Hyperglycaemia and PAD

There is a positive correlation between hyperglycaemia and the risk of developing PAD (Figure 8.1). In the UK Prospective Diabetes Study (UKPDS), for example, a

15-1

15-1

PVD 8 17 12 8 8 8 All 681 676 443 285 158 155

PVD 8 17 12 8 8 8 All 681 676 443 285 158 155

HbA1c (%) after 3 months' diet

120 130 140 150 160 170

PVD 13 All 1009

14 13 501 407

5 16 244 237

120 130 140 150 160 170

PVD 13 All 1009

14 13 501 407

5 16 244 237

Mean systolic blood presssure (mmHg)

Figure 8.1 Odds ratio for HbAlc (A) and SBP (B) by category adjusted for age, HDL cholesterol, previous cardiovascular disease, smoking, retinopathy, and peripheral sensory neuropathy in 61 patients with incident PVD at 6 years of a total 2,398 patients. A: Adjusted also for SBP. B: Adjusted also for HbAlc. Reference groups are HbAlc <6% and SBP <130 mmHg. Adapted from Adler et al. (2002) UKPDS 59: Hyperglycaemia and other potentially modifiable risk factors for peripheral arterial disease in type 2 diabetes. Diabetes Care 25: 894-9.

4987 4437 3935 2798 1338 323 56

Years from diagnosis of diabetes

Figure 8.2 Prevalence of PAD (95% CIs) defined as any two of the following: ABPI <0.8, absence of both DP and PT pulses to palpation in at least one leg, intermittent claudication at diagnosis of diabetes, and at 3-year intervals to 18 years. Adapted from Adler et al. (2002) UKPDS 59: Hyperglycaemia and other potentially modifiable risk factors for peripheral arterial disease in type 2 diabetes. Diabetes Care 25: 894-9.

1% increase in HbA1c was associated with a 28% increased risk of PAD (95% CI 12-46), independent of other factors including age, systolic blood pressure, smoking and prior cardiovascular disease (Adler etal., 2002). The incidence of PAD increases steadily with duration of diabetes, a reflection of prolonged exposure to high glucose concentrations (Figure 8.2) (Jude etal., 2001). Hyperglycaemia is well recognised to be an important pathogenic factor in the development of peripheral neuropathy, and several studies have shown that peripheral neuropathy, defined as the absence of Achilles tendon reflexes and impaired vibration sense in the great toe, is an independent predictor of amputation even after adjustment for age, sex and duration of diabetes (Nelson etal., 1988; Lehto etal., 1996). Thus, neuropathy compounds the problem of PAD by adding to the risk of amputation. Patients with peripheral neuropathy often fail to notice minor trauma resulting in foot ulceration, infection and gangrene. Hyperglycaemia contributes to small-vessel disease and probably impairs host defences against infection.

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