糖尿病前症、前糖尿病状態

関: prediabetes

WordNet

express in words; "He said that he wanted to marry her"; "tell me what is bothering you"; "state your opinion"; "state your name" (同)say, tell
a state of depression or agitation; "he was in such a state you just couldnt reason with him"
the way something is with respect to its main attributes; "the current state of knowledge"; "his state of health"; "in a weak financial state"
a politically organized body of people under a single government; "the state has elected a new president"; "African nations"; "students who had come to the nations capitol"; "the countrys largest manufacturer"; "an industrialized land" (同)nation, country, land, commonwealth, res publica, body_politic
the territory occupied by one of the constituent administrative districts of a nation; "his state is in the deep south" (同)province
the group of people comprising the government of a sovereign state; "the state has lowered its income tax"

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〈C〉(人・物事の)『状態』,ありさま,様子 / 〈C〉《a ~》《話》極度の緊張状態,異常な精神状態 / 〈U〉地位,階級,身分 / 〈C〉〈U〉《しばしばS-》『国家』,国,政府 / 〈C〉《時にS-》(アメリカ・オーストラリアなどの)『州』 / 《the States》《話》『米国』 / 〈U〉威厳;公式;堂々とした様子 / 国家の,国事に関する / 《しばしばS-》《米》州の,州立の / 公式の,儀式用の
…‘を'『はっきり述べる』,公式に申し立てる / 〈当局が〉…‘を'指定する,決める
決まった,規定の;定期の / はっきり述べられた,明言された;公認された

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/01/21 12:12:11」(JST)

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Prediabetes is the state in which some but not all of the diagnostic criteria for diabetes are met.^[1] It is often described as the “gray area” between normal blood sugar and diabetic levels.

Classification

Impaired fasting glycaemia

Impaired fasting glycaemia or impaired fasting glucose (IFG) refers to a condition in which the fasting blood glucose is elevated above what is considered normal levels but is not high enough to be classified as diabetes mellitus. It is considered a pre-diabetic state, associated with insulin resistance and increased risk of cardiovascular pathology, although of lesser risk than impaired glucose tolerance (IGT). IFG sometimes progresses to type 2 diabetes mellitus. There is a 50% risk over 10 years of progressing to overt diabetes. Many newly identified IFG patients progress to diabetes in less than three years.^[2] IFG is also a risk factor for mortality.^[3]

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

World Health Organization (WHO) criteria for impaired fasting glucose differs from the American Diabetes Association (ADA) criteria, because the normal range of glucose is defined differently. Fasting plasma glucose levels 100 mg/dL (5.5 mmol/L) and higher have been shown to increase complication rates significantly. However, WHO opted to keep its upper limit of normal at under 110 mg/dL for fear of causing too many people to be diagnosed as having impaired fasting glucose, whereas the ADA lowered the upper limit of normal to a fasting plasma glucose under 100 mg/dL.

WHO criteria: fasting plasma glucose level from 6.1 mmol/l (110 mg/dL) to 6.9 mmol/L (125 mg/dL).^[4]^[5]

ADA criteria: fasting plasma glucose level from 5.6 mmol/L (100 mg/dL) to 6.9 mmol/L (125 mg/dL).

Impaired glucose tolerance

Impaired glucose tolerance (IGT) is a pre-diabetic state of dysglycemia, that is associated with insulin resistance and increased risk of cardiovascular pathology. IGT may precede type 2 diabetes mellitus by many years. IGT is also a risk factor for mortality.^[3]

Signs and symptoms

Prediabetes typically has no distinct signs or symptoms. Patients should monitor for signs and symptoms of type 2 diabetes mellitus. These include the following:^[6]

Constant hunger
Unexplained weight loss
Weight gain
Flu-like symptoms, including weakness and fatigue
Blurred vision
Slow healing of cuts or bruises
Tingling or loss of feeling in hands or feet
Recurring gum or skin infections
Recurring vaginal or bladder infections

Cause

Sleep disorders
Family history of diabetes
Impaired glucose levels and/or metabolic syndrome
Cardiovascular disease
Hypertension (high blood pressure)
Increased triglycerides levels
Low levels of good cholesterol (HDL)
Overweight or obesity
Women who have had gestational diabetes, had high birth weight babies (greater than 9 lbs.), and/or has Polycystic Ovarian Syndrome (PCOS)^[7]

These are associated with insulin resistance and are risk factors for the development of type 2 diabetes mellitus. Those in this stratum (IGT or IFG) are at increased risk of cardiovascular disease. Of the two, impaired glucose tolerance better predicts cardiovascular disease and mortality.^[8]^[9]^[10]

In a way, prediabetes is a misnomer since it is an early stage of diabetes. It is now known that the health complications associated with type 2 diabetes often occur before the medical diagnosis of diabetes is made.^[11]

Genetics

As the human genome is further explored, it is likely that multiple genetic anomalies at different loci will be found that confer varying degrees of predisposition to type 2 diabetes.^[12] Type 2 DM, which is the condition for which prediabetes is a precursor, has 90-100% concordance in twins; there is no HLA association.^[13] However, genetics play a relatively small role in the widespread occurrence of type 2 diabetes. This can be logically deduced from the huge increase in the occurrence of type 2 diabetes which has correlated with the significant change in western lifestyle.^[13]

Pathophysiology

Diabetes mellitus (DM) is a group of metabolic diseases that are characterized by hyperglycemia and defects in insulin production in the pancreas and/or impaired tolerance to insulin effects. DM is a leading cause of morbidity and mortality. Because the disease can be insidious, the diagnosis is often delayed. Effects of the disease can be macrovascular, as seen in the cardiovascular system/arthrosclerosis, or microvascular, as seen with retinopathy, nephropathy, and neuropathy.^[13]

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

Insulin enters cells by first binding to target insulin receptors. DM and some of those with prediabetes have impaired glucose tolerance—in these individuals, blood glucose rises to abnormally high levels. This may be from a lack of pancreatic hormone release or failure of target tissues to respond to the insulin present or both.^[13]

Prevention

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

Healthy meals (a diet low in saturated fat, sugars and refined carbohydrates, as well as limited sodium and total calories)
Physical exercise (45 minutes of exercise per day, five days a week)
Reducing weight by as little as 5-10 percent can have a significant impact on overall health.

Screening

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

Family history (parent or sibling)
Dyslipidemia (triglycerides > 200 or HDL < 35)
Overweight or obesity (body mass index > 25)
History of gestational diabetes or infant born with birth weight greater than 9 lb (4 kg)
High risk ethnic group
Hypertension (systolic blood pressure >140 mmHg or diastolic blood pressure > 90 mmHg)
Prior fasting blood glucose > 99
Known vascular disease
Markers of insulin resistance (PCOS, acanthosis nigricans)^[14]^[15]

Diagnosis

Prediabetes is usually diagnosed with a blood test:^[16]

Fasting blood sugar (glucose) level of:
- 110 to 125 mg/dL (6.1 mM to 6.9 mM) - WHO criteria
- 100 to 125 mg/dL (5.6 mM to 6.9 mM) - ADA criteria
Two hour glucose tolerance test after ingesting the standardized 75 Gm glucose solution the blood sugar level of 140 to 199 mg/dL (7.8 to 11.0 mM).^[17]
Glycated hemoglobin between 5.7 and 6.4 percent ^[18]

Levels above these limits would be a diagnosis for diabetes.

Management

Intensive weight loss and lifestyle intervention, if sustained, can substantially improve glucose tolerance and prevent progression from IGT to type 2 diabetes. The Diabetes Prevention Program (DPP)^[19] study found a 16% reduction in diabetes risk for every kilogram of weight loss. Reducing weight by 7% through a low-fat diet and performing 150 minutes of exercise a week is the goal. The ADA guidelines^[20] recommend modest weight loss (5-10% body weight), moderate-intensity exercise (30 minutes daily), and smoking cessation.

For patients with severe risk factors, prescription medication may be appropriate. This can be considered in patients for whom lifestyle therapy has failed or is not sustainable and who are at high-risk for developing type 2 diabetes.^[21] Metformin^[22] and acarbose help prevent the development of frank diabetes, and also have a good safety profile. Evidence also supports thiazolidinediones but there are safety concerns, and data on newer agents such as GLP-1 receptor agonists, DPP4 inhibitors or meglitinides are lacking.^[23]

Prognosis

The progression to type 2 diabetes mellitus is not inevitable for those with prediabetes. The progression into diabetes mellitus from prediabetes is approximately 25% over three to five years.^[24]

Epidemiology

Studies conducted from 1988-1994 indicated that at that time, of the US population 40–74 years of age, 33.8% had IFG, 15.4% had IGT, and 40.1% had prediabetes (IFG, IGT, or both). Eighteen million people (6.3% of the population) had type 2 diabetes in 2002.^[25]

References

^ "prediabetes" at Dorland's Medical Dictionary
^ Nichols GA, Hillier TA, Brown JB (2007). "Progression From Newly Acquired Impaired Fasting Glusose to Type 2 Diabetes". Diabetes Care 30 (2): 228–233. doi:10.2337/dc06-1392. PMC 1851903. PMID 17259486.
^ ^a ^b Barr EL, Zimmet PZ, Welborn TA, et al. (2007). "Risk of cardiovascular and all-cause mortality in individuals with diabetes mellitus, impaired fasting glucose, and impaired glucose tolerance: the Australian Diabetes, Obesity, and Lifestyle Study (AusDiab)". Circulation 116 (2): 151–7. doi:10.1161/CIRCULATIONAHA.106.685628. PMID 17576864.
^ .World Health Organization. "Definition, diagnosis and classification of diabetes mellitus and its complications: Report of a WHO Consultation. Part 1. Diagnosis and classification of diabetes mellitus". Retrieved 2007-05-29.
^ "Diagnosis and classification of diabetes mellitus". Diabetes Care. 28 Suppl 1: S37–42. 2005. doi:10.2337/diacare.28.suppl_1.s37. PMID 15618111.
^ Mayo Clinic Diabetes: "Prediabetes". [1]. Accessed Jan. 27, 2009.
^ Power of Prevention, American College of Endocrinology. Vol. 1, issue 2, May 2009. http://www.powerofprevention.com/
^ "The Prevention or Delay of Type 2 Diabetes," ADA, Diabetes Care, 25: 742-749, 2002.
^ National Diabetes Fact Sheet
^ Tominaga et al. (Jun 1999). "Impaired glucose tolerance is a risk factor for cardiovascular disease, but not impaired fasting glucose. The Funagata Diabetes Study". Diabetes Care 22 (6): 920–4. doi:10.2337/diacare.22.6.920.
^ WebMD: Prediabetes. Accessed Jan. 27, 2009.
^ UpToDate: Classification of diabetes mellitis and genetic diabetic syndromes, Nov 14, 2007
^ ^a ^b ^c ^d Cotran, Kumar, Collins; Robbins Pathologic Basis of Disease, Saunders Sixth Edition, 1999; 913-926.
^ "ADA: Standards of Medical Care in Diabetes", Diabetes Care 27: Supp 1.515, 2004.
^ "Diabetes Guidelines Taskforce: AACE Guidelines for the Management of DM", Endocrin Pract 1995, 1.149
^ http://www.diabetes.co.uk/pre-diabetes.html
^ Jellinger, Paul S. "What You Need to Know about Prediabetes." Power of Prevention, American College of Endocrinology. Vol. 1, issue 2, May 2009. http://www.powerofprevention.com/
^ New Guidelines Urge A1C Test for Diabetes Diagnosis. HealthDay. December 29, 2009.
^ http://diabetes.niddk.nih.gov/dm/pubs/preventionprogram/
^ https://www.diabetes.org/diabetes-prevention/how-to-prevent-diabetes.jsp
^ UptoDate: Prediction and prevention of type 2 diabetes mellitus; www.utdol.com/utd/content/topic.do?topicKey=diabetes.
^ Lilly M, Godwin M (Apr 2009). "Treating prediabetes with metformin: systematic review and meta-analysis". Canadian Family Physician 55 (4): 363–9.
^ "American College of Endocrinology Consensus Statement on the diagnosis and management of pre-diabetes in the continuum of hyperglycemia—When do the risks of diabetes begin?" (PDF). American College of Endocrinology Task Force on Pre-Diabetes. Retrieved 2008-07-24.
^ Nathan et al. (Mar 2007). "Impaired fasting glucose and impaired glucose tolerance: implications for care". Diabetes Care 30 (3): 753–9. doi:10.2337/dc07-9920. PMID 17327355.
^ CDC: Diabetes. National Diabetes Fact Sheet; United States, 2003.

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 小児および思春期における2型糖尿病の疫学、症状、および診断 epidemiology presentation and diagnosis of type 2 diabetes mellitus in children and adolescents
2. 2型糖尿病の予測及び予防 prediction and prevention of type 2 diabetes mellitus
3. 糖尿病性多発性神経障害の臨床症状および診断 clinical manifestations and diagnosis of diabetic polyneuropathy
4. 妊娠糖尿病の内科的管理およびフォローアップ medical management and follow up of gestational diabetes mellitus
5. 妊娠中の糖尿病のスクリーニングおよび診断 screening and diagnosis of diabetes mellitus during pregnancy

English Journal

The effects of insulin resistance on skeletal muscle growth and exercise capacity in type 2 diabetic mouse models.

Ostler JE, Maurya SK, Dials J, Roof SR, Devor ST, Ziolo MT, Periasamy M.Author information 1The Ohio State University College of Medicine.AbstractType 2 diabetes mellitus is associated with an accelerated muscle loss during aging, decreased muscle function, and increased disability. To better understand the mechanisms causing this muscle deterioration in type 2 diabetes, we assessed muscle weight, exercise capacity, and biochemistry in db/db and TallyHo mice at prediabetic and overtly diabetic ages. Maximum running speeds and muscle weights were already reduced in prediabetic db/db mice when compared to lean controls and more severely reduced in the overtly diabetic db/db mice. In contrast to db/db mice, TallyHo muscle size dramatically increased and maximum running speed was maintained during the progression from prediabetes to overt diabetes. Analysis of mechanisms that may contribute to decreased muscle weight in db/db mice demonstrated that insulin-dependent phosphorylation of enzymes that promote protein synthesis was severely blunted in db/db muscle. In addition, prediabetic (6 week old) and diabetic (12 week old) db/db muscle exhibited an increase in a marker of proteasomal protein degradation - the level of polyubiquitinated proteins. Chronic treadmill training of db/db mice improved glucose tolerance, exercise capacity, and reduced markers of protein degradation, but only mildly increased muscle weight. The differences in muscle phenotype between these models of type 2 diabetes suggest that insulin resistance and chronic hyperglycemia alone are insufficient to rapidly decrease muscle size and function and that the effects of diabetes on muscle growth and function are animal model-dependent.
American journal of physiology. Endocrinology and metabolism.Am J Physiol Endocrinol Metab.2014 Jan 14. [Epub ahead of print]
Type 2 diabetes mellitus is associated with an accelerated muscle loss during aging, decreased muscle function, and increased disability. To better understand the mechanisms causing this muscle deterioration in type 2 diabetes, we assessed muscle weight, exercise capacity, and biochemistry in db/db
PMID 24425761

Prediabetes and Short-Term Outcomes in Nondiabetic Patients after Acute ST-Elevation Myocardial Infarction.

Tian L, Zhu J, Liu L, Liang Y, Li J, Yang Y.Author information State Key Laboratory of Cardiovascular Disease and Cardiovascular Department, Emergency and Critical Care Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.AbstractObjectives: A prediabetic state is defined as the time period before the development of symptomatic diabetes. Limited evidence is available for evaluating the correlation between prediabetes and short-term outcomes in nondiabetic patients with ST-elevation of myocardial infarction (STEMI). Methods: 4,787 nondiabetic patients with a diagnosis of STEMI based on typical onset of chest pain within 12 h were enrolled. Patients were followed up for 7 and 30 days after hospital admission. According to the 2013 Standards of Medical Care in Diabetes, the study population was stratified into three groups: normal, prediabetic and newly diagnosed diabetic patients. The primary outcomes of our study were all-cause mortality and major adverse cardiac events (MACE) on days 7 day and 30. Results: The proportions of patients with prediabetes and newly diagnosed diabetes were 31.1 and 19.2%, respectively. Rates of 7- and 30-day mortality and MACE were similar among the different HbA1c groups. Multivariable Cox regression analysis showed that compared with normal glucose metabolism, prediabetes (hazard ratio, HR, 1.003; 95% CI, 0.865-1.165) and newly diagnosed diabetes (HR, 0.887; 95% CI, 0.739-1.064) were not correlated with 30-day MACE. However, admission glucose was an independent predictor of short-term MACE (HR, 1.031; 95% CI, 1.017-1.046). Conclusions: In nondiabetic patients after STEMI, the incidence of latent diabetes mellitus was increased. Newly diagnosed diabetes and prediabetes were not correlated with short-term outcome in nondiabetic patients with STEMI, yet admission glucose level was an independent predictor of short-term MACE. To reduce the incidence of short-term MACE after STEMI, more attention should be paid to the control of increased glucose levels and intrinsic stress states. © 2013 S. Karger AG, Basel.
Cardiology.Cardiology.2014;127(1):55-61. doi: 10.1159/000354998. Epub 2013 Nov 13.
Objectives: A prediabetic state is defined as the time period before the development of symptomatic diabetes. Limited evidence is available for evaluating the correlation between prediabetes and short-term outcomes in nondiabetic patients with ST-elevation of myocardial infarction (STEMI). Methods:
PMID 24247598

The impact of prediabetes on glycemic control and clinical outcomes postburn injury.

Somerset A, Coffey R, Jones L, Murphy CV.Author information From the *The Ohio State University College of Medicine, Columbus; and †Division of Trauma, Department of Surgery, and ‡Department of Pharmacy, Critical Care and Burn, The Ohio State University Wexner Medical Center, Columbus.AbstractPoor glucose control and clinical outcomes have been observed in diabetic versus nondiabetic patients postburn injury. Prediabetes is a precursor to diabetes. The purpose of this study was to assess the effects of prediabetes on postinjury glucose control and clinical outcomes. A retrospective review was conducted comparing prediabetics and euglycemic controls. Patients who were admitted for burn care were 18 to 89 years of age and had a hemoglobin A1c (HbA1c) obtained on admission. Prediabetics were defined by an HbA1c of 5.7 to 6.4% and controls by HbA1c < 5.7%. Inpatient glucose levels were recorded, in addition to clinical outcomes. Two hundred eight patients were included: 54 prediabetics and 154 controls. The prediabetic population was older (50.7 vs 39 years; P < .001) with more hypertensives (44.4 vs 16.9%; P < .001), consisted of more African-Americans (20.4 vs 12%; P = .04), and had larger areas of full-thickness burns (4.5 vs 1.75%; P = .02). Median admission HbA1c was 5.9 (5.7-6.0)% among prediabetics and 5.3 (5-5.45)% among controls (P < .001). Prediabetics had significantly higher time-weighted glucose levels (127.7 [105.5-147.6] vs 108.0 [97.1-122.2] mg/dl; P < .001) and more had an average inpatient glucose >150 mg/dl (20.4 vs 9.1%; P = .028). There was no difference in rates of hypoglycemia (glucose <70 mg/dl) or glycemic variability. Prediabetics had lower survival rates (92.6 vs 98.7%; P = .041), but similar rates of unplanned readmission (1.9 vs 3.9%; P = .68), intensive care unit admission (29.6 vs 23.4%; P = .36), mechanical ventilation (24.1 vs 16.2%; P = .20), length of hospital stay (4 [2-8] vs 3 [2-11]; P = .71), and infection (11.1 vs 11.7%; P = .99). Prediabetic status has a significant impact on glucose control and mortality after burn injury.
Journal of burn care & research : official publication of the American Burn Association.J Burn Care Res.2014 Jan-Feb;35(1):5-10. doi: 10.1097/BCR.0b013e3182a2adea.
Poor glucose control and clinical outcomes have been observed in diabetic versus nondiabetic patients postburn injury. Prediabetes is a precursor to diabetes. The purpose of this study was to assess the effects of prediabetes on postinjury glucose control and clinical outcomes. A retrospective revie
PMID 24043230

Japanese Journal

Reactive Hypoglycemia Associated with Transient Hyperthyroidism in the Background of the Prediabetic Stage

Nagai Takashi,Kotake Mie,Takahashi Gen [他],Tonouchi Kazunori,Tonooka Naoko
北関東医学 60(2), 151-154, 2010
… Transient hyperthyroid state with little uptake by 123I-thyroid scintigram was shown and diagnosed as silent thyroiditis. … Hypoglycemia did not occur after glucose intake in the euthyroid state. … Reactive hypoglycemia may have been the result of transient hyperthyroid state in the background of the pre-diabetic stage. …
NAID 130000259032

Sudden Cardiac Death and Coronary Artery Disease : Pathophysiology and Risk Stratification

EL-SHERIF Nabil,KHAN Abdullah,SAVARESE Joseph,TURITTO Gioia
Journal of arrhythmia 25(3), 122-129, 2009-10-25
… Better understanding of pathophysiological processes, such as postmyocardial infarction remodeling, the transition from compensated hypertrophy to heart failure, and the increased cardiovascular risk of coronary artery disease in the presence of diabetes or even a prediabetic state will help to improve both risk stratification and management. …
NAID 10027737727

雄性自然発症2型糖尿病モデルSpontaneously Diabetic Torii(SDT)ラットの糖尿病進行に伴った肝臓糖代謝異常(生理学)

森長寿代,山本裕美,坂田薫 [他],福田純明,伊藤誠,笹瀬智彦,美谷島克宏,上田順久,太田毅,松下睦佳
The journal of veterinary medical science 70(11), 1239-1245, 2008-11-25
SDTラットはinsulin分泌不全を伴う非肥満型糖尿病モデルラットである.本研究では,糖尿病発症に関わる分子の探索を行なうことを目的に,SDTラットの糖尿病発症前後における肝糖代謝の変化について検討した.SDTラットは20週齢付近で糖尿病を発症するので,発症前の16週齢および発症後の24,32週齢を用い,対照として同週齢のSDラットを用いた.その結果,糖尿病発症前においてグルコキナーゼmRNAと …
NAID 110006987061