General practice management of type 2 diabetes

Impaired fasting glucose or impaired glucose tolerance
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The definition of diabetes is based on a collection of symptoms based on an agreed glycaemic measure. On glucose challenge testing, patients with elevated glucose not high enough to be diagnosed with type 2 diabetes, are considered to have either IFG or IGT (Figure 1). To apply the diagnostic algorithm, refer to Table 2.

These states are not considered to be benign and reflect a risk of developing diabetes in the future. In addition, as CVD risk is distributed across a continuum of post-challenge glucose levels, any degree of post-challenge hyperglycaemia may be associated with the development of premature CVD.33

Microvascular complications are commonly present at the time of diagnosis of type 2 diabetes in symptomatic and asymptomatic individuals.25

Table 2. Apply the diagnostic algorithm




Fasting blood glucose (FBG) venous blood

Fasting (eight hours)

Additionally may be used to detect impaired fasting glucose (IFG)

Glycated haemoglobin (HbA1c)  ≥48 mmol/mol  or ≥6.5%

Note that HbA1c may lack accuracy (specificity and/or sensitivity) in:

  • acute onset glycaemic states such as post-traumatic type 2 diabetes (eg pancreatitis), rapid onset of glycaemia with sepsis and steroid use, etc
  • people with haemoglobinopathy or haemolysis, or advanced chronic kidney disease
  • people with iron deficiency (artificially elevated). In such cases, a fasting venous blood glucose or oral glucose tolerance test (OGTT) may assist diagnosis Abnormal HbA1c values generally should be repeated in asymptomatic patients and confirmed on a different day, unless two abnormal tests (eg FBG and HbA1c) are already available from the same day

Not useful for assessment of impaired glucose tolerance (IGT)

Threshold of  48 mmol/mol is linked to escalating microvascular disease, and HbA1c is a better predictor of macrovascular disease than FBG and twohour post-glucose34,35 Lacks sensitivity with acute glycaemic states


Fasting (eight hours)
75 g glucose administered orally Blood is collected from a fasting venous sample and two-hour post-glucose challenge venous sample

Only standard method used to detect IGT. May concurrently detect IFG

HbA1c as a diagnostic tool

HbA1c has recently been approved as a diagnostic test for diabetes under the Medicare Benefits Schedule (MBS) and by the World Health Organization (WHO). The Australian Diabetes Society (ADS), the Royal College of Pathologists of Australasia (RCPA), and the Australasian Association of Clinical Biochemists (AACB) have reviewed the available evidence and confirmed that HbA1c can be used to diagnose diabetes.38

Diagnostic dilemmas

Discordant testing

If diagnosing diabetes, due to the different physiological measures of glycaemia, confirmatory tests at times may give discordant results especially if you do not repeat the initial diagnostic test. For example, HbA1c levels may not be elevated in acute glycaemic states in newly diagnosed diabetes, such that a value of <48 mmol/mol (<6.5%) does not exclude diabetes in the presence of an elevated blood glucose testing (≥7 mmol/L fasting or ≥11.1 mmol/L random). When the results of more than one test are discordant, the laboratory result that is above the diagnostic cut-off point should be repeated to make the diagnosis.

Alternative diagnoses

Alternative diagnoses to type 2 diabetes include unusual presentations of:

Type 1 diabetes

Consider type 1 diabetes if there is the presence of:

  • ketosis/ketonuria (which may be absent)
  • polyuria, polydipsia
  • weight loss or BMI <25 kg/m2
  • <50 years of age
  • personal and family history of autoimmune disease
  • rapid onset of symptoms.

If suspicious of type 1 diabetes:

  • Management of any hyperglycaemia should not be delayed and should include immediate assessment for possible ketosis and metabolic disorders such as hyperosmolar states. If blood ketone level is elevated seek help immediately.  Blood ketones >0.6 mmol/L are abnormal and require investigation in the presence of hyperglycaemia.
  • Non-urgent confirmatory tests for glutamic acid decarboxylase (GAD) and/or insulinoma antigen-2 (IA-2) antibodies. These will be present in 90% of patients with type 1 diabetes. When measuring antibodies, higher rates of false negative results occur early in the development of type 1 diabetes. However, false negative results decrease when two different antibody tests are measured.
  • Test for plasma C-peptide level.39 Levels <0.2 nmol/L on non-fasting sampling, support the diagnosis of type 1 diabetes. This will determine those patients with hyperglycaemia in the absence of or with minimal insulin production. This may not be low in acute early onset type 1 diabetes.

Latent autoimmune diabetes of adults

Latent autoimmune diabetes of adults (LADA) is diabetes with ß-islet cell antibodies more commonly occurring in adulthood, with a more rapid course of ß-cell destruction, a poorer metabolic response to sulphonylurea therapy and a more rapid progression to insulin requirement to control hyperglycaemia due to ß-cell failure.40

Monogenic diabetes

Monogenic diabetes is a disorder with the following characteristics:

  • onset before 25 years of age
  • non-ketotic diabetes mellitus often with a stable lower level hyperglycaemia
  • autosomal dominant inheritance
  • primary defect in the function of the pancreatic ß-cells.

Monogenic diabetes is genetically heterogeneous and all forms are dominantly inherited. There is variance among the forms with two main types – neonatal diabetes mellitus (rare) and maturity onset diabetes of the young (MODY). MODY subtypes may vary in the severity of hyperglycaemia, need for insulin and risk for future complications. Apart from MODY type 2, all other forms of monogenic diabetes are due to transcription factor gene mutations. Not all forms of the MODY phenotype have yet been defined. Suspected cases should be referred to a specialist endocrinologist, and management options and possible genetic diagnosis should be considered.41

Gestational diabetes mellitus

Refer to Section 13.3. Gestational diabetes mellitus.

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  2. Colagiuri S, Davies D, Girgis S, Colagiuri R. National evidence based guideline for case detection and diagnosis of type 2 diabetes. Canberra: Diabetes Australia, NHMRC, 2009.
  3. d’Emden MC, Shaw JE, Jones GR, Cheung NW. Guidance concerning the use of glycated haemoglobin (HbA1c) for the diagnosis of diabetes mellitus. Med J Aust 2015;203(2):89–90.
  4. Naik RG, Brooks-Worrell BM, Palmer JP. Latent autoimmune diabetes in adults. J Clin Endocrinol Metab 2009;94(12):4635–44.
  5. Kavvoura FK, Owen KR. Maturity onset diabetes of the young: clinical characteristics, diagnosis and management. Pediatr Endocrinol Rev 2012;10(2):234–42.