3.3.
Glycosuria (the presence of glucose in the urine) is responsible for the classic diabetic symptoms and was previously regarded as a diagnostic hallmark of the disease. Nowadays, it indicates the need to test blood glucose, but cannot be used to diagnose diabetes because of the poor relationship between blood and urine glucose (Figure 3.6). This is for several reasons: the renal threshold for glucose reabsorption varies considerably within and between individuals, the urine glucose concentration is affected by the subject’s state of hydration and the result reflects the average blood glucose during the period that urine has accumulated in the bladder. The average renal threshold is 10 mmol/L (i.e. blood glucose concentration above this level will ‘spill over’ into the urine), but a negative urine test can be associated with marked hyperglycaemia.
Figure 3.3 Diagnosis of diabetes and IGT by the oral glucose tolerance test.
Longer term indices of hyperglycaemia include the HbA1c, a measure of integrated blood glucose control over the preceding few weeks. HbA1c is used primarily to assess glycaemic control among people with diabetes on treatment. HbA1c analyses are now being calibrated to the IFCC assay. Thus the units of HbA1c in many countries have changed from percent to mmol/mol (Table 3.3).
Table 3.3 Historically, HbA1c has been reported in percentage values describing the proportion of haemoglobin that is glycated. The assay was aligned to that used in the Diabetes Control and Complications (DCCT) trial. The International Federation of Clinical Chemistry (IFCC) has now established a new reference system, and values will be reported in mmol HbA1c per mol haemoglobin without glucose attached. Conversion for HbA1c is shown below.
| DCCT (%) | IFCC (mmol/mol) | DCCT (%) | IFCC (mmol/mol) |
|---|---|---|---|
| 6.0 | 42 | 9.0 | 75 |
| 6.2 | 44 | 9.2 | 77 |
| 6.4 | 46 | 9.4 | 79 |
| 6.5 | 48 | 9.5 | 80 |
| 6.6 | 49 | 9.6 | 81 |
| 6.8 | 51 | 9.8 | 84 |
| 7.0 | 53 | 10.0 | 86 |
| 7.2 | 55 | 10.2 | 88 |
| 7.4 | 57 | 10.4 | 90 |
| 7.5 | 58 | 10.5 | 91 |
| 7.6 | 60 | 10.6 | 92 |
| 7.8 | 62 | 10.8 | 95 |
| 8.0 | 64 | 11.0 | 97 |
| 8.2 | 66 | 11.2 | 99 |
| 8.4 | 68 | 11.4 | 101 |
| 8.5 | 69 | 11.5 | 102 |
| 8.6 | 70 | 11.6 | 103 |
| 8.8 | 73 | 11.8 | 105 |
Figure 3.4 The prevalence of retinopathy in type 2 diabetes relative to the time of clinical diagnosis. Note the presence of retinopathy at diagnosis and the likely onset of retinopathy and diabetes some years before diagnosis. From Paisey. Diabetologia 1980; 19: 31 – 34.
The potential value of screening for diabetes is to facilitate early diagnosis and treatment. About 20% of newly diagnosed type 2 diabetic subjects already have evidence of vascular complications, such as retinopathy, the prevalence of which increases with diabetes duration. This suggests that complications begin about 5–6 years before a diagnosis is made, and that the actual onset of (type 2) diabetes may be several years before the clinical diagnosis.
Figure 3.5 High‐risk patients who should be screened annually for type 2 diabetes.
In most countries, there is no systematic screening policy for diabetes, yet there are estimates that up to 50% of patients with diabetes are undiagnosed. Ad‐hoc screening of high‐risk groups is becoming more common. The fasting plasma glucose is simple, quick, acceptable to patients and of low cost, but can miss those with isolated post‐challenge hyperglycaemia and requires patient to be fasted. The OGTT is more difficult to perform, impractical for large numbers and expensive, but is the only way to identify post‐load hyperglycaemia. Screening should focus on high‐risk groups. HbA1c is widely used to screen individuals at high risk of developing diabetes.
Figure 3.6 Classification of diabetes.
Figure