Type 1 diabetes mellitus
Type 1 diabetes mellitus is an insulin-deficient state from autoimmune (type 1A) or idiopathic (type 1B) destruction of pancreatic beta cells, presenting with hyperglycemia that can range from mild to life-threatening diabetic ketoacidosis. Diagnosis combines standard glycemic criteria with autoantibody testing (GAD65, IA-2), and lifelong insulin therapy, generally as a basal-bolus regimen, is required from diagnosis, with self-monitoring or continuous glucose monitoring to guide dosing.
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What this article covers
- Overview
An insulin-deficient form of diabetes caused by destruction of the insulin-producing pancreatic beta cells, most often autoimmune (type 1A) but occasionally idiopathic (type 1B) or acquired (pancreatectomy, pancreatitis).
- Epidemiology
Accounts for 5% to 10% of newly diagnosed diabetes (immune-mediated type 1A), with the remainder overwhelmingly type 2 diabetes.
- Risk factors
Genetic susceptibility conferred by specific human leukocyte antigen (HLA) alleles, interacting with environmental factors to trigger autoimmune beta-cell destruction.
- Pathophysiology
In immune-mediated (type 1A) diabetes, environmental factors acting on a genetically susceptible individual trigger T-cell-mediated beta-cell destruction, with HLA alleles conferring the strongest known genetic association.
- Clinical features
The diagnosis rests on standard hyperglycemic criteria plus evidence of insulin deficiency, most reliably islet autoantibody positivity and a low or undetectable C-peptide, distinguishing it from type 2 diabetes and monogenic forms.
- Differential diagnosis
Type 2 diabetes mellitus: shares hyperglycemia and its symptoms, but distinguished by insulin resistance with preserved (often elevated) C-peptide, an older or overweight patient profile, negative…
- Diagnosis
The diagnosis of diabetes requires classic hyperglycemic symptoms with a random glucose of 200 mg/dL or higher, or one of the confirmatory laboratory criteria below; in the absence of unequivocal…
- Management
First, initiate insulin therapy immediately at diagnosis; insulin is never optional or delayed in type 1 diabetes, since endogenous secretion is absent or minimal.
- Complications
Diabetic ketoacidosis, the most common acute, life-threatening complication, which can be the initial presentation of the disease and recurs with missed insulin doses or intercurrent illness.
- Prognosis
With consistent insulin therapy and glycemic monitoring, most patients with type 1 diabetes achieve near-normal life expectancy, though risk of microvascular and macrovascular complications rises with cumulative hyperglycemic burden.
- Prevention
There is no established primary prevention for autoimmune beta-cell destruction; management instead focuses on early diagnosis and prevention of acute and chronic complications.
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Related articles
- Diabetic ketoacidosis
Diabetic ketoacidosis is a life-threatening hyperglycemic crisis of near-absolute insulin deficiency, most common in type 1 diabetes, producing an anion-gap ketoacidosis from unrestrained lipolysis and osmotic diuresis from severe hyperglycemia. It is diagnosed by hyperglycemia, ketonemia, and an anion-gap metabolic acidosis, and treated with intravenous isotonic saline, an intravenous regular insulin bolus and infusion, and aggressive potassium repletion guided by frequent electrolyte monitoring.
- Insulin therapy in diabetes mellitus
Insulin therapy replaces or supplements endogenous insulin to control hyperglycemia, and is lifelong and mandatory in type 1 diabetes because of absolute beta-cell failure, while in type 2 diabetes it is added when oral and noninjectable agents fail to reach glycemic goals. First-line therapy is a basal-bolus regimen started at 0.4-1.0 units/kg/day in type 1 diabetes, or basal insulin glargine 10 units/day (or 0.1-0.2 units/kg/day) in type 2 diabetes, titrated to a fasting glucose target.
- Latent autoimmune diabetes in adults
Latent autoimmune diabetes in adults (LADA) is a slowly progressive autoimmune beta-cell destruction that presents in adulthood without an initial insulin requirement, so it is frequently misclassified as type 2 diabetes until positive islet autoantibodies are identified. First-line management follows a standard stepwise diabetes approach, but basal insulin should be started proactively as beta-cell failure progresses, since earlier insulin reduces stress on the remaining beta cells.
- Type 2 diabetes mellitus
Type 2 diabetes is hyperglycemia from insulin resistance with progressive relative insulin deficiency, diagnosed by a hemoglobin A1c of 6.5% or higher, a fasting glucose of 126 mg/dL or higher, or a 2-hour oral glucose tolerance test value of 200 mg/dL or higher. First-line treatment is lifestyle modification plus metformin, with an SGLT2 inhibitor or GLP-1 receptor agonist added early for patients with atherosclerotic disease, kidney disease, or heart failure.