Clinical presentations, investigations and management

1. DIABETES MELLITUS
CLINICAL PRESENTATION, INVESTIGATIONS AND
TREATMENT
BY
DR. HOPE INEGBENOSUN

2. OUTLINE
 Introduction
 Epidemiology
 Classification of diabetes mellitus
 Prediabetes: Impaired glucose tolerance and Impaired fasting glucose
 Clinical presentation
 Initial assessment – History taking and examination
 Investigations
 Diagnostic criteria
 General objective of diabetes management
 Management of diabetes mellitus
 Complications of diabetes mellitus
 Conclusion
 References

3. INTRODUCTION
o 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.
o The effects of diabetes mellitus include long–term damage,
dysfunction and failure of various organs.

4. EPIDEMIOLOGY
 The worldwide prevalence of diabetes has continued to increase
dramatically. Globally, as of 2011, an estimated 366 million people had DM,
with type 2 making up about 90% of the cases [Chen L, et al, 2014].
 The worldwide prevalence of DM was 425 million in 2017 [Carrillo-Larco RM, et al,
2019].
 The prevalence of DM in Nigeria has increased from 2.2% as reported by
Akinkugbe in 1997 from a national survey to 5.0% by 2013 estimates of the
International Diabetes Federation (IDF) [Akinkugbe OO, 1997 & IDF, 2013].
 The prevalence of DM in South Western Nigeria is 4.76% with 2.38% as
undiagnosed DM [Oyegbade OO, et al, 2007].
 The prevalence of undiagnosed DM in Edo state is 4.5% [Ojehanon PI, Akhionbare O,
2006].

5. CLASSIFICATION OF DIABETES MELLITUS
I. Primary (No associated disease present)
A. Type 1 DM – formerly Insulin Dependent Diabetes Mellitus (IDDM)
• Immune mediated
• Idiopathic (or Type 1b DM)
LADA (latent autoimmune diabetes in adults)
B. Type 2 DM - formerly Non-insulin Dependent Diabetes Mellitus
(NIDDM)
• Non- Autoimmune

6. II. Secondary diabetes (identifiable
disease/conditions present)
A. Genetic defects in β-cell function
1. Chromosome 12, HNF-1α (MODY 3)
2. Chromosome 7, glycosidase (MODY 2)
3. Chromosome 20, HNF-4α (MODY 1)
4. Mitochondrial DNA
5. Monogenic diabetes
B. Genetic defects in insulin action
1. Type A insulin resistance
2. Leprechaunism
3. Rabson-Mendenhall syndrome
4. Lipotrophic diabetes
C. Disease of the exocrine pancreas
1. Pancreatitis
2. Pancreatectomy/trauma
3. Neoplasia
4. Cystic fibrosis
5. Hemochromatosis
6. Fibrocalcific pancreatopathy
D. Endocrinopathies
1. Acromegaly
2. Cushing syndrome
3. Glucagonoma
4. Pheochromocytoma
5. Hyperthyroidism
6. Somatostatinoma
7. Aldosteronoma
E. Pharmacologically or chemically induced
1. Vacor
2. Pentamidine
3. Nicotinic acid
4. Glucocorticoids
5. Thyroid hormones
6. Diazoxide
7. β-adrenergic agonists
8. Thiazides
9. Dilantin
10. α interferon
F. Infections
1. Congenital rubeola
2. Cytomegalovirus
G. Infrequent forms of autoimmune diabetes
1. Stiff-man syndrome
2. Antibodies against insulin receptors
H. Other syndromes occasionally associated with diabetes
1. Down syndrome
2. Klinefelter syndrome
3. Turner syndrome
4. Wolfram syndrome
5. Friedreich ataxia
6. Huntington’s chorea
7. Lawrence-Moon-Biedel syndrome
8. Myotonic dystrophy
9. Porphyria
10. Prader-Willi syndrome
III. Gestational diabetes

7. TYPE 1 DIABETES
o Was previously called insulin-dependent diabetes mellitus (IDDM) or
juvenile-onset diabetes.
o 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.
o This form of diabetes usually strikes children and young adults,
although disease onset can occur at any age.
o Type 1 diabetes may account for 5% to 10% of all diagnosed cases
of diabetes.
o Risk factors for type 1 diabetes may include autoimmune, genetic,
and environmental factors.

8. o 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.
o 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“.
o Often, patients with LADA are mistakenly thought to have type 2 diabetes,
based on their age at the time of diagnosis.
o LADA is associated with slower loss of beta cell function. Rapid failure of
oral anti-diabetics is to be expected. Analysis of GAD antibodies is
recommended for cases of suspicion of LADA.
LADA

10. TYPE 2 DIABETES
o Was previously called non-insulin-dependent diabetes mellitus
(NIDDM) or adult-onset diabetes.
o Type 2 diabetes may account for about 90% to 95% of all diagnosed
cases of diabetes.
o 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.

11. o 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.
o 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.

12. PATHOPHYSIOLOGY

13. DIFFERENTIAL DIAGNOSTIC CRITERIA FOR TYPE 1 AND TYPE 2 DIABETES.
Type 1 Diabetes Type 2 Diabetes
Manifestation age Usually but not always before 30
years old
Often above 35 years old, though recently
occurring more often in youth
Onset Acute to subacute Usually gradual
Symptoms Frequently polyuria, polydipsia,
weight loss, fatigue
Frequently no complaints
Body weight Usually normal Usually overweight
Predisposition to ketosis Pronounced None or only slight
Insulin secretion Reduced or none Below normal to high, qualitatively always
impaired
Insulin resistance None (or only low) Often pronounced
Concordance with
identical twins
30 to 50 % Over 50 %
Heredity Multifactorial (polygenetic) Multifactorial (most likely polygenetic, but
genetic heterogeneity is possible)

14. Association with HLA (human
leukocyte antigen)
system
Present Not present
Antibodies associated with
diabetes
Approx. 90-95 % at onset
(GAD, ICA, IA-2, IAA)
None
Metabolism Unstable Stable
Response to insulin secretion
stimulating antidiabetics
Usually none Usually good at first
Insulin therapy Required Usually not required until
insulin secretion has
decreased after years of
disease

15.  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.
MODY

17.  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.
MODY (CONT.)

18. GESTATIONAL DIABETES
o A form of glucose intolerance that is diagnosed in some women
during pregnancy.
o 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.
o During pregnancy, gestational diabetes requires treatment to
normalize maternal blood glucose levels to avoid complications in
the infant and mother.
o After pregnancy, 5% to 10% of women with gestational diabetes are
found to have type 2 diabetes.

19. o Atypical Antipsychotics - Alter receptor binding characteristics, leading to increased
insulin resistance.
o Beta-blockers - Inhibit insulin secretion.
o Calcium Channel Blockers - Inhibits secretion of insulin by interfering with cytosolic
calcium release.
o Corticosteroids - Cause peripheral insulin resistance and gluconeogensis.
o Fluoroquinolones - Inhibits insulin secretion by blocking ATP sensitive potassium
channels.
o Niacin - They cause increased insulin resistance due to increased free fatty acid
mobilization.
o Phenothiazines - Inhibit insulin secretion.
o Protease Inhibitors - Inhibit the conversion of proinsulin to insulin.
o Thiazide Diuretics - Inhibit insulin secretion due to hypokalemia. They also cause
increased insulin resistance due to increased free fatty acid mobilization.
DRUG INDUCED HYPERGLYCEMIA

20. PREDIABETES: IMPAIRED GLUCOSE TOLERANCE AND
IMPAIRED FASTING GLUCOSE
 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 plasma sugar level is elevated
(100 to 125mg/dL) after an overnight fast but is not high enough to be
classified as diabetes.
 IGT is a condition in which the plasma 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.

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.

22. CLINICAL PRESENTATION
 Most of the symptoms are similar in both
types of diabetes but they vary in their
degree and develop more rapidly in type 1
diabetes and more typical.
 Symptoms of type 2 diabetes are insidious lin production usually
because insulin production decreases
over time.
 Common symptoms include:
 Polyuria, increased thirst and nocturia –
due to hyperglycemia
 Fatigue – due to the inability to use glucose
as an energy source

23.  These symptoms are usually accompanied by a rapid unhealthy
weight loss due to the breakdown of protein and fat as an alternative
energy source
 Blurred vision, caused by a change in lens refraction, may occur.
 Some patients also experience infections – especially Candida spp
and urinary tract infections – because raised serum glucose impairs
phagocyte function and provides a growth medium in which micro-
organisms can flourish.

24.  Undiagnosed diabetic patients often present at first with diabetic
complications as a result of sustained hyperglycemia (e.g
cardiovascular or renal disease); or retinopathy might be the first
symptom detected during a routine opthalmological examination.
 Patients with neuropathy, peripheral vascular disease and infection
could present with non-healing lower limb ulceration
 In acute cases, they can present with hyperosmolar non-ketotic
hyperglycemia or diabetic ketoacidosis.

25. INITIAL ASSESSMENT – HISTORY TAKING
 A full history is needed. In addition to the presenting symptoms,
emphasis should be placed on:
 Risk factors of cardiovascular diseases, such as smoking,
hypertension, obesity, hyperlipidaemia and family history
 Symptoms of cardiovascular complications including angina, heart
failure and claudication
 Visual symptoms
 Symptoms of neuropathic complications such as numbness, pain,
muscle weakness, gastrointestinal symptoms including diarrhoea,
impotence and bladder dysfunction
 Drug history
 Gestational history.

26. EXAMINATION
 A complete examination is part of the minimum requirements.
Certain aspects of the physical examination should receive special
attention. These include:
 Height and weight measurements
 Blood pressure (lying and standing positions to detect postural
change)
 Cardiovascular examination for abnormal signs and assessment of
peripheral pulses
 Examination of the lower limbs for peripheral pulses, sensation,
ankle jerk and foot lesions
 Ophthalmoscopy with dilated pupils.

27. INVESTIGATIONS
A. DIAGNOSTIC TESTS
1. Fasting plasma glucose test
2. Random plasma glucose test
3. Oral glucose tolerance test
4. Glycated haemoglobin (HbA1c)*
5. Urine glucose - +ve result, suggestive not diagnostic
6. Urine ketones -+ve result, marker of insulin deficiency & potential DKA
7. Random C-peptide test – Measures pancreatic cell function. A C-peptide
level of less than 0.2 nmol/L is associated with a diagnosis of T1DM
8. Autoantibodies to β cell test
B. MONITORING TESTS
1. Glycated haemoglobin (HbA1c)
2. Fructosamine/Glycated albumin test
* ADA 2010 recommendation

28. INVESTIGATIONS (CONT.)
C. OTHERS
1. Urinary albumin excretion - Slightly increased albumin excretion rate (AER), referred
to as microalbuminuria, is an indicator of risk for diabetic nephropathy.
2. Renal function test – to rule out already existing renal dysfunction before
administration of metformin and also to rule out diabetic nephropathy
3. Thyroid function test - Untreated thyroid disease interfere with DM management
4. Lipid profiles - Hyperlipidemia is common with poor metabolic control
5. Serum creatinine measurement in all hypertensive patients and those with proteinuria
6. Arterial blood gas – only indicated when urine ketones is +ve
7. Baseline stress test - may be indicated (especially older adults with 2 or more risk
factors for CAD)
8. Electrocardiography

29. Oral glucose tolerance test pursuant to WHO guidelines
 When random plasma glucose test is 160-200 mg/dl and the fasting plasma
test is 110-125 mg/dl, then this test is conducted.
 75g OGTT must be performed in the morning after 10 – 16 hours abstention
from nutrients (and alcohol) after at least 3 days of a diet rich in
carbohydrates (≥ 150 g carbohydrates per day) while sitting or lying down
(no muscular effort), no smoking before or during the test
 At time 0, patient drink 75 g glucose (or equivalent quantity of hydrolysed
starch) dissolved in 250 – 300 ml water within 5 minutes.
 Blood samples are taken at times 0 and 120 minutes.
 A fasting level of 126 mg/dl or greater and two hour glucose level of 200
mg/dl or higher confirms a diabetes diagnosis.

30. Glycated hemoglobin
 The life span of hemoglobin in vivo is 90 to 120 days during this time
glycated hemoglobin A forms.
 A1C test provide a retrospective measure of average blood glucose
concentration over a period of 2 to 3 months
 The A1C has several advantages to the FPG and OGTT, including greater
convenience (fasting not required), greater preanalytical stability, and less
day-to-day pertubations during stress and illness.
 These advantages must be balanced by greater cost, the limited availability
of A1C testing in certain regions of the developing world and the incomplete
correlation between A1C and average glucose in certain individuals.

31.  It is important to take age and race/ethnicity into consideration when
using the A1C to diagnose diabetes.
 The epidemiological studies that formed the framework for
recommending A1C to diagnose diabetes only included adult
populations.
 Therefore it remain unclear if the same A1C cut points should be used
to diagnose diabetes in children and adolescents [Nowicka P et al, 2011].
 Recent epidemiological study showed that African Americans had
higher A1C levels than non-Hispanic whites despite similar fasting and
post-glucose load levels [Ziemer DC et al, 2010].

32. Conditions which can lead to an inaccurate measurement of the HbA1c
level.
1. Haemoglobin variants (HbS, HbE, HbF, HbC, HbD and others)
2. Conditions with increased or decreased lifetime of the erythrocytes
(haemolytic anaemia, iron deficiency anaemia, blood formation in the context
of anaemia treatment, liver disease, kidney disease)
3. Chemical modifications of haemoglobin
Uraemia (carbamylated Hb), high dosage long-time therapy with
acetylsalicylic acid (acetylated Hb)
4. In conditions associated with increased red cell turnover, such as pregnancy,
recent blood loss or transfusion, erythropoietin therapy.
5. Inhibition of glycation (e. g. long-time therapy with ascorbic acid or Vit. E)

33. DIAGNOSTIC CRITERIA
ADA CRITERIA FOR DIAGNOSIS OF DIABETES
A1C ≥ 6.5%. This test should be performed in a laboratory using a method that is NGSP
certified and standardized to the DCCT assay.*
OR
FPG ≥ 126mg/dl (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8h.*
OR
2-h PG ≥ 200mg/dL (11.1 mmol/L) during an OGTT. This test should be performed as
prescribed by the WHO, using a glucose load containing the equivalent of 75g anhydrous
glucose dissolved in water.*
OR
In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a RPG ≥
200mg/dL (11.1mmol/L)
* In the absence of unequivocal hyperglycemia, results should be confirmed by at least one additional
result, obtained on another day. [ADA, 2010]

34. GENERAL OBJECTIVES OF DIABETES MANAGEMENT
1. To relieve symptoms
2. To correct associated health problems and to reduce morbidity,
mortality and economic costs of diabetes
3. To prevent as much as possible acute and long-term complications; to
monitor the development of such complications and to provide timely
intervention
4. To improve the quality of life and productivity of the individual with
diabetes

35. MANAGEMENT OF DM
 The major components of the treatment of diabetes are:

36.  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
DIET

37. 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.

38.  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.
EXERCISE

39. ORAL ANTI-DIABETIC AGENTS
Drug Class Drug Name Brand Name Mechanism of Action
Biguanide Metformin Diabetmin®
Glucophage®
Diamet®
Decreases hepatic glucose output
Sulphonyureas
(Second
generation)
Gilbenclamide
(Glyburide in US
and Canada)
Chlorpropamide
Gliclazide
Glimepiride
Glipizide
Clamide®
Glucotrol®
Diabeta®
Glynase PresTab®
Micronase®
Amaryl®
Stimulates insulin secretion by pancreatic
beta cells
Meglitinides Rapaglinide
Nateglinide
Prandin®
Starlix®
Stimulates insulin secretion by pancreatic
beta cells
Thiazolidinediones
(or glitazones)
Pioglitazone
Rosiglitazone
Actos®
Avandia®
They increase the sensitivity of muscle, fat
and liver to endogenous and exogenous
insulin (“Insulin sensitizers”)
Alpha-glucosidase
inhibitors
Acarbose
Miglitol
Precose®
Glyset®
Reduce the rate of digestion of
polysacharrides in the proximal small
intestine

40.  If glycaemic control is not achieved (HbA1c > 6.5% and/or; FPG > 7.0
mmol/L or; RPG >11.1mmol/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.
ORAL AGENT MONOTHERAPY

41. 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 metformin, acarbose or TZDs is
recommended. If targets are still not achieved, insulin secretagogues may be
added

42. Combination oral agents is indicated in:
 Newly diagnosed symptomatic patients with HbA1c >10%
 Patients who are not reaching targets after 3 months on monotherapy
COMBINATION ORAL AGENTS

43. o If targets have not been reached after optimal dose of combination therapy for
3 months, consider adding intermediate-acting/long-acting insulin.
o Combination of insulin + oral anti-diabetic agents has been shown to improve
glycaemic control in those not achieving target despite maximal combination
oral anti-diabetic agents.
o Insulin dose can be increased until target FPG is achieved.
COMBINATION OF ORAL AGENTS AND INSULIN

45. o 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.
o Twice-daily mixtures of short- and intermediate-acting insulin is a commonly used regimen
(Split-mix regimen).
o 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.
o In basal-bolus regimen, a single dose Glargine is given in the evening with twice or thrice a
day short acting
o 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.
INSULIN REGIMENS

46. OVERVIEW OF INSULIN AND ACTION

47. Diabetes
Management
Algorithm

48. METABOLIC AND VASCULAR COMPLICATIONS OF
DIABETES
ACUTE COMPLICATIONS
 Hypoglycemia (≤ 72mg/dL/4mmol/L)
 Hyperglycemic crises
 Diabetes Ketoacidosis (DKA)
 Hyperglycemic hyperosmolar state (HHS)
CHRONIC COMPLICATIONS
 Micro vascular complications
 Diabetic retinopathy
 Diabetic nephropathy
 Diabetic neuropathy
 Macro vascular complications
 Cerebrovascular disease
 Cardiovascular disease
 Peripheral vascular disease

49. CHRONIC SYSTEMIC COMPLICATIONS
1. Central and peripheral nervous systems
• Brain stroke
• Autonomic neuropathy
• Peripheral neuropathy (Motor & sensory dysfunctions)
2. Eye
• Retinopathy
• Cataracts
• Blindness
3. Cardiovascular system
• Cardiomyopathy
• Myocardial infarction
• Atherosclerosis
• Hypertension
• Endothelial cell dysfunction
4. Oral cavity
• Oral disease (Caries, gingivitis, periodontitis and infections)
5. Renal system
• Nephropathy
• Proteinuria
• Glucosuria
• Kidney failure
6. Gastrointestinal system
• Delayed gastric emptying
• Diarrhea
• Constipation
• Dyspepsia
• Exocrine gland insufficiency
7. Genital system
• Impotence
• Sexual dysfunction
• Urogenital dysfunction
8. Skin and soft tissues
• Wound healing impairment
• Skin infection
9. Bone
• Osteopenia, fractures
10. Foot
• Foot ulceration
• Foot amputation

50. ORAL COMPLICATIONS OF DIABETES
 The most common oral health problems associated with diabetes are:
• Periodontal disease.
Periodontal disease is considered the sixth complication of DM both in
Type 1 and Type 2 DM. Periodontitis has been identified as a possible risk
factor for poor glycemic control and the development of other clinical
complications of diabetes. [Loe H, 1993].
• Salivary gland dysfunction.
• Fungal infections.
• Mouth burning and taste impairment.
• Oral mucosal diseases including lichen planus and recurrent aphthous
stomatitis.
• Dental caries.
• Traumatic ulcers and irritation fibroma.
[Guggenheimer J et al, 2000]

51. CONCLUSION
 Since the average dentist attends to over 100 diabetic patients per
year, it is important for the dentist to be aware with the medical
management of the patients with DM, and to recognize the signs and
symptoms of the undiagnosed or poorly controlled disease [Azodo CC,
2009].
 By taking an active role in the diagnosis and treatment of oral
conditions associated with DM, dentist may also contribute to the
maintenance of optimal health in patients with this disease.

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