Diabetes mellitus: Difference between revisions

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{{Infobox_Disease
'''This page contains general information about Diabetes mellitus. For more information on specific types, please visit the pages:'''
| Name          = Diabetes mellitus  
* [[Diabetes mellitus type 1]]
| Image          = Blue circle for diabetes.svg
* [[Diabetes mellitus type 2]]
| Caption        = United Nations blue circle symbol for diabetes.<ref>{{cite web| title=IDF Chooses Blue Circle to Represent UN Resolution Campaign |url=http://www.unitefordiabetes.org/news/campaign/idf_chooses_blue_circle_to_represent_un_resolution_campaign/index.html |date=17 March 2006 |publisher=Unite for Diabetes}}</ref>
* [[Gestational diabetes]]
| ICD10          = {{ICD10|E|10||e|10}}–{{ICD10|E|14||e|10}}
| ICD9          = {{ICD9|250}}
| ICDO          =
| OMIM          =
| MedlinePlus    =
| MeshName      = Diabetes
| MeshNumber    = C18.452.394.750
}}


{{Diabetes mellitus }}
<div style="-webkit-user-select: none;">
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org]; {{CZ}}
__NOTOC__
{{Diabetes mellitus}}


==Overview==
{{CMG}}; {{AE}}{{MehdiP}}{{MJ}}
'''Diabetes mellitus''' ({{IPAEng|ˌdaɪəˈbiːtiːz}} or {{IPA|/ˌdaɪəˈbiːtəs/}}, {{IPA|/məˈlaɪtəs/}} or {{IPA|/ˈmɛlətəs/}}), often simply '''diabetes''' , is a [[syndrome]] characterized by disordered [[metabolism]] and inappropriately high [[blood sugar]] ([[hyperglycaemia]]) resulting from either low levels of the [[hormone]] [[insulin]] or from abnormal [[insulin resistance|resistance to insulin's effects]] coupled with inadequate levels of insulin secretion to compensate.<ref name="diag">{{cite book | last = L M Tierney, S J McPhee | first = M A Papadakis | title = Current medical Diagnosis & Treatment. International edition | publisher = Lange Medical Books/McGraw-Hill | date = 2002 | pages = 1203-1215 | location = New York | isbn = 0-07-137688-7 }}</ref> The characteristic symptoms are excessive urine production ([[polyuria]]), excessive thirst and increased fluid intake ([[polydipsia]]), and blurred vision. These symptoms are likely absent if the blood sugar is only mildly elevated.


The [[World Health Organization]] recognizes three main forms of diabetes mellitus: ''[[diabetes mellitus type 1|type 1]]'', ''[[diabetes mellitus type 2|type 2]]'', and ''[[gestational diabetes]]'' (occurring during [[pregnancy]]),<ref name "WHO1999-DefDiagClass">{{cite web | author=[[World Health Organisation]] Department of Noncommunicable Disease Surveillance | title=Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications | year=1999 | url=http://whqlibdoc.who.int/hq/1999/WHO_NCD_NCS_99.2.pdf | format=PDF}}</ref> which have different causes and population distributions. While, ultimately, all forms are due to the [[beta cell]]s of the [[pancreas]] being unable to produce sufficient insulin to prevent hyperglycemia, the causes are different.<ref name=Rother>{{cite journal |last=Rother |first=KI |year=2007 |title=Diabetes Treatment — Bridging the Divide |journal=N Engl J Med |volume=356 |issue=15 |pages=1499-1501 |id= |url=http://content.nejm.org/cgi/content/full/356/15/1499}}</ref> Type 1 diabetes is usually due to [[autoimmune disease|autoimmune]] destruction of the pancreatic beta cells. Type 2 diabetes is characterized by [[insulin resistance]] in target tissues. This causes a need for abnormally high amounts of insulin and diabetes develops when the beta cells cannot meet this demand. Gestational diabetes is similar to type 2 diabetes in that it involves insulin resistance; the hormones of [[pregnancy]] can cause insulin resistance in women genetically predisposed to developing this condition.
{{SK}} Diabetes; DM


Gestational diabetes typically resolves with delivery of the child, however types 1 and 2 diabetes are [[chronic disease|chronic conditions]].<ref name="diag"/> All types have been treatable since [[insulin]] became medically available in 1921. Type 1 diabetes, in which insulin is not secreted by the pancreas, is directly treatable only with injected or inhaled insulin, although dietary and other lifestyle adjustments are part of management. Type 2 may be managed with a combination of [[Diet (nutrition)|dietary treatment]], [[Anti-diabetic drug|tablets and injections]] and, frequently, insulin supplementation. While insulin was originally produced from natural sources such as porcine pancreas, most insulin used today is produced through genetic engineering, either as a direct copy of human insulin, or human insulin with modified molecules that provide different onset and duration of action. Insulin can also be delivered continuously by a specialized pump which subcutaneously provides insulin through a changeable catheter.
==Overview==
[[Diabetes mellitus]] ([[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 [[Metabolism|metabolic]] disarrangement that may result in [[hyperglycemia]] will define the pathologic feature of each type of [[Diabetes|DM]]. Decreased [[insulin]] secretion, [[insulin resistance]], decreased [[glucose]] utilization and increased [[glucose]] production are the main metabolic dysregulations that are known to cause [[hyperglycemia]].


Diabetes can cause many complications. [[Acute (medical)|Acute]] complications ([[hypoglycemia]], [[ketoacidosis]] or [[nonketotic hyperosmolar coma]]) may occur if the disease is not adequately controlled. Serious long-term complications include [[cardiovascular disease]] (doubled risk), [[chronic renal failure]], [[diabetic retinopathy|retinal damage]] (which can lead to [[blindness]]), [[diabetic neuropathy|nerve damage]] (of several kinds), and microvascular damage, which may cause [[erectile dysfunction|impotence]] and poor healing. Poor healing of wounds, particularly of the feet, can lead to [[gangrene]], which may require [[amputation]]. Adequate treatment of diabetes, as well as increased emphasis on [[blood pressure]] control and lifestyle factors (such as not [[tobacco smoking|smoking]] and keeping a healthy [[human weight|body weight]]), may improve the risk profile of most aforementioned complications. In the developed world, diabetes is the most significant cause of adult blindness in the non-elderly, the leading cause of non-traumatic amputation in adults, and [[diabetic nephropathy]] is the main illness requiring [[renal dialysis]] in the United States.<ref>{{cite web|url={{cite web /url=http://patients.uptodate.com/topic.asp?file=dialysis/15147 /title=UpToDate Dialysis in diabetic nephropathy /accessdate=2007-12-07 /format= /work=}} |title=UpToDate Dialysis in diabetic nephropathy |accessdate=2007-12-07 |last=Mailloux |first=Lionel |date=2007-02-13 |publisher=UpToDate }}</ref>
[[Hyperglycemia]] may cause secondary changes in [[metabolic]] arrangement in different systems and it can involve every [[Organ (anatomy)|organ]] systems. [[Diabetes|DM]] is the leading cause of [[end-stage renal disease]] ([[Chronic renal failure|ESRD]]), non-traumatic [[lower extremity]] [[Amputation|amputations]], and adult [[blindness]] worldwide.  
{{Diabetes}}


== Classification ==
Accordingly, early [[diagnosis]] and [[treatment]] can result in significant decrease in [[mortality]] and [[morbidity]]. The [[incidence]] of [[diabetes]] has been increased constantly. 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 [[Diabetes|DM]] [[complications]] is more common in developing countries.


The term ''diabetes'', without qualification, usually refers to diabetes mellitus, which is associated with excessive sweet urine (known as "[[glycosuria]]") but there are several rarer conditions also named diabetes. The most common of these is [[diabetes insipidus]] in which the urine is not sweet (insipidus meaning "without taste" in Latin); it can be caused by either [[kidney]] (nephrogenic DI) or [[pituitary gland]] (central DI) damage.
The [[prevalence]] of [[diabetes type 2]] is more common than [[type 1 diabetes]]. [[Diabetes]] can cause many [[complications]]. [[Acute]] [[complications]] ([[hypoglycemia]], [[DKA|ketoacidosis]] or [[Diabetic coma Nonketotic hyperosmolar coma|nonketotic hyperosmolar coma]]) may occur if the [[disease]] is not adequately controlled.<ref name="pmid16757028">{{cite journal |vauthors=Pasquale LR, Kang JH, Manson JE, Willett WC, Rosner BA, Hankinson SE |title=Prospective study of type 2 diabetes mellitus and risk of primary open-angle glaucoma in women |journal=Ophthalmology |volume=113 |issue=7 |pages=1081–6 |year=2006 |pmid=16757028 |doi=10.1016/j.ophtha.2006.01.066 |url=}}</ref> Serious long-term [[complications]] include [[Macrovascular disease|macrovascular]] ([[coronary heart disease]], [[peripheral arterial disease]] and [[cerebrovascular disease]]), [[Microvascular disease|microvascular]] ([[retinopathy]], [[neuropathy]] and [[nephropathy]]) and other organ involvement ([[gastrointestinal]], [[genitourinary]], [[Dermatologic disorders|dermatologic]], [[infectious]], [[Cataract|cataracts]], [[glaucoma]], [[periodontal disease]] and [[hearing loss]]). The main goals of [[treatment]] are:


The principal two idiopathic forms of diabetes mellitus are known as types 1 and 2. The term "type 1 diabetes" has universally replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes (IDDM). Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and non-insulin-dependent diabetes (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature.  Various sources have defined "type 3 diabetes" as, among others, [[gestational diabetes]],<ref>{{cite web | url= http://www.diabetes.org/other-types.jsp | title=Other "types" of diabetes |publisher=[[American Diabetes Association]] |date=August 25, 2005}}</ref> insulin-resistant type 1 diabetes (or "double diabetes"), type 2 diabetes which has progressed to require injected insulin, and [[latent autoimmune diabetes]] of adults (or LADA or "[[Diabetes Type 1.5|type 1.5]]" diabetes.<ref>{{cite web |url=http://autoimmune.pathology.jhmi.edu/diseases.cfm?systemID=3&DiseaseID=23 |title=Diseases: Johns Hopkins Autoimmune Disease Research Center |accessdate=2007-09-23 |format= |work=}}</ref>) There is also [[maturity onset diabetes of the young]] (MODY) which is a group of several single gene disorders with strong family histories that present as type 2 diabetes before 30 years of age.
#Elimination of [[hyperglycemic]] [[symptoms]]
#[[Control]] of the long term [[complications]]
#Improvement of the patient's [[quality of life]]


=== Type 1 Diabetes Mellitus ===
==Classification==
{{main|Diabetes mellitus type 1}}


[[Type 1 diabetes mellitus]] is characterized by loss of the insulin-producing [[beta cell]]s of the [[islets of Langerhans]] in the pancreas, leading to a deficiency of insulin. The main cause of this beta cell loss is a T-cell mediated [[autoimmunity|autoimmune]] attack.<ref name=Rother/> There is no known preventative measure that can be taken against type 1 diabetes, which comprises up to 10% of diabetes mellitus cases in North America and Europe (though this varies by geographical location). Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults but was traditionally termed "juvenile diabetes" because it represents a majority of cases of diabetes affecting children.
* [[Diabetes mellitus]] is classified into 3 types based on the pathogenic process that lead to [[hyperglycemia]]:
**[[Diabetes mellitus type 1]]
**[[Diabetes mellitus type 2]]
**[[Gestational diabetes]]


The principal treatment of type 1 diabetes, even from the earliest stages, is replacement of insulin combined with careful monitoring of blood glucose levels using blood testing monitors. Without insulin, [[diabetic ketoacidosis]] can develop and may result in coma or death. Emphasis is also placed on lifestyle adjustments (diet and exercise) though these can do absolutely nothing to reverse the loss. Apart from the common [[subcutaneous]] injections, it is also possible to deliver insulin by a [[insulin pump|pump]], which allows continuous infusion of insulin 24 hours a day at preset levels, and the ability to program doses (a [[Bolus (medicine)|bolus]]) of insulin as needed at meal times. An inhaled form of insulin, [[Exubera]], was approved by the FDA in January 2006, although Pfizer discontinued Exubera in October 2007. <ref>{{cite web |url=http://www.fda.gov/bbs/topics/news/2006/NEW01304.html |title=FDA Approves First Ever Inhaled Insulin Combination Product for Treatment of Diabetes |accessdate=2007-09-09 |format= |work=}}</ref>
==Differential diagnosis==


Type 1 treatment must be continued indefinitely. Treatment does not significantly impair normal activities, if sufficient patient training, awareness, appropriate care, discipline in testing and dosing of insulin is taken.  However, treatment is burdensome for patients, chronic and insulin is replaced in a non-physiological manner, and is therefore is far from ideal.  The average glucose level for the type 1 patient should be as close to normal (80–120&nbsp;mg/dl, 4–6&nbsp;mmol/l) as is ''safely'' possible. Some physicians suggest up to 140–150&nbsp;mg/dl (7-7.5&nbsp;mmol/l) for those having trouble with lower values, such as frequent hypoglycemic events. Values above 200&nbsp;mg/dl (10&nbsp;mmol/l) is sometimes accompanied by discomfort and frequent urination leading to [[dehydration]]. Values above 300&nbsp;mg/dl (15&nbsp;mmol/l) usually require treatment and may lead to [[ketoacidosis]], although is not immediately life-threatening.  However, low levels of blood glucose, called [[hypoglycemia]], may lead to seizures or episodes of unconsciousness and absolutely must be treated immediately.
{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
! rowspan="2" style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Disease}}
! colspan="5" style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|History and symptoms}}
! colspan="8" style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Laboratory findings}}
! rowspan="2" style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Additional findings}}
|-
! style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Polyuria}}
! style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Polydipsia}}
! style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Polyphagia}}
! style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|="center" style="background:#DCDCDC;"|Weight loss}}
! style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Weight gain}}
! style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Serum glucose}}
! style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Urinary Glucose}}
! style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Urine PH}}
! style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Serum Sodium}}
! style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Urinary Glucose}}
! style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|24 hrs cortisol level}}
! style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|C-peptide level}}
! style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Serum glucagon}}
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Diabetes mellitus type 1|Type 1 Diabetes mellitus]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''''↑'''''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |N/'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Auto antibodies present
([[GAD65|Anti GAD-65]] and anti insulin anti bodies)
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Diabetes mellitus type 2|Type 2 Diabetes mellitus]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Acanthosis nigricans]]
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[MODY]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |N
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Psychogenic polydipsia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Diabetes insipidus]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |Transient [[hyperglycemia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |N/'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |In hospitalized patients especially in [[ICU]] and [[CCU]]
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Steroid]] therapy
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |N/'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |N/'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Acanthosis nigricans|Acanthosis nigricans,]]
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[RTA|RTA 1]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hypokalemia]], [[nephrolithiasis]]
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Glucagonoma]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Necrolytic migratory erythema]]
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |[[Cushing's syndrome|Cushing syndrome]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | +
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" | -
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |N/'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Moon face]], [[obesity]], [[buffalo hump]], easy [[Bruising|bruisibility]]
|}


=== Type 2 Diabetes Mellitus===
==Complications==
{{main|Diabetes mellitus type 2}}


Type 2 diabetes mellitus is due to insulin resistance or reduced insulin sensitivity, combined with reduced insulin secretion. The defective responsiveness of body tissues to insulin almost certainly involves the [[insulin receptor]] in cell membranes. In the early stage the predominant abnormality is reduced insulin sensitivity, characterized by elevated levels of insulin in the blood. At this stage hyperglycemia can be reversed by a variety of measures and [[Anti-diabetic drug|medication]]s that improve insulin sensitivity or reduce glucose production by the [[liver]]. As the disease progresses the impairment of insulin secretion worsens, and therapeutic replacement of insulin often becomes necessary.
* [[Complications]] of [[diabetes mellitus]] may be classified as [[Acute (medicine)|acute]] or [[Chronic (medical)|chronic]]. Acute [[Complication (medicine)|complications]] of [[diabetes mellitus]] may occur in [[Diabetes mellitus type 1|type 1]], [[Diabetes mellitus type 2|type 2]], or [[gestational diabetes]]. Chronic [[Complication (medicine)|complications]] of [[diabetes mellitus]] are more likely to occur in long standing [[Diabetes mellitus type 1|type 1]] or [[Diabetes mellitus type 2|type 2]] diabetes and may be further classified as [[Macrovascular disease|macrovascular,]] [[Microvascular disease|microvascular]], or other (unspecified [[etiology]]) as follows:<ref name="pmid21366474">{{cite journal |vauthors=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 |title=Diabetes mellitus, fasting glucose, and risk of cause-specific death |journal=N. Engl. J. Med. |volume=364 |issue=9 |pages=829–41 |year=2011 |pmid=21366474 |pmc=4109980 |doi=10.1056/NEJMoa1008862 |url=}}</ref><ref name="pmid17563022">{{cite journal |vauthors=Franco OH, Steyerberg EW, Hu FB, Mackenbach J, Nusselder W |title=Associations of diabetes mellitus with total life expectancy and life expectancy with and without cardiovascular disease |journal=Arch. Intern. Med. |volume=167 |issue=11 |pages=1145–51 |year=2007 |pmid=17563022 |doi=10.1001/archinte.167.11.1145 |url=}}</ref><ref name="pmid25562264">{{cite journal |vauthors=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 |title=Estimated life expectancy in a Scottish cohort with type 1 diabetes, 2008-2010 |journal=JAMA |volume=313 |issue=1 |pages=37–44 |year=2015 |pmid=25562264 |pmc=4426486 |doi=10.1001/jama.2014.16425 |url=}}</ref>


There are numerous theories as to the exact cause and mechanism in type 2 diabetes. [[Central obesity]] (fat concentrated around the waist in relation to abdominal organs, but not subcutaneous fat) is known to predispose individuals for insulin resistance. Abdominal fat is especially active hormonally, secreting a group of hormones called [[adipokine]]s that may possibly impair glucose tolerance. Obesity is found in approximately 55% of patients diagnosed with type 2 diabetes.<ref>{{cite journal | last = Eberhart | first = MS | coauthors = Ogden C, Engelgau M, Cadwell B, Hedley AA, Saydah SH | title = Prevalence of Overweight and Obesity Among Adults with Diagnosed Diabetes --- United States, 1988--1994 and 1999--2002 | journal = Morbidity and Mortality Weekly Report | volume = 53 | issue = 45 | pages = 1066-1068 | publisher = Centers for Disease Control and Prevention | date = November 19, 2004 | url = http://www.cdc.gov/mmwR/preview/mmwrhtml/mm5345a2.htm | accessdate = 2007-03-11}}</ref>  Other factors include aging (about 20% of elderly patients in North America have diabetes) and family history (type 2 is much more common in those with close relatives who have had it). In the last decade, type 2 diabetes has increasingly begun to affect children and adolescents, likely in connection with the increased prevalence of childhood obesity seen in recent decades in some places.<ref>{{cite book
===Acute complications===
| last =  Arlan Rosenbloom
| first = Janet H Silverstein
| title = Type 2 Diabetes in Children and Adolescents: A Clinician's Guide to Diagnosis, Epidemiology, Pathogenesis, Prevention, and Treatment
| publisher = American Diabetes Association,U.S.
| date = 2003
| pages = 1
| isbn = 978-1580401555
}}</ref>


Type 2 diabetes may go unnoticed for years because visible symptoms are typically mild, non-existent or sporadic, and usually there are no [[Diabetic ketoacidosis|ketoacidotic episodes]]. However, severe long-term complications can result from unnoticed type 2 diabetes, including [[renal failure]] due to [[diabetic nephropathy]], vascular disease (including [[coronary artery disease]]), vision damage due to [[diabetic retinopathy]], loss of sensation or pain due to [[diabetic neuropathy]], and liver damage from [[non-alcoholic steatohepatitis]].
* They include [[diabetic ketoacidosis]] ([[Diabetic ketoacidosis|DKA]]) and [[Hyperosmolar hyperglycemic state]] ([[Hyperosmolar hyperglycemic state|HHS]]). [[Diabetic ketoacidosis|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 [[Diabetes mellitus type 2|type 2 diabetic]] patients. [[Hyperosmolar hyperglycemic state|HHS]] is mostly seen in the [[elderly]] and it is more common in [[type 2 diabetes]].
 
Type 2 diabetes is usually first treated by increasing physical activity, decreasing [[carbohydrate]] intake, and [[weight loss|losing weight]]. These can restore insulin sensitivity even when the weight loss is modest, for example around 5&nbsp;kg (10 to 15&nbsp;lb), most especially when it is in abdominal fat deposits. It is sometimes possible to achieve long-term, satisfactory glucose control with these measures alone. However, the underlying tendency to insulin resistance is not lost, and so attention to diet, exercise, and weight loss must continue. The usual next step, if necessary, is treatment with oral [[antidiabetic drug]]s. Insulin production is initially only moderately impaired in type 2 diabetes, so oral medication (often used in various combinations) can be used to improve insulin production (e.g., sulfonylureas), to regulate inappropriate release of glucose by the liver and attenuate insulin resistance to some extent (e.g., [[metformin]]), and to substantially attenuate insulin resistance (e.g., [[thiazolidinedione]]s). According to one study, overweight patients treated with metformin compared with diet alone, had [[relative risk reduction]]s of 32% for any diabetes endpoint, 42% for diabetes related death and 36% for all cause mortality and stroke.<ref>{{cite journal |author= |title=Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). UK Prospective Diabetes Study (UKPDS) Group |journal=Lancet |volume=352 |issue=9131 |pages=854-65 |year=1998 |pmid=9742977}}</ref> Oral medication may eventually fail due to further impairment of beta cell insulin secretion. At this point, insulin therapy is necessary to maintain normal or near normal glucose levels.
===Chronic complications===
 
===Gestational diabetes===
====Macrovascular====
{{main|Gestational diabetes}}
*[[Coronary heart disease]]<ref name="pmid18997199">{{cite journal |vauthors=Nicolucci A |title=Aspirin for primary prevention of cardiovascular events in diabetes: still an open question |journal=JAMA |volume=300 |issue=18 |pages=2180–1 |year=2008 |pmid=18997199 |doi=10.1001/jama.2008.625 |url=}}</ref>
 
*[[Peripheral arterial disease]]<ref name="pmid27979887">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2017: Summary of Revisions |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S4–S5 |year=2017 |pmid=27979887 |doi=10.2337/dc17-S003 |url=}}</ref>
Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2%–5% of all [[pregnancy|pregnancies]] and may improve or disappear after delivery. Gestational diabetes is fully treatable but requires careful medical supervision throughout the pregnancy. About 20%&ndash;50% of affected women develop type 2 diabetes later in life.
*[[Cerebrovascular disease]]<ref name="pmid27979887">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2017: Summary of Revisions |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S4–S5 |year=2017 |pmid=27979887 |doi=10.2337/dc17-S003 |url=}}</ref>
 
Even though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include [[macrosomia]] (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal [[surfactant]] production and cause [[Infant respiratory distress syndrome|respiratory distress syndrome]]. [[Hyperbilirubinemia]] may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental profusion due to vascular impairment. [[Induction (birth)|Induction]] may be indicated with decreased placental function. A [[Caesarean section|cesarean section]] may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder [[dystocia]].
 
===Other types===
There are several rare causes of diabetes mellitus that do not fit into type 1, type 2, or gestational diabetes; attempts to classify them remain controversial. Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon.  Genetic mutations ([[Autosomal dominant|autosomal]] or [[mitochondrial]]) can lead to defects in beta cell function. Abnormal insulin action may also been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, [[chronic pancreatitis]] , [[pancreatectomy]] , [[neoplasia]], [[hemachromatosis]], [[fibrocalculous pancreatopathy]] and [[cystic fibrosis]]).  Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion such as [[glucocorticoids]] , [[thyroid hormone]] , [[ Alpha-interferon]] , [[protease inhibitors]] , [[Beta-adrenergic agonists]] , [[thiazides]] , [[nicotinic acid]] , [[phenytoin]] and some toxins damage pancreatic beta cells. The [[ICD]]-10 (1992) diagnostic entity, ''malnutrition-related diabetes mellitus'' (MRDM or MMDM, ICD-10 code E12), was deprecated by the [[World Health Organization]] when the current taxonomy was introduced in 1999.<ref name "WHO1999-DefDiagClass"/>
 
== Signs and symptoms ==
The classical triad of diabetes symptoms is [[polyuria]], [[polydipsia]] and [[polyphagia]], which are, respectively, frequent urination; increased thirst and consequent increased fluid intake; and increased appetite. Symptoms may develop quite rapidly (weeks or months) in type 1 diabetes, particularly in children. However, in type 2 diabetes the symptoms develop much more slowly and may be subtle or completely absent. Type 1 diabetes may also cause a rapid yet significant weight loss (despite normal or even increased eating) and irreducible fatigue. All of these symptoms except weight loss can also manifest in type 2 diabetes in patients whose diabetes is poorly controlled.
 
When the glucose concentration in the blood is raised beyond the [[renal threshold]], [[reabsorption]] of glucose in the [[proximal tubule|proximal renal tubuli]] is incomplete, and part of the glucose remains in the [[urine]]([[glycosuria]]). This increases the [[osmotic pressure]] of the urine and inhibits the reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells, causing [[dehydration]] and increased thirst.
 
Prolonged high blood glucose causes glucose absorption, which leads to changes in the shape of the lenses of the eyes, resulting in vision changes. Blurred vision is a common complaint leading to a diabetes diagnosis; type 1 should always be suspected in cases of rapid vision change whereas type 2 is generally more gradual, but should still be suspected.
 
Patients (usually with type 1 diabetes) may also present with diabetic ketoacidosis (DKA), an extreme state of metabolic dysregulation characterized by the smell of [[acetone]] on the patient's breath; a rapid, deep breathing known as [[Kussmaul breathing]]; polyuria; nausea; vomiting and [[abdominal pain]]; and any of many altered states of consciousness or arousal (such as hostility and mania or, equally, confusion and lethargy). In severe DKA, [[coma]] may follow, progressing to death. Diabetic ketoacidosis is a medical emergency and requires hospital admission.
 
A rarer but equally severe possibility is [[Nonketotic hyperosmolar coma|hyperosmolar nonketotic state]], which is more common in type 2 diabetes and is mainly the result of dehydration due to loss of body water. Often, the patient has been drinking extreme amounts of sugar-containing drinks, leading to a [[positive feedback|vicious circle]] in regard to the water loss.
 
== Genetics ==
Both type 1 and type 2 diabetes are at least partly inherited. Type 1 diabetes appears to be triggered by some (mainly viral) infections, or in a less common group, by stress or environmental exposure (such as exposure to certain chemicals or drugs). There is a genetic element in individual susceptibility to some of these triggers which has been traced to particular [[Human leukocyte antigen|HLA]] [[genotype]]s (i.e., the genetic "self" identifiers relied upon by the immune system). However, even in those who have inherited the susceptibility, type 1 diabetes mellitus seems to require an environmental trigger. A small proportion of people with type 1 diabetes carry a [[mutation|mutated gene]] that causes [[maturity onset diabetes of the young]] (MODY).


There is a stronger inheritance pattern for type 2 diabetes. Those with first-degree relatives with type 2 have a much higher risk of developing type 2, increasing with the number of those relatives. [[Concordance (genetics)|Concordance]] among [[Twin#Identical twins|monozygotic twins]] is close to 100%, and about 25% of those with the disease have a family history of diabetes. Candidate genes include ''KCNJ11'' ([[Inward-rectifier potassium ion channel|potassium inwardly rectifying channel]], subfamily J, member 11), which encodes the islet ATP-sensitive potassium channel Kir6.2, and ''TCF7L2'' (transcription factor 7–like 2), which regulates [[proglucagon]] gene expression and thus the production of [[glucagon-like peptide-1]].<ref name=Rother/> Moreover, obesity (which is an independent risk factor for type 2 diabetes) is strongly inherited.<ref>{{cite journal |author=Walley AJ, Blakemore AI, Froguel P |title=Genetics of obesity and the prediction of risk for health |journal=Hum. Mol. Genet. |volume=15 Spec No 2 |issue= |pages=R124-30 |year=2006 |pmid=16987875 |doi=10.1093/hmg/ddl215}}</ref>
===='''Microvascular'''====
=====Ophthalmic=====
*[[Retinopathy]] (nonproliferative/proliferative)<ref name="pmid27979887">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2017: Summary of Revisions |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S4–S5 |year=2017 |pmid=27979887 |doi=10.2337/dc17-S003 |url=}}</ref>
*[[Macular edema]]<ref name="pmid27979887">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2017: Summary of Revisions |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S4–S5 |year=2017 |pmid=27979887 |doi=10.2337/dc17-S003 |url=}}</ref>


Various hereditary conditions may feature diabetes, for example [[myotonic dystrophy]] and [[Friedreich's ataxia]]. [[Wolfram's syndrome]] is an [[autosomal recessive]] [[neurodegenerative disorder]] that first becomes evident in childhood. It consists of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness, hence the acronym DIDMOAD.<ref name=AMN>{{cite journal |author=Barrett TG |title=Mitochondrial diabetes, DIDMOAD and other inherited diabetes syndromes |journal=Best Pract. Res. Clin. Endocrinol. Metab. |volume=15 |issue=3 |pages=325-43 |year=2001 |pmid=11554774 |doi=10.1053/beem.2001.0149}}</ref>
=====Neuropathy=====
*[[Sensory neuropathy|Sensory]] and [[Motor neuron disease|motor]] ([[Mononeuropathy|mono]]- and [[polyneuropathy]])<ref name="pmid27979887">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2017: Summary of Revisions |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S4–S5 |year=2017 |pmid=27979887 |doi=10.2337/dc17-S003 |url=}}</ref>
*[[Autonomic neuropathy]]<ref name="pmid27979887">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2017: Summary of Revisions |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S4–S5 |year=2017 |pmid=27979887 |doi=10.2337/dc17-S003 |url=}}</ref>
=====Nephropathy=====
*[[Albuminuria]] and declining [[renal function]]<ref name="pmid27979887">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2017: Summary of Revisions |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S4–S5 |year=2017 |pmid=27979887 |doi=10.2337/dc17-S003 |url=}}</ref>


== Pathophysiology ==
===Other organs<ref name="pmid27979887">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2017: Summary of Revisions |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S4–S5 |year=2017 |pmid=27979887 |doi=10.2337/dc17-S003 |url=}}</ref>===
[[Image:Glucose-insulin-release.png|right|thumb|400px|Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells, irrespective of blood glucose levels. It is stored within vacuoles pending release, via exocytosis, which is triggered by increased blood glucose levels.]]
*[[Gastrointestinal tract|Gastrointestinal]] ([[gastroparesis]], [[diarrhea]])
Insulin is the principal hormone that regulates uptake of [[glucose]] from the blood into most cells (primarily muscle and fat cells, but not central nervous system cells). Therefore deficiency of insulin or the insensitivity of its [[Receptor (biochemistry)|receptors]] plays a central role in all forms of diabetes mellitus.
*[[Genitourinary system|Genitourinary]] ([[uropathy]]/[[sexual dysfunction]])
*[[List of skin diseases|Dermatologic]]
*[[Infection|Infections]]
*[[Cataract|Cataracts]]
*[[Glaucoma]]
*[[Periodontal disease]]
*[[Hearing loss]]


Much of the carbohydrate in food is converted within a few hours to the [[monosaccharide]] glucose, the principal carbohydrate found in blood and used by the body as fuel. Some carbohydrates are not so converted. Notable examples include fruit sugar ([[fructose]]), usable as cellular fuel but it is not converted to glucose, and which therefore does not participate in the insulin/glucose metabolic regulatory mechanism. Additionally, the carbohydrate [[cellulose]] (though it is actually many glucose molecules in long chains) is not converted to glucose, as humans and many animals have no digestive pathway capable of breaking up cellulose.


Insulin is released into the blood by beta cells (β-cells), found in the Islets of Langerhans in the pancreas, in response to rising levels of blood glucose after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Insulin is also the principal control signal for conversion of glucose to [[glycogen]] for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly controlled by the hormone [[glucagon]] which acts in an opposite manner to insulin. Glucose thus recovered by the liver re-enters the bloodstream; muscle cells lack the necessary export mechanism.
* [[Complication (medicine)|Complications]] of [[gestational diabetes]] differs from [[Diabetes mellitus type 1|type 1]] and [[Diabetes mellitus type 2|type 2 diabetes]] primarily due to its [[pregnancy]]-specific effects on the mother as well as its effects on the [[fetus]].


Higher insulin levels increase some [[anabolism|anabolic]] ("building up") processes such as cell growth and duplication, [[protein biosynthesis|protein synthesis]], and [[lipid|fat]] storage. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolism from a [[catabolism|catabolic]] to an anabolic direction, and vice versa. In particular, a low insulin level is the trigger for entering or leaving ketosis (the fat burning metabolic phase).
* '''For more information on maternal complications of gestational diabetes [[Gestational diabetes maternal complications|click here]].'''
 
* '''For more information on fetal complications of gestational diabetes [[Gestational diabetes fetal complications|click here]].'''
If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or [[insulin resistance|resistance]]), or if the insulin itself is defective, then glucose will not be absorbed properly by those body cells that require it nor will it be stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as [[acidosis]].


==Diagnosis==
==Diagnosis==
The diagnosis of type 1 diabetes, and many cases of type 2, is usually prompted by recent-onset symptoms of excessive urination (polyuria) and excessive thirst (polydipsia), often accompanied by weight loss. These symptoms typically worsen over days to weeks; about a quarter of people with new type 1 diabetes have developed some degree of diabetic ketoacidosis by the time the diabetes is recognized. The diagnosis of other types of diabetes is usually made in other ways. These include ordinary health screening; detection of hyperglycemia during other medical investigations; and secondary symptoms such as vision changes or unexplainable fatigue. Diabetes is often detected when a person suffers a problem that is frequently caused by diabetes, such as a [[myocardial infarction|heart attack]], [[stroke]], [[neuropathy]], poor wound healing or a foot ulcer, certain eye problems, certain [[fungal infection]]s, or delivering a baby with macrosomia or [[hypoglycemia]].
===Diabetes mellitus type 1 and type 2===


Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:<ref name "WHO1999-DefDiagClass"/>
* A [[fasting plasma glucose]] ([[Fasting blood sugar|FPG]]) <5.6 mmol/L (100 mg/dL), a [[plasma glucose]] <140 mg/dL (11.1 mmol/L) following an [[Oral glucose tolerance test|oral glucose challenge]] and an [[HbA1c]] <5.7% are considered normal.<br> Diagnostic criteria for [[Diabetes|DM]] are:
* fasting plasma glucose level at or above 126&nbsp;mg/dL (7.0&nbsp;mmol/l).
**Symptoms of [[diabetes]] plus random blood glucose concentration ≥11.1 mmol/L (200 mg/dL)<sup>†</sup> '''OR'''
* plasma glucose at or above 200&nbsp;mg/dL (11.1&nbsp;mmol/l) two hours after a 75&nbsp;g oral glucose load as in a [[glucose tolerance test]].
**[[Fasting plasma glucose]] ≥7.0 mmol/L (126 mg/dL)<sup>‡</sup> '''OR'''
* random plasma glucose at or above 200&nbsp;mg/dL (11.1&nbsp;mmol/l).
**[[Hemoglobin A1c]] ≥ 6.5% '''OR'''
**2-hours[[plasma glucose]] ≥11.1 mmol/L (200 mg/dL) during an [[oral glucose tolerance test]]<sup>¶</sup>


A positive result, in the absence of clinical symptoms of diabetes, should be confirmed by another of the above-listed methods on a different day. Most physicians prefer to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete. According to the current definition, two fasting glucose measurements above 126 mg/dL (7.0 mmol/l) is considered diagnostic for diabetes mellitus.
'''American Diabetes Association Diabetes Diagnostic Criteria 2018 (DO NOT EDIT)'''


Patients with fasting glucose levels between 100 and 125&nbsp;mg/dL (6.1 and 7.0&nbsp;mmol/l) are considered to have [[impaired fasting glycaemia|impaired fasting glycemia]]. Patients with plasma glucose at or above 140&nbsp;mg/dL or 7.8&nbsp;mmol/l two hours after a 75 g oral glucose load are considered to have [[impaired glucose tolerance]]. Of these two pre-diabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus as well as cardiovascular disease.
{| class="wikitable"
|+ADA evidence-grading system for “Standards of Medical Care in Diabetes”
!Level of evidence
!Description
|-
|A
|
* Clear evidence from well-conducted, generalizable [[Randomized controlled trial|randomized controlled trials]] that are adequately powered, including
** Evidence from a well-conducted multi-center trial
** Evidence from a [[meta-analysis]] that incorporated quality ratings in the analysis


While not used for diagnosis, an elevated level of glucose irreversibly bound to [[hemoglobin]] (termed [[glycosylated hemoglobin]] or ''HbA1c'') of 6.0% or higher (the 2003 revised U.S. standard) is considered abnormal by most labs; HbA1c is primarily used as a treatment-tracking test reflecting average blood glucose levels over the preceding 90 days (approximately). However, some physicians may order this test at the time of diagnosis to track changes over time. The current recommended goal for HbA1c in patients with diabetes is <7.0%, which is considered good [[Diabetes management#Glycemic control|glycemic control]], although some guidelines are stricter (<6.5%). People with diabetes who have HbA1c levels within this range have a significantly lower incidence of complications from diabetes, including [[retinopathy]] and [[diabetic nephropathy]].<ref name="pmid17510078">{{cite journal |last=Sniderman|first=AD|coauthors=Bhopal R, Prabhakaran D, Sarrafzadegan N, Tchernof A |title=Why might South Asians be so susceptible to central obesity and its atherogenic consequences? The adipose tissue overflow hypothesis |journal=International journal of epidemiology |volume=36 |issue=1 |pages=220–225 |year=2007 |pmid=17510078 |doi=10.1093/ije/dyl245}}</ref><ref>{{cite journal | author = Genuth S | title = Insights from the diabetes control and complications trial/epidemiology of diabetes interventions and complications study on the use of intensive glycemic treatment to reduce the risk of complications of type 1 diabetes. | journal = Endocr Pract | issn = 1530-891X |volume = 12 | issue = Suppl 1 | pages = 34-41 | year =2006 | month = Jan-Feb| pmid=16627378}}</ref>
* Compelling non-experimental evidence, i.e., “all or none” rule developed by the Center for Evidence-Based Medicine at the University of Oxford.


=== Physical Examination ===
* Supportive evidence from well-conducted randomized controlled trials that are adequately powered, including
==== Extremities ====
** Evidence from a well-conducted trial at one or more institutions
[[Image:Diabetic foot ulcer.jpg|thumb|left|Diabetic foot ulcer<ref>http://picasaweb.google.com/mcmumbi/USMLEIIImages</ref>]]
** Evidence from a [[meta-analysis]] that incorporated quality ratings in the analysis
{{clr}}
|-
|B
|
* Supportive evidence from well-conducted [[Cohort study|cohort studies]]
** Evidence from a well-conducted [[prospective cohort study]] or registry
** Evidence from a well-conducted [[meta-analysis]] of [[Cohort study|cohort studies]]
* Supportive evidence from a well-conducted [[Case-control|case-control study]]
|-
|C
|
* Supportive evidence from poorly controlled or uncontrolled studies
** Evidence from randomized [[Clinical trial|clinical trials]] with one or more major or three or more minor flaws that could invalidate the results
** Evidence from [[Observational study|observational studies]] with high potential for [[bias]] (such as [[case series]] with comparison with historical controls)
** Evidence from [[case series]] or [[Case report|case reports]]
* Conflicting evidence with the weight of evidence supporting the recommendation
|-
|D
|
* Supportive evidence from poorly controlled or uncontrolled studies
** Evidence from [[Randomized controlled trial|randomized clinical trials]] with one or more major or three or more minor methodological flaws that could invalidate the results
** Evidence from [[Observational study|observational studies]] with high potential for [[bias]] (such as case series with comparison with historical controls)
** Evidence from [[case series]] or [[Case report|case reports]]
* Conflicting evidence with the weight of evidence supporting the recommendation
|-
|E
|Expert consensus or clinical experience
|}


==Screening==
* Recommendations for [[Glycosylated hemoglobin|HbA1c]]:
Diabetes screening is recommended for many people at various stages of life, and for those with any of several risk factors. The screening test varies according to circumstances and local policy, and may be a random blood glucose test, a fasting blood glucose test, a blood glucose test two hours after 75&nbsp;g of glucose, or an even more formal [[glucose tolerance test]]. Many healthcare providers recommend universal screening for adults at age 40 or 50, and often periodically thereafter. Earlier screening is typically recommended for those with risk factors such as obesity, [[family history (medicine)|family history]] of diabetes, high-risk ethnicity (Mestizo/Hispanic, Native American, Afro-Caribbean, Pacific Island, and South Asian ancestry).<ref name="pmid17215197">{{cite journal |author=Lee CM, Huxley RR, Lam TH, ''et al'' |title=Prevalence of diabetes mellitus and population attributable fractions for coronary heart disease and stroke mortality in the WHO South-East Asia and Western Pacific regions |journal=Asia Pacific journal of clinical nutrition |volume=16 |issue=1 |pages=187–92 |year=2007 |pmid=17215197 |doi=}}</ref><ref name="pmid10889785">{{cite journal |author=Seidell JC |title=Obesity, insulin resistance and diabetes--a worldwide epidemic |journal=Br. J. Nutr. |volume=83 Suppl 1 |issue= |pages=S5–8 |year=2000 |pmid=10889785 |doi=}}</ref>
** To avoid misdiagnosis or missed diagnosis, the [[Glycosylated hemoglobin|A1C]] test should be performed using a method that is certified by the NGSP and standardized to the Diabetes Control and Complications Trial (DCCT) assay. B
**Marked discordance between measured [[Glycosylated hemoglobin|A1C]] and [[Plasma glucose|plasma glucose levels]] should raise the possibility of [[Glycosylated hemoglobin|A1C]] assay interference due to [[hemoglobin]] variants (i.e., [[Hemoglobinopathy|hemoglobinopathies]]) and consideration of using an assay without interference or [[Blood sugar|plasma blood glucose]] criteria to diagnose [[diabetes]]. B
**In conditions associated with increased [[red blood cell]] turnover, such as [[Sickle-cell disease|sickle cell disease]], [[pregnancy]] (second and third [[trimesters]]), [[hemodialysis]], recent [[Bleeding|blood loss]] or [[Blood transfusion|transfusion]], or [[erythropoietin]] therapy, only [[Blood glucose|plasma blood glucose]] criteria should be used to diagnose [[diabetes]]. B


Many medical conditions are associated with diabetes and warrant screening. A partial list includes: high blood pressure, [[dyslipidemia|elevated cholesterol levels]], coronary artery disease, past gestational diabetes, [[polycystic ovary syndrome]], chronic pancreatitis, [[fatty liver]], [[hemochromatosis]], [[cystic fibrosis]], several mitochondrial neuropathies and myopathies, [[myotonic dystrophy]], [[Friedreich's ataxia]], some of the inherited forms of neonatal hyperinsulinism. The risk of diabetes is higher with chronic use of several medications, including high-dose [[glucocorticoid]]s, some [[chemotherapy]] agents (especially [[L-asparaginase]]), as well as some of the antipsychotics and mood stabilizers (especially [[phenothiazine]]s and some [[atypical antipsychotics]]).
<br>Note:<br>
<small>
†:Random is defined as without regard to time since the last meal.


==Prevention==
‡:Fasting is defined as no caloric intake for at least 8 hours.
Type 1 diabetes risk is known to depend upon a genetic predisposition based on [[Human leukocyte antigen|HLA]] types (particularly types DR3 and DR4), an unknown environmental trigger (suspected to be an infection, although none has proven definitive in all cases), and an uncontrolled [[autoimmune]] response that attacks the insulin producing [[beta cells]].<ref>{{cite journal |author=Daneman D |title=Type 1 diabetes |journal=Lancet |volume=367 |issue=9513 |pages=847-58 |year=2006 |pmid=16530579}}</ref> Some research has suggested that [[breastfeeding]] decreased the risk; <ref>{{cite journal |author=Borch-Johnsen K, Joner G, Mandrup-Poulsen T, Christy M, Zachau-Christiansen B, Kastrup K, Nerup J |title=Relation between breast-feeding and incidence rates of insulin-dependent diabetes mellitus. A hypothesis |journal=Lancet |volume=2 |issue=8411 |pages=1083-6 |year=1984 |pmid=6150150}}</ref><ref>{{cite journal |author=Naim Shehadeh, Raanan Shamir, Moshe Berant, Amos Etzioni |title=Insulin in human milk and the prevention of type 1 diabetes |journal=Pediatric Diabetes |volume=2 |issue=4 |pages=175-177 |year=2001 |url=http://www.blackwell-synergy.com/doi/abs/10.1034/j.1399-5448.2001.20406.x?journalCode=pdi }}</ref> various other nutritional risk factors are being studied, but no firm evidence has been found. <ref>{{cite journal |author=Virtanen S, Knip M |title=Nutritional risk predictors of beta cell autoimmunity and type 1 diabetes at a young age |journal=Am J Clin Nutr |volume=78 |issue=6 |pages=1053-67 |year=2003 |pmid=14668264}}</ref>
Giving children 2000 IU of Vitamin D during their first year of life is associated with reduced risk of type 1 diabetes. <ref>{{cite journal |author=Hyppönen E, Läärä E, Reunanen A, Järvelin MR, Virtanen SM |title=Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study |journal=Lancet |year=2001 |pmid=11705562}}</ref>


Type 2 diabetes risk can be reduced in many cases by making changes in diet and increasing physical activity.<ref name=pmid17098085>{{cite journal | author = Lindström J, Ilanne-Parikka P, Peltonen M, Aunola S, Eriksson J, Hemiö K, Hämäläinen H, Härkönen P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Mannelin M, Paturi M, Sundvall J, Valle T, Uusitupa M, Tuomilehto J | title = Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study. | journal = Lancet | volume = 368 | issue = 9548 | pages = 1673-9 | year = 2006 | id = PMID 17098085}}</ref><ref name=Knowler>{{cite journal | author = Knowler W, Barrett-Connor E, Fowler S, Hamman R, Lachin J, Walker E, Nathan D | title = Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. | journal = N Engl J Med | volume = 346 | issue = 6 | pages = 393-403 | year = 2002 | id = PMID 11832527}}</ref> The [[American Diabetes Association]] (ADA) recommends maintaining a healthy weight, getting at least 2½ hours of exercise per week (a brisk sustained walk appears sufficient), having a modest fat intake, and eating a good amount of fiber and whole grains. The ADA does not recommend [[Alcohol consumption and health|alcohol consumption]] as a preventative, but it is interesting to note that moderate alcohol intake may reduce the risk (though heavy consumption clearly increases damage to body systems significantly). There is inadequate evidence that eating foods of low [[glycemic index]] is clinically helpful.<ref>{{cite journal |author=Bantle JP, Wylie-Rosett J, Albright AL, ''et al'' |title=Nutrition recommendations and interventions for diabetes--2006: a position statement of the American Diabetes Association |journal=Diabetes Care |volume=29 |issue=9 |pages=2140–57 |year=2006 |pmid=16936169 |doi=10.2337/dc06-9914| url=http://care.diabetesjournals.org/cgi/content/full/29/9/2140}}</ref>
¶: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.
</small>
==== American Diabetes Association Diabetes Diagnostic Criteria 2018 (DO NOT EDIT)<ref name="pmid27979887">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2017: Summary of Revisions |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S4–S5 |year=2017 |pmid=27979887 |doi=10.2337/dc17-S003 |url=}}</ref>====


Some studies have shown delayed progression to diabetes in predisposed patients through prophylactic use of metformin,<ref name=Knowler/> [[rosiglitazone]],<ref>{{cite journal | author = Gerstein H, Yusuf S, Bosch J, Pogue J, Sheridan P, Dinccag N, Hanefeld M, Hoogwerf B, Laakso M, Mohan V, Shaw J, Zinman B, Holman R | title = Effect of rosiglitazone on the frequency of diabetes in patients with impaired glucose tolerance or impaired fasting glucose: a randomised controlled trial | journal = Lancet | volume = 368 | issue = 9541 | pages = 1096-105 | year = 2006 | id = PMID 16997664}}</ref> or [[valsartan]].<ref>{{cite journal | author =Kjeldsen SE, Julius S, Mancia G, McInnes GT, Hua T, Weber MA, Coca A, Ekman S, Girerd X, Jamerson K, Larochelle P, Macdonald TM, Schmieder RE, Schork MA, Stolt P, Viskoper R, Widimsky J, Zanchetti A; for the VALUE Trial Investigators | title = Effects of valsartan compared to amlodipine on preventing type 2 diabetes in high-risk hypertensive patients: the VALUE trial. | journal = J Hypertens | volume = 24 | issue = 7 | pages = 1405-1412 | year = 2006 | id = PMID 16794491}}</ref> In patients on [[hydroxychloroquine]] for [[rheumatoid arthritis]], incidence of diabetes was reduced by 77%.<ref>{{cite journal |author=Wasko MC, Hubert HB, Lingala VB, ''et al'' |title=Hydroxychloroquine and risk of diabetes in patients with rheumatoid arthritis |journal=JAMA |volume=298 |issue=2 |pages=187-93 |year=2007 |pmid=17622600 |doi=10.1001/jama.298.2.187}}</ref>
{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
Breastfeeding might also be associated with the prevention of type 2 of the disease in mothers.<!--
! align="center" style="background:#DCDCDC;" |'''Criteria for the diagnosis of diabetes'''
  --><ref name="JAMA2005-Stuebe">{{cite journal | author=Stuebe AM, Rich-Edwards JW, Willett WC, Manson JE, Michels KB | title=Duration of lactation and incidence of type 2 diabetes | journal=JAMA | year=2005 | pages=2601&ndash;10 | volume=294 | issue=20 | id=PMID 16304074}}</ref>
|-
| align="left" style="background:#F5F5F5;" |[[Fasting plasma glucose|FPG]] ≥126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 hours.
|-
| align="center" style="background:#F5F5F5;" |'''OR'''
|-
| align="left" style="background:#F5F5F5;" |2-h [[Blood glucose|Plasma Glucose]] (PG)  ≥200 mg/dL (11.1 mmol/L) during an [[Glucose tolerance test|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.
|-
| align="center" style="background:#F5F5F5;" |'''OR'''
|-
| align="left" style="background:#F5F5F5;" |[[A1C]] ≥6.5% (48 mmol/mol).  
* The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.


It is possible that adequate [[copper]] could help prevent insulin dependant diabetes since it does so for ATZ poisoned mice <ref> Sitasawad S, Deshpande M, Katdare M, Tirth S, Parab P. (2001) Beneficial effect of supplementation with copper sulfate on STZ diabetic mice (IDDM). Diabetes Res Clin Pract  May;52(2):77-84. </ref> and copper in drinking water has somewhat of a protective affect <ref> Zhao HX, Mold MD, Stenhouse EA, Bird SC, Wright DE, Demaine AG, Millward BA. (2001) Drinking water composition and childhood-onset Type 1 diabetes mellitus in Devon and Cornwall, England. Diabetic Med 18(9) p709-717.This article modified in November 2007.</ref>. It could be that copper produces its effects through super oxidase dismutase (SOD) because metaloporpherin based superoxide dismutase can prevent or delay the onset of the autoimmune cascade in diabetes, using mice <ref> Haskins K, et al (2003) "Immunology of diabetes II. Pathogenesis from mouse to man." Ann. N.Y. Academy of Sciences 1005: 43. doi. 10.1196/annals.1288.006.</ref>.  However, there are sufficient differences in human and animal models to indicate this is only a theory at the present time.
* In the absence of unequivocal [[hyperglycemia]], results should be confirmed by repeat testing.
|-
| align="center" style="background:#F5F5F5;" |'''OR'''
|-
| align="left" style="background:#F5F5F5;" |In a patient with classic symptoms of [[hyperglycemia]] or [[hyperglycemic]] crisis, a random [[plasma glucose]] ≥200 mg/dL (11.1 mmol/L).
|}


Children with antibodies treated with vitamin B-3 ([[niacin]]) had less than half the onset of diabetes incidence in a 7-year time span as the general population and even lower incidence relative to those with antibodies as above, but no vitamin B-3 <ref> Elliott RB Pilcher CC Fergusson DM Stewart AW 1996 A population based strategy to prevent insulin-dependent diabetes using nicotinamide. J Pediatr Endocrinol Metab. 1996 Sep-Oct;9(5):501-9.</ref>
===Gestational diabetes===


==Treatment and Management==
* There are 2 strategies to confirm the [[Gestational diabetes|GDM]] diagnosis.
{{main|Diabetes management}}
**'''One-step''' 75-g Oral [[glucose tolerance test]] ([[Glucose tolerance test|OGTT]]) '''OR'''
{{dablink|For more on the treatment of diabetics with coronary artery disease click [[Treatment of Diabetics with Coronary Artery Disease|here]].}}
** '''Two-step''' approach with a 50-g (non-fasting) screen followed by a 100-g [[Glucose tolerance test|OGTT]] for those who screen positive.<ref name="pmid26807004">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2016 Abridged for Primary Care Providers |journal=Clin Diabetes |volume=34 |issue=1 |pages=3–21 |year=2016 |pmid=26807004 |doi=10.2337/diaclin.34.1.3 |url=}}</ref>


Diabetes mellitus is currently a [[chronic disease]], without a cure, and medical emphasis must necessarily be on managing/avoiding possible short-term as well as long-term diabetes-related problems. There is an exceptionally important role for patient education, dietetic support, sensible exercise, self glucose monitoring, with the goal of keeping both short-term blood glucose levels, and long term levels as well,  [[Diabetes management#Glycemic control|within acceptable bounds]]. Careful control is needed to reduce the risk of long term complications. This is theoretically achievable with combinations of diet, exercise and weight loss (type 2), various oral diabetic drugs (type 2 only), and insulin use (type 1 and increasingly for type 2 not responding to oral medications). In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications should be undertaken to control blood pressure<ref>{{cite journal|last=Adler|first=A.I.|coauthors=Stratton, I. M.; Neil, H.A.; ''et al''|title=Association of systolic blood pressure with macrovascular and microvascular complications of type 2 diabetes (UKPDS 36): prospective observational study|url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=27454&rendertype=abstract|journal=BMJ|volume=321|issn=0959-8146|issue=7258|pages=412–419|year=2000|pmid=10938049|doi=}}</ref> and cholesterol by exercising more, smoking cessation, consuming an appropriate [[Diabetic diet|diet]], wearing [[diabetic sock]]s, and if necessary, taking any of several drugs to reduce pressure. Many Type 1 treatments include the combination use of regular or NPH insulin, and/or synthetic insulin analogs such as Humalog,  Novolog or Apidra; the combination of Lantus/Levemir and Humalog, Novolog or Apidra. Another Type 1 treatment option is the use of the insulin pump with the some of most popular pump brands being: Cozmo, Animas, Medtronic Minimed, and Omnipod.
====One Step Strategy====


In countries using a [[general practitioner]] system, such as the [[United Kingdom]], care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care of a patient in a team approach. [[Optometry|Optometrists]], [[podiatry|podiatrists]]/chiropodists, [[dietitian]]s, [[Physical therapy|physiotherapists]], clinical nurse specialists (eg, [[Certified diabetes educator|Certified Diabetes Educators]] and DSNs (Diabetic Specialist Nurse)), or [[nurse practitioner]]s may jointly provide multidisciplinary expertise. In countries where patients must provide their own health care, the impact of out-of-pocket costs of diabetic care can be high. In addition to the medications and supplies needed, patients are often advised to receive regular consultation from a physician (e.g., at least every three to six months).
* Perform a 75 g [[glucose tolerance test]] in 24-28 weeks of [[pregnancy]] and read the measures 1 h and 2 hours after [[glucose]] ingestion as well as fasting glucose.<ref name="pmid26807004">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2016 Abridged for Primary Care Providers |journal=Clin Diabetes |volume=34 |issue=1 |pages=3–21 |year=2016 |pmid=26807004 |doi=10.2337/diaclin.34.1.3 |url=}}</ref> The [[Glucose tolerance test|OGTT]] should be performed in the morning after an overnight fast of at least 8 hours. The diagnosis of [[Gestational diabetes|GDM]] is made when any of the following [[Blood sugar|plasma glucose]] values are met or exceeded:
** Fasting: 92 mg/dL (5.1 mmol/L)
** 1 hour: 180 mg/dL (10.0 mmol/L)
** 2 hours: 153 mg/dL (8.5 mmol/L)


==Cure==
====Two Step Strategy====
===Cures for type 1 diabetes===
{{main|Cure for diabetes mellitus type 1}}
There is no practical cure now for type 1 diabetes. The fact that type 1 diabetes is due to the failure of one of the cell types of a single organ with a relatively simple function (i.e. the failure of the islets of Langerhans) has led to the study of several possible schemes to cure this form diabetes mostly by replacing the pancreas or just the beta cells.<ref name=Vinik>{{cite journal |author=Vinik AI, Fishwick DT, Pittenger G |title=Advances in diabetes for the millennium: toward a cure for diabetes |journal=MedGenMed : Medscape general medicine |volume=6 |issue=3 Suppl |pages=12 |year=2004 |pmid=15647717 |doi=}}</ref> Only those type 1 diabetics who have received either a pancreas or a kidney-pancreas transplant (when they have developed diabetic nephropathy) and become insulin-independent may now be considered "cured" from their diabetes. A simultaneous pancreas-kidney transplant is a promising solution, showing similar or improved survival rates over a kidney transplant alone. <ref name=Stratta>


{{cite journal  
* In this approach, screening with a 1 hour 50-g [[glucose]] load test (GLT) followed by a 3 hours 100-g [[Glucose tolerance test|OGTT]] for those who screen positive.<ref name="pmid26696673">{{cite journal |vauthors= |title=Professional Practice Committee for the Standards of Medical Care in Diabetes-2016 |journal=Diabetes Care |volume=39 Suppl 1 |issue= |pages=S107–8 |year=2016 |pmid=26696673 |doi=10.2337/dc16-S018 |url=}}</ref>
| author=Stratta RJ, Alloway RR.| title=Pancreas transplantation for diabetes mellitus: a guide to recipient selection and optimum immunosuppression.| journal=BioDrugs. | year=1998 | pages=347-357 | volume=10 | issue=5 | id=PMID 18020607 


}}</ref>Still, they generally remain on long-term [[immunosuppressive drug]]s and there is a possibility that the immune system will mount a [[host versus graft]] response against the transplanted organ.<ref name=Vinik/>
* The diagnosis of [[Gestational diabetes|GDM]] is made when at least 2 out of 4 measures of 3 hours 100-g [[Glucose tolerance test|OGTT]] became abnormal.


Transplants of exogenous beta cells have been performed experimentally in both mice and humans, but this measure is not yet practical in regular clinical practice. Thus far, like any such transplant, it has provoked an immune reaction and long-term immunosuppressive drugs will be needed to protect the transplanted tissue.<ref>{{cite journal |author=Shapiro AM, Ricordi C, Hering BJ, ''et al'' |title=International trial of the Edmonton protocol for islet transplantation |journal=N. Engl. J. Med. |volume=355 |issue=13 |pages=1318-30 |year=2006 |pmid=17005949 |doi=10.1056/NEJMoa061267}}</ref> An alternative technique has been proposed to place transplanted beta cells in a semi-permeable container, isolating and protecting them from the immune system. [[Stem cell research]] has also been suggested as a potential avenue for a cure since it may permit regrowth of Islet cells which are genetically part of the treated individual, thus perhaps eliminating the need for immuno-suppressants.<ref name=Vinik/> A 2007 trial of 15 newly diagnosed patients with type 1 diabetes treated with [[stem cell]]s raised from their own [[bone marrow]] after [[immune suppression]] showed that the majority did not require any insulin treatment for prolonged periods of time.<ref>{{cite journal |last= Voltarelli |first=JC |coauthors=Couri CE, Stracieri AB, Oliveira MC, Moraes DA, Pieroni F, Coutinho M, Malmegrim KC, Foss-Freitas MC, Simoes BP, Foss MC, Squiers E, Burt RK. |year = 2007 |title=Autologous nonmyeloablative hematopoietic stem cell transplantation in newly diagnosed type 1 diabetes mellitus. |journal=JAMA |volume=297 |issue=14 |pages=1568-76 |id=PMID 17426276 |url=http://jama.ama-assn.org/cgi/content/full/297/14/1568}}</ref>
*The following table summarizes the diagnostic approach for [[gestational diabetes]].


Microscopic or nanotechnological approaches are under investigation as well, in one proposed case with implanted stores of insulin metered out by a rapid response valve sensitive to blood glucose levels. At least two approaches have been demonstrated ''in vitro''. These are, in some sense, closed-loop insulin pumps.
{| class="wikitable"
! rowspan="2" |
! colspan="4" |Cut off (mg/dl)
|-
!Fasting
!1 Hour
!2 Hours
!3 Hours
|-
|
: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<ref name="pmid7148898">{{cite journal |vauthors=Carpenter MW, Coustan DR |title=Criteria for screening tests for gestational diabetes |journal=Am. J. Obstet. Gynecol. |volume=144 |issue=7 |pages=768–73 |year=1982 |pmid=7148898 |doi= |url=}}</ref>
|95
|180
|155
|140
|-
|
:::::National Diabetes Data Group (NDDG) approach<ref name="pmid510803">{{cite journal |vauthors= |title=Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. National Diabetes Data Group |journal=Diabetes |volume=28 |issue=12 |pages=1039–57 |year=1979 |pmid=510803 |doi= |url=}}</ref>
|105
|190
|165
|145
|}


===Cures for type 2 diabetes===
==Screening==
Type 2 diabetes can be cured by one type of [[gastric bypass surgery]] in 80-100% of severely obese patients. The effect is not due to weight loss because it usually occurs within days of surgery, which is before significant weight loss occurs. The pattern of secretion of gastrointestinal hormones is changed by the bypass and removal of the [[duodenum]] and proximal [[jejunum]], which together form the upper (proximal) part of the [[small intestine]].<ref name=pmid12409659>{{cite journal
|last=Rubino |first=F |coauthors=Gagner M
|title=Potential of surgery for curing type 2 diabetes mellitus
|journal=Ann. Surg. |issn=0003-4932
|volume=236 |issue=5 |pages=554-9 |year=2002
|pmid=12409659
|url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12409659
}}</ref> One hypothesis is that the proximal small intestine is dysfunctional in type 2 diabetes; its removal eliminates the source of an unknown hormone that contributes to insulin resistance.<ref name=pmid17060767>{{cite journal
|last=Rubino |first=F |coauthors=Forgione A, Cummings DE, ''et al''
|title=The mechanism of diabetes control after gastrointestinal bypass surgery reveals a role of the proximal small intestine in the pathophysiology of type 2 diabetes
|journal=Ann. Surg.
|volume=244 |issue=5 |pages=741–9 |year=2006
|pmid=17060767
|url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17060767
}}</ref> This surgery has been widely performed on morbidly obese patients and has the benefit of reducing the death rate from all causes by up to 40%.<ref name=pmid17715409>{{cite journal
|last=Adams |first=TD |coauthors=Gress RE, Smith SC, ''et al''
|title=Long-term mortality after gastric bypass surgery
|journal=N. Engl. J. Med. |issn=0028-4793
|volume=357 |issue=8 |pages=753–61 |year=2007
|pmid=17715409 |doi=10.1056/NEJMoa066603
}}</ref> A small number of normal to moderately obese patients with type 2 diabetes have successfully undergone similar operations.<ref name=pmid17386401>{{cite journal
|last=Cohen |first=RV |coauthors=Schiavon CA, Pinheiro JS, Correa JL, Rubino F
|title=Duodenal-jejunal bypass for the treatment of type 2 diabetes in patients with body mass index of 22-34 kg/m2: a report of 2 cases
|journal=Surg Obes Relat Dis.
|volume=3 |issue=2 |pages=195–7 |year=2007
|pmid=17386401 |doi=10.1016/j.soard.2007.01.009
}}</ref><ref name=NS>{{cite journal
|last=Vasonconcelos |first=Alberto
|date=[[2007-09-01]]
|title= Could type 2 diabetes be reversed using surgery?
|journal=[[New Scientist]]
|issue=2619 |pages=11-13
|url= http://www.newscientist.com/channel/health/mg19526193.100-could-type-2-diabetes-be-reversed-using-surgery.html
|accessdate=2007-09-26
}}</ref>


==Prognosis==
* Comparing developed and developing countries shows lower rate of progression from [[glucose intolerance]] to [[diabetes]], due to better [[Screening (medicine)|screening]] in developed and high-income areas.<ref name="LiuLi2013">{{cite journal|last1=Liu|first1=Xiaoqian|last2=Li|first2=Changping|last3=Gong|first3=Hui|last4=Cui|first4=Zhuang|last5=Fan|first5=Linlin|last6=Yu|first6=Wenhua|last7=Zhang|first7=Cui|last8=Ma|first8=Jun|title=An economic evaluation for prevention of diabetes mellitus in a developing country: a modelling study|journal=BMC Public Health|volume=13|issue=1|year=2013|issn=1471-2458|doi=10.1186/1471-2458-13-729}}</ref>
Patient education, understanding, and participation is vital since the complications of diabetes are far less common and less severe in people who have well-[[Diabetes management#Glycemic control|controlled]] blood sugar levels.<!--
--><ref>{{cite journal|last=Nathan|first=D.M.|coauthors=Cleary P.A., Backlund J.Y., ''et al'' |title=Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes |journal=N. Engl. J. Med. |volume=353 |issue=25 |pages=2643-53 |year=2005 |pmid=16371630 |doi=10.1056/NEJMoa052187}}</ref><ref>{{cite journal|author=The Diabetes Control and Complications Trial Research Group|year=1995|title=The effect of intensive diabetes therapy on the development and progression of neuropathy|url=http://www.annals.org/cgi/content/abstract/122/8/561|journal=Annals of Internal Medicine|issn=0003-4819|volume=122|issue=8|pages=561-568|pmid=7887548}}</ref>
Wider health issues accelerate the deleterious effects of diabetes. These include [[tobacco smoking|smoking]], [[hypercholesterolemia|elevated cholesterol]] levels, [[obesity]], [[hypertension|high blood pressure]], and lack of regular [[exercise]]. According to a study, women with high [[blood pressure]] have a threefold risk of developing diabetes.


Anecdotal evidence suggests that some of those with type 2 diabetes who exercise regularly, lose weight, and eat healthy diets may be able to keep some of disease or some of the effects of the disease in 'remission.'  Certainly these tips can help prevent people predisposed to type 2 diabetes and those at pre-diabetic stages from actually developing the disorder as it helps restore insulin sensitivity.  However patients should talk to their doctors about this for real expectations before undertaking it (esp. to avoid hypoglycemia or other complications); few people actually seem to go into total 'remission,' but some may find they need less of their insulin medications since the body tends to have lower insulin requirements during and shortly following exercise.  Regardless of whether it works that way or not for an individual, there are certainly other benefits to this healthy lifestyle for both diabetics and nondiabetics.
===Diabetes mellitus type 1===
The way diabetes is managed changes with age. Insulin production decreases due to age-related impairment of pancreatic beta cells. Additionally, insulin resistance increases due to the loss of lean tissue and the accumulation of fat, particularly intra-abdominal fat, and the decreased tissue sensitivity to insulin. Glucose tolerance progressively declines with age, leading to a high prevalence of type 2 diabetes and postchallenge hyperglycemia in the older population.<ref name="health"/> Age-related glucose intolerance in humans is often accompanied by insulin resistance, but circulating insulin levels are similar to those of younger people. <ref name=ajp>{{cite web | author = Annette M. Chang and Jeffrey B. Halter | title =Aging and insulin secretion | url=http://ajpendo.physiology.org/cgi/content/full/284/1/E7?ck=nck | year = 2003 | publisher=AJP - Endocrinology and Metabolism | accessdate=2007-05-14 }}</ref> Treatment goals for older patients with diabetes vary with the individual, and take into account health status, as well as life expectancy, level of dependence, and willingness to adhere to a treatment regimen.<ref name=nidkk>{{cite web | title = Diabetes and Aging | work =Diabetes Dateline | url=http://diabetes.niddk.nih.gov/about/dateline/spri02/8.htm | year = 2002 | publisher=National Institute of Diabetes and Digestive and Kidney Diseases | accessdate=2007-05-14}}</ref>


===Acute complications===
* According to the American Diabetic Association, screening for [[Diabetes mellitus type 1|type 1 DM]] is not recommended.
{{Main | Diabetic ketoacidosis | Nonketotic hyperosmolar coma | Hypoglycemia | Diabetic coma }}
===Diabetes mellitus type 2===


;Diabetic ketoacidosis
* [[Screening (medicine)|Screening]] is recommended for many people at various stages of life, and for those with [[Risk factor|risk factors]]. American Diabetes Association Recommendations for [[Diabetes]] [[Screening (medicine)|screening]] include:<ref name="pmid27979889">{{cite journal |vauthors= |title=2. Classification and Diagnosis of Diabetes |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S11–S24 |year=2017 |pmid=27979889 |doi=10.2337/dc17-S005 |url=}}</ref><ref name="pmid19502545">{{cite journal |vauthors= |title=International Expert Committee report on the role of the A1C assay in the diagnosis of diabetes |journal=Diabetes Care |volume=32 |issue=7 |pages=1327–34 |year=2009 |pmid=19502545 |pmc=2699715 |doi=10.2337/dc09-9033 |url=}}</ref><ref name="pmid24126648">{{cite journal |vauthors=Schellenberg ES, Dryden DM, Vandermeer B, Ha C, Korownyk C |title=Lifestyle interventions for patients with and at risk for type 2 diabetes: a systematic review and meta-analysis |journal=Ann. Intern. Med. |volume=159 |issue=8 |pages=543–51 |year=2013 |pmid=24126648 |doi=10.7326/0003-4819-159-8-201310150-00007 |url=}}</ref><ref name="pmid22683134">{{cite journal |vauthors=Perreault L, Pan Q, Mather KJ, Watson KE, Hamman RF, Kahn SE |title=Effect of regression from prediabetes to normal glucose regulation on long-term reduction in diabetes risk: results from the Diabetes Prevention Program Outcomes Study |journal=Lancet |volume=379 |issue=9833 |pages=2243–51 |year=2012 |pmid=22683134 |pmc=3555407 |doi=10.1016/S0140-6736(12)60525-X |url=}}</ref>
[[Diabetic ketoacidosis]] (DKA) is an acute and dangerous complication that is always a [[medical emergency]]. Lack of insulin causes the [[liver]] to turn fat into [[ketone bodies]], a fuel mainly used by the brain. Elevated levels of ketone bodies in the blood decrease the blood's [[pH]], leading to most of the symptoms of DKA. On presentation at hospital, the patient in DKA is typically dehydrated and is breathing rapidly and deeply. Abdominal pain is common and may be severe. The level of consciousness is typically normal until late in the process, when lethargy may progress to coma. Ketoacidosis can become severe enough to cause [[hypotension]], [[Shock (medical)|shock]], and death.  Analysis of the urine reveals significant levels of ketone bodies present (which spill over from the blood when the kidneys filter blood). Prompt proper treatment usually results in full recovery, though death can result from inadequate or delayed treatment, or from complications. Ketoacidosis is much more common in type 1 diabetes than type 2.


;Nonketotic hyperosmolar coma
==== Categories of Increased Risk for [[Diabetes]] ([[Prediabetes|Prediabetics]]) Recommendations: ====
The [[Nonketotic hyperosmolar coma|hyperosmolar nonketotic state]] (HNS) is an acute complication with many symptoms in common with DKA, but an entirely different cause and different treatment. In a person with very high blood glucose levels (usually considered to be above 300 mg/dl (16 mmol/l)), water is drawn out of cells into the blood by [[osmosis]] and the kidneys dump glucose into the urine. This results in loss of water and an increase in blood [[osmolality]]. If fluid is not replaced (by mouth or intravenously), the osmotic effect of high glucose levels combined with the loss of water will eventually lead to [[dehydration]]. The body's cells become progressively dehydrated as water is taken from them and excreted. Electrolyte imbalances are also common and dangerous. As with DKA, urgent medical treatment is necessary, especially volume replacement. Lethargy may ultimately progress to a coma, which is more common in type 2 diabetes than type 1.


;Hypoglycemia
*[[Screening (medicine)|Screening]] for [[prediabetes]] and risk for future [[diabetes]] with an informal assessment of [[Risk factor|risk factors]] or validated tools should be considered in [[asymptomatic]] adults. B
[[Hypoglycemia]], or abnormally low blood glucose, is a complication of several diabetes treatments. It may develop if the glucose intake does not cover the treatment. The patient may become agitated, sweaty, and have many symptoms of [[Autonomic nervous system|sympathetic]] activation of the autonomic nervous system resulting in feelings similar to dread and immobilized panic. Consciousness can be altered or even lost in extreme cases, leading to coma, [[seizure]]s, or even brain damage and death. In patients with diabetes, this may be caused by several factors, such as too much or incorrectly timed insulin, too much or incorrectly timed exercise (exercise decreases insulin requirements) or not enough food (specifically glucose-producing carbohydrates), but this is an over-simplification.


It is more accurate to note that iatogenic (caused by medical treatment) hypoglycemia is typically the result of the interplay of absolute (or relative) insulin excess and compromised glucose counterregulation in type 1 and advanced type 2 diabetes. Decrements in insulin, increments in glucagon, and, absent the latter, increments in epinephrine stand high in the hierarchy of redundant glucose counterregulatory factors that normally prevent or rapidly correct hypoglycemia. In insulin-deficient diabetes (exogenous) insulin levels do not decrease as glucose levels fall, and the combination of deficient glucagon and epinephrine responses causes defective glucose counterregulation.
* Testing for [[prediabetes]] and risk for future [[diabetes]] in [[asymptomatic]] people should be considered in adults of any age who are [[overweight]] or [[Obesity|obese]] ([[Body mass index|BMI]] >25 kg/m2 or >23 kg/m2 in Asian Americans) and who have one or more additional [[Risk factor|risk factors]] for [[diabetes]]. B
* For all people, testing should begin at age 45 years. B
* If tests are normal, repeat testing carried out at a minimum of 3-year intervals is reasonable. C
* To test for [[prediabetes]], [[Blood sugar|fasting plasma glucose]], 2-hours [[Blood sugar|plasma glucose]] during 75-g oral [[glucose tolerance test]], and [[Glycosylated hemoglobin|HbA1C]] are equally appropriate. B
* In [[Prediabetes|prediabetic]] patients, identify and, if appropriate, treat other [[Risk factor|risk factors]] of [[cardiovascular disease]]. B
* Testing for [[prediabetes]] should be considered in children and adolescents who are [[overweight]] or [[Obesity|obese]] ([[Body mass index|BMI]] = 85th [[percentile]] for age and sex, weight for height = 85th [[percentile]], or weight 120% of ideal for height) and who have additional [[Risk factor|risk factors]] for [[diabetes]] (Table 2.5). E


Furthermore, reduced sympathoadrenal responses can cause hypoglycemia unawareness. The concept of hypoglycemia-associated autonomic failure (HAAF) in diabetes posits that recent incidents of hypoglycemia causes both defective glucose counterregulation and hypoglycemia unawareness. By shifting glycemic thresholds for the sympathoadrenal (including epinephrine) and the resulting neurogenic responses to lower plasma glucose concentrations, antecedent hypoglycemia leads to a vicious cycle of recurrent hypoglycemia and further impairment of glucose counterregulation. In many cases (but not all), short-term avoidance of hypoglycemia reverses hypoglycemia unawareness in most affected patients, although this is easier in theory than it is in practice.


In most cases, hypoglycemia is treated with sugary drinks or food. In severe cases, an injection of [[glucagon]] (a hormone with the opposite effects of insulin) or an [[intravenous]] infusion of dextrose is used for treatment, but usually only if the person is unconscious. In hospitals, intravenous dextrose is often used.
{| class="wikitable"
|+ADA 2018 [DO NOT EDIT]
!Criteria for testing for diabetes or prediabetes in asymptomatic adults
|-
|1. Testing should be considered in [[overweight]] or [[Obesity|obese]] (BMI 25 kg/m2 or 23 kg/m2 in Asian Americans) adults who have one or more of the following [[Risk factor|risk factors]]:


===Chronic complications===
* First-degree relative with [[diabetes]]
;Vascular disease
* High-risk [[race]]/[[Ethnicity and health|ethnicity]] (e.g., African American, Latino, Native American, Asian American, Pacific Islander)
Chronic elevation of blood glucose level leads to damage of [[blood vessel]]s ([[angiopathy]]). The [[endothelial cell]]s lining the blood vessels take in more glucose than normal, since they don't depend on insulin. They then form more surface [[glycoprotein]]s than normal, and cause the [[basement membrane]] to grow thicker and weaker. In diabetes, the resulting problems are grouped under "[[microvascular disease]]" (due to damage to small blood vessels) and "[[macrovascular disease]]" (due to damage to the [[artery|arteries]]).
* History of [[Cardiovascular disease|CVD]]
[[Image:Fundus photo showing scatter laser surgery for diabetic retinopathy EDA09.JPG|thumb|Image of [[Fundus (eye)|fundus]] showing scatter [[Laser scalpel|laser surgery]] for [[diabetic retinopathy]]]]
*[[Hypertension]] (140/90 mmHg or on therapy for hypertension)
The damage to small blood vessels leads to a [[microangiopathy]], which can cause one or more of the following:
*[[High density lipoprotein|HDL]] [[cholesterol]] level <35 mg/dL (0.90 mmol/L) and/or a [[triglyceride]] level >250 mg/dL (2.82 mmol/L)
* ''[[Diabetic retinopathy]]'', growth of friable and poor-quality new blood vessels in the [[retina]] as well as [[macular edema]] (swelling of the [[macula]]), which can lead to severe [[vision loss]] or blindness. Retinal damage (from microangiopathy) makes it the most common cause of blindness among non-elderly adults in the US.
* Women with [[polycystic ovary syndrome]]
* ''[[Diabetic neuropathy]]'', abnormal and decreased sensation, usually in a 'glove and stocking' distribution starting with the feet but potentially in other nerves, later often fingers and hands. When combined with damaged blood vessels this can lead to ''[[diabetic foot]]'' (see below). Other forms of diabetic neuropathy may present as mononeuritis or [[autonomic neuropathy]]. [[Diabetic amyotrophy]] is muscle weakness due to neuropathy.
* Physical inactivity
* ''[[Diabetic nephropathy]]'', damage to the [[kidney]] which can lead to chronic renal failure, eventually requiring [[dialysis]]. Diabetes mellitus is the most common cause of adult kidney failure worldwide in the developed world.
* Other clinical conditions associated with [[insulin resistance]] (e.g., severe [[obesity]], [[acanthosis nigricans]])
|-
|2. Patients with [[prediabetes]] ([[Glycosylated hemoglobin|A1C]] > 5.7% [39 mmol/mol], IGT, or IFG) should be tested yearly.
|-
|3. Women who were diagnosed with [[Gestational diabetes|GDM]] should have lifelong testing at least every 3 years.
|-
|4. For all other patients, testing should begin at age 45 years.
|-
|5. If results are normal, testing should be repeated at a minimum of 3-year intervals, with consideration of more frequent testing depending on initial results and risk status.
|}


[[Macrovascular disease]] leads to cardiovascular disease, to which  accelerated [[atherosclerosis]] is a contributor:
* To test for [[Diabetes mellitus type 2|type 2 diabetes]], [[fasting plasma glucose]], 2-h plasma glucose after 75-g [[Glucose tolerance test|oral glucose tolerance test]], and [[HbA1C]] are equally appropriate.
*[[Coronary artery disease]], leading to [[Angina pectoris|angina]] or [[myocardial infarction]] ("heart attack")
*[[Stroke]] (mainly the ischemic type)
*[[Peripheral artery occlusive disease|Peripheral vascular disease]], which contributes to [[intermittent claudication]] (exertion-related leg and foot pain) as well as diabetic foot.
*[[Diabetic myonecrosis]] ('muscle wasting')


Diabetic foot, often due to a combination of neuropathy and arterial disease, may cause skin [[ulcer]] and [[infection]] and, in serious cases, [[necrosis]] and gangrene. It is why diabetics are prone to leg and foot infections and why it takes longer for them to heal from leg and foot wounds. It is the most common cause of adult amputation, usually of toes and or feet, in the developed world.
{| class="wikitable"
|+
!Categories of increased risk for diabetes (prediabetes)
|-
|FPG 100 mg/dL (5.6 mmol/L) to 125 mg/dL (6.9 mmol/L) (IFG)
|-
| align="center" |OR
|-
|2-h PG during 75-g [[Glucose tolerance test|OGTT]] 140 mg/dL (7.8 mmol/L) to 199 mg/dL (11.0 mmol/L) (IGT)
|-
| align="center" |OR
|-
|[[Glycosylated hemoglobin|A1C]] 5.7–6.4% (39–47 mmol/mol)
|}


[[Carotid artery stenosis]] does not occur more often in diabetes, and there appears to be a lower prevalence of [[abdominal aortic aneurysm]]. However, diabetes does cause higher morbidity, mortality and operative risks with these conditions.<!--
===Gestational diabetes===
--><ref>{{cite journal | author = Weiss J, Sumpio B | title = Review of prevalence and outcome of vascular disease in patients with diabetes mellitus. | journal = Eur J Vasc Endovasc Surg | volume = 31 | issue = 2 | pages = 143-50 | year = 2006 | id = PMID 16203161}}</ref>


==Epidemiology==
* All [[Pregnancy|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 factor|risk factors]] include:<ref name="pmid26696675">{{cite journal |vauthors= |title=2. Classification and Diagnosis of Diabetes |journal=Diabetes Care |volume=39 Suppl 1 |issue= |pages=S13–22 |year=2016 |pmid=26696675 |doi=10.2337/dc16-S005 |url=}}</ref><ref name="pmid24424622">{{cite journal |vauthors=Moyer VA |title=Screening for gestational diabetes mellitus: U.S. Preventive Services Task Force recommendation statement |journal=Ann. Intern. Med. |volume=160 |issue=6 |pages=414–20 |year=2014 |pmid=24424622 |doi=10.7326/M13-2905 |url=}}</ref>
In 2000, according to the World Health Organization, at least 171 million people worldwide suffer from diabetes. Its incidence is increasing rapidly, and it is estimated that by the year 2030, this number will double. Diabetes mellitus occurs throughout the world, but is more common (especially type 2) in the more developed countries. The greatest increase in prevalence is, however, expected to occur in Asia and Africa, where most patients will likely be found by 2030. The increase in incidence of diabetes in developing countries follows the trend of urbanization and lifestyle changes, perhaps most importantly a "Western-style" diet. This has suggested an environmental (i.e., dietary) effect, but there is little understanding of the mechanism(s) at present, though there is much speculation, some of it most compellingly presented.
** A [[Family history (medicine)|family history]] of [[diabetes]] especially in first degree relatives
** Maternal age >25 yrs
** Certain [[Ethnic group|ethnic]] groups (such as Native American, Hispanic-American, African-American, South or East Asian, Pacific Islander)
**[[Body mass index]] greater than 25 kg/m<sup>2</sup>
**[[Gestational diabetes]] or impaired [[glucose tolerance test]] in previous [[Pregnancy|pregnancies]]
** Previous [[Childbirth|delivery]] of a baby >9 pounds
** Personal history of  [[impaired glucose tolerance]] or [[impared fasting glucose|impaired fasting glucose]] ([[Prediabetes|pre-diabetes]])
**[[Glycosuria]] at the first prenatal visit
** Certain medical conditions (such as [[metabolic syndrome]], [[polycystic ovary syndrome]] ([[Polycystic ovary syndrome|PCOS]]), current use of [[glucocorticoids]], [[hypertension]])
** Previous history of unexplained [[miscarriage (patient information)|miscarriage]] or [[stillbirth]]
**[[Smoking]] doubles the risk of [[gestational diabetes]]
**[[Multiple gestation]]
** Genetic predisposition (.e.g. [[glucokinase]] [[mutation]])


Diabetes is in the top 10, and perhaps the top 5, of the most significant diseases in the developed world, and is gaining in significance there and elsewhere (see [[big killer]]s).


For at least 20 years, diabetes rates in North America have been increasing substantially. In 2005 there were about 20.8 million people with diabetes in the United States alone. According to the American Diabetes Association, there are about 6.2 million people undiagnosed and about 41 million people that would be considered prediabetic.<!--
  --><ref name="AA2005-Stats">{{cite web | author = American Diabetes Association | year = 2005 | url = http://www.diabetes.org/diabetes-statistics/prevalence.jsp | title = Total Prevalence of Diabetes & Pre-diabetes | accessdate = 2006-03-17}}</ref>
However, the criteria for diagnosing diabetes in the USA means that it is more readily diagnosed than in some other countries. The [[Centers for Disease Control]] has termed the change an [[epidemic]]. The [[National Diabetes Information Clearinghouse]] estimates that diabetes costs $132 billion in the United States alone every year. About 5%&ndash;10% of diabetes cases in North America are type 1, with the rest being type 2.  The fraction of type 1 in other parts of the world differs; this is likely due to both differences in the rate of type 1 and differences in the rate of other types, most prominently type 2. Most of this difference is not currently understood. The American Diabetes Association point out the 2003 assessment of the National Center for Chronic Disease Prevention and Health Promotion (Centers for Disease Control and Prevention) that 1 in 3 Americans born after 2000 will develop diabetes in their lifetime.<!--
  --><ref>{{cite journal |author=Narayan K, Boyle J, Thompson T, Sorensen S, Williamson D |title=Lifetime risk for diabetes mellitus in the United States |journal=JAMA |volume=290 |issue=14 |pages=1884-90 |year=2003 |id=PMID 14532317}}</ref><!--
  --><ref name="AA2005-Stats">{{cite web | author = American Diabetes Association | year = 2005 | url = http://www.diabetes.org/diabetes-statistics/prevalence.jsp | title = Total Prevalence of Diabetes & Pre-diabetes | accessdate = 2006-03-17}}</ref>


According to the American Diabetes Association, approximately 18.3% (8.6 million) of Americans age 60 and older have diabetes. <ref name=dlife>{{cite web | title = Seniors and Diabetes | work =Elderly And Diabetes - Diabetes and Seniors | url=http://www.dlife.com/dLife/do/ShowContent/daily_living/seniors/ | year = 2006 | publisher=LifeMed Media | accessdate=2007-05-14}}</ref> Diabetes mellitus prevalence increases with age, and the numbers of older persons with diabetes are expected to grow as the elderly population increases in number. The National Health and Nutrition Examination Survey (NHANES III) demonstrated that, in the population over 65 years old, 18% to 20% have diabetes, with 40% having either diabetes or its precursor form of [[impaired glucose tolerance]].<ref name="health">{{cite journal |author=Harris MI, Flegal KM, Cowie CC, ''et al'' |title=Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The Third National Health and Nutrition Examination Survey, 1988-1994 |journal=Diabetes Care |volume=21 |issue=4 |pages=518-24 |year=1998 |pmid=9571335 |doi=}}</ref>
==Prevention==
 
==History==
The term ''diabetes'' was coined by [[Aretaeus of Cappadocia]]. It was derived from the Greek verb διαβαίνειν, ''diabaínein'',  itself formed from the prefix ''dia''-, "across, apart," and the verb ''bainein'', "to walk, stand."  The verb ''diabeinein'' meant "to stride, walk, or stand with legs asunder"; hence, its derivative ''diabētēs'' meant "one that straddles," or specifically "a compass, siphon." The sense "siphon" gave rise to the use of ''diabētēs'' as the name for a disease involving the discharge of excessive amounts of urine. Diabetes is first recorded in English, in the form diabete, in a medical text written around 1425. In 1675, [[Thomas Willis]] added the word ''mellitus'', from the Latin meaning "honey", a reference to the sweet taste of the urine. This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, and Indians. In 1776, Matthew Dobson confirmed that the sweet taste was because of an excess of a kind of sugar in the urine and blood of people with diabetes.<ref>{{cite journal|last=Dobson|first=M.|coauthors=|year=1776|title=Nature of the urine in diabetes|url=|journal=Medical Observations and Inquiries|volume=5|pages=298–310|doi=}}</ref>


The ancient Indians tested for diabetes by observing whether ants were attracted to a person's urine, and called the ailment "sweet urine disease" (Madhumeha). The Korean, Chinese, and Japanese words for diabetes are based on the same ideographs (糖尿病) which mean "sugar urine disease".
* Life style modification is the mainstay of prevention of [[diabetes mellitus]]. It includes, changes in diet, weight reduction and [[Physical exercise|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 [[Diabetes mellitus type 2|type 2 diabetes]] by 58% over 3 years.<ref name="pmid17098085">{{cite journal |vauthors=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 |title=Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study |journal=Lancet |volume=368 |issue=9548 |pages=1673–9 |year=2006 |pmid=17098085 |doi=10.1016/S0140-6736(06)69701-8 |url=}}</ref>
Although diabetes has been recognized since antiquity, and treatments of various efficacy have been known in various regions since the Middle Ages, and in legend for much longer, pathogenesis of diabetes has only been understood experimentally since about 1900.<!--
*Based on a study, life style modification can improve glucose tolerance and decrease the [[cardiovascular]] [[Complication (medicine)|complications]]. Even [[Obesity|obese]] [[Diabetes|diabetic]] patients in this study showed reduced chance of [[diabetes mellitus]] development after 2 years of life style interventions.<ref name="Lindstrom2003">{{cite journal|last1=Lindstrom|first1=J.|title=Prevention of Diabetes Mellitus in Subjects with Impaired Glucose Tolerance in the Finnish Diabetes Prevention Study: Results From a Randomized Clinical Trial|journal=Journal of the American Society of Nephrology|volume=14|issue=90002|year=2003|pages=108S–113|issn=1046-6673|doi=10.1097/01.ASN.0000070157.96264.13}}</ref>
  --><ref name="FASEBJ2002-Patlak">{{cite journal | author=Patlak M | title=New weapons to combat an ancient disease: treating diabetes | journal=FASEB J | year=2002 | pages=1853 | volume=16 | issue=14 | url=http://www.fasebj.org/cgi/content/full/16/14/1853e | id=PMID 12468446 }}</ref>
*Patients with a modified life style had 58% less chance to develop [[diabetes]], compared to the [[Scientific control|control group]] after a 3 years study.<ref name="TuomilehtoLindström2001">{{cite journal|last1=Tuomilehto|first1=Jaakko|last2=Lindström|first2=Jaana|last3=Eriksson|first3=Johan G.|last4=Valle|first4=Timo T.|last5=Hämäläinen|first5=Helena|last6=Ilanne-Parikka|first6=Pirjo|last7=Keinänen-Kiukaanniemi|first7=Sirkka|last8=Laakso|first8=Mauri|last9=Louheranta|first9=Anne|last10=Rastas|first10=Merja|last11=Salminen|first11=Virpi|last12=Aunola|first12=Sirkka|last13=Cepaitis|first13=Zygimantas|last14=Moltchanov|first14=Vladislav|last15=Hakumäki|first15=Martti|last16=Mannelin|first16=Marjo|last17=Martikkala|first17=Vesa|last18=Sundvall|first18=Jouko|last19=Uusitupa|first19=Matti|title=Prevention of Type 2 Diabetes Mellitus by Changes in Lifestyle among Subjects with Impaired Glucose Tolerance|journal=New England Journal of Medicine|volume=344|issue=18|year=2001|pages=1343–1350|issn=0028-4793|doi=10.1056/NEJM200105033441801}}</ref> This life style modification includes [[Physical exercise|physical activity]], [[weight loss]], limiting the total dietary intake, lowering intake of [[saturated fat]] and increasing [[dietary fiber]].<ref>{{cite journal|title=Primary Prevention of Type 2 Diabetes Mellitus by Lifestyle Intervention: Implications for Health Policy|journal=Annals of Internal Medicine|volume=140|issue=11|year=2004|pages=951|issn=0003-4819|doi=10.7326/0003-4819-140-11-200406010-00036}}</ref>
The discovery of a role for the pancreas in diabetes is generally ascribed to [[Joseph von Mering]] and [[Oskar Minkowski]], who in 1889 found that dogs whose pancreas was removed developed all the signs and symptoms of diabetes and died shortly afterwards.<!--
*Traditionally, life style modifications mainly focused on [[weight loss]], which is still one of the main components. Nevertheless other factors, such as better [[Diabetes management|glycemic control]], careful food selection, regular [[Physical exercise|physical activity]] and consistent visits and behavioral interventions to maintain adherence are also considered crucial in new approaches.<ref name="BuseGinsberg2007">{{cite journal|last1=Buse|first1=John B.|last2=Ginsberg|first2=Henry N.|last3=Bakris|first3=George L.|last4=Clark|first4=Nathaniel G.|last5=Costa|first5=Fernando|last6=Eckel|first6=Robert|last7=Fonseca|first7=Vivian|last8=Gerstein|first8=Hertzel C.|last9=Grundy|first9=Scott|last10=Nesto|first10=Richard W.|last11=Pignone|first11=Michael P.|last12=Plutzky|first12=Jorge|last13=Porte|first13=Daniel|last14=Redberg|first14=Rita|last15=Stitzel|first15=Kimberly F.|last16=Stone|first16=Neil J.|title=Primary Prevention of Cardiovascular Diseases in People With Diabetes Mellitus|journal=Circulation|volume=115|issue=1|year=2007|pages=114–126|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.106.179294}}</ref>  
  --><ref>{{cite journal | author=Von Mehring J, Minkowski O. | title=Diabetes mellitus nach pankreasexstirpation. | journal=Arch Exp Pathol Pharmakol | year=1890 | volume=26 | pages=371-387}}</ref>
*Intensive interdisciplinary intervention (II) on [[Diet (nutrition)|dietary]] habits and [[Physical exercise|physical activity]] was related to lower [[blood pressure]], [[Blood sugar|plasma glucose]] and [[binge eating disorder]] ([[Binge eating disorder|BED]]) frequency, compared to 9-month traditional (TI) intervention in patients at risk for [[diabetes]]. Furthermore, both interventions were effective in lowering the frequency of [[depression]] in these people.<ref name="CezarettoSiqueira-Catania2011">{{cite journal|last1=Cezaretto|first1=Adriana|last2=Siqueira-Catania|first2=Antonela|last3=de Barros|first3=Camila Risso|last4=Salvador|first4=Emanuel Péricles|last5=Ferreira|first5=Sandra Roberta G.|title=Benefits on quality of life concomitant to metabolic improvement in intervention program for prevention of diabetes mellitus|journal=Quality of Life Research|volume=21|issue=1|year=2011|pages=105–113|issn=0962-9343|doi=10.1007/s11136-011-9919-2}}</ref>
In 1910, Sir [[Edward Albert Sharpey-Schafer]] suggested that people with diabetes were deficient in a single chemical that was normally produced by the pancreas—he proposed calling this substance ''insulin'', from the Latin ''insula'', meaning island, in reference to the insulin-producing [[islets of Langerhans]] in the pancreas.<ref name="FASEBJ2002-Patlak"/>
*Study on [[aspirin]] in [[Diabetes|diabetic]] patients with no previous history of [[cardiovascular disease]] showed significant reduction in serious vascular events. Nevertheless, the high risk of [[bleeding]] with [[aspirin]] use overshadows this desirable outcome.<ref>{{cite journal|title=Effects of Aspirin for Primary Prevention in Persons with Diabetes Mellitus|journal=New England Journal of Medicine|volume=379|issue=16|year=2018|pages=1529–1539|issn=0028-4793|doi=10.1056/NEJMoa1804988}}</ref>
 
*An intervention done on 682 patients with impaired [[glucose tolerance test]], evaluated the effect of [[acarbose]] as a possible agent for preventing the [[diabetes]] development. Based on this study, after 3 months, patients who received [[acarbose]] showed significant conversion to normal [[glucose]] level. On the other hand, patients who received [[placebo]], had increased conversion to [[Diabetes|diabetic]] states.<ref name="ChiassonJosse2002">{{cite journal|last1=Chiasson|first1=Jean-Louis|last2=Josse|first2=Robert G|last3=Gomis|first3=Ramon|last4=Hanefeld|first4=Markolf|last5=Karasik|first5=Avraham|last6=Laakso|first6=Markku|title=Acarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM randomised trial|journal=The Lancet|volume=359|issue=9323|year=2002|pages=2072–2077|issn=01406736|doi=10.1016/S0140-6736(02)08905-5}}</ref>
The endocrine role of the pancreas in metabolism, and indeed the existence of insulin, was not further clarified until 1921, when Sir [[Frederick Grant Banting]] and [[Charles Herbert Best]] repeated the work of Von Mering and Minkowski, and went further to demonstrate they could reverse induced diabetes in dogs by giving them an extract from the pancreatic islets of Langerhans of healthy dogs.<!--
  --><ref name="CanadMedAssocJ1922-Banting">{{cite journal | url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=1933711 | author= Banting FG, Best CH, Collip JB, Campbell WR, Fletcher AA | title=Pancreatic extracts in the treatment of diabetes mellitus | journal= Canad Med Assoc J | year=1922 | pages=141&ndash;146 | volume=12}}</ref>
Banting, Best, and colleagues (especially the chemist [[James Collip|Collip]]) went on to purify the hormone insulin from bovine pancreases at the [[University of Toronto]]. This led to the availability of an effective treatment—insulin injections—and the first patient was treated in 1922. For this, Banting and laboratory director MacLeod received the [[Nobel Prize in Physiology or Medicine]] in 1923; both shared their Prize money with others in the team who were not recognized, in particular Best and Collip.  Banting and Best made the patent available without charge and did not attempt to control commercial production. [[Insulin]] production and therapy rapidly spread around the world, largely as a result of this decision.
 
The distinction between what is now known as type 1 diabetes and type 2 diabetes was first clearly made by Sir [[Harold Percival Himsworth|Harold Percival (Harry) Himsworth]], and published in January 1936.<ref name="Lancet1936-Himsworth">{{cite journal | author= Himsworth | title=''Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive types | journal= Lancet | year=1936 | pages=127&ndash;130 | volume=i}}</ref>
 
Despite the availability of treatment, diabetes has remained a major cause of death. For instance, [[statistics]] reveal that the cause-specific [[mortality rate]] during 1927 amounted to about 47.7 per 100,000 population in Malta.<!--
  --><ref> Department of Health (Malta), 1897&ndash;1972:Annual Reports.</ref>
 
Other landmark discoveries include:<ref name="FASEBJ2002-Patlak" />
* identification of the first of the [[sulfonylurea]]s in 1942
* reintroduction of the use of [[biguanides]] for Type 2 diabetes in the late 1950s. The initial [[phenformin]] was withdrawn worldwide (in the U.S. in 1977) due to its potential for sometimes fatal lactic acidosis and [[metformin]] was first marketed in France in 1979, but not until 1994 in the US.
* the determination of the [[amino acid sequence]] of insulin (by Sir [[Frederick Sanger]], for which he received a Nobel Prize)
* the [[radioimmunoassay]] for insulin, as discovered by [[Rosalyn Yalow]] and [[Solomon Berson]] (gaining Yalow the 1977 Nobel Prize in Physiology or Medicine)<ref>{{cite journal |author=Yalow RS, Berson SA |title=Immunoassay of endogenous plasma insulin in man |journal=J. Clin. Invest. |volume=39 |issue= |pages=1157-75 |year=1960 |pmid=13846364 |doi=}}</ref>
* the three-dimensional structure of insulin ({{PDB|2INS}})
* Dr [[Gerald Reaven]]'s identification of the constellation of symptoms now called [[metabolic syndrome]] in 1988
* demonstration that intensive [[Diabetes management#Glycemic control|glycemic control]] in type 1 diabetes reduces chronic side effects more as glucose levels approach 'normal' in a large longitudinal study,<ref>{{cite journal | author = | title = The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial Research Group. | journal = N Engl J Med | volume = 329 | issue = 14 | pages = 977-86 | year = 1993 | id = PMID 8366922}}</ref> and also in type 2 diabetics in other large studies
* identification of the first [[thiazolidinedione]] as an effective insulin sensitizer during the 1990s
 
==Social issues==
The 1989 Declaration of St Vincent was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important both in terms of quality of life and life expectancy but also economically - expenses to diabetes have been shown to be a major drain on health- and productivity-related resources for healthcare systems and governments.
 
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.<ref name="EO005-Dubois&Bankauskaite">{{cite journal | author= Dubois, HFW and Bankauskaite, V| title=Type 2 diabetes programmes in Europe | url= http://www.euro.who.int/Document/Obs/EuroObserver7_3.pdf | format=PDF | journal=Euro Observer | year=2005 | pages=5&ndash;6 | volume=7 | issue=2}}</ref>
 
A study shows that diabetic patients with neuropathic symptoms such as [[Paresthesia|numb]]ness or tingling in feet or hands are twice more likely to be unemployed than those without the symptoms.<ref name="pmid17563611">{{cite journal
|author=Stewart WF, Ricci JA, Chee E, Hirsch AG, Brandenburg NA
|title=Lost productive time and costs due to diabetes and diabetic neuropathic pain in the US workforce
|journal=J. Occup. Environ. Med.
|volume=49
|issue=6
|pages=672–9
|year=2007
|pmid=17563611
|doi=10.1097/JOM.0b013e318065b83a
}}</ref>
 
==See also==
*[[List of terms associated with diabetes]]


==References==
==References==
{{reflist|2}}
{{reflist|2}}
Data from the Report of the Expert Committee on the diagnosis and classification of diabetes mellitus
==External links==
{{refbegin|2}}
*[http://www.diabetes.org/ American Diabetes Association]
*[http://healthy-ojas.com/diabetes/diabetes-details.html Diabetes]
*[http://www.diabetesnsw.com.au/ Diabetes Australia-NSW]
*[http://www.diabetes.ca/ Canadian Diabetes Association]
*[http://www.who.int/nutrition/topics/dietnutrition_and_chronicdiseases/en/ Diet, Nutrition and the prevention of chronic diseases] (including diabetes) by a Joint [[WHO]]/[[FAO]] Expert consultation (2003)
*[http://www.cdc.gov/diabetes/ Centers for Disease Control Diabetes Section]
*[http://www.diabetes.org.uk  Diabetes UK]
*[http://www.dhealth.org/ Diabetes Health Institute]
*[http://www.diabetesinstitute.org/ Diabetes Institute for Immunology and Transplantion]
*[http://www.idsoc.org/ The Immunology of Diabetes Society]
*[http://www.idf.org/ International Diabetes Federation]
*[http://www.jdrf.org/ Juvenile Diabetes Research Foundation]
*[http://www.nlm.nih.gov/medlineplus/diabetes.html MedlinePlus Diabetes from the U.S. National Library of Medicine]
*[http://ndep.nih.gov/ National Diabetes Education Program]
*[http://www.diabetes.niddk.nih.gov/ National Diabetes Information Clearinghouse]
*[http://www.pcdeurope.org/ Primary Care Diabetes Europe]
*[http://www.who.int/mediacentre/factsheets/fs312/en/ World Health Organization fact sheet on diabetes]
*[http://www.who.int/diabetes/en/ World Health Organization—The Diabetes Programme]
*[http://www.mydogtag.ca/medical Diabetic Medical ID Tag]
{{refend}}
{{Endocrine pathology}}
{{SIB}}
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Latest revision as of 12:57, 9 September 2020

This page contains general information about Diabetes mellitus. For more information on specific types, please visit the pages:

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]Mehrian Jafarizade, M.D [3]

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.

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), non-traumatic lower extremity amputations, and adult blindness worldwide.

Accordingly, early diagnosis and treatment can result in significant decrease in mortality and morbidity. The incidence of diabetes has been increased constantly. 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.[1] 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). 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

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

Acute complications

Chronic complications

Macrovascular

Microvascular

Ophthalmic
Neuropathy
Nephropathy

Other organs[6]


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

Diagnosis

Diabetes mellitus type 1 and type 2

American Diabetes Association Diabetes Diagnostic Criteria 2018 (DO NOT EDIT)

ADA evidence-grading system for “Standards of Medical Care in Diabetes”
Level of evidence Description
A
  • Clear evidence from well-conducted, generalizable randomized controlled trials that are adequately powered, including
    • Evidence from a well-conducted multi-center trial
    • Evidence from a meta-analysis that incorporated quality ratings in the analysis
  • Compelling non-experimental evidence, i.e., “all or none” rule developed by the Center for Evidence-Based Medicine at the University of Oxford.
  • Supportive evidence from well-conducted randomized controlled trials that are adequately powered, including
    • Evidence from a well-conducted trial at one or more institutions
    • Evidence from a meta-analysis that incorporated quality ratings in the analysis
B
C
  • Supportive evidence from poorly controlled or uncontrolled studies
  • Conflicting evidence with the weight of evidence supporting the recommendation
D
  • Supportive evidence from poorly controlled or uncontrolled studies
  • Conflicting evidence with the weight of evidence supporting the recommendation
E Expert consensus or clinical experience


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

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

¶: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 2018 (DO NOT EDIT)[6]

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 hours.
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).
  • The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.
  • In the absence of unequivocal hyperglycemia, results should be confirmed by repeat testing.
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 Strategy

  • Perform a 75 g glucose tolerance test in 24-28 weeks of pregnancy and read the measures 1 h and 2 hours after glucose ingestion as well as fasting glucose.[7] The OGTT should be performed in the morning after an overnight fast of at least 8 hours. 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 hour: 180 mg/dL (10.0 mmol/L)
    • 2 hours: 153 mg/dL (8.5 mmol/L)

Two Step Strategy

  • In this approach, screening with a 1 hour 50-g glucose load test (GLT) followed by a 3 hours 100-g OGTT for those who screen positive.[8]
  • The diagnosis of GDM is made when at least 2 out of 4 measures of 3 hours 100-g OGTT became abnormal.
Cut off (mg/dl)
Fasting 1 Hour 2 Hours 3 Hours
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[9]
 95 180 155 140
National Diabetes Data Group (NDDG) approach[10]
 105 190 165 145

Screening

Diabetes mellitus type 1

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

Diabetes mellitus type 2

Categories of Increased Risk for Diabetes (Prediabetics) Recommendations:


ADA 2018 [DO NOT EDIT]
Criteria for testing for diabetes or prediabetes in asymptomatic adults
1. Testing should be considered in overweight or obese (BMI 25 kg/m2 or 23 kg/m2 in Asian Americans) adults who have one or more of the following risk factors:
2. Patients with prediabetes (A1C > 5.7% [39 mmol/mol], IGT, or IFG) should be tested yearly.
3. Women who were diagnosed with GDM should have lifelong testing at least every 3 years.
4. For all other patients, testing should begin at age 45 years.
5. If results are normal, testing should be repeated at a minimum of 3-year intervals, with consideration of more frequent testing depending on initial results and risk status.
Categories of increased risk for diabetes (prediabetes)
FPG 100 mg/dL (5.6 mmol/L) to 125 mg/dL (6.9 mmol/L) (IFG)
OR
2-h PG during 75-g OGTT 140 mg/dL (7.8 mmol/L) to 199 mg/dL (11.0 mmol/L) (IGT)
OR
A1C 5.7–6.4% (39–47 mmol/mol)

Gestational diabetes


Prevention

References

  1. ↑ 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.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 6.8 "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.
  7. ↑ 7.0 7.1 "Standards of Medical Care in Diabetes-2016 Abridged for Primary Care Providers". Clin Diabetes. 34 (1): 3–21. 2016. doi:10.2337/diaclin.34.1.3. PMID 26807004.
  8. ↑ "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.
  9. ↑ Carpenter MW, Coustan DR (1982). "Criteria for screening tests for gestational diabetes". Am. J. Obstet. Gynecol. 144 (7): 768–73. PMID 7148898.
  10. ↑ "Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. National Diabetes Data Group". Diabetes. 28 (12): 1039–57. 1979. PMID 510803.
  11. ↑ Liu, Xiaoqian; Li, Changping; Gong, Hui; Cui, Zhuang; Fan, Linlin; Yu, Wenhua; Zhang, Cui; Ma, Jun (2013). "An economic evaluation for prevention of diabetes mellitus in a developing country: a modelling study". BMC Public Health. 13 (1). doi:10.1186/1471-2458-13-729. ISSN 1471-2458.
  12. ↑ "2. Classification and Diagnosis of Diabetes". Diabetes Care. 40 (Suppl 1): S11–S24. 2017. doi:10.2337/dc17-S005. PMID 27979889.
  13. ↑ "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.
  14. ↑ 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.
  15. ↑ 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.
  16. ↑ "2. Classification and Diagnosis of Diabetes". Diabetes Care. 39 Suppl 1: S13–22. 2016. doi:10.2337/dc16-S005. PMID 26696675.
  17. ↑ Moyer VA (2014). "Screening for gestational diabetes mellitus: U.S. Preventive Services Task Force recommendation statement". Ann. Intern. Med. 160 (6): 414–20. doi:10.7326/M13-2905. PMID 24424622.
  18. ↑ 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.
  19. ↑ Lindstrom, J. (2003). "Prevention of Diabetes Mellitus in Subjects with Impaired Glucose Tolerance in the Finnish Diabetes Prevention Study: Results From a Randomized Clinical Trial". Journal of the American Society of Nephrology. 14 (90002): 108S–113. doi:10.1097/01.ASN.0000070157.96264.13. ISSN 1046-6673.
  20. ↑ Tuomilehto, Jaakko; Lindström, Jaana; Eriksson, Johan G.; Valle, Timo T.; Hämäläinen, Helena; Ilanne-Parikka, Pirjo; Keinänen-Kiukaanniemi, Sirkka; Laakso, Mauri; Louheranta, Anne; Rastas, Merja; Salminen, Virpi; Aunola, Sirkka; Cepaitis, Zygimantas; Moltchanov, Vladislav; Hakumäki, Martti; Mannelin, Marjo; Martikkala, Vesa; Sundvall, Jouko; Uusitupa, Matti (2001). "Prevention of Type 2 Diabetes Mellitus by Changes in Lifestyle among Subjects with Impaired Glucose Tolerance". New England Journal of Medicine. 344 (18): 1343–1350. doi:10.1056/NEJM200105033441801. ISSN 0028-4793.
  21. ↑ "Primary Prevention of Type 2 Diabetes Mellitus by Lifestyle Intervention: Implications for Health Policy". Annals of Internal Medicine. 140 (11): 951. 2004. doi:10.7326/0003-4819-140-11-200406010-00036. ISSN 0003-4819.
  22. ↑ Buse, John B.; Ginsberg, Henry N.; Bakris, George L.; Clark, Nathaniel G.; Costa, Fernando; Eckel, Robert; Fonseca, Vivian; Gerstein, Hertzel C.; Grundy, Scott; Nesto, Richard W.; Pignone, Michael P.; Plutzky, Jorge; Porte, Daniel; Redberg, Rita; Stitzel, Kimberly F.; Stone, Neil J. (2007). "Primary Prevention of Cardiovascular Diseases in People With Diabetes Mellitus". Circulation. 115 (1): 114–126. doi:10.1161/CIRCULATIONAHA.106.179294. ISSN 0009-7322.
  23. ↑ Cezaretto, Adriana; Siqueira-Catania, Antonela; de Barros, Camila Risso; Salvador, Emanuel Péricles; Ferreira, Sandra Roberta G. (2011). "Benefits on quality of life concomitant to metabolic improvement in intervention program for prevention of diabetes mellitus". Quality of Life Research. 21 (1): 105–113. doi:10.1007/s11136-011-9919-2. ISSN 0962-9343.
  24. ↑ "Effects of Aspirin for Primary Prevention in Persons with Diabetes Mellitus". New England Journal of Medicine. 379 (16): 1529–1539. 2018. doi:10.1056/NEJMoa1804988. ISSN 0028-4793.
  25. ↑ Chiasson, Jean-Louis; Josse, Robert G; Gomis, Ramon; Hanefeld, Markolf; Karasik, Avraham; Laakso, Markku (2002). "Acarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM randomised trial". The Lancet. 359 (9323): 2072–2077. doi:10.1016/S0140-6736(02)08905-5. ISSN 0140-6736.
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