Management of type 2 diabetes: A handbook for general practice

Defining and diagnosing type 2 diabetes

Management of type 2 diabetes: A handbook for general practice
Download PDF

Defining and diagnosing type 2 diabetes

Recommendation 

Grade 

References 

Recommended as of:

General population of normal risk 

Assessing the risk of diabetes is recommended every 3 years for those in the general population aged >40 years without specific risk factors. Use a validated screening tool to assess the risk of diabetes, such as the Australian type 2 diabetes risk assessment tool (AUSDRISK). 

Conditionally recommended 

1 

 14/11/2024

Aboriginal and Torres Strait Islander people 

All adults aged 18 years and over should be screened on an opportunistic basis and/or annually. 

  1. Measure fasting blood glucose (FBG) or glycated haemoglobin (HbA1c): A laboratory test is preferable, but fingerprick testing is an alternative. If an FBG is impractical, perform a random (non-fasting) venous test or an HbA1c (which is not affected by fasting status). 

  1. Perform an oral glucose tolerance test (OGTT) in those with equivocal results (FBG 5.5–6.9 mmol/L, or random glucose 5.5–11.0 mmol/L*). 

Children/adolescents with the following additional risk factors should be screened** from the age of 10 years (or at the onset of puberty, whichever occurs first): 

  • overweight or obesity (body mass index*** [BMI] ≥85th or ≥95th percentile, respectively, and/or waist circumference to height ratio >0.5) 
  • maternal history of diabetes or gestational diabetes (GDM) 
  • first-degree relative with type 2 diabetes 
  • signs of insulin resistance (acanthosis nigricans) 
  • other conditions associated with obesity and metabolic syndrome (eg dyslipidaemia, polycystic ovary syndrome [PCOS]) 
  • use of psychotropic medication. 

*Impaired fasting glucose (IFG) = fasting glucose 6.1–6.9 mmol/L; impaired glucose tolerance (IGT) = non fasting glucose ≥7.8 to <11.0 mmol/L. 

**Repeat annually if HbA1c <5.7%; repeat in six months if HbA1c 5.7–6.4%. 

***BMI should be calculated using age- and gender-appropriate calculator/percentile growth charts. 

Recommended (Strong) 

2 

 14/11/2024

High-risk population* 

In asymptomatic adults at high risk* of developing type 2 diabetes, screen using fasting blood glucose (FBG) or glycated haemoglobin (HbA1c) every 3 years (every 12 months for people with impaired glucose tolerance [IGT] and impaired fasting glucose [IFG]**) 

*Adults at high risk of developing type 2 diabetes include people with any one of the following: 

  • overweight or obesity and age ≥40 years 
  • overweight or obesity, age 18–40 years and hypertension 
  • overweight or obesity, age 18–40 years and clinical evidence of insulin resistance (acanthosis nigricans, dyslipidaemia) 
  • a first-degree relative with type 2 diabetes 
  • a history of a cardiovascular event (eg acute myocardial infarction, angina, peripheral vascular disease or stroke) 
  • certain ethnicities (Aboriginal and Torres Strait Islander***, South Asian, South-east Asian, North African, Latin American, Middle Eastern, Māori or Pacific Islander people [includes individuals of mixed ethnicity]) 
  • a history of GDM 
  • PCOS 
  • taking antipsychotic medication. 

An AUSDRISK score ≥12 also indicates high risk. 

**IFG = fasting glucose 6.1–6.9 mmol/L; IGT = non fasting glucose ≥7.8 to <11.0 mmol/L. 

***Aboriginal and Torres Strait Islander people refer to recommendation above 

Conditionally recommended 

1 

 14/11/2024

Individuals with impaired glucose metabolism, defined by fasting glucose, OGTT or HbA1c should be screened: 

  • with FBG or HbA1c* 
  • every 12 months. 

*If impaired glucose metabolism was diagnosed only on the two-hour plasma glucose of the OGTT, consider using the OGTT for subsequent screenings. 

 

B
C 

3, 4 

 14/11/2024

Diabetes is a group of disorders and the tenth leading cause of death in Australia.5 There are four clinical classes of diabetes:6 

  • type 1 diabetes – results from β-cell destruction due to an autoimmune process usually leading to insulin deficiency 
  • type 2 diabetes – results from a progressive insulin secretory defect on a background of insulin resistance 
  • GDM – defined as glucose intolerance with onset or first recognition during pregnancy 
  • other specific types of diabetes – for example, monogenic diabetes and diabetes secondary to other causes (see below). 

Type 2 diabetes is a chronic and progressive medical condition that results from two major metabolic dysfunctions: insulin resistance followed by pancreatic islet cell dysfunction, causing a relative insulin deficiency. These occur due to modifiable lifestyle-related risk factors interacting with non-modifiable (eg age) and genetic risk factors.7 

The relative insulin deficiency leads to chronic hyperglycaemia and multiple disturbances in carbohydrate, protein and fat metabolism.7 

Type 2 diabetes is the most common form of diabetes in Australia. Almost 1.2 million (4.6%) people were living with type 2 diabetes in 2021, although this is likely to be an underestimate of the true prevalence.5 In addition, almost one in six adults are affected by impaired glucose tolerance (IGT) or impaired fasting glucose (IFG).8 

Clinical suspicion for type 2 diabetes needs to remain high, because type 2 diabetes is often asymptomatic and is increasingly developing in younger people (refer to ‘Early-onset type 2 diabetes’).6 Causes of secondary diabetes, such as diseases of the exocrine pancreas (eg pancreatic cancer, cystic fibrosis, haemochromatosis), metabolic or drug-induced causes (eg treatment of human immunodeficiency virus [HIV]), should also be considered in the presence of symptoms suggestive of diabetes.8 

Type 2 diabetes in specific populations 

There is a higher prevalence of type 2 diabetes among Australians from lower socioeconomic backgrounds compared with higher socioeconomic groups,5 and people with certain ethnicities (Aboriginal and Torres Strait Islander people, South Asian, South-east Asian, North African, Latin American, Middle Eastern, Māori or Pacific Islander people [includes individuals of mixed ethnicity]).1 

Aboriginal and Torres Strait Islander peoples have almost three times the rate of type 2 diabetes than other Australians, with onset at an earlier age.9 Type 2 diabetes is a direct or indirect cause of 20% of deaths among Aboriginal and Torres Strait Islander people.10 There are many structural barriers to access to and affordability of healthy foods for many Aboriginal and Torres Strait Islander people, and colonisation has disrupted traditional diets and knowledge of food systems.2 (Refer to the National Aboriginal Community Controlled Health Organisation [NACCHO]–Royal Australian College of General Practitioners [RACGP] National guide to preventive healthcare for Aboriginal and Torres Strait Islander people). 

Assessing diabetes risk 

People should be assessed for diabetes risk every three years from the age of 40 years using the Australian type 2 diabetes risk assessment tool (AUSDRISK; Table 1).3  

Aboriginal and Torres Strait Islander people 

Given the high background prevalence of type 2 diabetes in Aboriginal and Torres Strait Islander adults, AUSDRISK has limited use as a screening tool in this population. 

Aboriginal or Torres Strait Islander people should instead proceed directly to blood testing for diabetes, in conjunction with other opportunistic screening (such as for cardiovascular risk assessment) from the age of 18 years.2 

Refer to the NACCHO-RACGP National guide to preventive healthcare for Aboriginal and Torres Strait Islander people. 

An AUSDRISK score of ≥12 is considered ‘high risk’ for developing type 2 diabetes (Table 1). The following people are also considered at high risk, regardless of AUSDRISK score:1,3 

  • any age with IGT or IFG 
  • overweight or obesity and age ≥40 years 
  • overweight or obesity, age 18–40 years and hypertension 
  • overweight or obesity, age 18–40 years and clinical evidence of insulin resistance (acanthosis nigricans, dyslipidaemia) 
  • a first-degree relative with type 2 diabetes 
  • a history of a cardiovascular event (eg acute myocardial infarction, angina, peripheral vascular disease or stroke) 
  • certain ethnicities (Aboriginal and Torres Strait Islander, South Asian, South-east Asian, North African, Latin American, Middle Eastern, Māori or Pacific Islander people [includes individuals of mixed ethnicity]) 
  • a history of GDM 
  • PCOS 
  • taking antipsychotic medication. 

It is recommended that all people at high risk are tested every three years for diabetes with either FBG or a non-fasting HbA1c (refer to ‘Diagnosing diabetes in asymptomatic people’).1,3 People with IGT or IFG should be tested annually.3 For recommended management of people at high risk of developing diabetes, refer to ‘Preventing progression to type 2 diabetes’. 

For recommendations on screening in pregnancy, refer to ‘Type 2 diabetes, reproductive health and pregnancy’. 

Aboriginal and Torres Strait Islander people 

Obesity is a major cause of type 2 diabetes; Aboriginal and Torres Strait Islander adults who are obese are sevenfold more likely as those of healthy weight or underweight to have diabetes (17% versus 2.4%, respectively).10 Obesity is a very strong predictor of who may get type 2 diabetes in the future; a study of non-diabetic Aboriginal adults in Central Australia found that those who were overweight or obese were 3.3-fold more likely to develop diabetes than those who were not.2,3 

The AusDiab study found that BMI, waist circumference and waist-to-hip ratio all had similar correlations with diabetes and cardiovascular disease (CVD) risk.11 However, a later study of diabetes risk in an Aboriginal community found that in women, central obesity (defined as waist circumference ≥88 cm) or BMI ≥25 kg/m2 were better predictors of type 2 diabetes and CVD risk; many women with ‘normal’ BMIs were found to have central obesity. For men, a BMI ≥25 kg/m2 was a better predictor than BMI ≥30 kg/m2 or a waist circumference ≥102 cm.12 

Table 1. AUSDRISK tool for assessing type 2 diabetes risk13 

AUSDRISK score 

Risk of developing type 2 diabetes within five years* 

≤5 

1 in 100 

6–8  

1 in 50 

9–11 

1 in 30 

12–15 

1 in 14 

16–19 

1 in 17 

≥20 

1 in 3 

*The overall score may overestimate the risk of diabetes in those aged <25 years and underestimate the risk in Aboriginal and Torres Strait Islander people.1


IFG and IGT 

The definition of diabetes is based on a collection of symptoms and agreed glycaemic measures associated with escalating retinopathy risk. People with elevated glucose not high enough to be diagnosed with type 2 diabetes might have either IFG or IGT, also known as ‘dysglycaemic states’ or ‘intermediate hyperglycaemia’. IFG is identified by a FBG test, and IGT can be identified by a two-hour OGTT (Figure 1).14 

These states are not considered benign, and they reflect a risk of developing diabetes in the future; however, IFG and IGT have been shown to regress over three years in 18% of cases if people follow standard (ie non-intensive) lifestyle recommendations.15 

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.16 

Refer also to ‘Preventing progression to type 2 diabetes’. 

Clinical symptoms suggestive of diabetes 

Symptoms of diabetes include: 

  • lethargy, polyuria, polydipsia 
  • frequent fungal or bacterial infections 
  • blurred vision 
  • loss of sensation (ie touch, vibration, cold) 
  • poor wound healing 
  • weight loss. 

Clinical signs of insulin resistance 

Signs of insulin resistance may include the following:17 

  • Acanthosis nigricans – typically characterised by hyperpigmentation (darkening of skin pigment) and usually accompanied by a velvety change in the texture of the affected skin. Common sites are the neck and axillae. 
  • Skin tags – benign (non-cancerous) skin growths on the body or face. They can be smooth or wrinkled, skin-coloured or just slightly darker than skin colour and can vary in size. 
  • Central obesity – defined by a high waist-to-hip ratio, waist-to-thigh ratio and waist circumference. 
  • Signs of PCOS – such as excess facial and body hair and menstrual irregularity.18,19 

Box 1 provides information about testing insulin levels. 

Box 1. Testing insulin levels to assess insulin resistance 

  • There is no role for routine testing of insulin levels to assess insulin resistance in IGT or IFG, or in the evaluation of type 2 diabetes. 
  • Although measuring insulin C-peptide (along with relevant auto-antibodies) can be helpful when type 1 diabetes is suspected, it has no clinical role in characterising insulin resistance in prediabetes or type 2 diabetes. No studies have shown that measuring C-peptide in prediabetes or type 2 diabetes assists with management. 

Diagnosing type 2 diabetes 

Three laboratory tests can be used to diagnose type 2 diabetes: 

  • FBG 
  • HbA1c 
  • OGTT. 

Notes about the use of each in making a diagnosis are provided in Table 2. 

Diagnostic criteria differ depending on whether a person is symptomatic or asymptomatic (see below). Asymptomatic people should be assessed for diabetes risk prior to testing and screened as shown in Figure 1. 

Table 2. Diagnostic tests for type 2 diabetes 

Diagnostic method 

Use when diagnosing diabetes 

Further notes 

FBG 

Fasting (eight hours) 

May also be used to detect IFG 

HbA1c 

Non-fasting 

Abnormal HbA1c values should be repeated in asymptomatic people and confirmed on a different day, unless two abnormal tests (eg FBG and HbA1c) are already available from the same day 

Note that HbA1c may lack accuracy (specificity and/or sensitivity) in the following cases, when FBG or OGTT may assist diagnosis: 

  • acute-onset glycaemic states such as post-traumatic type 2 diabetes (eg pancreatitis), rapid onset of glycaemia with sepsis and steroid use 

  • within four months postpartum 

  • people with haemoglobinopathy or haemolysis, or advanced chronic kidney disease 

  • people with iron deficiency (artificially elevated HbA1c) 

  • people who have recently had a blood or iron transfusion20,21 

Not useful for assessment of IGT 

A threshold of 6.5% (48 mmol/ mol) is linked to escalating microvascular disease, and HbA1c is a better predictor of macrovascular disease than FBG and two-hour post-glucose22,23 

OGTT 

Fasting (eight hours) 

75 g glucose administered orally 

Blood is collected from a fasting venous sample and two-hour post-glucose challenge venous sample 

Abnormal glucose values should be repeated in asymptomatic people and confirmed on a different day 

Only method able to detect IGT 

May concurrently detect IFG 

FBG, fasting blood glucose; HbA1c, glycated haemoglobin; IFG, impaired fasting glucose; IGT, impaired glucose tolerance; OGTT, oral glucose tolerance test 



Figure 1. Screening and diagnosing type 2 diabetes in asymptomatic people3,24–27 
 

Diagnosing diabetes in asymptomatic people 

People who do not have symptoms of hyperglycaemia but who fall in the high-risk categories cited above, or people for whom there is clinical suspicion of diabetes, should be tested using FBG, HbA1c or OGTT (Box 2). 

A second concordant laboratory result is required to confirm a diagnosis of diabetes in asymptomatic people (Figure 1). It is recommended that the same laboratory test be repeated, using a new blood sample, for a greater likelihood of concurrence. 

Box 2. Diagnostic criteria for type 2 diabetes in asymptomatic people 

  • HbA1c ≥6.5% (48 mmol/mol) on two separate occasions 

or 

  • FBG ≥7.0 mmol/L or random blood glucose ≥11.1 mmol/L confirmed by a second abnormal FBG on a separate day 

or 

  • OGTT before (fasting) and two hours after an oral 75-g glucose load is taken. Diabetes is diagnosed as FBG ≥7.0 mmol/L or two-hour post-challenge blood glucose ≥11.1 mmol/L 

These tests are undertaken on venous blood samples. 

For clinical purposes, the diagnosis of diabetes should always be confirmed by repeating the abnormal test on another day, unless there is unequivocal hyperglycaemia with acute metabolic decompensation or obvious symptoms. 

Diagnosing diabetes in symptomatic people 

The presence of symptoms suggestive of hyperglycaemia (refer to ‘Clinical symptoms suggestive of diabetes’) with one of the following is confirmatory of a diagnosis of diabetes: 

  • a single elevated FBG ≥7.0 mmol/L or single HbA1c ≥6.5% 
  • a random blood glucose ≥11.1 mmol/L. 

A second laboratory test is not required to confirm the diagnosis, unless diagnostic uncertainty remains. 

Discordant testing 

Due to the different physiological measures of glycaemia, confirmatory tests at times may give discordant results, especially if the second diagnostic test used is not the same as the initial one. For example, HbA1c levels may not be elevated in acute glycaemic states in newly diagnosed diabetes, such that a value of <6.5% (48 mmol/mol) does not exclude diabetes in the presence of an elevated result on blood glucose testing (≥7.0 mmol/L fasting or ≥11.1 mmol/L random). 

When the results of more than one type of test are discordant, the result that is above the diagnostic cut-off point should be repeated to make the diagnosis. 

Problems with the testing process, such as incorrect fasting or laboratory error, can also lead to discordant results. 

Alternative types of diabetes are listed below. (Also refer to the comparison [table 1] in ‘Early-onset type 2 diabetes’.) 

Type 1 diabetes 

Type 1 diabetes is typically considered a disease of children and the young; however, the majority of people with type 1 diabetes are adults and, in as many as 42% of cases of type 1 diabetes, onset occurs in people between the ages of 30 and 60 years.28 

Consider type 1 diabetes if there is the presence of: 

  • ketosis/ketonuria (which may be absent) 
  • polyuria, polydipsia 
  • acute weight loss (>5% in less than four weeks) 
  • age <50 years 
  • personal and family history of autoimmune disease 
  • acute onset of symptoms. 

If suspicious of type 1 diabetes: 

  • management of hyperglycaemia should not be delayed, and should include immediate assessment for possible ketosis and metabolic disorders, such as hyperosmolar states, while seeking specialist endocrinology assessment. If the blood ketone level is >1.5 mmol/L, seek help immediately. Blood ketones >0.5 mmol/L are abnormal in the presence of hyperglycaemia. Refer to the RACGP’s position statement on Emergency management of hyperglycaemia in primary care. 
  • consider non-urgent confirmatory tests for glutamic acid decarboxylase (GAD) and/or insulinoma antigen-2 (IA-2) antibodies. These will be present in 90% of people 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 performed. 
  • consider testing for plasma C-peptide level.29 Levels <0.2 nmol/L in a non-fasting sampling support the diagnosis of type 1 diabetes; however, the diagnostic accuracy of this test varies in presymptomatic type 1 diabetes. Specialist endocrinology evaluation will assist in the case of diagnostic uncertainty. 

Latent autoimmune diabetes of adults 

Latent autoimmune diabetes of adults (LADA) is diabetes with islet β-cell antibodies that occurs more commonly in adulthood. LADA often presents similarly to type 2 diabetes, but involves a more rapid course of β-cell destruction, a poorer metabolic response to non-insulin therapy and a more rapid progression to requiring insulin to control hyperglycaemia due to β-cell failure.30 

Monogenic diabetes 

Monogenic diabetes is a collection of single-gene-mutation disorders that accounts for 1–2% of cases of diabetes. Monogenic diabetes usually develops before the age of 25 years and is often non-insulin requiring. Monogenic diabetes can be misdiagnosed as either type 1 or type 2 diabetes.31 

Monogenic diabetes is genetically heterogeneous, but all forms are dominantly inherited, unless they occur as a result of a de novo mutation. There is variance among the forms, with two main types: neonatal diabetes mellitus, occurring in the first six months of life (rare); and monogenic diabetes. Monogenic diabetes subtypes may vary in the severity of hyperglycaemia. The most prevalent subtypes are due to mutations in the HNF1A, GCK and HNF4A genes. Not all forms of the monogenic diabetes phenotype have yet been defined.32 Suspected cases should be referred to a specialist endocrinologist, and management options and possible genetic diagnosis should be considered.33 

Gestational diabetes 

Refer to ‘Gestational diabetes’.

  1. The Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice.10th edn. RACGP, 2024 [Accessed 4 September 2024].
  2. National Aboriginal Community Controlled Health Organisation and The Royal Australian College of General Practitioners (RACGP). National guide to preventive healthcare for Aboriginal and Torres Strait Islander people. 4th edn. RACGP, 2024 [Accessed 4 September 2024].
  3. Colagiuri S, Davies D, Girgis S, Colagiuri R. National evidence based guideline for case detection and diagnosis of type 2 diabetes. Diabetes Australia and the National Health and Medical Research Council, 2009.
  4. Bell K, Shaw JE, Maple-Brown L, et al. A position statement on screening and management of prediabetes in adults in primary care in Australia. Diabetes Res Clin Pract 2020;164:108188. doi: 10.1016/j.diabres.2020.108188.
  5. Australian Institute of Health and Welfare (AIHW). Diabetes: Australian facts. AIHW, 2024 [Accessed 4 September 2024].
  6. American Diabetes Association Professional Practice Committee. 2. Diagnosis and classification of diabetes: Standards of care in diabetes – 2024. Diabetes Care 2024;47(Suppl 1):S20–42. doi: 10.2337/dc24-S002.
  7. Nolan CJ, Damm P, Prentki M. Type 2 diabetes across generations: From pathophysiology to prevention and management. Lancet 2011;378(9786):169–81. doi: 10.1016/S0140-6736(11)60614-4.
  8. Shaw J, Tanamas S, editors. Diabetes: The silent pandemic and its impact on Australia. Baker IDI Heart and Diabetes Institute, 2012.
  9. Australian Bureau of Statistics (ABS). National Aboriginal and Torres Strait Islander health survey 2018–19. ABS, 2019 [Accessed 4 September 2024].
  10. Australian Institute of Health and Welfare (AIHW). The health and welfare of Australia’s Aboriginal and Torres Strait Islander peoples 2015. AIHW, 2015.
  11. Daniel M, Rowley KG, McDermott R, Mylvaganam A, O’Dea K. Diabetes incidence in an Australian aboriginal population. An 8-year follow-up study. Diabetes Care 1999;22(12):1993–98. doi: 10.2337/diacare.22.12.1993.
  12. Bambrick H. Relationships between BMI, waist circumference, hypertension and fasting glucose: Rethinking risk factors in Indigenous diabetes. Aust Indigen Health Bull 2005;5(4):Original article 1.
  13. Chen L, Magliano DJ, Balkau B, et al. AUSDRISK: An Australian type 2 diabetes risk assessment tool based on demographic, lifestyle and simple anthropometric measures. Med J Aust 2010;192(4):197–202. doi: 10.5694/j.1326-5377.2010.tb03478.x.
  14. Barry E, Roberts S, Oke J, Vijayaraghavan S, Normansell R, Greenhalgh T. Efficacy and effectiveness of screen and treat policies in prevention of type 2 diabetes: Systematic review and meta-analysis of screening tests and interventions. BMJ 2017;356:i6538. doi: 10.1136/bmj.i6538.
  15. Perreault L, Kahn SE, Christophi CA, Knowler WC, Hamman RF; Diabetes Prevention Program Research Group. Regression from pre-diabetes to normal glucose regulation in the diabetes prevention program. Diabetes Care 2009;32(9):1583–88. doi: 10.2337/dc09-0523.
  16. Twigg SM, Kamp MC, et al. Prediabetes: A position statement from the Australian Diabetes Society and Australian Diabetes Educators Association. Med J Aust 2007;186(9):461–65. doi: 10.5694/j.1326-5377.2007.tb00998.x.
  17. González-Saldivar G, Rodríguez-Gutiérrez R, Ocampo-Candiani J, González-González JG, Gómez-Flores M. Skin manifestations of insulin resistance: From a biochemical stance to a clinical diagnosis and management. Dermatol Ther (Heidelb) 2017;7(1):37–51. doi: 10.1007/s13555-016-0160-3.
  18. Freeman AM, Acevedo LA, Pennings N. Insulin resistance. StatPearls Publishing, 2023 [Accessed 4 September 2024].
  19. Teede HJ, Tay CT, Laven JEJ, et al. Recommendations from the 2023 international evidence-based guideline for the assessment and management of polycystic ovary syndrome. Eur J Endocrinol 2023;189(2):G43–64. doi: 10.1093/ejendo/lvad096.
  20. Sugimoto T, Hashimoto M, Hayakawa I, et al. Alterations in HbA1c resulting from the donation of autologous blood for elective surgery in patients with diabetes mellitus. Blood Transfus 2014;12(Suppl 1):s209–13.
  21. Schindler C, Birkenfeld AL, Hanefeld M, et al. Intravenous ferric carboxymaltose in patients with type 2 diabetes mellitus and iron deficiency: CLEVER trial study design and protocol. Diabetes Ther 2018;9(1):37–47. doi: 10.1007/s13300-017-0330-z.
  22. Selvin E, Steffes MW, Zhu H, et al. Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults. N Engl J Med 2010;362(9):800–11. doi: 10.1056/NEJMoa0908359.
  23. Sarwar N, Aspelund T, Eiriksdottir G, et al. Markers of dysglycaemia and risk of coronary heart disease in people without diabetes: Reykjavik prospective study and systematic review. PLoS Med 2010;7(5):e1000278. doi: 10.1371/journal.pmed.1000278.
  24. World Health Organization (WHO). Use of glycated haemoglobin (HbA1c) in the diagnosis of diabetes mellitus. WHO, 2011.
  25. d’Emden MC, Shaw JE, Colman PG, et al. The role of HbA1c in the diagnosis of diabetes mellitus in Australia. Med J Aust 2012;197(4):220–21. doi: 10.5694/mja12.10988.
  26. Diabetes Canada Clinical Practice Guidelines Expert Committee. Diabetes Canada 2018 clinical practice guidelines for the prevention and management of diabetes in Canada. Can J Diabetes 2018;42(Suppl 1):S1–326.
  27. Colman PG, Thomas DW, Zimmet PZ, Welborn TA, Garcia-Webb P, Moore MP. New classification and criteria for diagnosis of diabetes mellitus. Position Statement from the Australian Diabetes Society, New Zealand Society for the Study of Diabetes, Royal College of Pathologists of Australasia and Australasian Association of Clinical Biochemists. Med J Aust 1999;170(8):375–78. doi: 10.5694/j.1326-5377.1999.tb139171.x.
  28. Thomas N, Jones SE, Weedon MN, Shields BM, Oram RA, Hattersley AT. Frequency and phenotype of type 1 diabetes in the first six decades of life: A cross-sectional, genetically stratified survival analysis from UK Biobank. Lancet Diabetes Endocrinol 2018;6(2):122–29. doi: 10.1016/S2213-8587(17)30362-5.
  29. Jones AG, Hattersley AT. The clinical utility of C-peptide measurement in the care of patients with diabetes. Diabet Med 2013;30(7):803–17. doi: 10.1111/dme.12159.
  30. Naik RG, Brooks-Worrell BM, Palmer JP. Latent autoimmune diabetes in adults. J Clin Endocrinol Metab 2009;94(12):4635–44. doi: 10.1210/jc.2009-1120.
  31. Amed S, Oram R. Maturity-onset diabetes of the young (MODY): Making the right diagnosis to optimize treatment. Can J Diabetes 2016;40(5):449–54. doi: 10.1016/j.jcjd.2016.03.002.
  32. Timsit J, Saint-Martin C, Dubois-Laforgue D, Bellanné-Chantelot C. Searching for maturity-onset diabetes of the young (MODY): When and what for? Can J Diabetes 2016;40(5):455–61. doi: 10.1016/j.jcjd.2015.12.005.
  33. Kavvoura FK, Owen KR. Maturity onset diabetes of the young: Clinical characteristics, diagnosis and management. Pediatr Endocrinol Rev 2012;10(2):234–42.
This event attracts CPD points and can be self recorded

Did you know you can now log your CPD with a click of a button?

Create Quick log


 

Related documents

Advertising