Diabetes mellitus

Un article de Vev.

Modèle:Infobox Disease</ref>//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>

| ICD10          = Modèle:ICD10–Modèle:ICD10
| ICD9           = Modèle:ICD9
| ICDO           = 
| OMIM           = 
| MedlinePlus    = 001214
| eMedicineSubj  = med
| eMedicineTopic = 546
| eMedicine_mult = Modèle:EMedicine2
| MeshName       = Diabetes
| MeshNumber     = C18.452.394.750

}} Modèle:Two other uses

Diabetes mellitus (Modèle:IPAEng or Modèle:IPA, Modèle:IPA or Modèle:IPA), often simply diabetes (Modèle:Lang-el), 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 resistance to insulin's effects coupled with inadequate levels of insulin secretion to compensate.<ref name="diag">Modèle:Cite book</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.

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 cells of the pancreas being unable to produce sufficient insulin to prevent hyperglycemia, the causes are different.<ref name=Rother>Modèle:Cite journal</ref> Type 1 diabetes is usually due to 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.//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 cells of the pancreas being unable to produce sufficient insulin to prevent hyperglycemia, the causes are different.<ref name=Rother>Modèle:Cite journal</ref> Type 1 diabetes is usually due to 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.

Gestational diabetes typically resolves with delivery of the child, however types 1 and 2 diabetes are 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 dietary treatment, 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.

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>//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> Modèle:Diabetes

Classification

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.

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 "type 1.5" diabetes.<ref> Diseases: Johns Hopkins Autoimmune Disease Research Center

. Retrieved on 2007-09-23. </ref>) There is also maturity onset diabetes of the young (MODY) which is a single gene disorder with strong family history that presents as type 2 diabetes before 30 years of age.//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 "type 1.5" diabetes.<ref> Diseases: Johns Hopkins Autoimmune Disease Research Center

. Retrieved on 2007-09-23. </ref>) There is also maturity onset diabetes of the young (MODY) which is a single gene disorder with strong family history that presents as type 2 diabetes before 30 years of age.

Type 1 diabetes mellitus

Main article: Diabetes mellitus type 1

Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells 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 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.

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>//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>

Type 1 treatment must be continued indefinitely. Treatment does not impair normal activities, if sufficient awareness, appropriate care, and discipline in testing and medication is taken. The average glucose level for the type 1 patient should be as close to normal (80–120 mg/dl, 4–6 mmol/l) as possible. Some physicians suggest up to 140–150 mg/dl (7-7.5 mmol/l) for those having trouble with lower values, such as frequent hypoglycemic events. Values above 200 mg/dl (10 mmol/l) are often accompanied by discomfort and frequent urination leading to dehydration. Values above 300 mg/dl (15 mmol/l) usually require immediate treatment and may lead to ketoacidosis. Low levels of blood glucose, called hypoglycemia, may lead to seizures or episodes of unconsciousness.

Type 2 Diabetes Mellitus

Main article: 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 medications 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.

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>Modèle:Cite book//www.cdc.gov/mmwR/preview/mmwrhtml/mm5345a2.htm</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>Modèle:Cite book</ref>

Type 2 diabetes may go unnoticed for years because visible symptoms are typically mild, non-existent or sporadic, and usually there are no 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 diabetes neuropathy, and liver damage from non-alcoholic steatohepatitis.

Type 2 diabetes is usually first treated by increasing physical activity, decreasing carbohydrate intake, and losing weight. These can restore insulin sensitivity even when the weight loss is modest, for example around 5 kg (10 to 15 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 drugs. 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., thiazolidinediones). According to one study, overweight patients treated with metformin compared with diet alone, had relative risk reductions of 32% for any diabetes endpoint, 42% for diabetes related death and 36% for all cause mortality and stroke.<ref>Modèle:Cite journal</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.

Gestational diabetes

Main article: Gestational diabetes

Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a combination of inadequate insulin secretion and responsiveness. It occurs in about 2%–5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes is fully treatable but requires careful medical supervision throughout the pregnancy. About 20%–50% of affected women develop type 2 diabetes later in life.

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 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 may be indicated with decreased placental function. A 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 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 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 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 weight loss (despite normal or increased eating) and irreducible fatigue. These symptoms 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 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 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 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 HLA genotypes (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 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 among monozygotic twins is close to 100%, and about 25% of those with the disease have a family history of diabetes. Candidate genes include KCNJ11 (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>Modèle:Cite journal</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>Modèle:Cite journal</ref>

Pathophysiology

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 receptors plays a central role in all forms of diabetes mellitus.

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.

Higher insulin levels increase many anabolic ("building up") processes such as cell growth and duplication, protein synthesis, and fat storage. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolism from a 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).

If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or 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

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 heart attack, stroke, neuropathy, poor wound healing or a foot ulcer, certain eye problems, certain fungal infections, or delivering a baby with macrosomia or hypoglycemia.

Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:<ref name "WHO1999-DefDiagClass"/>

• fasting plasma glucose level at or above 126 mg/dL (7.0 mmol/l).
• plasma glucose at or above 200 mg/dL (11.1 mmol/l) two hours after a 75 g oral glucose load as in a glucose tolerance test.
• random plasma glucose at or above 200 mg/dL (11.1 mmol/l).

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.

Patients with fasting glucose levels between 110 and 125 mg/dL (6.1 and 7.0 mmol/l) are considered to have impaired fasting glycemia. Patients with plasma glucose at or above 140 mg/dL or 7.8 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.

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 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">Modèle:Cite journal</ref><ref>Modèle:Cite journal</ref>

Screening

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 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 of diabetes, high-risk ethnicity (Mestizo/Hispanic, Native American, Afro-Caribbean, Pacific Island, and South Asian ancestry).<ref name="pmid17215197">Modèle:Cite journal</ref><ref name="pmid10889785">Modèle:Cite journal</ref>

Many medical conditions are associated with diabetes and warrant screening. A partial list includes: high blood pressure, 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 glucocorticoids, some chemotherapy agents (especially L-asparaginase), as well as some of the antipsychotics and mood stabilizers (especially phenothiazines and some atypical antipsychotics).

Prevention

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>Modèle:Cite journal</ref>//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>Modèle:Cite journal</ref>

care.diabetesjournals.org/cgi/content/full/29/9/2140}}</ref>//care.diabetesjournals.org/cgi/content/full/29/9/2140}}</ref>

Some studies have shown delayed progression to diabetes in predisposed patients through prophylactic use of metformin,<ref name=Knowler/> rosiglitazone,<ref>Modèle:Cite journal</ref> or valsartan.<ref>Modèle:Cite journal</ref> In patients on hydroxychloroquine for rheumatoid arthritis, incidence of diabetes was reduced by 77%.<ref>Modèle:Cite journal</ref> Breastfeeding might also be correlated with the prevention of type 2 of the disease in mothers.<ref name="JAMA2005-Stuebe">Modèle:Cite journal</ref>

Treatment and management

Main article: Diabetes management

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 diet, wearing diabetic socks, and if necessary, taking any of several drugs to reduce pressure.//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 diet, wearing diabetic socks, and if necessary, taking any of several drugs to reduce pressure.

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. Optometrists, podiatrists/chiropodists, dietitians, physiotherapists, clinical nurse specialists (eg, Certified Diabetes Educators and DSNs (Diabetic Specialist Nurse)), or nurse practitioners 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 (eg, at least every three to six months).

Cure

Cures for type 1 diabetes

Main article: 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>Modèle:Cite journal</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>

Modèle:Cite journal</ref>Still, they generally remain on long-term immunosuppressive drugs and there is a possibility that the immune system will mount a host versus graft response against the transplanted organ.<ref name=Vinik/>

jama.ama-assn.org/cgi/content/full/297/14/1568}}</ref>//jama.ama-assn.org/cgi/content/full/297/14/1568}}</ref>

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.

Cures for type 2 diabetes

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>Modèle:Cite journal</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>Modèle:Cite journal</ref> A small number of normal to moderately obese patients with type 2 diabetes have successfully undergone similar operations.<ref name=pmid17386401>Modèle:Cite journal</ref><ref name=NS>«  »</ref>//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>Modèle:Cite journal</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>Modèle:Cite journal</ref> A small number of normal to moderately obese patients with type 2 diabetes have successfully undergone similar operations.<ref name=pmid17386401>Modèle:Cite journal</ref><ref name=NS>«  »</ref>

Prognosis

Patient education, understanding, and participation is vital since the complications of diabetes are far less common and less severe in people who have well-controlled blood sugar levels.<ref>Modèle:Cite journal</ref>

Epidemiology

In 2006, 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.

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 killers).

For at least 20 years, diabetes rates in North America have been increasing substantially. In 2005 there are 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>Modèle:Cite journal</ref><ref>Modèle:Cite journal</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"/>

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> Department of Health (Malta), 1897–1972:Annual Reports.</ref>

Other landmark discoveries include:<ref name="FASEBJ2002-Patlak" />

• identification of the first of the sulfonylureas 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>Modèle:Cite journal</ref>
• the three-dimensional structure of insulin (Modèle:PDB)
• Dr Gerald Reaven's identification of the constellation of symptoms now called metabolic syndrome in 1988
• demonstration that intensive glycemic control in type 1 diabetes reduces chronic side effects more as glucose levels approach 'normal' in a large longitudinal study,<ref>Modèle:Cite journal</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.

www.euro.who.int/Document/Obs/EuroObserver7_3.pdf | format=PDF | journal=Euro Observer | year=2005 | pages=5–6 | volume=7 | issue=2}}</ref>//www.euro.who.int/Document/Obs/EuroObserver7_3.pdf | format=PDF | journal=Euro Observer | year=2005 | pages=5–6 | volume=7 | issue=2}}</ref>

A study shows that diabetic patients with neuropathic symptoms such as numbness or tingling in feet or hands are twice more likely to be unemployed than those without the symptoms.<ref name="pmid17563611">Modèle:Cite journal</ref>

See also

• List of terms associated with diabetes

References

External links

www.diabetes.org/ American Diabetes Association]//www.diabetes.org/ American Diabetes Association] www.diabetes.org/ American Diabetes Association]//www.diabetesnsw.com.au/ Diabetes Australia-NSW] www.diabetes.org/ American Diabetes Association]//www.diabetes.ca/ Canadian Diabetes Association] www.diabetes.org/ American Diabetes Association]//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) www.diabetes.org/ American Diabetes Association]//www.cdc.gov/diabetes/ Centers for Disease Control Diabetes Section] www.diabetes.org/ American Diabetes Association]//www.diabetes.org.uk Diabetes UK] www.diabetes.org/ American Diabetes Association]//www.dhealth.org/ Diabetes Health Institute] www.diabetes.org/ American Diabetes Association]//www.diabetesinstitute.org/ Diabetes Institute for Immunology and Transplantion] www.diabetes.org/ American Diabetes Association]//www.joinleenow.org The Iacocca Foundation] www.diabetes.org/ American Diabetes Association]//www.idsoc.org/ The Immunology of Diabetes Society] www.diabetes.org/ American Diabetes Association]//www.idf.org/ International Diabetes Federation] www.diabetes.org/ American Diabetes Association]//www.jdrf.org/ Juvenile Diabetes Research Foundation] www.diabetes.org/ American Diabetes Association]//www.nlm.nih.gov/medlineplus/diabetes.html MedlinePlus Diabetes from the U.S. National Library of Medicine] www.diabetes.org/ American Diabetes Association]//ndep.nih.gov/ National Diabetes Education Program] www.diabetes.org/ American Diabetes Association]//www.diabetes.niddk.nih.gov/ National Diabetes Information Clearinghouse] www.diabetes.org/ American Diabetes Association]//www.pcdeurope.org/ Primary Care Diabetes Europe] www.diabetes.org/ American Diabetes Association]//www.who.int/mediacentre/factsheets/fs312/en/ World Health Organization fact sheet on diabetes] www.diabetes.org/ American Diabetes Association]//www.who.int/diabetes/en/ World Health Organization—The Diabetes Programme]

Modèle:Endocrine pathologyaf:Diabetes mellitus ar:مرض السكري ast:Diabetes zh-min-nan:Thn̂g-jiō-pēⁿ bs:Diabetes mellitus bg:Диабет ca:Diabetis mellitus cs:Diabetes mellitus cy:Clefyd y siwgr da:Sukkersyge de:Diabetes mellitus et:Suhkurtõbi el:Διαβήτης es:Diabetes mellitus eo:Diabeto eu:Diabete fa:مرض قند fr:Diabète sucré gl:Diabetes mellitus ko:당뇨병 hi:मधुमेह hr:Diabetes mellitus id:Diabetes mellitus is:sykursýki it:Diabete mellito he:סוכרת ka:დიაბეტი lb:Diabetes mellitus hu:Cukorbetegség ml:പ്രമേഹം ms:Penyakit kencing manis nl:Diabetes mellitus ne:मधुमेह new:मधुमेह ja:糖尿病 no:Diabetes mellitus nn:Diabetes mellitus om:Diabetes pl:Cukrzyca pt:Diabetes mellitus ro:Diabet qu:Misk'i unquy ru:Сахарный диабет sq:Diabetes mellitus simple:Diabetes mellitus sk:Cukrovka sl:Sladkorna bolezen sr:Шећерна болест sh:Dijabetes fi:Diabetes sv:Diabetes ta:நீரிழிவு நோய் te:మధుమేహం th:เบาหวาน vi:Đái tháo đường tr:Diyabet uk:Діабет yi:דיעביטיס zh:糖尿病