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Type 1 diabetes
Diabetes mellitus type 1, commonly known as type 1 diabetes (T1D), and formerly known as juvenile diabetes, is an autoimmune disease that occurs when the body's immune system destroys pancreatic cells (beta cells). In healthy persons, beta cells produce insulin. Insulin is a hormone required by the body to store and convert blood sugar into energy. T1D results in high blood sugar levels in the body prior to treatment. Common symptoms include frequent urination, increased thirst, increased hunger, weight loss, and other complications. Additional symptoms may include blurry vision, tiredness, and slow wound healing (owing to impaired blood flow). While some cases take longer, symptoms usually appear within weeks or a few months.
The cause of type 1 diabetes is not completely understood, but it is believed to involve a combination of genetic and environmental factors. The underlying mechanism involves an autoimmune destruction of the insulin-producing beta cells in the pancreas. Diabetes is diagnosed by testing the level of sugar or glycated hemoglobin (HbA1C) in the blood.
Type 1 diabetes can typically be distinguished from type 2 by testing for the presence of autoantibodies and/or declining levels/absence of C-peptide.
There is no known way to prevent type 1 diabetes. Treatment with insulin is required for survival. Insulin therapy is usually given by injection just under the skin but can also be delivered by an insulin pump. A diabetic diet, exercise, and lifestyle modifications are considered cornerstones of management. If left untreated, diabetes can cause many complications. Complications of relatively rapid onset include diabetic ketoacidosis and nonketotic hyperosmolar coma. Long-term complications include heart disease, stroke, kidney failure, foot ulcers, and damage to the eyes. Furthermore, since insulin lowers blood sugar levels, complications may arise from low blood sugar if more insulin is taken than necessary.
Type 1 diabetes makes up an estimated 5–10% of all diabetes cases. The number of people affected globally is unknown, although it is estimated that about 80,000 children develop the disease each year. Within the United States the number of people affected is estimated to be one to three million. Rates of disease vary widely, with approximately one new case per 100,000 per year in East Asia and Latin America and around 30 new cases per 100,000 per year in Scandinavia and Kuwait. It typically begins in children and young adults but can begin at any age.
Type 1 diabetes can develop at any age, with a peak in onsets during childhood and adolescence. Adult onsets on the other hand are often initially misdiagnosed as type 2. The major sign of type 1 diabetes is very high blood sugar, which typically manifests in children as a few days to weeks of polyuria (increased urination), polydipsia (increased thirst), and weight loss after being exposed to a triggering factor including infections, strenuous exercise, dehydration. Children may also experience increased appetite, blurred vision, bedwetting, recurrent skin infections, candidiasis of the perineum, irritability, and reduced mental acumen. Adults with type 1 diabetes tend to have more varied symptoms, which come on over months, rather than days or weeks.
Prolonged lack of insulin can cause diabetic ketoacidosis, characterized by fruity breath odor, mental confusion, persistent fatigue, dry or flushed skin, abdominal pain, nausea or vomiting, and labored breathing. Blood and urine tests reveal unusually high glucose and ketones in the blood and urine. Untreated ketoacidosis can rapidly progress to loss of consciousness, coma, and death. The percentage of children whose type 1 diabetes begins with an episode of diabetic ketoacidosis varies widely by geography, as low as 15% in parts of Europe and North America, and as high as 80% in the developing world.
Type 1 diabetes is caused by the destruction of β-cells—the only cells in the body that produce insulin—and the consequent progressive insulin deficiency. Without insulin, the body cannot respond effectively to increases in blood sugar. Due to this, people with diabetes have persistent hyperglycemia. In 70–90% of cases, β-cells are destroyed by one's own immune system, for reasons that are not entirely clear. The best-studied components of this autoimmune response are β-cell-targeted antibodies that begin to develop in the months or years before symptoms arise. Typically, someone will first develop antibodies against insulin or the protein GAD65, followed eventually by antibodies against the proteins IA-2, IA-2β, and/or ZNT8. People with a higher level of these antibodies, especially those who develop them earlier in life, are at higher risk for developing symptomatic type 1 diabetes. The trigger for the development of these antibodies remains unclear. Several explanatory theories have been put forward, and the cause may involve genetic susceptibility, a diabetogenic trigger, and/or exposure to an antigen. The remaining 10–30% of type 1 diabetics have β-cell destruction but no sign of autoimmunity; this is called idiopathic type 1 diabetes (its cause is unknown).
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Type 1 diabetes
Diabetes mellitus type 1, commonly known as type 1 diabetes (T1D), and formerly known as juvenile diabetes, is an autoimmune disease that occurs when the body's immune system destroys pancreatic cells (beta cells). In healthy persons, beta cells produce insulin. Insulin is a hormone required by the body to store and convert blood sugar into energy. T1D results in high blood sugar levels in the body prior to treatment. Common symptoms include frequent urination, increased thirst, increased hunger, weight loss, and other complications. Additional symptoms may include blurry vision, tiredness, and slow wound healing (owing to impaired blood flow). While some cases take longer, symptoms usually appear within weeks or a few months.
The cause of type 1 diabetes is not completely understood, but it is believed to involve a combination of genetic and environmental factors. The underlying mechanism involves an autoimmune destruction of the insulin-producing beta cells in the pancreas. Diabetes is diagnosed by testing the level of sugar or glycated hemoglobin (HbA1C) in the blood.
Type 1 diabetes can typically be distinguished from type 2 by testing for the presence of autoantibodies and/or declining levels/absence of C-peptide.
There is no known way to prevent type 1 diabetes. Treatment with insulin is required for survival. Insulin therapy is usually given by injection just under the skin but can also be delivered by an insulin pump. A diabetic diet, exercise, and lifestyle modifications are considered cornerstones of management. If left untreated, diabetes can cause many complications. Complications of relatively rapid onset include diabetic ketoacidosis and nonketotic hyperosmolar coma. Long-term complications include heart disease, stroke, kidney failure, foot ulcers, and damage to the eyes. Furthermore, since insulin lowers blood sugar levels, complications may arise from low blood sugar if more insulin is taken than necessary.
Type 1 diabetes makes up an estimated 5–10% of all diabetes cases. The number of people affected globally is unknown, although it is estimated that about 80,000 children develop the disease each year. Within the United States the number of people affected is estimated to be one to three million. Rates of disease vary widely, with approximately one new case per 100,000 per year in East Asia and Latin America and around 30 new cases per 100,000 per year in Scandinavia and Kuwait. It typically begins in children and young adults but can begin at any age.
Type 1 diabetes can develop at any age, with a peak in onsets during childhood and adolescence. Adult onsets on the other hand are often initially misdiagnosed as type 2. The major sign of type 1 diabetes is very high blood sugar, which typically manifests in children as a few days to weeks of polyuria (increased urination), polydipsia (increased thirst), and weight loss after being exposed to a triggering factor including infections, strenuous exercise, dehydration. Children may also experience increased appetite, blurred vision, bedwetting, recurrent skin infections, candidiasis of the perineum, irritability, and reduced mental acumen. Adults with type 1 diabetes tend to have more varied symptoms, which come on over months, rather than days or weeks.
Prolonged lack of insulin can cause diabetic ketoacidosis, characterized by fruity breath odor, mental confusion, persistent fatigue, dry or flushed skin, abdominal pain, nausea or vomiting, and labored breathing. Blood and urine tests reveal unusually high glucose and ketones in the blood and urine. Untreated ketoacidosis can rapidly progress to loss of consciousness, coma, and death. The percentage of children whose type 1 diabetes begins with an episode of diabetic ketoacidosis varies widely by geography, as low as 15% in parts of Europe and North America, and as high as 80% in the developing world.
Type 1 diabetes is caused by the destruction of β-cells—the only cells in the body that produce insulin—and the consequent progressive insulin deficiency. Without insulin, the body cannot respond effectively to increases in blood sugar. Due to this, people with diabetes have persistent hyperglycemia. In 70–90% of cases, β-cells are destroyed by one's own immune system, for reasons that are not entirely clear. The best-studied components of this autoimmune response are β-cell-targeted antibodies that begin to develop in the months or years before symptoms arise. Typically, someone will first develop antibodies against insulin or the protein GAD65, followed eventually by antibodies against the proteins IA-2, IA-2β, and/or ZNT8. People with a higher level of these antibodies, especially those who develop them earlier in life, are at higher risk for developing symptomatic type 1 diabetes. The trigger for the development of these antibodies remains unclear. Several explanatory theories have been put forward, and the cause may involve genetic susceptibility, a diabetogenic trigger, and/or exposure to an antigen. The remaining 10–30% of type 1 diabetics have β-cell destruction but no sign of autoimmunity; this is called idiopathic type 1 diabetes (its cause is unknown).