Diabetes and its Complication

Diabetes and its Complication

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2. Diabetes mellitus (DM) is a group of diseases
characterized by high levels of blood glucose resulting from
defects in insulin production, insulin action, or both.
The term diabetes mellitus describes a metabolic disorder
of multiple aetiology characterized by chronic
hyperglycaemia with disturbances of carbohydrate, fat and
protein metabolism resulting from defects in insulin
secretion, insulin action, or both.
The effects of diabetes mellitus include long–term damage,
dysfunction and failure of various organs.
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3. Diabetes mellitus may present with characteristic
symptoms such as thirst, polyuria, blurring of vision, and
weight loss.
In its most severe forms, ketoacidosis or a non–ketotic
hyperosmolar state may develop and lead to stupor, coma
and, in absence of effective treatment, death.
Often symptoms are not severe, or may be absent, and
consequently hyperglycaemia sufficient to cause
pathological and functional changes may be present for a
long time before the diagnosis is made.
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4. The long–term effects of diabetes mellitus include
progressive development of the specific complications
of retinopathy with potential blindness, nephropathy
that may lead to renal failure, and/or neuropathy with
risk of foot ulcers, amputation, Charcot joints, and
features of autonomic dysfunction, including sexual
dysfunction.
People with diabetes are at increased risk of
cardiovascular, peripheral vascular and
cerebrovascular disease.
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5. The development of diabetes is projected to reach
pandemic proportions over the next10-20 years.
International Diabetes Federation (IDF) data indicate that
by the year 2025, the number of people affected will reach
333 million –90% of these people will have Type 2
diabetes.
In most Western societies, the overall prevalence has
reached 4-6%, and is as high as 10-12% among 60-70-
year-old people.
The annual health costs caused by diabetes and its
complications account for around 6-12% of all health-care
expenditure.
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6. Type 1 Diabetes Mellitus
Type 2 Diabetes Mellitus
Gestational Diabetes
Other types:
LADA (
MODY (maturity-onset diabetes of youth)
Secondary Diabetes Mellitus
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7. Was previously called insulin-dependent diabetes
mellitus (IDDM) or juvenile-onset diabetes.
Type 1 diabetes develops when the body’s immune
system destroys pancreatic beta cells, the only cells
in the body that make the hormone insulin that
regulates blood glucose.
This form of diabetes usually strikes children and
young adults, although disease onset can occur at any
age.
Type 1 diabetes may account for 5% to 10% of all
diagnosed cases of diabetes.
Risk factors for type 1 diabetes may include
autoimmune, genetic, and environmental factors.
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8. Was previously called non-insulin-dependent diabetes
mellitus (NIDDM) or adult-onset diabetes.
Type 2 diabetes may account for about 90% to 95% of all
diagnosed cases of diabetes.
It usually begins as insulin resistance, a disorder in which
the cells do not use insulin properly. As the need for insulin
rises, the pancreas gradually loses its ability to produce
insulin.
Type 2 diabetes is associated with older age, obesity, family
history of diabetes, history of gestational diabetes, impaired
glucose metabolism, physical inactivity, and race/ethnicity.
African Americans, Hispanic/Latino Americans, American
Indians, and some Asian Americans and Native Hawaiians or
Other Pacific Islanders are at particularly high risk for type 2
diabetes.
Type 2 diabetes is increasingly being diagnosed in children
and adolescents.
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11. A form of glucose intolerance that is diagnosed in
some women during pregnancy.
Gestational diabetes occurs more frequently among
African Americans, Hispanic/Latino Americans, and
American Indians. It is also more common among
obese women and women with a family history of
diabetes.
During pregnancy, gestational diabetes requires
treatment to normalize maternal blood glucose levels
to avoid complications in the infant.
After pregnancy, 5% to 10% of women with gestational
diabetes are found to have type 2 diabetes.
Women who have had gestational diabetes have a
20% to 50% chance of developing diabetes in the next
5-10 years.
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12. Other specific types of diabetes result
from specific genetic conditions (such as
maturity-onset diabetes of youth), surgery,
drugs, malnutrition, infections, and other
illnesses.
Such types of diabetes may account for
1% to 5% of all diagnosed cases of
diabetes.
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13. Latent Autoimmune Diabetes in Adults (LADA) is a
form of autoimmune (type 1 diabetes) which is
diagnosed in individuals who are older than the usual
age of onset of type 1 diabetes.
Alternate terms that have been used for "LADA"
include Late-onset Autoimmune Diabetes of
Adulthood, "Slow Onset Type 1" diabetes, and
sometimes also "Type 1.5
Often, patients with LADA are mistakenly thought to
have type 2 diabetes, based on their age at the
time of diagnosis.
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15. About 80% of adults apparently with recently
diagnosed Type 2 diabetes but with GAD auto-
antibodies (i.e. LADA) progress to insulin
requirement within 6 years.
The potential value of identifying this group at high
risk of progression to insulin dependence
includes:
◦the avoidance of using metformin treatment
◦the early introduction of insulin therapy
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16. MODY – Maturity Onset Diabetes of the Young
MODY is a monogenic form of diabetes with an autosomal
dominant mode of inheritance:
◦Mutations in any one of several transcription factors or in the enzyme
glucokinase lead to insufficient insulin release from pancreatic ß-cells,
causing MODY.
◦Different subtypes of MODY are identified based on the mutated gene.
Originally, diagnosis of MODY was based on presence of non-
ketotic hyperglycemia in adolescents or young adults in
conjunction with a family history of diabetes.
However, genetic testing has shown that MODY can occur at
any age and that a family history of diabetes is not always
obvious.
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18. Within MODY, the different subtypes can essentially
be divided into 2 distinct groups: glucokinase MODY
and transcription factor MODY, distinguished by
characteristic phenotypic features and pattern on oral
glucose tolerance testing.
Glucokinase MODY requires no treatment, while
transcription factor MODY (i.e. Hepatocyte nuclear
factor -1alpha) requires low-dose sulfonylurea therapy
and PNDM (caused by Kir6.2 mutation) requires high-
dose sulfonylurea therapy.
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19. Secondary causes of Diabetes mellitus include:
Acromegaly,
Cushing syndrome,
Thyrotoxicosis,
Pheochromocytoma
Chronic pancreatitis,
Cancer
Drug induced hyperglycemia:
◦Atypical Antipsychotics - Alter receptor binding characteristics, leading to increased insulin
resistance.
◦Beta-blockers - Inhibit insulin secretion.
◦Calcium Channel Blockers - Inhibits secretion of insulin by interfering with cytosolic calcium
release.
◦Corticosteroids - Cause peripheral insulin resistance and gluconeogensis.
◦Fluoroquinolones - Inhibits insulin secretion by blocking ATP sensitive potassium channels.
◦Naicin - They cause increased insulin resistance due to increased free fatty acid mobilization.
◦Phenothiazines - Inhibit insulin secretion.
◦Protease Inhibitors - Inhibit the conversion of proinsulin to insulin.
◦Thiazide Diuretics - Inhibit insulin secretion due to hypokalemia. They also cause increased
insulin resistance due to increased free fatty acid mobilization.
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20. Prediabetes is a term used to distinguish people who are at
increased risk of developing diabetes. People with
prediabetes have impaired fasting glucose (IFG) or
impaired glucose tolerance (IGT). Some people may have
both IFG and IGT.
IFG is a condition in which the fasting blood sugar level is
elevated (100 to 125 milligrams per decilitre or mg/dL) after
an overnight fast but is not high enough to be classified as
diabetes.
IGT is a condition in which the blood sugar level is elevated
(140 to 199 mg/dL after a 2-hour oral glucose tolerance
test), but is not high enough to be classified as diabetes.
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21. Progression to diabetes among those with prediabetes is
not inevitable. Studies suggest that weight loss and
increased physical activity among people with
prediabetes prevent or delay diabetes and may return
blood glucose levels to normal.
People with prediabetes are already at increased risk for
other adverse health outcomes such as heart disease
and stroke.
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24. Research studies have found that lifestyle changes can
prevent or delay the onset of type 2 diabetes among high-
risk adults.
These studies included people with IGT and other high-risk
characteristics for developing diabetes.
Lifestyle interventions included diet and moderate-intensity
physical activity (such as walking for 2 1/2 hours each
week).
In the Diabetes Prevention Program, a large prevention
study of people at high risk for diabetes, the development
of diabetes was reduced 58% over 3 years.
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25. Studies have shown that medications have been successful in
preventing diabetes in some population groups.
In the Diabetes Prevention Program, people treated with the drug
metformin reduced their risk of developing diabetes by 31% over 3
years.
Treatment with metformin was most effective among younger, heavier
people (those 25-40 years of age who were 50 to 80 pounds
overweight) and less effective among older people and people who
were not as overweight.
Similarly, in the STOP-NIDDM Trial, treatment of people with IGT with
the drug acarbose reduced the risk of developing diabetes by 25% over
3 years.
Other medication studies are ongoing. In addition to preventing
progression from IGT to diabetes, both lifestyle changes and medication
have also been shown to increase the probability of reverting from IGT
to normal glucose tolerance.
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26. The major components of the treatment of
diabetes are:
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27. Diet is a basic part of management in every case.
Treatment cannot be effective unless adequate
attention is given to ensuring appropriate nutrition.
Dietary treatment should aim at:
◦ensuring weight control
◦providing nutritional requirements
◦allowing good glycaemic control with blood glucose
levels as close to normal as possible
◦correcting any associated blood lipid abnormalities
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28. The following principles are recommended as dietary
guidelines for people with diabetes:
Dietary fat should provide 25-35% of total intake of calories but
saturated fat intake should not exceed 10% of total energy. Cholesterol
consumption should be restricted and limited to 300 mg or less daily.
Protein intake can range between 10-15% total energy (0.8-1 g/kg of
desirable body weight). Requirements increase for children and during
pregnancy. Protein should be derived from both animal and vegetable
sources.
Carbohydrates provide 50-60% of total caloric content of the diet.
Carbohydrates should be complex and high in fibre.
Excessive salt intake is to be avoided. It should be particularly restricted
in people with hypertension and those with nephropathy.
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29. Physical activity promotes weight reduction and
improves insulin sensitivity, thus lowering blood
glucose levels.
Together with dietary treatment, a programme of
regular physical activity and exercise should be
considered for each person. Such a programme must
be tailored to the individual’s health status and fitness.
People should, however, be educated about the
potential risk of hypoglycaemia and how to avoid it.
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30. There are currently four classes of oral anti-
diabetic agents:
i. Biguanides
ii. Insulin Secretagogues – Sulphonylureas
iii. Insulin Secretagogues – Non-sulphonylureas
iv. α-glucosidase inhibitors
v. Thiazolidinediones (TZDs)
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31. If glycaemic control is not achieved (HbA1c > 6.5%
and/or; FPG > 7.0 mmol/L or; RPG >11.0mmol/L) with
lifestyle modification within 1 –3 months, ORAL ANTI-
DIABETIC AGENT should be initiated.
In the presence of marked hyperglycaemia in newly
diagnosed symptomatic type 2 diabetes (HbA1c > 8%,
FPG > 11.1 mmol/L, or RPG > 14 mmol/L), oral anti-
diabetic agents can be considered at the outset
together with lifestyle modification.
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32. As first line therapy:
Obese type 2 patients, consider use of metformin, acarbose or
TZD.
Non-obese type 2 patients, consider the use of metformin or
insulin secretagogues
Metformin is the drug of choice in overweight/obese patients.
TZDs and acarbose are acceptable alternatives in those who are
intolerant to metformin.
If monotherapy fails, a combination of TZDs, acarbose and
metformin is recommended. If targets are still not achieved,
insulin secretagogues may be added
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33. Combination oral agents is indicated in:
Newly diagnosed symptomatic patients with
HbA1c >10
Patients who are not reaching targets after 3
months on monotherapy
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34. If targets have not been reached after optimal dose of combination
therapy for 3 months, consider adding intermediate-acting/long-acting
insulin (BIDS).
Combination of insulin+ oral anti-diabetic agents (BIDS) has been
shown to improve glycaemic control in those not achieving target
despite maximal combination oral anti-diabetic agents.
Combining insulin and the following oral anti-diabetic agents has been
shown to be effective in people with type 2 diabetes:
◦Biguanide (metformin)
◦Insulin secretagogues (sulphonylureas)
◦Insulin sensitizers (TZDs)(the combination of a TZD plus insulin is not an approved
indication)
◦α-glucosidase inhibitor (acarbose)
Insulin dose can be increased until target FPG is achieved.
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Diabetes
Management
Algorithm

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37. In elderly non-obese patients, short acting insulin secretagogues can be
started but long acting Sulphonylureas are to be avoided. Renal
function should be monitored.
Oral anti-diabetic agent s are not recommended for diabetes in
pregnancy
Oral anti-diabetic agents are usually not the first line therapy in diabetes
diagnosed during stress, such as infections. Insulin therapy is
recommended for both the above
Targets for control are applicable for all age groups. However, in
patients with co-morbidities, targets are individualized
When indicated, start with a minimal dose of oral anti-diabetic agent,
while reemphasizing diet and physical activity. An appropriate duration
of time (2-16 weeks depending on agents used) between increments
should be given to allow achievement of steady state blood glucose
control
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38. Short-term use:
Acute illness, surgery, stress and emergencies
Pregnancy
Breast-feeding
Insulin may be used as initial therapy in type 2 diabetes
in marked hyperglycaemia
Severe metabolic decompensation (diabetic ketoacidosis, hyperosmolar
nonketotic coma, lactic acidosis, severe hypertriglyceridaemia)
Long-term use:
If targets have not been reached after optimal dose of combination
therapy or BIDS, consider change to multi-dose insulin therapy. When
initiating this,insulin secretagogues should be stopped and insulin
sensitisers e.g. Metformin or TZDs, can be continued.
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39. The majority of patients will require more than one daily injection if
good glycaemic control is to be achieved. However, a once-daily
injection of an intermediate acting preparation may be effectively
used in some patients.
Twice-daily mixtures of short- and intermediate-acting insulin is a
commonly used regimen.
 In some cases, a mixture of short- and intermediate-acting
insulin may be given in the morning. Further doses of short-acting
insulin are given before lunch and the evening meal and an evening
dose of intermediate-acting insulin is given at bedtime.
Other regimens based on the same principles may be used.
A regimen of multiple injections of short-acting insulin before the main
meals, with an appropriate dose of an intermediate-acting insulin given
at bedtime, may be used, particularly when strict glycaemic control is
mandatory.
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42. Patients should be educated to practice self-care.
This allows the patient to assume responsibility and
control of his / her own diabetes management. Self-
care should include:
◦Blood glucose monitoring
◦Body weight monitoring
◦Foot-care
◦Personal hygiene
◦Healthy lifestyle/diet or physical activity
◦Identify targets for control
◦Stopping smoking
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43. The complications of diabetes mellitus are far less common and less
severe in people who have well-controlled blood sugar levels.
Wider health problems accelerate the deleterious effects of diabetes. These
include smoking, elevated cholesterol levels, obesity,high blood pressure,
and lack of regular exercise.
1.Acute
◦1.1Diabetic ketoacidosis
◦1.2Hyperglycemia hyperosmolar state
◦1.3Hypoglycemia
◦1.4Diabetic coma
◦1.5Respiratory infections
◦1.6Periodontal disease
2.Chronic
◦2.1Mechanisms of chronic complications
◦2.2Examples of chronic complications
3.Statistics
4.Management
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44. Acute
Diabetic ketoacidosis
Diabetic ketoacidosis (DKA) is an acute and dangerous complication that is always a medical
emergency and requires prompt medical attention. Low insulin levels cause the liver to turn fatty
acid to ketone for fuel (i.e., ketosis); ketone bodies are intermediate substrates in that metabolic
sequence. This is normal when periodic, but can become a serious problem if sustained.
Elevated levels of ketone bodies in the blood decrease the blood's pH, leading to DKA. On
presentation at hospital, the patient in DKA is typically dehydrated, and breathing rapidly and
deeply. Abdominal pain is common and may be severe. The level of consciousness is typically
normal until late in the process, when lethargy may progress to coma. Ketoacidosis can easily
become severe enough to cause hypotension, shock, and death. Urine analysis will reveal
significant levels of ketone bodies (which have exceeded their renal threshold blood levels to
appear in the urine, often before other overt symptoms). Prompt, proper treatment usually results
in full recovery, though death can result from inadequate or delayed treatment, or from
complications (e.g., brain edema). Ketoacidosis is much more common in type 1 diabetes than
type 2.
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45. Hypoglycemia
Hypoglycemia, or abnormally low blood glucose, is an acute complication of several diabetes treatments. It is rare
otherwise, either in diabetic or non-diabetic patients. The patient may become agitated, sweaty, weak, and have
many symptoms of sympathetic activation of the autonomic nervous system resulting in feelings akin to dread
and immobilized panic. Consciousness can be altered or even lost in extreme cases, leading to coma, seizures,
or even brain damage and death. In patients with diabetes, this may be caused by several factors, such as too
much or incorrectly timed insulin, too much or incorrectly timed exercise (exercise decreases insulin
requirements) or not enough food (specifically glucose containing carbohydrates). The variety of interactions
makes cause identification difficult in many instances.
It is more accurate to note that iatrogenic hypoglycemia is typically the result of the interplay of absolute (or
relative) insulin excess and compromised glucose counterregulation in type 1 and advanced type 2 diabetes.
Decrements in insulin, increments in glucagon, and, absent the latter, increments in epinephrine are the primary
glucose counterregulatory factors that normally prevent or (more or less rapidly) correct hypoglycemia. In insulin-
deficient diabetes (exogenous) insulin levels do not decrease as glucose levels fall, and the combination of
deficient glucagon and epinephrine responses causes defective glucose counterregulation.
Furthermore, reduced sympathoadrenal responses can cause hypoglycemia unawareness. The concept of
hypoglycemia-associated autonomic failure (HAAF) in diabetes posits that recent incidents of hypoglycemia
causes both defective glucose counterregulation and hypoglycemia unawareness. By shifting glycemic thresholds
for the sympathoadrenal (including epinephrine) and the resulting neurogenic responses to lower plasma glucose
concentrations, antecedent hypoglycemia leads to a vicious cycle of recurrent hypoglycemia and further
impairment of glucose counterregulation. In many cases (but not all), short-term avoidance of hypoglycemia
reverses hypoglycemia unawareness in affected patients, although this is easier in theory than in clinical
experience.
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46. Hyperglycemia hyperosmolar state
Hyperosmolar nonketotic state (HNS) is an acute complication sharing
many symptoms with DKA, but an entirely different origin and different
treatment. A person with very high (usually considered to be above
300 mg/dl (16 mmol/L)) blood glucose levels, water is osmotically drawn
out of cells into the blood and the kidneys eventually begin to dump
glucose into the urine. This results in loss of water and an increase in
blood osmolarity. If fluid is not replaced (by mouth or intravenously), the
osmotic effect of high glucose levels, combined with the loss of water,
will eventually lead to dehydration. The body's cells become
progressively dehydrated as water is taken from them and excreted.
Electrolyte imbalances are also common and are always dangerous. As
with DKA, urgent medical treatment is necessary, commonly beginning
with fluid volume replacement. Lethargy may ultimately progress to a
coma, though this is more common in type 2 diabetes than type 1.
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47. Diabetic coma
Diabetic coma is a medical emergency in which a person with diabetes mellitus is comatose
 (unconscious) because of one of the acute complications of diabetes:
Severe diabetic hypoglycemia
Diabetic ketoacidosis advanced enough to result in unconsciousness from a combination of
severe hyperglycemia, dehydration and shock, and exhaustion
Hyperosmolar nonketotic coma in which extreme hyperglycemia and dehydration alone are
sufficient to cause unconsciousness.
In most medical contexts, the term diabetic coma refers to the diagnostical dilemma posed when
a physician is confronted with an unconscious patient about whom nothing is known except that
he has diabetes. An example might be a physician working in an emergency department who
receives an unconscious patient wearing a medical identification tag saying DIABETIC. 
Paramedics may be called to rescue an unconscious person by friends who identify him as
diabetic. Brief descriptions of the three major conditions are followed by a discussion of the 
diagnostic process used to distinguish among them, as well as a few other conditions which must
be considered.
An estimated 2 to 15 percent of diabetics will suffer from at least one episode of diabetic coma in
their lifetimes as a result of severe hypoglycemia.
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48. Respiratory infections
The immune response is impaired in individuals with diabetes mellitus. Cellular
studies have shown that hyperglycemia both reduces the function of immune
cells and increases inflammation. The vascular effects of diabetes also tend to
alter lung function, all of which leads to an increase in susceptibility to
respiratory infections such as pneumonia and influenza among individuals with
diabetes. Several studies also show diabetes associated with a worse disease
course and slower recovery from respiratory infections.
Periodontal disease
Diabetes is associated with periodontal disease (gum disease) and may make
diabetes more difficult to treat.[6] Gum disease is frequently related to bacterial
infection by organisms such as Porphyromonas gingivalis and Actinobacillus
actinomycetemcomitans. A number of trials have found improved blood sugar
levels in type 2 diabetics who have undergone peridontal treatment.
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49. Chronic
Mechanisms of chronic complications
Chronic elevation of blood glucose level leads to damage of blood vessels (angiopathy). The 
endothelial cells lining the blood vessels take in more glucose than normal, since they do not
depend on insulin. They then form more surface glycoproteins than normal, and cause the
basement membrane to grow thicker and weaker. In diabetes, the resulting problems are
grouped under "microvascular disease" (due to damage to small blood vessels) and "
macrovascular disease" (due to damage to the arteries).
However, some research challenges the theory of hyperglycemia as the cause of diabetic
complications. The fact that 40% of diabetics who carefully control their blood sugar nevertheless
develop neuropathy,
[8]
 requires explanation. It has been discovered that the serum of diabetics
with neuropathy is toxic to nerves even if its blood sugar content is normal.
[9]
 Recent research
suggests that in type 1 diabetics, the continuing autoimmune disease which initially destroyed
the beta cells of the pancreas may also cause retinopathy,
[10]
 neuropathy,
[11]
and nephropathy.
[12]
 One researcher has even suggested that retinopathy may be better treated by drugs to
suppress the abnormal immune system of diabetics than by blood sugar control.
[13]
 The familial
clustering of the degree and type of diabetic complications
[14]
 indicates that genetics may also play
a role in causing complications such as diabetic retinopathy
[15]
 and nephropathy.
[16]
 Non-diabetic
offspring of type 2 diabetics have been found to have increased arterial stiffness and neuropathy
despite normal blood glucose levels,
[17]
 and elevated enzyme levels associated with diabetic renal
disease have been found in non-diabetic first-degree relatives of diabetics
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50. Examples of chronic complications
The damage to small blood vessels leads to a microangiopathy, which can cause one or more of
the following:
Diabetic cardiomyopathy, damage to the heart muscle, leading to impaired relaxation and filling
of the heart with blood (diastolic dysfunction) and eventually heart failure; this condition can
occur independent of damage done to the blood vessels over time from high levels of blood
glucose.
[24]
Diabetic nephropathy, damage to the kidney which can lead to chronic renal failure, eventually
requiring dialysis. Diabetes mellitus is the most common cause of adult kidney failure in the
developed world.
Diabetic neuropathy, abnormal and decreased sensation, usually in a 'glove and stocking'
distribution starting with the feet but potentially in other nerves, later often fingers and hands.
When combined with damaged blood vessels this can lead to diabetic foot (see below). Other
forms of diabetic neuropathy may present as mononeuritis or autonomic neuropathy. 
Diabetic amyotrophy is muscle weakness due to neuropathy.
Diabetic retinopathy, growth of friable and poor-quality new blood vessels in the retina as well as 
macular edema (swelling of the macula), which can lead to severe vision lossor blindness.
Retinal damage (from microangiopathy) makes it the most common cause of blindness among
non-elderly adults in the US.
Diabetic encephalopathy
[25]
 is the increased cognitive decline and risk of dementia- including (but
not limited to) the Alzheimer's type- observed in diabetes. Various mechanisms are proposed,
including alterations to the vascular supply of the brain and the interaction of insulin with the
brain itself.
[26][27]
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51. Examples of chronic complications
Macrovascular disease leads to cardiovascular disease, to which accelerated atherosclerosis is a contributor:
Coronary artery disease, leading to angina or myocardial infarction ("heart attack")
Diabetic myonecrosis ('muscle wasting')
Peripheral vascular disease, which contributes to intermittent claudication (exertion-related leg and foot pain) as well as
diabetic foot.
[28]
Stroke (mainly the ischemic type)
Diabetic foot, often due to a combination of sensory neuropathy (numbness or insensitivity) and vascular damage,
increases rates of skin ulcers (diabetic foot ulcers) andinfection and, in serious cases, necrosis and gangrene. It is why
diabetics are prone to leg and foot infections and why it takes longer for them to heal from leg and foot wounds. It is the
most common cause of non-traumatic adult amputation, usually of toes and or feet, in the developed world.
[28]
Carotid artery stenosis does not occur more often in diabetes, and there appears to be a lower prevalence of 
abdominal aortic aneurysm. However, diabetes does cause higher morbidity, mortality and operative risks with these
conditions.
[29]
In the developed world, diabetes is the most significant cause of adult blindness in the non-elderly and the leading cause of
non-traumatic amputation in adults, and diabetic nephropathy is the main illness requiring renal dialysis in the United States.
[30]
A review of type 1 diabetes came to the result that, despite modern treatment, women with diabetes are at increased risk of 
female infertility, such as reflected by delayed puberty and menarche, menstrual irregularities (especially oligomenorrhoea),
mild hyperandrogenism, polycystic ovarian syndrome, fewer live born children and possibly earliermenopause.
[31]
 Animal
models indicate that abnormalities on the molecular level caused by diabetes include defective leptin, insulin and kisspeptin
 signalling.
[31]
Restrictive lung defect is known to be associated with diabetes. Lung restriction in diabetes could result from chronic low-
grade tissue inflammation, microangiopathy, and/or accumulation of advanced glycation end products.
[32]
 In fact the presence
restrictive lung defect in association with diabetes has been shown even in presence of obstructive lung diseases like
asthma and copd in diabetic patients.
[33]
Lipohypertrophy may be caused by insulin therapy. Repeated insulin injections at the same site, or near to, causes an
accumulation of extra subcutaneous fat and may present as a large lump under the skin. It may be unsightly, mildly painful,
and may change the timing or completeness of insulin action.
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52. Statistics
In the United States, there were approximately 675,000 diabetes-related emergency department (ED) visits in
2010 that involved neurological complications, 409,000 ED visits with kidney complications, and 186,000 ED
visits with eye complications.
Management
Modulating and ameliorating diabetic complications may in turn improve the overall quality of life for diabetic
patients. For example; when elevated blood pressure was tightly controlled, diabetic related deaths were reduced
by 32% compared to those with less controlled blood pressure. Many observational and clinical studies had been
conducted to investigate the role of several vitamins on diabetic complications, the results of these studies
elevated a suggested beneficial role of vitamins on diabetic complications. In the First National Health and
Nutrition Examination Survey (NHANES I)
Epidemiologic Follow-up Study, vitamin supplementations were observed to be associated with 24% reduction on
the risk of diabetes was observed during 20 years of follow-up. Many observational studies and clinical trials have
linked several vitamins with the pathological process of diabetes; these vitamin include folate, thiamine, β-
carotene, and vitamin E, C,B12, and D.
However, numerous researches had been shown inconsistent results about the roles of vitamins on diabetic risk
and complications. Most of these researches performed to investigate effect of individual vitamin without looking
to status of other vitamins. Even though, it is expected that vitamin(s) supplementation might be more effective
and might induce a beneficial role on diabetic process when deficiency exists.
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53. Thiamine: Thiamine acts as an essential cofactor in glucose metabolism,therefore, it may modulate diabetic
complications by controlling glycemic status in diabetic patients.
[46][47]
 Additionally, deficiency of thiamine was
observed to be associated with dysfunction of β-cells and impaired glucose tolerance.
[47]
 
Different studies indicated possible role of thiamin supplementation on the prevention or reversal of early stage
diabetic nephropathy,
[48][49]
 as well as significant improvement on lipid profile.
[47]
vitamin B12: Low serum B12 level is common finding in diabetic patients especially those taking Metformin or
advanced age patients.
[50]
 
Vitamin B12 deficiency has been linked to two diabetic complications; atherosclerosis and diabetic neuropathy.
Folic acid: Low plasma concentrations of folic acid were found to be associated with high plasma homocysteine
concentrations.
Antioxidants: Three vitamins, ascorbic acid; α-tocopherol; and β-carotene, are well recognized for their
antioxidant activities in human.
[38]
 Free radical-scavenging ability of antioxidants may reduce the oxidative stress
and thus may protect against oxidative damage.
[
 improving lipid metabolism and insulin-mediated glucose disposal, as well as by enhancing endothelial function.
[38]
[59][60]
 In addition to its antioxidant capacity, vitamin C has been proposed to induce beneficial effects on diabetes by
two other mechanisms. Firstly; vitamin C may replace the glucose in many chemical reactions due to their
similarity in structure, thus, it may prevent the non-enzymatic glycosylation of proteins,
[44]
 and therefore it might
reduce glycated hemoglobin (HbA1c) levels.
Secondly, vitamin C has also been suggested to play an important role in lipid regulation as a controller of
catabolism of cholesterol to bile acid.

Vitamin D: The insufficiency of vitamin D is a common finding in diabetic patients.
[39]
 Observational studies showed
that serum vitamin D is inversely associated with biomarkers of diabetes; impaired insulin secretion, insulin
resistance, and glucose intolerance.
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54. National Diabetes Fact Sheet 2003, DEPARTMENT OF HEALTH AND HUMAN SERVICES Centres for Disease Control
and Prevention
World Health Organization. Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications. Report of WHO.
Department of Non-communicable Disease Surveillance. Geneva 1999
Academy of Medicine. Clinical Practice Guidelines. Management of type 2 diabetes mellitus. MOH/P/PAK/87.04(GU), 2004
NHS. Diabetes - insulin initiation - University Hospitals of Leicester NHS Trust Working in partnership with PCTs across
Leicestershire and Rutland, May 2008.
https://en.wikipedia.org/wiki/Compl
ications_of_diabetes_mellitus
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55. Thank You
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