Diabetes mellitus management - targets for glycaemic control and other metabolic parameters
Individualised targets
- There is no single target. The target is set by the person, not the disease
- Tighten for: newly diagnosed, long life expectancy, no CVD, low hypoglycaemia risk, agents that do not cause hypoglycaemia
- Relax for: hypoglycaemia unawareness, severe hypoglycaemia history, established microvascular/macrovascular disease, limited life expectancy, frailty, CKD, cognitive impairment, living alone
The evidence behind the number
- DCCT/UKPDS - tight control reduces microvascular complications; macrovascular benefit emerges only over decades (legacy effect)
- ACCORD - HbA1c <6.0% in high-risk T2DM *increased mortality*
- -> there is a floor: pushing HbA1c below ~6.5% with hypoglycaemia-causing agents in established CVD does harm
- Modern position: cardiorenal protection is prescribed on indication, not on HbA1c
Where Australia sits
- ~50% of Australians with T2DM are above an HbA1c of 7%
- Therapeutic inertia (a year or more before intensification) is the commonest reason
- Older adults are more often over-treated than under-treated - hypoglycaemia risk rises steeply with age, CKD and sulfonylurea/insulin use
HbA1c and when it misleads
- HbA1c = non-enzymatic glycation of haemoglobin, reflecting mean glycaemia over ~8-12 weeks, weighted to the most recent 4 weeks
- Unreliable when red cell survival is abnormal:
- Falsely low - haemolysis, blood loss, transfusion, splenomegaly, pregnancy, erythropoietin, iron/B12 replacement
- Falsely high - iron deficiency, B12/folate deficiency, splenectomy, alcohol, CKD/uraemia, some haemoglobinopathies
- *Haemoglobinopathy: HbA1c is unreliable - use an OGTT for diagnosis and CGM/fructosamine for monitoring*
- HbA1c is a mean, and a mean hides variability - two people with the same HbA1c can have very different hypoglycaemia burdens
| HbA1c % | mmol/mol | Mean glucose (mmol/L) |
|---|---|---|
| 6.0 | 42 | ~7.0 |
| 7.0 | 53 | ~8.6 |
| 8.0 | 64 | ~10.2 |
| 9.0 | 75 | ~11.8 |
Glycaemic targets
Glycaemic targets
| Situation | HbA1c |
|---|---|
| General adult target | <=7.0% (53 mmol/mol) |
| T2DM on lifestyle +/- metformin, short duration, no CVD | <=6.5% (48) |
| T1DM | <=7.0% (individualised) |
| Hypoglycaemia unawareness, severe hypoglycaemia, comorbidity, limited life expectancy | <=8.0% (64), or symptom-driven only |
| Frail/residential aged care | 7.5-8.5%; avoid hypoglycaemia and symptomatic hyperglycaemia rather than chasing a number |
| Pregnancy (pre-existing diabetes) | <=6.0-6.5% pre-conception and in pregnancy, if achievable without hypoglycaemia |
Capillary glucose targets
- Preprandial 4-7 mmol/L; 2 h postprandial 5-10 mmol/L
- Pregnancy: fasting <5.0-5.3; 1 h <7.4-7.8; 2 h <6.7 mmol/L
CGM targets - increasingly the primary metric
CGM targets - increasingly the primary metric
| Metric | Target (most adults with T1/T2DM) |
|---|---|
| Time in range 3.9-10.0 mmol/L | >70% |
| Time below 3.9 | <4% |
| Time below 3.0 | <1% |
| Time above 10.0 | <25% |
| Time above 13.9 | <5% |
| Coefficient of variation | <=36% |
| High risk / older / frail | TBR <1%, TIR >50% |
| Pregnancy (T1DM) | TIR 3.5-7.8 mmol/L >70%, TBR <4% |
- *Fix the time below range before chasing the time in range* - the order matters
- Each 10% increase in TIR ~ 0.5-0.8% fall in HbA1c
Non-glycaemic targets - where most of the mortality benefit lives
| Domain | Target |
|---|---|
| Blood pressure | *<130/80 mmHg where tolerated[[c3]] - the older 140/80 (with microalbuminuria) and 140/90 figures are superseded* |
| Lipids | Statin in essentially all adults >40y with diabetes; LDL-C goal <1.8 mmol/L in established ASCVD (<1.4 mmol/L if very high risk), <2.0 mmol/L in high-risk primary prevention |
| Albuminuria | ACR reduction >=30% is a treatment target in its own right |
| Weight | 5-10% loss for metabolic benefit; >=15% can induce T2DM remission |
| Smoking | Cessation |
Monitoring frequency
- HbA1c 3-monthly if not at target or after any change; 6-monthly if stable and at target
- CGM ambulatory glucose profile reviewed at each visit for insulin-treated diabetes
Getting to the target
- Metformin remains first-line for most T2DM on glycaemic grounds
- *But cardiorenal indications override HbA1c* - prescribe regardless of whether glycaemic control is at target:
- Established ASCVD -> GLP-1 RA and/or SGLT2 inhibitor with proven benefit
- Heart failure (any EF) -> SGLT2 inhibitor
- CKD (eGFR <60 or albuminuria) -> SGLT2 inhibitor; add finerenone if albuminuria persists on maximal ACEi/ARB; GLP-1 RA (semaglutide) now has CKD outcome evidence
- Obesity -> GLP-1 RA or tirzepatide (dual GIP/GLP-1)
- Sulfonylureas and insulin: effective, but hypoglycaemia and weight gain - the reason they have fallen down the list
- Add insulin when the target is unmet despite combination therapy, or with catabolic features/very high HbA1c
Reviewing a target that is not being met
Ask in this order
1. Adherence and access (cost, complexity, device problems)
2. Technique - injection sites, lipohypertrophy, pump/CGM use
3. Diet, alcohol, activity, sleep, mental health, diabetes distress
4. Intercurrent - infection, steroids, antipsychotics, thyroid disease, MASLD, coeliac
5. Regimen - is the drug class right for this phenotype?
De-intensification - as important as intensification
- HbA1c <6.5% on a sulfonylurea or insulin in an older person is a signal to reduce, not to celebrate
- Withdraw sulfonylureas first in frailty, falls or CKD
- Reassess the target at every change in health status
Structural care
Structural
- Structured education, dietitian, diabetes educator
- Annual cycle of care; complication screening as scheduled
- Sick day management plan; driving and hypoglycaemia advice
Constraints on tight control
- Hypoglycaemia (the main constraint on tight control)
- Weight gain with insulin, sulfonylureas, thiazolidinediones
- CKD - alters drug choice and dosing, and raises hypoglycaemia risk
- Haemoglobinopathy, anaemia, pregnancy, recent transfusion - all invalidate HbA1c
- Depression and diabetes distress - a major driver of unmet targets
- Obstructive sleep apnoea, MASLD, periodontal disease
Progression and legacy effect
- T2DM is progressive - beta-cell function declines, so a regimen that works today will not work in 5 years; expect and plan intensification
- Legacy effect: good control early yields benefit decades later; late intensification in established CVD yields much less
- *Achieving a number at the cost of severe hypoglycaemia is a net harm* - severe hypoglycaemia independently predicts mortality, dementia and cardiovascular events
- Sustained weight loss >=15% can produce T2DM remission (DiRECT), most likely within 6 years of diagnosis
- The target should be re-negotiated whenever health status, life expectancy or the person's priorities change - it is not set once at diagnosis
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