Diabetes mellitus type 1 Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Priyamvada Singh, M.B.B.S. [2]; Cafer Zorkun, M.D., Ph.D. [3]Vishal Devarkonda, M.B.B.S[4]Fatemeh Dehghani Firouzabadi, MD [5]
Diabetes mellitus type 1(T1D ) is a metabolic disorder that is primarily characterized by deficiency in insulin. T1D has 2 forms of presentations 1) Classic new onset, which commonly present with persistent thirst, frequent urination, and dehydration 2) Diabetic ketoacidosis, which commonly presents with abdominal pain, vomiting and flu-like symptoms. Patients with classic onset presentation of T1D are usually well appearing. Whereas T1D patients presenting with diabetic ketoacidosis is usually remarkable for tachycardia, tachypnea (kussumal breathing) and dehydration. T1D is characterized by an absolute insulin deficiency. For these patients, a basal-bolus regimen with a long-acting analog and a short- or rapid-acting insulin analog is the most physiologic insulin regimen and the best option for optimal glycemic control.
Term "diabetes" was first described in the literature by a Egyptian scientist Eberes papyrus in 1500 BC. Discovery of insulin by Friedrick Banting in 1921-22, was considered as an important landmark in understanding the nature of disease.
American Diabetic Association(ADA), classifies T1D based on etiology into 1) Immune mediated and 2) Idiopathic
Type 1 diabetes is a disorder characterized by abnormally high blood sugar levels. T1D is the result of interactions of genetic, environmental, and immunologic factors that ultimately lead to the destruction of the pancreatic beta cells and insulin deficiency.
There are no established causes for type 1 DM. Studies have found that cause of T1D is the result of interactions of genetic, environmental, and immunologic factors.
Type 1 DM must be differentiated from type 2 DM, MODY-DM, psychogenic polydipsia, diabetes insipidus, transient hyperglycemia, steroid therapy, renal tubular acidosis type-1, glucagonoma, cushing's syndrome, and hypothyroidism.
Epidemiology and demographics of type 1 DM varies with geography, age, race and genetic susceptibility.
Risk factors for type 1 DM include family history, genetics, geography, congenital rubella infection, maternal entero-viral infection, cesarean infection, higher birth weight, older maternal age, low maternal intake of vegetables, enteroviral infection, frequent respiratory or enteric infections, early exposure to cereals, root vegetables, eggs and cow's milk, infant weight gain, persistent or recurrent entero-viral infections, overweight or increased height velocity, high glycemic load, fructose intake, dietary nitrates or nitrosamines, puberty, psychological stress and low vitamin D levels.
According to the American Diabetic Association, screening for type 1 DM is not recommended.[1]
If left untreated, patients with [type 1 DM] may progress to develop complications of the hyperglycemia state, which commonly include diabetes ketoacidosis and hyperglycemia hyperosmolar state. Prognosis is generally good with compliance with medications.
The diagnosis of type 1 DM is based on the ADA criteria, which include FPG ≥126 mg/dL (7.0 mmol/L), or 2-h PG ≥200 mg/dL (11.1 mmol/L) during an OGTT, or A1C ≥6.5% (48 mmol/mol), or classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L).
Type 1 DM has 2 forms of presentations 1) Classic new onset, which commonly present with persistent thirst, frequent urination, and dehydration 2) Diabetic ketoacidosis, which commonly presents with abdominal pain, vomiting and flu-like symptoms.
Patients with classic onset presentation of type 1 DM are usually well appearing. Whereas patients with diabetic ketoacidosis present with tachycardia, tachypnea (kussumal breathing) and dehydration.
Laboratory findings consistent with the diagnosis of type 1 DM include FPG ≥126 mg/dL (7.0 mmol/L), or 2-h PG ≥200 mg/dL (11.1 mmol/L) during an OGTT, or A1C ≥6.5% (48 mmol/mol), or classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L).
Type 1 diabetes is characterized by an absolute insulin deficiency. For these patients, a basal-bolus regimen with a long-acting analog and a short- or rapid-acting insulin analog is the most physiologic insulin regimen and the best option for optimal glycemic control.
Surgery is not the first-line treatment option for patients with type 1 DM. β-Cell replacement therapy is usually reserved for patients with either who have an indication for kidney transplantation and are poorly controlled with large glycemic excursions or in patients who already received a kidney transplant.
Currently there are no primary preventive measures available for type 1 DM. However, there are clinical trials ongoing that aim to find methods of preventing or slowing its development.
Secondary prevention strategies following type 1 diabetes mellitus include: maintain optimal glycemic control, life style modifications, and monitoring for micro and macrovascular complications.
Future research mainly focuses of artificial pancreas, beta cell replacement, smart insulin, and gene therapy.