there is little objective data as yet to confirm such a
mechanism. Central renin angiotensin system may have a presser
effect in causing hypertension, may be also in diabetics which again its
relevance to diabetes in not clear.(20)
Diabetic nephropathy:
Hypertension
in
types
DM
often
relates
to
diabetic
nephropathy. The situation has become clearer with studies of the

early markers of diabetic renal disease particularly microalbuminuria.
Christensen, for example in a five year fallow up study, found a
correlation
between
severity
of
microalbuminuria and increased
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
patients with hypertension had atherosclerosis and there was a strong

correlation between the extent of the lesion and the level of blood
pressure.
Some
patients,
however,
were
found
to
have
glomerulonephritis, particularly of the membranous type. This supports

the suggestion that hypertension in diabetic patients with renal
involvement may be the result of renal lesions other than those of the
classic or typical diabetic nephropathy.(20, 52, 53)
The clinical diagnosis of diabetic nephropathy requires not only
the detection of persistent proteinuria but also the presence of diabetic
retinopathy and the absence of other (i.e. non diabetic) renal disease if
there is deterioration in renal function without retinopathy, non
diabetic renal disease should be considered.(13)
The term microalbuminuria or microproteinuria (Albustixproteinuria) and macroalbuminuria and macroproteinuria (dipstick
(Albustix) + proteinuria) reflects continuum of increasing protein
excretion. It is generally considered that small increase in albumin
exertion (microalbuminuria) precedes the development of clinical
nephropathy by 10 -14 years. Initially there is renal hyperfunction with
an increase in glomerular filtration rate (GFR), resulting in an
increased
albumin
exertion.
Microalbuminuria
and
rising
blood
pressure (although not in a conventional hypertension range) Probably

indicates early-established diabetic renal disease. Progressive changes
in both renal structure and function may lead to increase in proteinuria
with a decline in renal function.(13)
An area of practical concern is renal artery stenosis. Diabetes

is associated with accelerated atherosclerosis and it is likely that some
diabetic patients have a degree of atheromatous renal artery stenosis.
Although this may contribute to hypertension in diabetics, its precise
prevalence in diabetic subjects with or without hypertension is not
clear and may in part be a reflection of the unwillingness to perform
renal angiogram. The use of ACE inhibitors in current therapy makes
study of this aspect important because of the potential deterioration in
renal function with this class of drugs in patients with renal artery
stenosis.(20)
Great studies have recently been made in the understanding
of platelet, coagulation, lipoprotein and endothelial abnormalities in
the pathogenesis of cardiovascular and renal disease associated with
diabetes mellitus and hypertension. Major progress has been made in
clarifying
the
pathophysiology
of
glomerulosclerosis
and
other
processes involved in the progression of diabetic nephropathy.

Furthermore, accumulating data surveyed in this view address new
and promising pharmacological interventions that specifically address
these pathophysiological mechanisms.(54)
Obesity:
Obesity may be a major factor linking hypertension and
diabetes.
Possible
reasons
for
this
association
may
be
that
hypertension
and
diabetes
have a
similar
predisposing
genetic
component and or similar environmental factors are in operation. In a

large Polish survey, a family history of hypertension was more
common among relatives with those with type II diabetes than among
relatives of patients with type I diabetes mellitus. Tarn and Drury also
found an increased prevalence of parental hypertension for young
males with type I diabetes mellitus and high blood pressure.
There is considerable data, in non-diabetic and diabetic
populations, showing a positive relationship between body mass index
and
blood
pressure.
The
pathological
mechanisms
for
these
relationships are poorly understood, although several hypotheses have

been proposed. Elevated blood pressure itself or anti hypertensive
drug therapy may result in an inappropriately high caloric intake, or
obesity itself may be due to either metabolic changes or be
consequential to an increased energy intake with lack of exercise,
which then may predispose to high blood pressure. There is also
evidence that weight loss achieved by dietary means is associated with
decreased indices of sympathetic nervous system activity.
It
is
possible
that
the
relation
between
obesity
and
hypertension may operate through the hyperinsulinaemia found in

association with obesity and type II diabetes. This hypothesis has been
broadened to include the other common features associated with

insulin resistance termed syndrome X.(20,55,56,57)
Increased total peripheral resistance:
May be due to altered vascular sensitivity to catecholamines
and angiotensin II. Insulin has been shown to stimulate sympathetic
activity, thereby promoting an increase in vascular tone.
Increase total peripheral resistance is due also to increased
blood viscosity as well as fibrinogen and a decreased arterial
compliance as a consequence of either glycation of proteins or
atherosclerosis. This later feature may lead to a loss of elastic
compliance and be a mechanism of isolated systolic hypertension in
subjects with diabetes particularly with increasing age. Another
mechanism for occurrence of increased total peripheral resistance is
the alteration in the concentration of intracellular cations leading to
vasoconstriction which has been shown in several studies including the
trans-membrane-sodium-lithium-hydrogen counter- transport is often
increased in the red cells in hypertensive compared with normotensive
diabetes (IDDM). The red cells sodium potassium counter-transporter,
often increased in essential hypertension, is not universally altered in
hypertension with NIDDM and also intracellular calcium is elevated in a
variety of tissues in patients with both essential hypertension and
diabetic hypertension. Insulin resistance may result in impaired
calmodulin-dependent calcium ATPase activity producing increased

intracellular calcium, which in turn leads to increased vascular
resistance.(13,58,59)
Endocrine causes:
Some
secondary
to
patients
developed
endocrine
causes
hypertension
such
as
and
diabetes
thyrotoxicosis,
phaeochromocytoma, Cushing syndrome, Acromegally and synthetic

oestrogen/progesterone combination therapy. Although it is extremely
important to identify these cases as effective treatment may be
available, these conditions (except for thyrotoxicosis) are rare.(20)
Effect of hypertension on diabetes mellitus:

Cardiovascular effects:
Large-vessel (macrovascular) disease:
Many diabetic patients, particularly those with non-insulin
dependent DM have several or all of these. The incidence of large
vessel disease is dramatically increased in both insulin-dependent
diabetes type I and type II and is the major cause of morbidity and
premature cerebral and peripheral vessels and occurs at an earlier age
and
with
greater
frequency
in
diabetic
patients,
although
the
pathological features do not appear to differ from those seen in non

diabetic subjects.
Alteration in endothehal cell platelet interactions and lipid and
lipoprotein metabolism have been implicated in the accelerated rate of
atherosclerosis in diabetic patients. Hypertension increases the risk of
vascular endothelial injury with subsequent macrophage and platelet
aggregation, release of growth factors that stimulate the proliferation
of smooth muscle cells and the deposition of lipid laden foam
cells.(14,17,18,20)
Coronary heart disease:
Patients with both diabetes and hypertension have two
important risk factors and are therefore, more likely to develop
coronary heart disease (CHD). Compared with non-diabetic subjects,
the overall frequency of CHD is increased particularly in women, whose

disease is often surprisingly more advanced. The generally high
mortality rate (2-3 fold increase) from CHD in diabetic patients may be
explained in part,
by the increased interplay of
multiple risk
factors.(20,24,32)
Cerebrovascular disease:
Hypertension
predisposes
to
cerebral
disease,
as
does
diabetes. Thus it is a major risk factor for cerebral infarction,

cerebrovascular accidents (CVA) and transient ischaemic episodes
have been reported to occur two to six times more in diabetic subjects
and within the subset of hypertensive diabetic, CVA occurs twice as
often as those with hypertension alone.(20)
Peripheral vascular disease:
This is an extremely common problem in diabetic patients and
may present with symptoms of intermittent claudication, rest pain,
arterial foot ulceration peripheral gangrene and infection. A diabetic
over the age of 70 years has a 70 fold increase risk of peripheral
gangrene compared with a non diabetic subject of the same age. In
other diabetic patients there appears to be a close correlation between
systolic hypertension and peripheral vascular disease. It is not clear
however,
whether
hypertension
causes
the
vascular disease or merely reflects the altered physical properties of

the vessels.(60,61,62,63)
Small vessel disease (microangiopathy):
Microangiopathy a disorder of the small blood vessels specific
to
diabetes
and
is
clinically
apparent
in
the
eyes,
kidneys
vasonervosum of peripheral nerves and sometimes in the myocardium

of the heart (cardiomyopathy). It is responsible for much of the
morbidity and mortality of diabetes.
Hypertension appears to be a contributory factor in both the
pathogenesis of these disorders and their further evolution. The
sequences of events which lead to haemostatic abnormalities in
microangiopathy such as increased platelet aggregation, increased
factor VIII, decreased fibrinolysis and increased fibrinogen all these
culminate in capillary basement membrane abnormalities, protein
leakage microthrombus formation and tissue ischaemia, these factors,
together with haemodynamic abnormalities including hypertension,
genetic susceptibility and insulin like growth factors, result in the
microvascular changes seen in susceptible target organs.
Hypertension has an influence on the various clinical important
complication
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
patients. There are reports of an association of hypertension with hard

exudates, haemorrhages and other forms of retinopathy, and other
studies have found a positive relationship between proliferative
retinopathy and elevated diastolic blood pressure. There has been no
prospective reports for type I. DM although there have been
retrospective reports of a high incidence of hypertension in patient
with type I DM and retinopathy compared with matched patients but

without hypertension. In another study factors protective against
retinopathy for 30 years included lower diastolic blood pressure at the
time of analysis. In conclusion, it is possible but not firmly established,
that hypertension may play a causative role in the development of
retinopathy.(20) Hypertension increase glaucoma and ischaemic optic
glaucoma in patient with
DM.(31,67,68,69)
Nephropathy:
Hypertension is also a risk factor for diabetic nephropathy. It
accelerates progression of diabetic renal disease. The clinical syndrome
of diabetic nephropathy is characterized by persistent albuminuria,
associated with a relentless decline in glomerular filtration rate and
raised arterial blood pressure. Roughly about 40% of all insulin
dependent and NIDD develop nephropathy.(16,23,70,71)
Hypertension has been implicated as both a cause and
consequences of diabetic nephropathy. Some patients with proteinuria
have elevated levels Qf erythrocyte Na-lithium counter transport
activity which is a possible genetic markers for essential hypertension.
Nephropathy is the main cause of increased morbidity and mortality in
patients
with
NIDDM.
The
assessed
mortality of IDDM with nephropathy is 80-100 times that of the age

and sex match back ground population.(72,73,74,75,76,77)
Other microvascular complications:
There is still uncertainty as to whether diabetic neuropathy is a
metabolic or microvascular based disorder. Both processes are likely to
be involved. If there is a microvascular element, hypertension may be
expected to be contributory but, so far, no studies have examined this.
A further complication, which may be caused by microvascular disease
is diabetic cardiomyopathy (or specific heart muscle disease of
diabetes). There are data suggesting that myocardial dysfunction may
be associated with diabetes in the absence of extensive coronary
atherosclerosis. The whole field of diabetic cardiomyopathy is still
controversial and awaits clarification.(20)
Management of hypertension in the diabetic patient:
Why should hypertension associated with diabetes be treated?
Many large prospective and other studies of the treatment of
hypertension were published, including the Medical Research Council
(MRC), trial of mild hypertension, the European working party on
hypertension
in
the
elderly,
the
Heart
Attack
Primary
Prevention Study in Hypertension (IPPPSH) and recently the joint

National Committee of Prevention Evaluation and Treatment of higher
blood pressure (JNC VI, 1997). As a result of these trials, it is now
generally accepted that treating mild or moderate hypertension
improves the prognosis of these patients. As for mild hypertensive,
inspite of the widely divergent protocols of the relevant studies, all
indicate benefit with treatment.
Trials
within
specific
groups
of
diabetics
have
been
undertaken, particularly in patients with diabetic nephropathy, results

have demonstrated clear evidence of delay in progression of this
complication with effective blood pressure lowering treatment. In the
recent UK prospective diabetes study, even moderate lowering of
blood pressure leads to major reduction in the risk of cardiovascular
and
renal
events.
The
accompanying
editorial
stated
that
antihypertensive treatment is more effective than tight glucose control

and the beneficial effect comes sooner. In the hypertensive optimal
treatment study, the risk of major CV event was 50% lower among
patients with type II DM whose target diastolic BP was 8OmmHg than
among patients whose target diastolic BP was 90mm Hg.(80,81)
In the hypertensive Cohort of the UK prospective diabetes
study (UKPDS), comparison of patients allocated either to tight.
blood pressure control using captopril or atenolol, or to a less tight

control, showed that tight control was associated with significant
reduction in the risk of death related to diabetes, and with reduction of
an all microvascular end points. Predictably, reduction in the risk of
heart failure stroke occurred, but 21% reductions in the risk of
myocardial infarction was not significant. The hypertension optimal
treatment (HOT) study also reported reduction in myocardial infarction
in patients treated to a target diastolic BP of 80 mmHg compared
with targets of 90 mmHg, but again the changes were not significant.
Based largely on these recent data, a target BP of < l3OmmHg systolic
and < 80 mmHg diastolic is now recommended for diabetic patients,
lower
targets
may
be
appropriate
for
diabetic
patients
with
microalbuminuria, in whom considerable data support the use of ACE

inhibitors for protecting against deterioration of the renal function, a
beneficial effect that occurs independently of BP reduction. However,
UKPDS reported that captopril or atenolol was similarly effective in
reducing the incidence of diabetic complications and concluded that for
most patients blood pressure reduction itself is more important than
the agent used.(82)
General measures as first line therapy for hypertension in

diabetics:
The 1st therapeutic step is usually not pharmacological, these
measures include:
- Exercise.
- Reduction of alcohol intake. Relaxation therapy.
- Weight reduction: there is now sound evidence that weight
reduction
benefits
hypertension
as
well
as
producing
reductions in insulin resistance and in cardiovascular risk.

A diet high in fibre and low in fat and sodium (the diabetic or
prudent diet). 50-60% unrefined carbohydrate and lowering
fat to 30% total energy intake per day. Reduction in sodium
intake is no more than 60gm per day and for those with
hypertension,
Randomized
restriction
blind
to
controlled
no
and
more
than
crossover
3gm/day.
studies
of
moderate Na+ restriction and Na+ supplements was carried in

hypertensive type II DM which revealed that, moderate dietary
sodium has a definite hypotensive effect, which may be useful
in mild hypertensive of type II DM.(83)
Drug treatment:
The Ideal drug for the hypertensive diabetic patients should:
- Lower the BP effectively.
-
Neither impair glucose tolerance or interact with

hypoglycaemics, nor impair the patients ability to recognize
or respond to hyper or hypoglycaemia.
Not adversely affect plasma lipids.
Not cause postural hypotension, impair limb

blood flow, raise risk of impotence or decrease renal
function.
Reduce susceptibility to ischemic heart disease

(cardio protective actions such as reducing arrthymias and
platelet aggregation and increasing coronary blood flow.(80)
Although many anti-hypertensive drugs are now available
most of those currently in use can be subdivided into four major
classes:
1- Thiazide diuretics:
These drugs are still commonly used, they are often effective
inexpensive and can be given once daily and are preferable to loop
diuretics in uncomplicated cases. They combat what may be two of the
major
contributory
factors
to
hypertension
in diabetes: An elevated pool of exchangeable sodium and an elevated

cardiovascular reactivity to noradrenaline. They have a number of
possible side effects, however, and show a dosage plateau above
which enhanced blood pressure reduction is rare and adverse
metabolic effects are made worse. In addition, there are several major
complications related to the use of thiazide e.g. they have adverse
effect on CHO metabolism. The diabetogenic effect is reversible with 712 months of stopping the drug, the mechanism of action of CHO is
not known, but may relate to hypokalaemia. Many diabetic patients
have severe coronary artery disease or cardiomyopathy and many
receive digoxin. In such patients even a small decrease in serum
potassium
may
produce
dangerous
arrhythmias.
Potassium
supplementation or the use of potassium sparing diuretics, either

alone or in combination may help overcome this and also improve
glycaemia, but may precipitate hyperkalaemia which is undesirable
particularly in patients with renal impairment, it is also possible that
thiazides have a direct effect on insulin producing beta cells of the
pancreas, thus blocking insulin release, an effect which may be
worsened when combined with a beta bloker.(80,84)
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
properties in non-diabetic patients who have sustained a previous

heart attack. Patients with diabetic nephropathy have an increased
cardiovascular mortality, but there are no studies directly addressing
the question of whether beta-blockers are cardioprotective in these
patients. Potential disadvantages of beta-blockers are that they alter
patients hypoglycaemia awareness, impaired the bodys ability to low
blood sugar and adversely affect lipid and glycaemic profile. They may
also cause impotence. The use of beta-blockers in diabetic subject,
however, remains controversial. Certainly cardioprotective and anti

anginal effect, the main advantage of beta-blocker are often required
in hypertensive patients as most deaths in this group are due to
cardiovascular
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
management of diabetes more difficult. They may increase plasma

lipids and have adverse effects on some of the complications of
diabetes. If a beta-blocker is to be used, then a relatively beta
selective
drug
is
preferable
and
beta-blockers
with
intrinsic
sympathomimetic activity may have less effect on lipids.(20,80)

3- Calcium antagonists:
These agents are effective often in a once or twice daily
dosage
and
have
the
added
advantage of having antianginal,
cardioprotective and/or anti-arrhythmic properties. In contrast to

diuretics, they usually preserve cerebral and renal blood flow. Their
antihypertensive action is based on their peripheral vasodilatation
properties causing a direct decrease in total peripheral resistance.
Unfortunately, calcium antagonist produce side effects, usually minor
and self limiting in a significant proportion of patients such as flushing,
headaches and peripheral oedema.
Some patients particularly those with autonomic neuropathy,
may respond well to these drugs because they do not experience the
reflex tachycardia which occurs in those with intact nervous system.(20)
Glucose induced insulin secretion is a calcium dependent
process, mobilization of glucose from the liver is also calcium
dependent and alpha adrenergic receptor mediated glycogenolysis
operates through calcium release from intramitochondrial pool.(80,86)
In a recent review of this subjects, however, no significant

effect on glucose homestasis in diabetic patients treated with calcium
antagonists emerge, no consistent change were reported in basal
plasma glucose and insulin levels over several months. Several small
short term clinical trials have suggested that nifidipine may be
potentially diabetogenic with an increase in fasting blood glucose
concentration and delay in insulin response.(87) Although in a better
control trial another group of researchers reported improvement in
glucose tolerance. Large studies involving both non diabetic and
diabetic patients did not suggest that nifidipine is diabetogenic.
Several larger term trials demonstrated that it has no significant effect
on insulin levels and did not impair long term glucose control in
hypertensive patients.
It must be concluded that despite evidence to the contrary
from some short term high dose trials; nifedipine at therapeutic doses,
is not diabetogenic in normal patients, nor does it significantly affect
glucose tolerance in NIDD. In addition it does not interact adversely
with oral hypoglycemic drugs.(80)
On the other hand verapamil, in the presence of calcium
inhibits the effect of glucagon on glucose output and inhibits insulin
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,
however, a short term study. The results of long term comparative

studies of calcium antagonists and ACE inhibitors are still awaited.(20)
In conclusion calcium antagonists should now be regarded as
first line treatment in patients with diabetes and hypertension. They
are relatively safe and well tolerated and appear to have no clinically
relevant metabolic side effects. In addition there is some evidence of
cardioprotective properties and the potential to improve, rather than
impair, peripheral circulation and renal function.(80)
4- Angiotensin Converting Enzyme (ACE) inhibitors:
There is at present, great interest in the role of ACE inhibitors
in the treatment of hypertension in patients with diabetic
nephropathy. ACE works by preventing the conversion of angiotensin I
to II. Angiotension II, stimulates aldosterone secretion
and causes vasoconstriction, both of which tend to raise BP. ACE
inhibitors exert their intra-renal effects predominately at the efferent
arteriole,
causing
vasorelaxation
and,
thus,
lowering
the
intraglomerular capillary pressure.(20) They lower BR by decreasing

elevated systemic vascular resistance, but do not (unlike vasodilator)
produce reflex sympathetic activation or other myocardial contractility.
They
enhance
perfusion
of
vital
organs,
reverse cardiac hypertrophy and had been reported to have beneficial

effects in patients with congestive heart failure (HF). Both preload and
afterload are decreased and, because there is no risk of reflex
tachycardia,
cardiac
oxygen
demands
are
decreased.
Potential
problems of ACE inhibitors include renal impairment and marrow

suppression, which may be closely related. The four
currently
available ACE inhibitors are captopril, enalapril, lisinopril and quinapril

(and recently perinodopril) are all eliminated by the kidneys and both
age and cardiovascular disease impair renal function, there is an
increased potential for adverse reactions. agents should be used with
caution in patients with renal impairment. There are several important
factors regarding treatment with ACE inhibitors in the hypetrensive
diabetic patients, including glucose homoestasis, the effect of these
drugs on glucose metabolism has been evaluated in several controlled
studies. They were found to be safe and effective in treating
hypertension, glucose metabolism was not affected and no patients
required changes in the doses of insulin or oral hypoglycemic drugs.
Other factor that ACE inhibitors have no significant effect on the lipid
profile, captopril however, has been shown to increase HDL-cholesterol
ration in hypertensive patients with or without hyperlipidaemia, which
is
likely
to
be
beneficial.
Reports
of
improvements in renal function even in patients with albuminuria who

are normotensive suggest that this improvement may be more
specifically related to ACE inhibitors rather than general effects on
systolic BP, this however, is still controversial. Reduction in the rate of
deterioration in GFR after treatment with captopril in patients with
diabetic nephropathy and hypertension, with no correlation between
the
fall
in
BP
and
reduced
deterioration
in
GFR,
has
been
demonstrated. ACE inhibitors dont cause impotence, and any effect on

peripheral vascular disease is likely to be beneficial. They have a
neutral effect on ischaemic HD. In a recent study these agents
produced an increase in coronary blood flow (BF) despite a moderate
reduction in coronary perfusion pressure.(93)
In conclusions ACE inhibitors are safe in diabetic patients, but
treatment should be commenced with caution in those receiving
diuretics or with autonomic neuropathy. Both diuretics and ACE
inhibitors are potent anti-hypertensives and may cause symptomatic
hypotension following the first dose, which may provoke deterioration
in renal function.(94,95) These side effects were more marked with
enalapril and it is now recommended that diuretics be stopped two to
three days before starting the drug. Generally ACE inhibitors should be
started at a low dose with the first dose taken at night to reduce the
risk
of
postural
hypotension.(80,96)ACE
acceptability
as
inhibitors
they
have
no
enjoy
high
demonstrable
level
of
patient
psychological
or
physiological effects. They may also have a specific effect on diabetic

nephropathy They are effective antihypertensive drugs, which do not
cause adverse metabolic effects or change in coronary heart diseaserisk profile. Provided that they are used with caution to avoid the
potent early hypotensive effect, they should now be considered as first
line treatment for hypertension in diabetic patients.(20,82,82)
Other drugs:
These include sympathetic inhibitors (e.g. methyl dopa,
clonidine and guanithidine), alpha blockers (prazocin and the newer
dexazocine which are postsynaptic alpha adrenergic blocker), and
direct
vasodilators
(hydralazine,
minoxidil).
These
can
not
be
considered as first line drugs for treatment of hypertension in diabetic

patients. The sympathetic inhibitors may cause problems of postural
hypotension, impotence and depression. The alpha blockers decrease
peripheral vascular resistance and cause venous dilatation, thus
decreasing venous return to the right side of the heart. This, however,
may be an advantage over direct vasodilators in patients with ischemic
heart disease, as they do not significantly increase cardiac output.
Alpha blockers should be used
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
to achieve adequate control, then combination therapy with different

classes of first line drugs should be used.(98,99,100)
OBJECTIVES
The objectives of this study:

1- To detect the prevalence of hypertension in diabetic patients
compared with non-diabetic subjects (control group).
2- To evaluate the effect of hypertension in diabetic patients.
3- To determine the best management of hypertension in diabetic
mellitus.
PATIENTS & METHODS
Study design and samples:

In this study descriptive and comparative, 160 adults
diabetics were examined, 100 of the them were type II
diabetics and 60 were type I diabetics. Another 100 non
diabetic individuals were taken as control.
Study area:
The diabetic patients were seen at Diabetic Clinic in
Khartoum Clinics, including Gabir Abu El Aiz Diabetic Center,
Fath El Rahman El Bashir and Khartoum Teaching Hospital.
Exclusion criteria:
Children (below 17 years) were excluded from the
study.
Data collection
All patients were studied by a unified protocol
consisting of a standard questionnaire and clinical examination.
The questionnaire included the following; personal
history (name, age, sex, occupation, tribe and residence),
known diabetic (the control were not diabetic, but might be
hypertensive), duration of diabetes, treatment of diabetes
including diet insulin and oral hypoglycaemic agents. Control of
DM (symptoms of DM + investigations including urine analysis,
fasting blood glucose (FBG), and 2 hours postprandial blood
glucose (2PPBG)). Family history of DM, history of

hypertension and its duration, family history of hypertension,
history of smoking, number of cigarette per day and its
duration, body mass index (BMI) was calculated by dividing
weight (kg) by height squared (m2).
Obesity was defined as BMI more than 25 kg/m2 in
males and BMI more than 24 kg/m2 in females. Subjects with
BMI less than 19 kg/m2 were considered underweight. BP was
measured in the supine position and standing position. A
standard mercury sphygmomanometer was used and
maintained regularly. Postural hypotension is generally
accepted when there is postural decrease in blood pressure
from the supine to standing position of at least 20mmHg
systolic and 10 mmHg in diastolic BP sustained at least for 3
minutes.
Cardiovascular features were assessed by symptoms of
angina or myocardial infarction, and ECG findings of ischaemic
changes, evidence of long standing hypertension and evidence
of myocardial infarction.
Neurological features were assessed by symptoms of
transient ischaemic attack (TIA) or stroke and funduscopy for
both hypertensive and diabetic changes.
Renal manifestation were assessed by urine analysis for

proteins, the frequency of proteinuria and its occurrence from
the time of development of DM, blood urea and serum
creatinine measurement.
Data analysis:
The data was coded and analyzed using SPSS
programme to calculate frequency distribution and (P) values.
The P. values was taken as significant if it is 0.05 and
insignificant if the P value is >0.05, finally the results were
evaluated and discussed to gain useful information from the
study.
RESULTS
One hundred and sixty known diabetic patients were

included in this study. Hundred of them were type II DM and 60
were type I DM.
Some of the demographic and behavioural
characteristics studied are summarized (Table 1).
In type 1 (IDDM), 13 patients were found to be
hypertensive and five of them were males (8.3%), while eight
were females (13.3%), (Table 2).
In type II (NIDDM), 53 patients were found to be
hypertensive. 27 of them are males (27%) and 26 were
females (26%), (Table 3).
Of the 100 subjects non diabetics were chosen as
control, 20 of them were found to be hypertensive, 13 were
males (13%) and 7 were females (7%), (Table 4). The
relationship between all these are summarized in (Table 5).
Table 6 showed the percentage of hypertensive patients
in each type of diabetes separately, type I (21.6%), type
II(53%) and the control group (20%), while Table 7 reveals
the prevalence of hypertension in both types of diabetes
(41.2%) and that of the control group 20%.
The numbers of the hypertensive patients according to

the age distribution were shown in Table 8 (type 1 DM) and
Table 9 (type II DM) and the control group (Table 10).
Type 1 (IDDM) hypertensive patients in relation to the
duration of diabetes are shown in Table 11, while Table 12
shows type II (NIDDM) with hypertension in relation to the
duration of DM.
Fig. 13 shows the percentage of types I hypertensive
patients in relation to the control of DM. Patients of good
control were 5% and poor control were 16.6%. Criteria for
good control are absence of symptoms, normal BMI, absence of
glucose in the urine and normoglycemia.
Table 14 shows the percentage of type II DM according
to the control of DM, while Table 15 involved the two groups of
DM in relation to the control.
Table 16 shows type I (IDDM) diabetics with
hypertension in relation to the BMI, while Table 17 shows the
same relationship with type II (NIDDM), and Table 18 was
applied to the two groups together.
Table 19 shows three patients from type I (IDDM)
developed ischemic heart disease (5%), while two patients
from type II without hypertension developed the IHD (3.3%),
(Table 20) shows 25 patients from type II diabetic with

hypertension developed IHD (25%), while eight patients (8%)
developed IHD.
Table 21 shows the percentage of IHD in both types of
DM with HTN (17.5%) and diabetics only (6.2%). There is
significant difference between the two groups.
Fig.1 demonstrates the neurological complications
(mainly TIA and stroke) in type I DM with hypertension
compared to diabetic without hypertension.
Fig.2 shows the same neurological complications with
type II DM with hypertension compared with diabetic without
hypertension.
Fig.3 shows the prevalence of neurological
complications in both types of DM with hypertension (14.3%)
compared with diabetic without hypertension (5%), there is
significant difference between the two groups.
The incidence of retinopathy in each type of DM was
obtained. In type I, it was found to be 5% and 15% in type II
DM with hypertension (Fig. 4).
The incidence of retinopathy in type II DM with
hypertension (15%) compared with diabetics without
hypertension (7%) (Fig. 5). Retinopathy in type I DM with
hypertension (5%) compared with DM without hypertension

(1.6%), (Fig. 6).
Fig. 7 demonstrates the prevalence of retinopathy in
both types of DM (10.2%) compared with that of DM without
hypertension (5%), there is also a significant difference
between the two groups.
The occurrence of nephropathy in type I DM (3.3%) and
type II DM with hypertension (14%) separately with total
percentage of 10% for both types is shown in Fig. 8.
Fig. 9 shows the incidence of nephropathy in type II DM
with hypertension (14%) and diabetics without hypertension
(0%).
Fig. 10 shows the incidence of nephropathy in type I DM
with hypertension (3.3%) and diabetics without hypertension
(5%).
Fig. 11 shows the prevalence of nephropathy in both
types of DM with hypertension (10%) and diabetics without
hypertension (1.9%), which indicate significant difference
between the two groups.
Table 1 : Demographic characteristics of the two groups

Variable
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)
25.3 (SD 2.3)
23.2 (SD 2.2)
Mean blood pressure:
Systolic
Diastolic
Type I
125
80
140
85
120
80
Gender frequency:
Mean age:
M + SD yrs
Mean duration of DM:

M SD yrs
Mean BMI (Kg/m2):
(IDDM)
Type II
(NIDDM)
Control
M = Mean
SD = Standard deviation
Table 2: Hypertensive patients in type I diabetes mellitus

according to sex in the study groups (n=60)
No. of hypertensive patients
Not hypertensive
Males
26
8.3%
Females
21
13.3%
Sex
P = 0.2817
X2 = 1.16
Table 3: Hypertensive patients in type II diabetes mellitus

according to sex in the study groups (n= 100)
Sex
No. of hypertensive patients
Not hypertensive
Males
27
22
27%
Females
26
25
26%
Total
53
47
P = 0.8411
Table 4 : Hypertensive patients in control group

according to sex in the study (n=100)
Sex
Males
Females
Total
P = 0.00000
No. of patients
Percentage
13
13%
7%
20
20%
Table 5: Hypertensive in both types of DM and the control

group according to sex (160 patients; 100 control)
Sex
Type I & Type II
Control group
DM
Males
32
51%
13
65%
Females
34
49%
35%
Total
66
100
20
100%
%
P = 0.8411
Table 6 : Hypertensive patients in both types of diabetes and

the control group in the study groups (n=260)
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
Table 7 : Prevalence of hypertension in diabetic patients

compared with non diabetic subjects (control group)
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
Table 8: Hypertensive patients in type I diabetes mellitus

according to age in the study groups (n=60)
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
Table 9: Hypertensive patients in type II diabetes mellitus

according to age in the study groups (n=100)
Not hypertensive
Total
20 30
31 40
41 50
55
14
19
51 60
16
17
33
> 60
30
13
43
Age group (in

years)
Total
53
47
P = 0.0186
Table 10: Hypertensive patients in control group

according to age (n=100)
Age group (in years)
No. of patients
20 30
31 40
41 50
51 60
> 60
11
100
Total
20
Table 11: Hypertensive patients in type I diabetes mellitus in

relation to duration of diabetes in the study groups (n=60)
Not hypertensive
15
17
6 10
17
11 15
16 20
Duration (in years)
> 20
Total
13
47
P = 0.01
Table 12: Hypertensive patients in type II diabetes mellitus in

relation to duration of diabetes in the study groups (n=100)
Duration (in years)
15
Not hypertensive
13
20
6 10
11 15
16
16 20
13
> 20
Total
53
43
P = 0.27
Table 13 : Hypertensive patients in type I diabetes mellitus in

relation to the control of diabetes in the study group (n=60)
Status
Not hypertensive
Good control
33
5%
Poor control
10
14
16.6
Total
13
47
P = 0.0021
Table 14 : Hypertensive patients in type II diabetes mellitus in

Status
Not hypertensive
Good control
20
34
20%
Poor control
33
13
33%
Total
53
47
100
P = 0.0176
Table 15: Hypertension in both types of diabetes mellitus in

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
Table 16: Hypertensive patients in type I diabetes mellitus in

relation to body mass index (BMI) in the study groups (n=60)
BMI (%)
Not hypertensive
10 20
15
20 25
27
25 30
30 40
> 40
Total
13
47
Table 17: Hypertensive patients in type II diabetes mellitus in

relation to body mass index (BMI) in the study groups
(n=100)
Not hypertensive
10 20
10
20 25
13
25 30
14
19
30 40
26
> 40
Total
53
47
BMI (%)
Table 18: Hypertensive patients in both types of diabetes

mellitus in relation to body mass index (BMI) in the study
groups (n=160)
BMI (%)
Total of type 1 + type
Percentage
II
10 20
9%
20 25
21.1%
25 30
17
27%
30 40
32
46%
> 40
4.5%
Total
66
Table 19: Ischaemic heart disease (IHD) in type I diabetic

patients with hypertension compared with diabetic patients
without hypertension (n=60)
Status
DM + HTN
DM only
Havent IHD
10
45
Total
13
47
3.3%
5%
Have IHD
Percentage
P = 0.0757
Table 20: Ischaemic heart disease (IHD) in type II diabetic

patients with hypertension compared with diabetic patients
without hypertension (n=100)
Status
DM + HTN
DM only
Have IHD
25
Havent IHD
28
39
Total
53
47
Percentage
8%
25%
P = 0.0757
Table 21: Ischaemic heart disease (IHD) in both typesof

diabetic patients with hypertension compared with diabetic
patients without hypertension (n=160)
Status
DM + HTN
DM only
Havent IHD
25
Total
28
10
17.5%
6.2%
Have IHD
Percentage
P = 0.0134
DISCUSSION
The prevalence of hypertension in diabetic Sudanese patients

(type I and type II) is found to be double that in the non diabetic
control group (as twice as common). This is consistent with similar
results obtained in several studies carried at different parts of the
world as shown below.
Data for several epidemological studies have suggested the
prevalence of hypertension in patients with DM is approximately 1.5 -2
times
greater
than
in
approximately
matched
non
diabetic
patients.(16,18,19)
In
USA
according
to
the national
high blood pressure
education programme working group report on hypertension in DM,

hypertension is as twice as common in people who have DM as in
those who do not as the population ages, becomes less active, and
grows more obese.(23)
The highest prevalence was obtained from study conducted in
Pima India age 18-62 years. Age and sex adjusted to Pima population,
the prevalence of HTNwas 7.1% for subjects with normal glucose
tolerance compared with 13.0% for subjects with impaired glucose
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
increase in the prevalence of HTN among diabetics, occurs in all areas

of Saudi Arabia. These observations are due to that Saudi Arabia has
undergone significant epidemiological transformation over the past two
to three decades. This has resulted in modification of life style to a
more sedentary way of living, with considerable reduction in the extent
of physical activity, increase in intake of (fast foots) and elevation of
stress related work and other activities. Females are particularly more
prone to sedentary life and due to climatic conditions i.e. high
temperatures particularly during the summer months, out door life is
significantly reduced. This has caused the precipitation of several
multifactorial traits both in males and females. Since associated
morbidity and complications are expected to increase, hence, control
of DM and hypertension by appropriate methods, particularly, dietary
restriction of calories, sodium and regular physical exercise must be
stressed. Of interest is the prospect of introduction of presymptomatic
diagnosis of susceptible individuals using genetic markers, where it is
expected to play an essential role in the control and prevention of non
communicable diseases. If this becomes a practical approach the
prevention of the complication will be of appreciable benefits to those
prone to DM and hypertension.(27)
The prevalence of hypertension in diabetic patients is similar
to the finding of Wokoma F.S in Nigeria. Of the 119 patients included
in his study, 78 were males and 41 were females (male: female =

1.9:1) NIDDM. The patients had been diabetic for 6 months to 35.
Fifty (41.2%) had coexisting hypertension with DM. He observed that
hypertensive NIDDM patients were older and more obese than, non
diabetic, though these differences were not statistically significant.(28)
In a large study of 662 diabetic patients with carefully matched
controls, for e.g. Pell and D' Alonzo found 54% greater prevalence of
hypertension among diabetic subjects compared with controls and this
was independent of obesity.(20)
Patient with type II (NIDDM) represent the majority of
hypertensive patients and in the group, the prevalence of hypertension
increases with age not like that of type I (IDDM), these findings are in
line with those reported in the literature, e.g. in a population based
study performed in Southern Wiscon (USA), 765 individuals diagnosed
as having DM when they were younger than 30 years and taking
insulin participated in based line, 4 years and 10 years examinations.
It was found that the prevalence of hypertension at base line was
17.3%. The ten years incidence of hypertension was 25.9%. The
incidence of HTN was greater with older age, long duration of DM, high
glycosylated haemoglobin level protinuria, more severe retinopathy
and male gender. This data suggested that control of hyperglycaemia
and prevention of gross protinuria may lead to a reduction in the long

term incidence of HNT.(22)
In a recent study Chuhwak EK (2001) in Jos Nigeria found
that, of 302 diabetic patients in Jos Nigeria, 36% were found to be
hypertensive. Patients with hypertension were older and more obese
than normotensive patients. This is similar to the findings of
Kumwenda, et al., in Malawi.(29)
In unselected but representative diabetic population, Brylogle
and Bradley found an over hypertension prevalence of 20% increasing
to 40% in patients over 50 years of age. The prevalence in men and
women younger than 50 years was equal but it was greater in women
above this age. The ratio (female : male) is 2.6 :1.(21)
El Bagir M, El Mahdi EM, studied a total of 377 diabetic
Sudanese
patients with age and sex matched controls, they found
that there was a high prevalence of diastolic hypertension (40%) in

NIDDM, that the blood pressure did not correlate with age or duration
of DM and that a higher prevalence of hypertension was observed in
females than in male subjects.(30) However, in our study there is slight
female predominance with overall ratio of female to male is 1.03:1,
while in type I
IDDM the female predominance is higher than that
1.6:1, in type II NIDDM there is no significant difference between the

two sexes since the ratio (Female : male) is 1.04: 1.
The high prevalence
of hypertension in Sudanese diabetic
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.
The high prevalence of overweight and obesity amongst hyperensive

and diabetic adult patients, might be explained because hypertension
is more prevalent in older obese population than in normal weight
control.(102)
John Kwals, over a 5 years period in his clinic of 442 newly
diagnosed type II, he found that 47% men were overweight and 41
women were overweight and 31 obese. Indeed some doctors stress
this
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
countries than in Europeans
and specially among blck females with hypertension and DM.

Weight reduction enhances the blood pressure lowering effect
of concurrent antihypertensive agents and can significantly reduce the
cardiovascular risk factors such as DM and dyslipidieamias.
The occurrence of hypertension in DM have an additive risk

factor for cardiocascular disease and worsening retinopathy and
nephropathy.
In our study the incidence of ischamic heart disease is
significantly higher in both types of DM with hypertension compared
with disbetics who have no hypertension. This reflects the effect of
hypertension in development of these complications in diabetic. This
observation was documented by Goodkin in his 20 years morbidity
study which showed increased incidence of large vessel disease in both
type I and type II DM and is the major cause of morbidity and
premature death. Atherosclerosis particularly involves the coronary,
cerebral and peripheral vessels also occur at an earlier age with
greater frequency in diabetic patients, although the pathological
features do not appear to differ from those seen in non diabetic
subject, this is also studied by Stambler J (USA).(20)
The
chance
of
occurrence
of
stroke
in
diabetic
with
hypertension is not high as seen in the literature (twice), This

observed by Asplund in his study about the national history of stroke
in DM, this difference can be explained by that many of our patients
are unable to reach the hospital and prefer to stay at home. However,
the incidence of TIA is significantly higher specially in type II (NIDDM)
with hypertension (3-4 times) that of the diabetic alone 10: 3. This is
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
predisposition to hypertension is associated with diabetic nephropathy

even when systolic blood pressure is not raised. Genetic predisposition
to hypertension is indicated by the presence of hypertension in a
parent which trebles the risk of nephropathy of by increased by
erythrocyte sodium-lithium counter transport, which is a fairly weak,
but positive marker for hypertension in family studies. This is studied

by Haslacher and Moghsen.(20)
However, in the literature many studies shoed the incidence of
nephropathy as high as 40% in both types.(16,71) This is observed by
McMillian.(20)
This reflect that hypertension had been implicated as both a
cause and consequence of diabetic nephropathy.
David M in his study to examine the putative pathogenic
mechanisms of long term specific complications of DM, his sources
were the literature reviews relevant to long-term diabetic complication
and their pathogenesis, he concluded that the level of chronic
glycaemia is the best established concomitant factor associated with
diabetic complications.(68)
Bertran and his colleagues assessed the relative effect of
different antihypertensive agents on proteinuria and renal function,
they concluded that ACE inhibitors can decrease protinuria and
preserve glomerular filtration rate in patients with DM. These effects
occur independent of changes in systemic blood pressure.(102)
CONCLUSION
The prevalence of hypertension in DM is double that in non

diabetic subjects in Sudanese population.
Type II DM is the commonest type of DM in Sudan.
No significant difference is found among gender regarding DM.
Hypertension
diabetics.
and
obesity
are
common
among
Sudanese
Large number of diabetic patients with hypertension are having

poor glycaemic control. This is reflected in the high incidence of
diabetic retinopathy.
Earlier detection and proper therapy of both conditions might

help
halting
the
serious
cardiovascular
and
cerebrovascular
complications of these two serious diseases.
RECOMMENDATIONS
1-
This study needs to be extended to include large number of

patients from both urban and rural areas.
2-
More diabetic clinics and trained personnel are needed to deal

with the increasing problems of DM and hypertension.
3-
Control
of
hyperglycaemia
should
follow
the
new
recommendations made by the WHO to reduce the long-term

incidence of HTN.
4-
Hypertensive therapy should first emphasize on life style

modification such as weight reduction, exercise, stress mangement,
alcohol consumption and moderate restriction of salt intake.
5-
Anti-hypertensive treatment must be particularly meticulous in

diabetics.
6-
Anti-hypertensive agents should be selected-based on the

advantages and disadvantages of the therapeutic agents in context
of individual patient's risk factors profile.
7-
The
goal
of
treatment
is
diastolic
blood
pressure
of
approximately 80 mmHg and lower than that in patients with

microalbuminurea.
8-
In general the preferred anti-hypertensive agents are ACE

inhibitors, which are glucose and lipid neutral and thus positively
impact the cardiovascular risk profile.
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inhibition in heart failure. Br Med J 1985; 53: 672.

96-
Carl EM. ACE inhibitors and diabetic nephropathy. Br Med J
304(8): 1992.
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Wilcox RG. Mitchell JR, Hampton JR. Treatment of high blood
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98-
Michael P, Cynthia MD. Using cardiovascular risk profiles to
individualize hypertensive treatment. Br Med J 2001; 322.

99-
Andrew FG, Tame O, Paul O. Effective of blood pressure
reduction what if any, should be the treatment of raised blood

pressure in diabetic patients. N Engl J Med 1990 Feb; 322(8).
100- Dennis B. Hypertension and DM. Post Graduate Doctor Middle
East 1994; 17(10): 428-35.
101- UKPDS
38.
Tight
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pressure
control
and
risk
of
macrovascular and microvascular complications in type II DM. Br

Med J 1998; 317: 703-13.
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1993; 93: 193-95.
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
First degree relative:

Second degree relative
No
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-

Prevalence of Hypertension in Sudanese Patients

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Prevalence of Hypertension in Sudanese Patients

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UNIVERSITY OF KHARTOUM

PREVALENCE OF HYPERTENSION IN SUDANESE PATIENTS

A thesis Submitted in partial fulfillment for the requirements

I am extremely grateful to my teacher and supervisor

Musa Mohamed Khier, for his confidence in delivering this subject to

calculating the sample size of this study.

Body mass index

Coronary heart disease

Diabetes complication control trial

Fasting blood glucose

Hypertension optimal treatment

Impaired glucose tolerance

Medical Research Council

2 hours post prandial blood glucose

Random blood sugar

United Kingdom Prospective diabetes study

World Health organization

interrelated diseases and frequently concomitant. They are worldwide

increasing problems with significant impact on patients, public health

hypertension. Other neurological complications as stroke was found to

LIST OF TABLES & FIGURES

Table 1: Demographic characteristic of the two groups

Table 2: Hypertensive patients in type I DM according to sex

Table 3: Hypertensive patients in type II DM according to sex

Table 4: Hypertensive patients in control group according to sex 73

Table 6: Hypertensive patients in both types of DM and

Table 8: Hypertensive patients in type I DM according to age

Table 9: Hypertensive patients in type II DM according to age

Table 10: Hypertensive patients in control group

Table 12: Hypertensive patients in type II DM in relation to

Table 13: Hypertensive patients in type I DM in relation to

Table 14: Hypertensive patients in type II DM in relation to

Table 16: Hypertensive patients in type I DM in relation to

hypertension compared with diabetic patients

Neurological complications in type I DM with

Neurological complications in type II DM with

Neurological complications in both types of DM

Retinopathy in both types diabetic patients with

Retinopathy in type II diabetic patients with

Retinopathy in type I diabetic patients with

Retinopathy in both types of diabetic patients

Nephropathy in both types of diabetic patients

Nephropathy in type II diabetic patients with

Nephropathy in types I diabetic patients with

Nephropathy in both types of diabetic patients

emphasized the sweet taste of urine.

(1621-1675) an English physician clearly

documented the sweet taste of urine. Mathew Dabson in 1776 showed

The Belgian, Jean de Meyer (1909) gave the name insulin to

sulphonylureas as hypoglycemic agents was obvious by 1942 and the

cardiovascular disease. Life style and genetic lactors are important in

In the classical young onset form of disorders there is near

microangiopathy, macroangiopthy, and peripheral nerve damage.

prospective treatment of hyperglycaemia and other cardiovascular risk

Type I diabetes mellitus: (Beta-cell destruction usually

exogenous insulin to prevent metabolic decompensation and

resistance caused by acute illness, therefore, insulin secretory

medical attention. Moreover, if the level of hyperglycaemia is

* 2 hours plasma glucose 11.1 mmol/L (200 mg/dl) during oral

IDDM in the countries in which the

population is predominately white, the reported yearly appearance

the US and Denmark the peak age of onset is between 10 and 14

The figure may be underestimated as patients who died at

there is no dividing line so is the relationship between arterial pressure