Synopsis
Recognise adult autoimmune diabetes and ketosis-prone phenotypes, treat acute insulin deficiency safely, and revisit long-term classification using antibodies and beta-cell reserve.
- Latent autoimmune diabetes in adults describes slower autoimmune beta-cell loss that initially resembles type 2 diabetes but progresses towards insulin dependence.
- GAD antibodies are commonly detected; local panels may include IA-2 or ZnT8, and testing is most informative close to diagnosis when clinical classification is uncertain.
- Rapid deterioration, catabolic weight loss, ketosis, personal autoimmunity or failure of non-insulin therapy should prompt reassessment for autoimmune diabetes.
- Ketosis-prone diabetes presents with DKA but may later show substantial endogenous insulin reserve and an antibody-negative phenotype; acute DKA care is unchanged.
- Classify ketosis-prone presentations after glucose toxicity resolves, using diabetes-specific antibodies and C-peptide measured with paired glucose under specialist supervision.
- Some people with recovered beta-cell reserve can reduce or stop insulin, but only through a planned process with glucose and ketone surveillance and rapid restart criteria.
- Avoid using ethnicity or body size as a deterministic diagnostic rule; both conditions occur across diverse populations and individual physiology must be measured.
- An SGLT2 inhibitor is hazardous when effective insulin deficiency or recurrent ketosis is possible and should not be introduced casually during diagnostic uncertainty.
Investigation priorities
Identify autoimmune beta-cell disease in an adult whose diabetes type is uncertain.
Management branches
An adult with any prior diabetes label has ketonaemia, acidosis and compatible illness.
- Start the current adult DKA protocol with fluid, fixed-rate insulin, potassium monitoring and precipitant treatment, regardless of body habitus or presumed type.
- Continue or establish background insulin according to the pathway and involve the inpatient diabetes team early for transition and education.
- Record diagnostic uncertainty and plan antibody and later C-peptide review, but discharge only with a safe insulin and ketone strategy owned by a named service.
A person is clinically stable after DKA and insulin requirements fall as glucose toxicity resolves.
- Allow metabolic recovery, then measure antibodies and stimulated or non-fasting C-peptide with paired glucose through specialist care.
- If reserve is adequate and glucose remains stable, reduce insulin stepwise with frequent glucose review, ready access to ketone testing and explicit relapse thresholds.
- Maintain long-term follow-up for glycaemia and complications, reconsider insulin promptly during illness or deterioration, and avoid medicines that amplify ketosis risk without expert justification.
Key medicines
Basal-bolus insulinUse an individual specialist-led basal and mealtime regimen, titrated from glucose patterns, carbohydrate intake, renal function and hypoglycaemia risk; continue basal insulin during illness.Requirements may fall substantially after reversal of glucose toxicity, creating hypoglycaemia unless reviewed frequently. Any planned withdrawal needs specialist supervision and a ketone safety plan.
Intravenous insulin for DKAFollow the current JBDS-aligned fixed-rate infusion and local protocol alongside fluid, potassium and glucose-containing solutions until biochemical resolution criteria are met.Do not stop because plasma glucose normalises while ketones or acidosis persist. Monitor potassium closely and overlap the transition to subcutaneous insulin safely.