Endocrine
AKT · Endocrine/Diabetes & glucose

Type 1 diabetes mellitus

Autoimmune β-cell destruction → absolute insulin deficiency

Overview

Autoimmune destruction of pancreatic β-cells (anti-GAD/IA-2/ZnT8 antibodies) causing absolute insulin deficiency, usually presenting in childhood/young adults with a short history of osmotic symptoms, weight loss and ketosis. Lifelong insulin is mandatory; DKA is the presenting or decompensating emergency.

Recognise

  • Short history of polyuria, polydipsia, weight loss, fatigue; often a lean young person
  • Ketosis/DKA at presentation (vomiting, abdominal pain, Kussmaul breathing, ketotic breath)
  • Associated autoimmune disease (coeliac, thyroid, Addison's); C-peptide low, autoantibodies positive

Red flags

  • DKA (ketonaemia + acidosis + hyperglycaemia) → emergency (see acute care)
  • Recurrent severe hypoglycaemia / impaired awareness → review regimen, DVLA implications

Differentials & how to tell them apart

Type 2 diabetesolder, overweight, insulin-resistant, gradual onset, no ketosis at presentation, antibody-negative
Maturity-onset diabetes of the young (MODY)young, strong autosomal-dominant family history, antibody-negative, C-peptide preserved — responds to sulfonylureas
Diabetic ketoacidosisthe acute decompensation — needs the DKA pathway (acute care)

Investigations

Random glucose ≥11.1 with symptoms (or fasting ≥7, HbA1c ≥48 mmol/mol — caution in acute T1DM). Ketones/blood gas if unwell. Confirm type: islet autoantibodies, low C-peptide. Screen for coeliac/thyroid.

Management

Lifelong basal-bolus insulin + structured education + CGM

  1. 1Start basal-bolus insulin (or pump) with carbohydrate counting and structured education; offer continuous/flash glucose monitoring. Target HbA1c ≤48 mmol/mol if achievable without disabling hypoglycaemia.Gate: Insulin must NEVER be omitted (even when not eating/ill) — stopping it precipitates DKA; during illness follow 'sick-day rules' (continue insulin, check ketones, maintain fluids/carbohydrate)
  2. 2Annual screening for complications (retinopathy, nephropathy [ACR], neuropathy/feet, lipids/BP); treat hypertension and microalbuminuria with an ACE-inhibitor/ARB.
Basal-bolus insulinfirst-line — multiple daily injections (long-acting basal + rapid-acting with meals) or pump
Carbohydrate counting + flexible dosingstructured education (e.g. DAFNE)
Continuous/flash glucose monitoringoffered to all (NICE); hybrid closed-loop in eligible patients

Key points

Lean young person + short osmotic history + weight loss + ketones = T1DM. The non-negotiable is that insulin is never stopped — omission causes DKA. Look for the autoimmune cluster (coeliac, thyroid, Addison's).

Monitor & prognosis

HbA1c 3–6 monthly; annual retinal/renal/foot screening; CGM time-in-range.

Excellent with good control; microvascular/macrovascular complications with poor control.

Source: NICE NG17 (T1DM); Diabetes UK