Diabetes mellitus

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This page contains general information about Diabetes mellitus. For more information on specific types, please visit the pages on Diabetes mellitus type 1, Diabetes mellitus type 2, and Gestational diabetes.

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Diabetes mellitus Main page

Patient Information

Type 1
Type 2

Overview

Classification

Diabetes mellitus type 1
Diabetes mellitus type 2
Gestational diabetes

Differential Diagnosis

Complications

Screening

Diagnosis

Prevention

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Synonyms and keywords: Diabetes; DM

Overview

Diabetes mellitus (DM) refers to a spectrum of disorders with different metabolic changes that result in hyperglycemia as a common feature. It is caused by interaction of environmental agents in a genetically susceptible person. The metabolic disarrangement that may result in hyperglycemia will define the pathologic feature of each type of DM. Decreased insulin secretion, insulin resistance, decreased glucose utilization and increased glucose production are the main metabolic dysregulations that are known to cause hyperglycemia.[1] Hyperglycemia may cause secondary changes in metabolic arrangement in different systems and it can involve every organ systems. DM is the leading cause of end-stage renal disease (ESRD), nontraumatic lower extremity amputations, and adult blindness worldwide.[2] Accordingly, early diagnosis and treatment can result in significant decrease in mortality and morbidity. The incidence of diabetes has been increasing constantly.[3] According to WHO reports, 346 million people worldwide have diabetes and it is projected to double by 2030. It's prevalence is more in developed countries but the death occurring from DM complications is more common in developing countries. The prevalence of diabetes type 2 is more common than type 1 diabetes. Diabetes can cause many complications. Acute complications (hypoglycemia, ketoacidosis or nonketotic hyperosmolar coma) may occur if the disease is not adequately controlled.[4] Serious long-term complications include macrovascular (coronary heart disease, peripheral arterial disease and cerebrovascular disease), microvascular (retinopathy, neuropathy and nephropathy) and other organ involvement (gastrointestinal, genitourinary, dermatologic, infectious, cataracts, glaucoma, periodontal disease and hearing loss).[5] The main goals of treatment are:

  1. Elimination of hyperglycemic symptoms
  2. Control of the long term complications
  3. Improvement of the patient's quality of life

Classification

Diabetes mellitus is classified into 3 types based on the pathogenic process that lead to hyperglycemia.

Differential diagnosis

Disease History and symptoms Laboratory findings Additional findings
Polyuria Polydipsia Polyphagia Weight loss Weight gain Serum glucose Urinary Glucose Urine PH Serum Sodium Urinary Glucose 24 hrs cortisol level C-peptide level Serum glucagon
Type 1 Diabetes mellitus + + + + - Normal Normal N/ Normal Normal Auto antibodies present

(Anti GAD-65 and anti insulin anti bodies)

Type 2 Diabetes mellitus + + + + - Normal Normal Normal Normal Acanthosis nigricans
MODY + + + - + Normal Normal Normal Normal N -
Psychogenic polydipsia + + - - - Normal Normal Normal Normal Normal Normal Normal -
Diabetes insipidus + + - - - Normal Normal Normal Normal Normal Normal Normal -
Transient hyperglycemia - - - - - Normal Normal Normal Normal N/ In hospitalized patients especially in ICU and CCU
Steroid therapy + - - - + Normal Normal N/ N/ Acanthosis nigricans,
RTA 1 - - - + - Normal Normal Normal Normal Normal Normal Hypokalemia, nephrolithiasis
Glucagonoma - - - - - Normal Normal Normal - Normal Normal Necrolytic migratory erythema
Cushing syndrome - - - - + - Normal N/ Normal Normal Moon face, obesity, buffalo hump, easy bruisibility

Complications

Complications of diabetes mellitus may be classified as acute or chronic. Acute complications of diabetes mellitus may occur in type 1, type 2, or gestational diabetes. Chronic complications of diabetes mellitus are more likely to occur in long standing type 1 or type 2 diabetes and may be further classified as macrovascular, microvascular, or other (unspecified etiology) as follows:[6][7][8]

Acute complications

They include diabetic ketoacidosis (DKA) and Hyperosmolar hyperglycemic state (HHS). DKA could be the presenting feature of type 1 diabetes and it is more common in type 1 diabetes although, it is sometimes seen in type 2 diabetic patients. HHS is mostly seen in the elderly and it is more common in type 2 diabetes.

Chronic complications

Macrovascular

Microvascular

Ophthalmic
Neuropathy
Nephropathy

Other organs[10]

Complications of gestational diabetes differs from type 1 and type 2 diabetes primarily due to its pregnancy-specific effects on the mother as well as its effects on the fetus.

For more information on maternal complications of gestational diabetes click here.

For more information on fetal complications of gestational diabetes click here.

Screening

Diabetes mellitus type 1

According to the American Diabetic Association, screening for type 1 DM is not recommended.

Diabetes mellitus type 2

Diabetes screening is recommended for many people at various stages of life, and for those with any of several risk factors. American Diabetes Association Recommendations for Diabetes Screening include:[11][12][13][14]

  • The general population should be screened every 3 years, beginning at age 45 (especially if their BMI>25kg/m2).
  • Younger individuals should be screened if they have BMI>25kg/m2 and at least one of the following risk factors:

To test for type 2 diabetes, fasting plasma glucose, 2-h plasma glucose after 75-g oral glucose tolerance test, and HbA1C are equally appropriate.

Gestational diabetes

All pregnant women should be screened for gestational diabetes in 24-28 weeks with 50 gram glucose test. Measurements greater than 130 mg/dL are considered positive and should proceed to 100 gram glucose test for diagnosis. High risk mothers should be screened as early as the first prenatal visit. These risk factors include:[15][16]

Diagnosis

Diabetes mellitus type 1 and type 2

A fasting plasma glucose (FPG) <5.6 mmol/L (100 mg/dL), a plasma glucose <140 mg/dL (11.1 mmol/L) following an oral glucose challenge and an HbA1c <5.7% are considered normal.
Diagnostic criteria for DM are:


Note:
†:Random is defined as without regard to time since the last meal.

‡:Fasting is defined as no caloric intake for at least 8 h.

¶:The test should be performed using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water, not recommended for routine clinical use.

American Diabetes Association Diabetes Diagnostic Criteria 2017 (DO NOT EDIT)[10]

Criteria for the diagnosis of diabetes
FPG ≥126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 h.
OR
2-h Plasma Glucose (PG) ≥200 mg/dL (11.1 mmol/L) during an OGTT. The test should be performed as described

by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.

OR
A1C ≥6.5% (48 mmol/mol).
OR
In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L).

Gestational diabetes

There are 2 strategies to confirm the GDM diagnosis.

  • One-step 75-g Oral glucose tolerance test (OGTT)
OR
  • Two-step approach with a 50-g (nonfasting) screen followed by a 100-g OGTT for those who screen positive.[17]

One Step Strategy=

Perform a 75 g glucose tolerance test in 24-28 weeks of pregnancy and read the measures 1 h and 2 h after glucose ingestion as well as fasting glucose.[17] The OGTT should be performed in the morning after an overnight fast of at least 8 h. The diagnosis of GDM is made when any of the following plasma glucose values are met or exceeded:

  • Fasting: 92 mg/dL (5.1 mmol/L)
  • 1 h: 180 mg/dL (10.0 mmol/L)
  • 2 h: 153 mg/dL (8.5 mmol/L)

Two Step Strategy

In this approach, screening with a 1 h 50-g glucose load test (GLT) followed by a 3 h 100-g OGTT for those who screen positive.[18]

The diagnosis of GDM is made when at least 2 out of 4 measures of 3 h 100-g OGTT became abnormal.

  • The following table summarizes the diagnostic approach for gestational diabetes.
Cut off (mg/dl)
Fasting 1 Hour 2 Hour 3 Hour
One step test
2 hour 75 g glucose tolerance test
92 180 153 ----
Two step test
1 hour 50 g screening test
---- 140 ---- ----
3 hour 100 g test if screening test became positive
Carpenter/Coustan approach[19]
95 180 155 140
National Diabetes Data Group (NDDG) approach[20]
105 190 165 145

Prevention

Life style modification is the mainstay of prevention of diabetes mellitus. It includes, changes in diet, weight reduction and exercise. The strongest evidence for diabetes prevention comes from the Diabetes Prevention Program (DPP). The DPP demonstrated that an intensive lifestyle intervention could reduce the incidence of type 2 diabetes by 58% over 3 years.[21]

References

  1. Li C, Balluz LS, Okoro CA, Strine TW, Lin JM, Town M, Garvin W, Murphy W, Bartoli W, Valluru B (2011). "Surveillance of certain health behaviors and conditions among states and selected local areas --- Behavioral Risk Factor Surveillance System, United States, 2009". MMWR Surveill Summ. 60 (9): 1–250. PMID 21849967.
  2. Mokdad AH, Ford ES, Bowman BA, Dietz WH, Vinicor F, Bales VS, Marks JS (2003). "Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001". JAMA. 289 (1): 76–9. PMID 12503980.
  3. Harris MI, Klein R, Welborn TA, Knuiman MW (1992). "Onset of NIDDM occurs at least 4-7 yr before clinical diagnosis". Diabetes Care. 15 (7): 815–9. PMID 1516497.
  4. Pasquale LR, Kang JH, Manson JE, Willett WC, Rosner BA, Hankinson SE (2006). "Prospective study of type 2 diabetes mellitus and risk of primary open-angle glaucoma in women". Ophthalmology. 113 (7): 1081–6. doi:10.1016/j.ophtha.2006.01.066. PMID 16757028.
  5. Obrosova IG, Chung SS, Kador PF (2010). "Diabetic cataracts: mechanisms and management". Diabetes Metab. Res. Rev. 26 (3): 172–80. doi:10.1002/dmrr.1075. PMID 20474067.
  6. Seshasai SR, Kaptoge S, Thompson A, Di Angelantonio E, Gao P, Sarwar N, Whincup PH, Mukamal KJ, Gillum RF, Holme I, Njølstad I, Fletcher A, Nilsson P, Lewington S, Collins R, Gudnason V, Thompson SG, Sattar N, Selvin E, Hu FB, Danesh J (2011). "Diabetes mellitus, fasting glucose, and risk of cause-specific death". N. Engl. J. Med. 364 (9): 829–41. doi:10.1056/NEJMoa1008862. PMC 4109980. PMID 21366474.
  7. Franco OH, Steyerberg EW, Hu FB, Mackenbach J, Nusselder W (2007). "Associations of diabetes mellitus with total life expectancy and life expectancy with and without cardiovascular disease". Arch. Intern. Med. 167 (11): 1145–51. doi:10.1001/archinte.167.11.1145. PMID 17563022.
  8. Livingstone SJ, Levin D, Looker HC, Lindsay RS, Wild SH, Joss N, Leese G, Leslie P, McCrimmon RJ, Metcalfe W, McKnight JA, Morris AD, Pearson DW, Petrie JR, Philip S, Sattar NA, Traynor JP, Colhoun HM (2015). "Estimated life expectancy in a Scottish cohort with type 1 diabetes, 2008-2010". JAMA. 313 (1): 37–44. doi:10.1001/jama.2014.16425. PMC 4426486. PMID 25562264.
  9. Nicolucci A (2008). "Aspirin for primary prevention of cardiovascular events in diabetes: still an open question". JAMA. 300 (18): 2180–1. doi:10.1001/jama.2008.625. PMID 18997199.
  10. 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 "Standards of Medical Care in Diabetes-2017: Summary of Revisions". Diabetes Care. 40 (Suppl 1): S4–S5. 2017. doi:10.2337/dc17-S003. PMID 27979887.
  11. "2. Classification and Diagnosis of Diabetes". Diabetes Care. 40 (Suppl 1): S11–S24. 2017. doi:10.2337/dc17-S005. PMID 27979889.
  12. "International Expert Committee report on the role of the A1C assay in the diagnosis of diabetes". Diabetes Care. 32 (7): 1327–34. 2009. doi:10.2337/dc09-9033. PMC 2699715. PMID 19502545.
  13. Schellenberg ES, Dryden DM, Vandermeer B, Ha C, Korownyk C (2013). "Lifestyle interventions for patients with and at risk for type 2 diabetes: a systematic review and meta-analysis". Ann. Intern. Med. 159 (8): 543–51. doi:10.7326/0003-4819-159-8-201310150-00007. PMID 24126648.
  14. Perreault L, Pan Q, Mather KJ, Watson KE, Hamman RF, Kahn SE (2012). "Effect of regression from prediabetes to normal glucose regulation on long-term reduction in diabetes risk: results from the Diabetes Prevention Program Outcomes Study". Lancet. 379 (9833): 2243–51. doi:10.1016/S0140-6736(12)60525-X. PMC 3555407. PMID 22683134.
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  18. "Professional Practice Committee for the Standards of Medical Care in Diabetes-2016". Diabetes Care. 39 Suppl 1: S107–8. 2016. doi:10.2337/dc16-S018. PMID 26696673.
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  20. "Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. National Diabetes Data Group". Diabetes. 28 (12): 1039–57. 1979. PMID 510803.
  21. Lindström J, Ilanne-Parikka P, Peltonen M, Aunola S, Eriksson JG, Hemiö K, Hämäläinen H, Härkönen P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Mannelin M, Paturi M, Sundvall J, Valle TT, Uusitupa M, Tuomilehto J (2006). "Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study". Lancet. 368 (9548): 1673–9. doi:10.1016/S0140-6736(06)69701-8. PMID 17098085.