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Prediabetes
ICD-10 R730
ICD-9 790.29
OMIM [2]
DiseasesDB [3]
MedlinePlus [4]
eMedicine /
MeSH {{{MeshNumber}}}

Prediabetes is the state in which some but not all of the diagnostic criteria for diabetes are met.[1] It is often described as the “gray area” between normal blood sugar and diabetic levels. While in this range, patients are at risk for not only developing type 2 diabetes, but also for cardiovascular complications.[2] It has been termed "America's largest healthcare epidemic," affecting more than 57 million Americans.[3] Prediabetes is also referred to as borderline diabetes, impaired glucose tolerance (IGT), and/or impaired fasting glucose (IFG).[citation needed]

Diabetes mellitus
Types of Diabetes
Diabetes mellitus type 1
Diabetes mellitus type 2
Gestational diabetes

Prediabetes:
Impaired fasting glycaemia
Impaired glucose tolerance

Disease Management
Diabetes management:
Diabetic diet
Anti-diabetic drugs
Conventional insulinotherapy
Intensive insulinotherapy
Other Concerns
Cardiovascular disease

Diabetic comas:
Diabetic hypoglycemia
Diabetic ketoacidosis
Nonketotic hyperosmolar

Diabetic myonecrosis
Diabetic nephropathy
Diabetic neuropathy
Diabetic retinopathy

Diabetes and pregnancy

Blood tests
Fructosamine
Glucose tolerance test
Glycosylated hemoglobin

ClassificationEdit

Impaired fasting glycaemiaEdit

Main article: Impaired fasting glycaemia

Impaired fasting glycaemia or impaired fasting glucose (IFG) refers to a condition in which the fasting blood glucose is elevated above what is considered normal levels but is not high enough to be classified as diabetes mellitus. It is considered a pre-diabetic state, associated with insulin resistance and increased risk of cardiovascular pathology, although of lesser risk than impaired glucose tolerance (IGT). IFG sometimes progresses to type 2 diabetes mellitus. There is a 50% risk over 10 years of progressing to overt diabetes. A recent study cited the average time for progression as less than three years.[4] IFG is also a risk factor for mortality.[5]

Fasting blood glucose levels are in a continuum within a given population, with higher fasting glucose levels corresponding to a higher risk for complications caused by the high glucose levels. Impaired fasting glucose is defined as a fasting glucose that is higher than the upper limit of normal, but not high enough to be classified as diabetes mellitus. Some patients with impaired fasting glucose can also be diagnosed with impaired glucose tolerance, but many have normal responses to a glucose tolerance test.

WHO criteria for impaired fasting glucose differs from the ADA criteria, because the normal range of glucose is defined differently. Fasting glucose levels 100 mg/dL and higher have been shown to increase complication rates significantly. However, WHO opted to keep its upper limit of normal at under 110 mg/dL for fear of causing too many people to be diagnosed as having impaired fasting glucose, whereas the ADA lowered the upper limit of normal to a fasting glucose under 100 mg/dL.

  • WHO criteria: fasting plasma glucose level from 6.1 mmol/l (110 mg/dL) to 6.9 mmol/l (125 mg/dL).[6][7]
  • ADA criteria: fasting plasma glucose level from 5.6 mmol/L (100 mg/dL) to 6.9 mmol/L (125 mg/dL).

Impaired Glucose ToleranceEdit

Main article: Impaired glucose tolerance

Impaired glucose tolerance (IGT) is a pre-diabetic state of dysglycemia, that is associated with insulin resistance and increased risk of cardiovascular pathology. IGT may precede type 2 diabetes mellitus by many years. IGT is also a risk factor for mortality.[5]

Signs and symptoms Edit

Prediabetes typically has no signs or symptoms. Patients should monitor for signs and symptoms of type 2 diabetes mellitus. These include the following:[8]

Cause Edit

These are associated with insulin resistance and are risk factors for the development of type 2 diabetes mellitus. Those in this stratum (IGT or IFG) are at increased risk of cardiovascular disease. Of the two, impaired glucose tolerance better predicts cardiovascular disease and mortality.[10][11][12]

In a way, prediabetes is a misnomer since it is an early stage of diabetes. It is now known that the health complications associated with type 2 diabetes often occur before the medical diagnosis of diabetes is made.[13]

Genetics Edit

As the human genome is further explored, it is likely that multiple genetic anomalies at different loci will be found that confer varying degrees of predisposition to type 2 diabetes.[14] Type 2 DM, which is the condition for which prediabetes is a precursor, has 90-100% concordance in twins; there is no HLA association.[15] However, genetics play a relatively small role in the widespread occurrence of type 2 diabetes. This can be logically deduced from the huge increase in the occurrence of type 2 diabetes which has correlated with the significant change in western lifestyle.[15]

Pathophysiology Edit

Diabetes mellitus (DM) is a group of metabolic diseases that are characterized by hyperglycemia and defects in insulin production in the pancreas and/or impaired tolerance to insulin effects. DM is a leading cause of morbidity and mortality. Because the disease can be insidious, the diagnosis is often delayed. Effects of the disease can be macrovascular, as seen in the cardiovascular system/arthrosclerosis, or microvascular, as seen with retinopathy, nephropathy, and neuropathy.[15]

Normal glucose homeostasis is controlled by three interrelated processes. There is gluconeogenesis (glucose production that occurs in the liver), uptake and utilization of glucose by the peripheral tissues of the body, and insulin secretion by the pancreatic islet cells. What triggers the production and release of insulin from the pancreas is the presence of glucose in the body. The main function of insulin is to increase the rate of transport of glucose into certain cells of the body, such as striated muscles, fibroblasts, and fat cells. It is also necessary for transport of amino acids, glycogen formation in the liver and skeletal muscles, triglyceride formation from glucose, nucleic acid synthesis, and protein synthesis.

Insulin enters cells by first binding to target insulin receptors. DM and some of those with prediabetes have impaired glucose tolerance—in these individuals, blood glucose rises to abnormally high levels. This may be from a lack of pancreatic hormone release or failure of target tissues to respond to the insulin present or both.[15]

PreventionEdit

The goals of prevention are to delay the onset of type 2 diabetes, preserving the function of the beta cells, and preventing or delaying the microvascular and cardiovascular complications. Obesity is an extremely important environmental influence, therefore, exercise, weight loss, and drug therapies have been studied. It has been found that lifestyle modification/intervention provides the greatest benefit in preventing the progression into type 2 diabetes.[16]

The American College of Endocrinology (ACE) and the American Association of Clinical Endocrinologists (AACE) have developed lifestyle intervention guidelines for preventing the onset of type 2 diabetes:

  • Healthy meals (low-fat, low-sugar, low-salt diet)
  • Physical exercise (45 minutes of exercise per day, five days a week)
  • Reducing weight by as little as 5-10 percent can have a significant impact on overall health.

Many studies showed that low-carb diet is a very valuable prevention and treatment tool in diabetes and prediabetes.[17][18] Previous advice focused on low-fat approach.[19]

Screening Edit

Fasting plasma glucose screening should begin at age 30-45 and be repeated at least every three years. Earlier and more frequent screening should be conducted in at-risk individuals. The risk factors for which are listed below:

Diagnosis Edit

Prediabetes is usually diagnosed with a blood test:

Levels above these limits would be a diagnosis for diabetes.

Management Edit

Persons with prediabetes actually have the same complications as persons with diabetes—only less frequently. They run the risk of developing diabetic eye disease, nerve damage, and early diabetic kidney disease with excess protein in the urine. Patients with prediabetes are also thought to already have an increased risk of heart and blood vessel disease.[3]

Intensive weight loss and lifestyle intervention, if sustained, can substantially improve glucose tolerance and prevent progression from IGT to type 2 diabetes. The Diabetes Prevention Program (DPP)[23] study found a 16% reduction in diabetes risk for every kilogram of weight loss. Reducing weight by 7% through a low-fat diet and performing 150 minutes of exercise a week is the goal. The ADA guidelines[24] recommend modest weight loss (5-10% body weight), moderate-intensity exercise (30 minutes daily), and smoking cessation.

For patients with severe risk factors, prescription medication may be appropriate. This can be considered in patients for whom lifestyle therapy has failed or is not sustainable and who are at high-risk for developing type 2 diabetes.[16] Metformin[25] and acarbose help prevent the development of frank diabetes, and also have a good safety profile. Evidence also supports thiazolidinediones but there are safety concerns, and data on newer agents such as GLP-1 receptor agonists, DPP4 inhibitors or meglitinides are lacking.[26]

Prognosis Edit

The progression to type 2 diabetes mellitus is not inevitable for those with prediabetes. The progression into diabetes mellitus from prediabetes is approximately 25% over three to five years [27]

Epidemiology Edit

Studies conducted from 1988-1994 indicated that at that time, 33.8% of the US population 40–74 years of age had IFG, 15.4% had IGT, and 40.1% had prediabetes (IFG, IGT, or both). Eighteen million people (6.3% of the population) had type 2 diabetes in 2002.[28]

References Edit

  1. Template:DorlandsDict
  2. Power of Prevention, American College of Endocrinology. Vol. 1, issue 1, January 2009. http://www.powerofprevention.com/POP_magazine_Jan2009_final.pdf/
  3. 3.0 3.1 3.2 Jellinger, Paul S. "What You Need to Know about Prediabetes." Power of Prevention, American College of Endocrinology. Vol. 1, issue 2, May 2009. http://www.powerofprevention.com/
  4. Nichols GA, Hillier TA, Brown JB (2007). Progression From Newly Acquired Impaired Fasting Glusose to Type 2 Diabetes. Diabetes Care 30: 228–233.
  5. 5.0 5.1 Barr EL, Zimmet PZ, Welborn TA, et al. (2007). Risk of cardiovascular and all-cause mortality in individuals with diabetes mellitus, impaired fasting glucose, and impaired glucose tolerance: the Australian Diabetes, Obesity, and Lifestyle Study (AusDiab). Circulation 116 (2): 151–7.
  6. .World Health Organization. Definition, diagnosis and classification of diabetes mellitus and its complications: Report of a WHO Consultation. Part 1. Diagnosis and classification of diabetes mellitus. URL accessed on 2007-05-29.
  7. (2005) Diagnosis and classification of diabetes mellitus. Diabetes Care 28 Suppl 1: S37–42.
  8. Mayo Clinic Diabetes: "Prediabetes". [1]. Accessed Jan. 27, 2009.
  9. Power of Prevention, American College of Endocrinology. Vol. 1, issue 2, May 2009. http://www.powerofprevention.com/
  10. "The Prevention or Delay of Type 2 Diabetes," ADA, Diabetes Care, 25: 742-749, 2002.
  11. National Diabetes Fact Sheet
  12. Tominaga et al. "Impaired glucose tolerance is a risk factor for cardiovascular disease, but not impaired fasting glucose. The Funagata Diabetes Study," Diabetes Care 1999 Jun;22(6):920-4.
  13. WebMD: Prediabetes. Accessed Jan. 27, 2009.
  14. UpToDate: Classification of diabetes mellitis and genetic diabetic syndromes, Nov 14, 2007
  15. 15.0 15.1 15.2 15.3 Cotran, Kumar, Collins; Robbins Pathologic Basis of Disease, Saunders Sixth Edition, 1999; 913-926.
  16. 16.0 16.1 UptoDate: Prediction and prevention of type 2 diabetes mellitus; www.utdol.com/utd/content/topic.do?topicKey=diabetes.
  17. Dyson, Pamela, Sue Beatty and David Matthews. "A Low Carbohydrate Diet Is More Effective for Reducing Weight, % Body Fat and HbA1c Than Healthy Eating in Both Diabetic and Non-Diabetic Subjects." abstract.
  18. http://intl-diabetes.diabetesjournals.org/cgi/content/full/53/9/2375
  19. http://www.dlife.com/dLife/do/ShowContent/food_and_nutrition/ada_backs_low_carbs.html
  20. "ADA: Standards of Medical Care in Diabetes", Diabetes Care 27: Supp 1.515, 2004.
  21. "Diabetes Guidelines Taskforce: AACE Guidelines for the Management of DM", Endocrin Pract 1995, 1.149
  22. New Guidelines Urge A1C Test for Diabetes Diagnosis. HealthDay. December 29, 2009.
  23. http://diabetes.niddk.nih.gov/dm/pubs/preventionprogram/
  24. https://www.diabetes.org/diabetes-prevention/how-to-prevent-diabetes.jsp
  25. Lilly M; Godwin M. "Treating prediabetes with metformin: systematic review and meta-analysis." Canadian Family Physician. 2009 Apr; Vol. 55 (4), pp. 363-9
  26. American College of Endocrinology Consensus Statement on the diagnosis and management of pre-diabetes in the continuum of hyperglycemia—When do the risks of diabetes begin?. (PDF) American College of Endocrinology Task Force on Pre-Diabetes. URL accessed on 2008-07-24.
  27. Nathan et al. "Impaired fasting glucose and impaired glucose tolerance: implications for care," Diabetes Care. 2007 Mar;30(3):753-9.
  28. CDC: Diabetes. National Diabetes Fact Sheet; United States, 2003.

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