Ketosis-prone diabetes
Ketosis-prone diabetes (KPD, formerly 'Flatbush diabetes') is a syndrome of episodic diabetic ketoacidosis in patients whose clinical picture otherwise resembles type 2 diabetes, with variable periods of insulin dependence and independence driven by reversible glucose toxicity rather than permanent beta-cell destruction. Acute DKA is treated with IV insulin like any other episode, but once resolved, fasting C-peptide and glutamic acid decarboxylase antibody testing determine whether insulin can later be transitioned to metformin or another noninsulin agent.
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What this article covers
- Overview
A syndrome, not a single disease: ketosis-prone diabetes (KPD) is an umbrella term for several previously separately named glycemic syndromes, including "Flatbush diabetes," ketosis-prone type 2…
- Epidemiology
Recognized wherever a patient without a classic type 1 phenotype presents in DKA: the syndrome is identified in patients who present with DKA but whose subsequent clinical and biochemical course does…
- Risk factors
A clinical phenotype otherwise consistent with type 2 diabetes: obesity, endogenous insulin production at baseline, and a strong family history of diabetes are the features most associated with the…
- Pathophysiology
Insulin deficiency at the time of DKA is real but can be transient: during the acute episode, insulin secretion is insufficient to suppress lipolysis and ketogenesis, producing DKA indistinguishable…
- Clinical features
Episodic diabetic ketoacidosis is the presenting feature: patients present acutely with the standard features of DKA (hyperglycemia, ketosis, and acidosis) rather than a gradual, progressive hyperglycemic course.
- Differential diagnosis
Classic autoimmune type 1 diabetes: DKA from permanent beta-cell destruction, distinguished from KPD by positive islet autoantibodies and a fasting C-peptide that remains below 1 ng/mL (0.33 nmol/L)…
- Diagnosis
The clinching basis is the pattern over the weeks to months after presentation, not a single test at the time of DKA: KPD is recognized when a patient presents with DKA whose subsequent clinical and…
- Management
First, treat the acute DKA episode with an IV insulin infusion as in any DKA episode, continuing until the anion gap has closed and the patient is tolerating oral intake, then transition to subcutaneous insulin.
- Complications
Recurrent DKA: patients remain at risk for further ketotic episodes, particularly if hyperglycemia is not adequately controlled or if insulin is discontinued in a patient who does not truly have preserved beta-cell function.
- Prognosis
Favorable in the antibody-negative, beta-cell-preserved subgroup: many of these patients are able to discontinue insulin within weeks to months and be managed on metformin, with a course closer to type 2 diabetes.
- Prevention
Reassess beta-cell function and antibody status after every DKA episode in a patient whose diabetes type is not already firmly established, since this determines whether future episodes can be…
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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.
- 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.
- 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.
- 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.