Aftab Aziz
19/12/13
1441 pt with T1DM

Secondary
Prevention

Primary Prevention
n=726

Conventional
therapy
n=378

•
•
•
•
•

Intensive therapy
n=348

n=715
Conventional
therapy
n=352

Intensive therapy
n=363

Randomised, multicentre trial
1441 pts recruited from 29 centres 1983-89
Av follow-up was 6.5 yrs (mean 3-9)
Inclusion age 13-39 yrs, Type 1 DM
Primary prevention arm
– 1-5 yrs DM, no retinopathy or nephropathy

• Secondary prevention arm
– 1-15yrs DM, M NPRetinopathy, Ur Microalb <200mg/24 hrs
Glycemic control
16.6

13.8

11.1

8.3

5.5

• HbA1c improvement in intensive vs. conventional treated
group (p0.001)
• Mean glucose level 8.6mmol/l vs. 12.8mmol/l (p<0.001)
Retinopathy

• Primary prevention group (Intensive vs. conventional)
– 23 vs 91 pts developed retinopathy in 6 years followup (Mean risk
reduction 76%)

• Secondary prevention group (Intensive vs. conventional)
– 77 vs 143 pts developed progressive retinopathy (Mean risk reduction
54%)
– 47% reduction of severe retinopathy, 56% reduction in laser
photocoagulation

• Transient worsening of retinopathy (22% vs. 13%) 18 months
Nephropathy

• Primary prevention group
– Mean risk reduction for microalbuminuria by 34% (p 0.04) intensive gp

• Secondary prevention group
– Mean risk reduction for microalbuminuria by 43% (p 0.001) intensive gp

• Risk reduction in albuminuria (54%) and microalbunimuria
(39%) in intensive treatment arms
Neuropathy

• Primary Prevention group
– 3% vs 10% developed neuropathy (69% reduction of neuropathy by 5
years, p0.006)

• Secondary Prevention group
– 7% vs 16% developed neuropathy (57% reduction of neuropathy by 5
years)
Secondary analysis

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•
•
•
•
•
•

Severe hypoglycemic episodes 62 vs. 19/100 pt yrs
Hypoglycemia Coma / seizure episodes 16 vs. 5/100 pt yrs
Hospitalisation 54/40 pts vs. 36/27 pts
Major accidents 20 vs. 22 (2 fatalities, 1 vs. 1)
No difference in neuropsycholgical function
No death, MI or stroke
Wt gain ( overweight 12.7 vs. 9.3 /100 pt yrs)
DCCT overview

DCCT overview

  • 1.
  • 2.
    1441 pt withT1DM Secondary Prevention Primary Prevention n=726 Conventional therapy n=378 • • • • • Intensive therapy n=348 n=715 Conventional therapy n=352 Intensive therapy n=363 Randomised, multicentre trial 1441 pts recruited from 29 centres 1983-89 Av follow-up was 6.5 yrs (mean 3-9) Inclusion age 13-39 yrs, Type 1 DM Primary prevention arm – 1-5 yrs DM, no retinopathy or nephropathy • Secondary prevention arm – 1-15yrs DM, M NPRetinopathy, Ur Microalb <200mg/24 hrs
  • 3.
    Glycemic control 16.6 13.8 11.1 8.3 5.5 • HbA1cimprovement in intensive vs. conventional treated group (p0.001) • Mean glucose level 8.6mmol/l vs. 12.8mmol/l (p<0.001)
  • 4.
    Retinopathy • Primary preventiongroup (Intensive vs. conventional) – 23 vs 91 pts developed retinopathy in 6 years followup (Mean risk reduction 76%) • Secondary prevention group (Intensive vs. conventional) – 77 vs 143 pts developed progressive retinopathy (Mean risk reduction 54%) – 47% reduction of severe retinopathy, 56% reduction in laser photocoagulation • Transient worsening of retinopathy (22% vs. 13%) 18 months
  • 5.
    Nephropathy • Primary preventiongroup – Mean risk reduction for microalbuminuria by 34% (p 0.04) intensive gp • Secondary prevention group – Mean risk reduction for microalbuminuria by 43% (p 0.001) intensive gp • Risk reduction in albuminuria (54%) and microalbunimuria (39%) in intensive treatment arms
  • 6.
    Neuropathy • Primary Preventiongroup – 3% vs 10% developed neuropathy (69% reduction of neuropathy by 5 years, p0.006) • Secondary Prevention group – 7% vs 16% developed neuropathy (57% reduction of neuropathy by 5 years)
  • 7.
    Secondary analysis • • • • • • • Severe hypoglycemicepisodes 62 vs. 19/100 pt yrs Hypoglycemia Coma / seizure episodes 16 vs. 5/100 pt yrs Hospitalisation 54/40 pts vs. 36/27 pts Major accidents 20 vs. 22 (2 fatalities, 1 vs. 1) No difference in neuropsycholgical function No death, MI or stroke Wt gain ( overweight 12.7 vs. 9.3 /100 pt yrs)