Diabetes mellitus

Last updated: March 22, 2022

Summarytoggle arrow icon

Diabetes mellitus (DM) describes a group of metabolic diseases that are characterized by chronic hyperglycemia. Type 1 diabetes mellitus (T1DM) is the result of an autoimmune response that triggers the destruction of insulin-producing β cells in the pancreas and results in an absolute insulin deficiency. It commonly manifests during childhood, often with an acute onset (e.g., diabetic ketoacidosis). Type 2 diabetes mellitus (T2DM), which is much more common, has a strong genetic component as well as a significant association with obesity and a sedentary lifestyle. T2DM is characterized by insulin resistance and impaired insulin secretion due to pancreatic β cell dysfunction, resulting in relative insulin deficiency. This type of diabetes usually remains undiagnosed for many years. Testing for hyperglycemia is recommended for patients with classic symptoms of diabetes mellitus, and screening is recommended for asymptomatic patients who are at high risk of prediabetes or diabetes (e.g., patients with overweight or obesity and additional risk factors for T2DM). The diagnosis is made based on blood glucose or HbA1c levels. The main goal of treatment is blood glucose control tailored to glucose targets while avoiding hypoglycemia. Diabetes care should be comprehensive and patient-centered, and it should include monitoring and management of ASCVD risk factors, microvascular complications (e.g., diabetic retinopathy, diabetic nephropathy, diabetic neuropathy), and macrovascular complications (e.g., CAD, stroke, PAD). Management should also include general lifestyle modifications (e.g., smoking cessation, exercise, nutritional support) and pharmacotherapy (e.g., antihyperglycemics, statins, ACE inhibitors or angiotensin receptor blockers, and aspirin).

For more information on the complications of type 1 and type 2 diabetes, see “Complications of diabetes mellitus.”

See also “Gestational diabetes mellitus,” “Insulin,” and “Hyperglycemic crises.”

Features Type 1 DM Type 2 DM [1]
Genetics
  • Negative HLA association
  • Strong familial predisposition [3]
  • Polygenic
Pathogenesis
Association with obesity
  • No
  • Yes
Onset
  • Childhood onset typically < 20 years but can occur at any age
  • Peaks at age 4–6 years and 10–14 years
  • Gradual; usually at age > 40 years
C-peptide (insulin)
  • Decreased or absent
  • Initially elevated, decreased in advanced stage
Glucose intolerance
  • Severe
  • Mild to moderate
Insulin sensitivity
  • High
  • Low
Risk of ketoacidosis
  • High
  • Low
β-cells in the islets
  • Decreased

Classic symptoms (i.e., polyuria, polydipsia, polyphagia, weight loss)

  • Common
  • Sometimes
Histology
Treatment

Type 1 DM

  • Prevalence [4]
    • ∼ 1.6 million in the US
    • ∼ 5–10% of all patients with diabetes
  • Age [4]
    • Childhood onset typically < 20 years but can occur at any age
    • Peaks at age 4–6 years and 10–14 years
  • Race: highest prevalence in non-Hispanic whites [5]

Type 2 DM

  • Prevalence [4]
    • ∼ 10.5% of adult population in the US
    • Near 34 million individuals in the US have diabetes with 7.3 million being undiagnosed.
  • Incidence: ∼ 6.7 per 1,000 among the US adults [4]
  • Age
    • Adult onset typically > 40 years [5]
    • Mean age of onset is decreasing
  • Gender: > [4]
  • Race: highest prevalence in Native Americans, Hispanics, African Americans, and Asian non-Hispanic Americans [4]

Epidemiological data refers to the US, unless otherwise specified.

Type 1 DM [6][7]

“If you buy 4 DiaMonds and only pay for 3, you get 1 for free:” DR4 and DR3 are associated with Diabetes Mellitus type 1.

Type 2 DM [8][9][10]

Classification according to the WHO and American Diabetes Association (ADA) [15][16]

Normal insulin physiology [17]

Type 1 diabetes [6]

Type 2 diabetes

Mechanisms [5]

Progression [1]

Clinical features of diabetes mellitus
Type 1 DM Type 2 DM [1]
Onset
  • Often sudden
  • Diabetic ketoacidosis (DKA) is the first manifestation in approx. one-third of cases. [10]
  • Alternatively, children may present with acute illness and classic symptoms.
  • Typically gradual
  • The majority of patients are asymptomatic.
  • Some patients may present with a hyperglycemic crisis.
    • Elderly patients especially may present in a hyperosmolar hyperglycemic state. [20]
    • Occasionally, patients with T2DM present with DKA , which mostly affects black and Hispanic individuals. [21]
  • Symptoms of complications may be the first clinical sign of disease.
Clinical features
  • A thin appearance is typical for patients with T1DM.

Diabetes mellitus should be suspected in patients with recurrent cellulitis, candidiasis, dermatophyte infections, gangrene, pneumonia (particularly tuberculosis reactivation), influenza, genitourinary infections (UTIs), osteomyelitis, and/or vascular dementia.

Indications for testing [10][24]

The indications listed below are consistent with the 2021 ADA guidelines. The 2021 USPSTF guideline recommends screening in adults aged 35–70 years with overweight or obesity. [25]

If results are normal, repeat testing in asymptomatic patients at least every three years. Patients with prediabetes should be tested at least annually to detect progression to diabetes. [10]

Diagnostic criteria for diabetes mellitus [10]

A combination of either of the tests described below may be performed to confirm the diagnosis and the same test can be used both for screening and diagnosis. If two separate blood samples are used, the second should be obtained soon after the first.

Hyperglycemia tests [10]

  • Random blood glucose: blood glucose measured at any time irrespective of recent meals
  • Fasting plasma glucose (FPG): blood glucose measured after > 8 hours of fasting
    • Inexpensive and widely available
    • Should not be used to diagnose diabetes in hospitalized patients or in patients with critical illness
  • Oral glucose tolerance test (OGTT): Measurement of fasting plasma glucose and blood glucose 2 hours after the consumption of 75 g of glucose
    • Most sensitive test
    • Less convenient and more expensive than other tests.
  • Hemoglobin A1C (HbA1c or A1C): Glycated hemoglobin, which reflects the average blood glucose levels of the prior 8–12 weeks
    • Can be measured at any time
    • Results may be altered by a variety of conditions.
Interpretation of diagnostic tests [10]
FPG 2-hour glucose value after OGTT HbA1c
Diabetes mellitus ≥ 126 mg/dL (≥ 7.0 mmol/L) ≥ 200 mg/dL (≥ 11.1 mmol/L) ≥ 6.5%
Prediabetes 100–125 mg/dL (5.6–6.9 mmol/L) = impaired fasting glucose 140–199 mg/dL (7.8–11.0 mmol/L) = impaired glucose tolerance 5.7–6.4%
Normal < 100 mg/dL (< 5.6 mmol/L) < 140 mg/dL (< 7.8 mmol/L) < 5.7%

Routine studies

Perform in all patients as part of the initial diagnostic workup and reassess at least annually.

Additional studies

These tests are not routinely indicated or required to establish a diagnosis.

While screening for T1DM with autoantibodies is not routinely recommended, it can be considered for patients with first-degree relatives with T1DM or in the setting of research trials. [10]

Consider specialist consultation if the differentiation between T2DM and T1DM is unclear.

The differential diagnoses listed here are not exhaustive.

General principles [29]

Diabetes care should be patient-centered and comprehensive, including lifestyle modifications and assessment of psychosocial health. Consider social determinants of health and formulate a treatment plan together with the patient.

The goals of diabetes management include eliminating symptoms of hyperglycemia, reducing or eliminating complications, and enabling as healthy a lifestyle as possible. [24]

Lifestyle modifications [32]

Lifestyle recommendations for patients with diabetes mellitus [32]
Physical activity
  • Exercise regularly.
    • 2 ½ hours of aerobic exercise spread over ≥ 3 days per week
    • 2–3 sessions of resistance exercise per week
  • Reduce the amount of time spent sedentary. and an increase in nonsedentary activities.
Balanced diet and nutrition
  • Refer to a registered nutritionist.
  • Individualize dietary recommendations taking into account the patient’s health status, preferences, and cultural background.
  • General recommendations include:
    • A high-fiber diet
    • Eating nonstarchy vegetables, whole foods
    • Avoiding refined sugar and grains
Weight management [33]
Other
  • Recommend smoking cessation for all patients; offer counseling if necessary. [34]
  • Alcohol consumption [34][35]
    • Should be limited to a moderate intake
    • To avoid hypoglycemia, consume alcohol together with food and monitor glucose after consumption.

Physical exercise reduces blood glucose and increases insulin sensitivity.

Glycemic targets in diabetes [36][37]

  • Consider the following patient factors when setting a glycemic target:
    • Risk of hypoglycemia or other adverse effects
    • Presence of vascular complications and comorbidities
    • Patient preferences and resources
    • Disease duration and life expectancy
  • Reevaluate glycemic targets continuously and adjust if necessary.
Common glycemic targets [36]
HbA1c

< 7%: suitable for most patients [36][37]

Preprandial capillary glucose

80–130 mg/dL

Peak postprandial capillary glucose

< 180 mg/dL

Glycemic targets should be individualized. A target of HbA1c < 7% is generally suitable for most nonpregnant adults. [36]

Assess for past episodes or risk of hypoglycemia regularly and adjust glycemic goals accordingly. Hypoglycemia is one of the major limitations for adequate glycemic control. [36]

In patients that meet preprandial glucose targets, HbA1c above target may be due to postprandial hyperglycemia that requires prandial insulin dose adjustments.

Glycemic monitoring [36][38]

HbA1c monitoring

  • HbA1c is measured at fixed intervals.
    • At least every 6 months if targets are met
    • At least every 3 months in the following situations:

Glucose monitoring

Glucose levels can be used to evaluate treatment and prevent hypoglycemia and hyperglycemia, especially in patients using insulin.

  • Self-monitoring of blood glucose (SMBG): at fixed times or as necessary
    • Indication: insulin therapy (particularly for intensive regimens)
    • Consider for any patient to assess for hypoglycemia or the impact of diet and/or exercise.
  • Continuous glucose monitoring (CGM): Interstitial glucose levels are measured continuously or intermittently using a device. [38]

Hypoglycemia

  • Assess for episodes of hypoglycemia (symptomatic or asymptomatic) at every follow-up visit.
  • In patients with at least one clinically significant hypoglycemia event or asymptomatic hypoglycemia
    • Check for possible contributors, e.g., medication interaction or errors.
    • Consider relaxing the glycemic targets and adjusting management.
    • Prescribing glucagon may be beneficial for some patients.

Reassess and adjust treatment at regular intervals, e.g., every 3–6 months.

Early morning hyperglycemia

  • Early morning hyperglycemia may be caused by:
    • Dawn phenomenon
      • A physiological increase of growth hormone levels; in the early morning hours stimulates hepatic gluconeogenesis and leads to a subsequent increase in insulin demand that cannot be met in insulin-dependent patients, resulting in elevated blood glucose levels.
      • Consider measurement of nocturnal blood glucose levels before initiating insulin therapy.
      • Long-acting insulin dose may be given later or increased under careful glycemic control.
    • Somogyi effect (widely taught but unproven hypothesis)
      • Description: Nocturnal hypoglycemia ; due to evening insulin injection triggers a counterregulatory secretion of hormones , leading to elevated blood glucose levels in the morning.
      • There is no evidence to support the existence of this effect. [39][40][41]

As there is little to no evidence to support the existence of the Somogyi effect, it should not be assumed that early morning hyperglycemia is due to nocturnal hypoglycemia. Rather, it is more likely caused by nocturnal hyperglycemia with or without hypoinsulinemia and/or the early morning secretion of counterregulatory hormones (e.g., cortisol). [39][40][41]

This section outlines the approach to pharmacological treatment of diabetes mellitus. See “Inpatient management of hyperglycemia” for details regarding, e.g., management of hyperglycemia in critically ill patients. See also “Perioperative medication management” for the adjustments to insulin and oral antidiabetics prior to surgery.

Type 1 diabetes mellitus

Insulin replacement therapy [29]

Educate patients on calculating insulin requirements throughout the day and in accordance with activities and meals. [29]

Other treatment strategies [29]

Type 2 diabetes mellitus

Approach [29]

  • Start treatment in all patients at diagnosis. [29][43]
    • Monotherapy with metformin is the first-line initial treatment for most patients.
    • If there are contraindications for metformin, choose a different noninsulin antidiabetic, depending on patient factors.
  • Consider initial or early dual therapy with a noninsulin antidiabetic in certain patients, e.g., those with:
  • Consider the necessity for early combination therapy with insulin (see “Indications for insulin therapy for T2DM” below).
  • Reevaluate treatment and treatment adherence every 3–6 months. [29]

Metformin should be part of every patient's treatment, unless contraindicated, and continued for as long as it is tolerated, as it is safe, effective, widely available, and has been shown to reduce cardiovascular events and mortality. [29]

Noninsulin antidiabetics

Noninsulin antidiabetics for the treatment of type 2 diabetes mellitus [29]
Drug class

Examples

Important considerations
Biguanides
  • Drug of choice, unless there are contradictions for metformin
Dipeptidyl peptidase-4 inhibitor
SGLT-2 inhibitors
GLP-1 receptor agonists
Sulfonylureas
Thiazolidinedione

Oral monotherapy usually lowers HbA1c levels by ∼ 1%. Every noninsulin drug added to metformin will lower the HbA1c by an additional ∼ 0.7–1.0%. [29]

Beware of drug interactions and drug incompatibilities. Combining GLP-1 receptor agonists with DPP4 inhibitors is not beneficial. Sulfonylureas should not be used together with insulin.

Many oral antidiabetic drugs should be avoided in patients undergoing surgery or experiencing severe illness. Instead, insulin therapy may be initiated.

Indications for insulin therapy in T2DM [29]

Approach to insulin treatment in T2DM [29]

GLP-1 receptor agonists should be part of the treatment strategy prior to starting insulin treatment in patients with T2DM, unless they are not appropriate or insulin therapy is preferred.

If treatment goals are not met in a patient on a basal insulin regimen, combination therapy with basal insulin and injectable GLP-1 receptor agonists may be considered.

Interested in the newest medical research, distilled down to just one minute? Sign up for the One-Minute Telegram in “Tips and links” below.

  1. Brunton S. Pathophysiology of Type 2 Diabetes: The Evolution of Our Understanding.. J Fam Pract. 2016; 65 (4 Suppl).
  2. Karl A. Metcalfe, Graham A. Hitman, Rachel E. Rowe, Mohammed Hawa, Xiaojian Huang, Timothy Stewart, and R. David G. Leslie. Concordance for Type 1 Diabetes in Identical Twins Is Affected by Insulin Genotype. American Diabetes Association. 2001 .
  3. Poulsen P, Esteller M, Vaag A, Fraga MF.. The Epigenetic Basis of Twin Discordance in Age-Related Diseases. Pediatric Research. 2007 .
  4. American Diabetes Association. 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Medical Care in Diabetes—2021. Diabetes Care. 2020; 44 (Supplement 1): p.S111-S124. doi: 10.2337/dc21-s009 . | Open in Read by QxMD
  5. American Diabetes Association. 10. Cardiovascular Disease and Risk Management: Standards of Medical Care in Diabetes—2021. Diabetes Care. 2020; 44 (Supplement 1): p.S125-S150. doi: 10.2337/dc21-s010 . | Open in Read by QxMD
  6. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2018; 139 (25). doi: 10.1161/cir.0000000000000625 . | Open in Read by QxMD
  7. American Diabetes Association. 5. Facilitating Behavior Change and Well-being to Improve Health Outcomes: Standards of Medical Care in Diabetes—2021. Diabetes Care. 2020; 44 (Supplement 1): p.S53-S72. doi: 10.2337/dc21-s005 . | Open in Read by QxMD
  8. Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2). McGraw-Hill Education / Medical ; 2018
  9. American Diabetes Association. 8. Obesity Management for the Treatment of Type 2 Diabetes: Standards of Medical Care in Diabetes—2021. Diabetes Care. 2020; 44 (Supplement 1): p.S100-S110. doi: 10.2337/dc21-s008 . | Open in Read by QxMD
  10. American Diabetes Association. 8. Obesity Management for the Treatment of Type 2 Diabetes: Standards of Medical Care in Diabetes—2020. Diabetes Care. 2019; 43 (Supplement 1): p.S89-S97. doi: 10.2337/dc20-s008 . | Open in Read by QxMD
  11. American Diabetes Associaton. Nutrition Recommendations and Interventions for Diabetes-2006: A position statement of the American Diabetes Association. Diabetes Care. 2006; 29 (9): p.2140-2157. doi: 10.2337/dc06-9914 . | Open in Read by QxMD
  12. American Diabetes Association. 6. Glycemic Targets: Standards of Medical Care in Diabetes—2021. Diabetes Care. 2020; 44 (Supplement 1): p.S73-S84. doi: 10.2337/dc21-s006 . | Open in Read by QxMD
  13. Qaseem A, Wilt TJ, Kansagara D, et al. Hemoglobin A1c Targets for Glycemic Control With Pharmacologic Therapy for Nonpregnant Adults With Type 2 Diabetes Mellitus: A Guidance Statement Update From the American College of Physicians. Ann Intern Med. 2018; 168 (8): p.569. doi: 10.7326/m17-0939 . | Open in Read by QxMD
  14. ADA. 7. Diabetes Technology: Standards of Medical Care in Diabetes—2021. Diabetes Care. 2020; 44 (Supplement 1): p.S85-S99. doi: 10.2337/dc21-s007 . | Open in Read by QxMD
  15. Hirsch IB, Smith LJ, Havlin CE, Shah SD, Clutter WE, Cryer PE. Failure of Nocturnal Hypoglycemia to Cause Daytime Hyperglycemia in Patients With IDDM. Diabetes Care. 1990; 13 (2): p.133-142. doi: 10.2337/diacare.13.2.133 . | Open in Read by QxMD
  16. Høi-Hansen T, Pedersen-Bjergaard U, Thorsteinsson B. The Somogyi phenomenon revisited using continuous glucose monitoring in daily life. Diabetologia. 2005; 48 (11): p.2437-2438. doi: 10.1007/s00125-005-1946-5 . | Open in Read by QxMD
  17. M. I. Schmidt, A. Hadji-Georgopoulos, M. Rendell, S. MargoliS, D. Kowarski, A. A. Kowarski. Fasting Hyperglycemia and Associated Free Insulin and Cortisol Changes in "Somogyi-Like" Patients. Diabetes Care. 1979; 2 (6): p.457-464. doi: 10.2337/diacare.2.6.457 . | Open in Read by QxMD
  18. American Diabetes Association. 4. Comprehensive Medical Evaluation and Assessment of Comorbidities: Standards of Medical Care in Diabetes—2021. Diabetes Care. 2020; 44 (Supplement 1): p.S40-S52. doi: 10.2337/dc21-s004 . | Open in Read by QxMD
  19. Nwosu BU. Partial Clinical Remission of Type 1 Diabetes Mellitus in Children: Clinical Applications and Challenges with its Definitions.. Eur Med J Diabetes. 2019; 4 (1): p.89-98.
  20. Johansen MY, MacDonald CS, Hansen KB, et al. Effect of an Intensive Lifestyle Intervention on Glycemic Control in Patients With Type 2 Diabetes. JAMA. 2017; 318 (7): p.637. doi: 10.1001/jama.2017.10169 . | Open in Read by QxMD
  21. National Diabetes Statistics Report. https://www.cdc.gov/diabetes/data/statistics-report/index.html. Updated: August 7, 2020. Accessed: August 23, 2020.
  22. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015
  23. Krzewska A, Ben-Skowronek I. Effect of Associated Autoimmune Diseases on Type 1 Diabetes Mellitus Incidence and Metabolic Control in Children and Adolescents. Biomed Res Int. 2016; 2016 : p.1-12. doi: 10.1155/2016/6219730 . | Open in Read by QxMD
  24. Thorn LM, Forsblom C, Waden J, et al. Effect of Parental Type 2 Diabetes on Offspring With Type 1 Diabetes. Diabetes Care. 2008; 32 (1): p.63-68. doi: 10.2337/dc08-0472 . | Open in Read by QxMD
  25. Kolb H, Martin S. Environmental/lifestyle factors in the pathogenesis and prevention of type 2 diabetes. BMC Med. 2017; 15 (1). doi: 10.1186/s12916-017-0901-x . | Open in Read by QxMD
  26. Fletcher B, Gulanick M, Lamendola C. Risk Factors for Type 2 Diabetes Mellitus. J Cardiovasc Nurs. 2002; 16 (2): p.17-23. doi: 10.1097/00005082-200201000-00003 . | Open in Read by QxMD
  27. American Diabetes Association. 2. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes—2021. Diabetes Care. 2020; 44 (Supplement 1): p.S15-S33. doi: 10.2337/dc21-s002 . | Open in Read by QxMD
  28. Medici F, Hawa M, Ianari A, Pyke DA, Leslie RDG. Concordance rate for Type II diabetes mellitus in monozygotic twins: actuarial analysis. Diabetologia. 1999; 42 (2): p.146-150. doi: 10.1007/s001250051132 . | Open in Read by QxMD
  29. Willemsen G, Ward KJ, Bell CG, et al. The Concordance and Heritability of Type 2 Diabetes in 34,166 Twin Pairs From International Twin Registers: The Discordant Twin (DISCOTWIN) Consortium. Twin Research and Human Genetics. 2019; 18 (6): p.762-771. doi: 10.1017/thg.2015.83 . | Open in Read by QxMD
  30. Ali O. Genetics of type 2 diabetes. World Journal of Diabetes. 2013; 4 (4): p.114. doi: 10.4239/wjd.v4.i4.114 . | Open in Read by QxMD
  31. Snijder MB, Zimmet PZ, Visser M, Dekker JM, Seidell JC, Shaw JE. Independent and opposite associations of waist and hip circumferences with diabetes, hypertension and dyslipidemia: the AusDiab Study. Int J Obes. 2004; 28 (3): p.402-409. doi: 10.1038/sj.ijo.0802567 . | Open in Read by QxMD
  32. American Diabetes Association. 2. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes—2020. Diabetes Care. 2019; 43 (Supplement 1): p.S14-S31. doi: 10.2337/dc20-s002 . | Open in Read by QxMD
  33. Classification of Diabetes. https://www.who.int/publications/i/item/classification-of-diabetes-mellitus. Updated: January 1, 2019. Accessed: March 1, 2022.
  34. Mayer JP, Zhang F, DiMarchi RD. Insulin structure and function. Biopolymers. 2007; 88 (5): p.687-713. doi: 10.1002/bip.20734 . | Open in Read by QxMD
  35. Draznin B. Molecular mechanisms of insulin resistance: Serine phosphorylation of insulin receptor substrate-1 and increased expression of p85 : The two sides of a coin. Diabetes. 2006; 55 (8): p.2392-2397. doi: 10.2337/db06-0391 . | Open in Read by QxMD
  36. Guthrie RA, Guthrie DW. Pathophysiology of Diabetes Mellitus. Crit Care Nurs Q. 2004; 27 (2): p.113-125. doi: 10.1097/00002727-200404000-00003 . | Open in Read by QxMD
  37. Pasquel FJ, Umpierrez GE. Hyperosmolar Hyperglycemic State: A Historic Review of the Clinical Presentation, Diagnosis, and Treatment. Diabetes Care. 2014; 37 (11): p.3124-3131. doi: 10.2337/dc14-0984 . | Open in Read by QxMD
  38. Umpierrez GE. Ketosis-Prone Type 2 Diabetes: Time to revise the classification of diabetes. Diabetes Care. 2006; 29 (12): p.2755-2757. doi: 10.2337/dc06-1870 . | Open in Read by QxMD
  39. Katzberg H, Kokokyi S, Halpern E, et al. Prevalence of Muscle Cramps in Patients With Diabetes: Table 1. Diabetes Care. 2013; 37 (1): p.e17-e18. doi: 10.2337/dc13-1163 . | Open in Read by QxMD
  40. Levy L, Zeicner JA. Dermatologic manifestation of diabetes. J Diabetes. 2012; 4 (1): p.68-76. doi: 10.1111/j.1753-0407.2011.00151.x . | Open in Read by QxMD
  41. US Preventive Services Task Force., Davidson KW, Barry MJ, et al. Screening for Prediabetes and Type 2 Diabetes: US Preventive Services Task Force Recommendation Statement.. JAMA. 2021; 326 (8): p.736-743. doi: 10.1001/jama.2021.12531 . | Open in Read by QxMD
  42. American Diabetes Association. 4. Comprehensive Medical Evaluation and Assessment of Comorbidities: Standards of Medical Care in Diabetes—2020. Diabetes Care. 2019; 43 (Supplement 1): p.S37-S47. doi: 10.2337/dc20-s004 . | Open in Read by QxMD
  43. Jones AG, Hattersley AT. The clinical utility of C-peptide measurement in the care of patients with diabetes. Diabetic Medicine. 2013; 30 (7): p.803-817. doi: 10.1111/dme.12159 . | Open in Read by QxMD
  44. Sacks DB, Arnold M, Bakris GL, et al. Guidelines and Recommendations for Laboratory Analysis in the Diagnosis and Management of Diabetes Mellitus. Clin Chem. 2011; 57 (6): p.e1-e47. doi: 10.1373/clinchem.2010.161596 . | Open in Read by QxMD

3 free articles remaining

You have 3 free member-only articles left this month. Sign up and get unlimited access.
 Evidence-based content, created and peer-reviewed by physicians. Read the disclaimer