Key Facts

T1DM requires lifelong insulin therapy. Technology (CGM, insulin pumps, hybrid closed-loop systems) has transformed management. Tight glycaemic control reduces microvascular complications (DCCT/EDIC). Structured education (DAFNE) is essential.

Epidemiology

UK prevalence ~400,000. Incidence ~25 per 100,000/year (children); increasing ~3-4% per year. Peak onset 10-14 years (pubertal) but can occur at any age. LADA (latent autoimmune diabetes in adults): slower-onset autoimmune diabetes in adults >30.

Aetiology

• Autoimmune: genetic predisposition (HLA-DR3/DR4, HLA-DQ2/DQ8) + environmental trigger → T-cell mediated destruction of beta cells
• Environmental triggers: enteroviral infection (coxsackievirus B), early cow's milk exposure, vitamin D deficiency (hypothesised)
• Genetic: concordance in monozygotic twins ~30-50%; polygenic (HLA region accounts for ~50% of genetic risk)

Pathophysiology

Autoimmune T-cell (CD8+ cytotoxic) attack on pancreatic beta cells → progressive beta cell destruction → absolute insulin deficiency. Symptoms appear when ~80-90% of beta cells are destroyed. Without insulin: unrestrained lipolysis → ketogenesis → DKA; hyperglycaemia → osmotic diuresis → dehydration.

Classic Presentation

• Polyuria, polydipsia, nocturia: osmotic diuresis from hyperglycaemia
• Weight loss: despite normal/increased appetite; catabolic state
• Fatigue, malaise
• Blurred vision: osmotic lens changes
• Onset: days to weeks (rapid in children)

DKA Presentation (~25% of New T1DM)

• Nausea, vomiting, abdominal pain
• Kussmaul breathing (deep, rapid — respiratory compensation for metabolic acidosis)
• Ketotic breath (pear drops/acetone)
• Dehydration, confusion → coma

LADA (Latent Autoimmune Diabetes in Adults)

• Initially misdiagnosed as T2DM (>30 years, slower onset)
• Progressive insulin requirement over months-years
• Positive autoantibodies (esp. anti-GAD)
• Consider in 'T2DM' patient who is lean, <50, rapidly requiring insulin

Red Flags

• Young, lean patient with diabetes → T1DM/LADA until proven otherwise
• DKA at presentation → manage as emergency (see DKA)
• Recurrent DKA → assess adherence, education, psychosocial factors

At Diagnosis

• Random blood glucose: ≥11.1 mmol/L with symptoms; or fasting ≥7.0 mmol/L; or HbA1c ≥48 mmol/mol
• Capillary/blood ketones: raised (≥0.6 mmol/L); ≥3.0 suggests DKA
• Autoantibodies: anti-GAD, anti-IA2, anti-ZnT8, anti-insulin (at least 1 positive in >90%)
• C-peptide: low/undetectable (measure when glucose >8 mmol/L for accurate interpretation)
• HbA1c: may be very high at presentation

Bloods

• FBC, U&Es, LFTs, TFTs (autoimmune thyroid disease in ~20%)
• Coeliac screen (anti-tTG): ~4-8% of T1DM have coeliac disease
• Lipid profile: cardiovascular risk

Ongoing Monitoring (NICE NG17)

• HbA1c: every 3-6 months; target ≤48 mmol/mol
• Annual review: renal function (ACR, eGFR), retinal screening, foot check, BP, lipids, TFTs, coeliac screen (if not done)
• CGM data: time in range (TIR) 70-180 mg/dL target >70%

Insulin Therapy (NICE NG17)

Basal-Bolus (MDI) — Standard:

• Basal: insulin glargine (Lantus/Toujeo) OD or insulin degludec (Tresiba) OD or insulin detemir (Levemir) BD
• Bolus: rapid-acting with meals — insulin aspart (NovoRapid), lispro (Humalog), faster aspart (Fiasp)
• Carbohydrate counting + insulin:carbohydrate ratios + correction doses

Insulin Pump (CSII):

• Continuous subcutaneous infusion of rapid-acting insulin
• NICE criteria: suboptimal control despite optimised MDI, disabling hypoglycaemia, very variable glucose
• Combined with CGM → hybrid closed-loop (automated insulin delivery — e.g., CamAPS FX, Omnipod 5, MiniMed 780G)

Hybrid Closed-Loop:

• Pump + CGM + algorithm automatically adjusts basal insulin
• Significantly improves TIR and HbA1c; reduces hypoglycaemia
• Increasingly standard of care (NICE NG17 update)

Continuous Glucose Monitoring

• Flash CGM (FreeStyle Libre): factory-calibrated sensor; scanned for readings; NICE recommended for all T1DM
• Real-time CGM (Dexcom, Guardian): continuous readings with alarms; recommended for pump users, pregnancy, hypoglycaemia unawareness

Structured Education

• DAFNE (Dose Adjustment for Normal Eating): NICE-recommended; teaches carbohydrate counting and insulin dose adjustment

Hypoglycaemia Management

• Mild: fast-acting glucose (dextrose tablets, juice — 15-20g)
• Severe (unconscious): IM glucagon 1mg or IV glucose 10% 200mL
• Hypoglycaemia unawareness: relaxed HbA1c target, CGM with alarms, hypoglycaemia avoidance programmes

Complication Screening (Annual — NICE NG17)

• Retinal screening: from age 12 (T1DM)
• Renal: ACR + eGFR annually; ACE inhibitor (ramipril) if microalbuminuria (ACR >3 mg/mmol)
• Foot: annual assessment; diabetic foot team if ulceration
• Cardiovascular: lipids, BP; statin if >40 years or additional CVD risk

Referral Criteria

• Specialist diabetes team: all T1DM (NICE NG17)
• Pump/closed-loop: specialist diabetes centre
• Pregnancy: pre-conception counselling + specialist diabetic antenatal care

Life expectancy reduced by ~8-12 years compared to general population (improving with modern management). DCCT/EDIC: intensive insulin therapy reduces microvascular complications by ~60% (retinopathy, nephropathy, neuropathy) and cardiovascular events by ~42%. HbA1c is the strongest modifiable predictor of complications. DKA mortality ~1% in UK. Technology (CGM, pumps, closed-loop) is transforming outcomes. Main causes of mortality: cardiovascular disease, renal disease, DKA.

Key T1DM Trials

T1DM vs T2DM