Type-2 diabetes, a progressive condition affecting glucose metabolism, is an increasing problem that all GPs in the UK have to deal with on a regular basis.
The current WHO diagnostic criteria define type-2 diabetes as a fasting plasma glucose of [s40]7mmol/l, or a two-hour plasma glucose of [s40]11.1mmol/l following oral ingestion of 75g glucose. Ideally glucose measurements should be on venous blood, not a finger-prick.
A less specific definition is a degree of hyperglycaemia sufficient to cause pathological and functional changes to target organs in people who do not require insulin.
One of the problems in preventing the complications of type-2 diabetes is that patients may be asymptomatic, yet have a degree of hyperglycaemia sufficient to cause target organ damage for years before the diagnosis is made.
The condition is due to a combination of insulin resistance and pancreatic beta-cell failure that results in insufficient insulin secretion to overcome the insulin resistance. Patients with type-2 diabetes rarely need insulin treatment to survive, but might be given it to maintain optimum health or delay the onset of complications when oral medications are not sufficiently effective.
Type-2 diabetes usually appears in people over the age of 40, but in South Asian and African-Caribbean people it often appears after the age of 25.
A worrying trend is that in recent years more children are being diagnosed, some as young as seven.
Altogether type-2 diabetes accounts for between 85 and 95 per cent of all diabetes. It is estimated that in the UK there are over 2.5 million people with diabetes, and probably more than half a million people undiagnosed.
It is estimated that there are 1.7 new diagnoses of type-2 diabetes per 1,000 persons per year in England and Wales, making a total of 90,000 cases per year.
Obesity is one of the most important risk factors, and the distribution of fat is relevant. Central obesity - around the trunk - is more diabetogenic than fat around the hips and thighs. It is a sobering thought that the risk of diabetes increases by about 5 per cent with every 1kg of weight gain.
Other risk factors include a lack of physical activity and a history of gestational diabetes. People with impaired glucose tolerance (fasting plasma glucose level <7.0mmol/l and a two-hour plasma glucose of between 7.8 and 11.1mmol/l) and impaired fasting glucose (fasting glucose >6.1 and <6.9mmol/l) also have an increased risk.
Drug therapy such as a combination of thiazide diuretics and beta-blockers can also increase the risk.
Cigarette smoking, a low fibre, high glycaemic index diet, metabolic syndrome and polycystic ovary syndrome all increase the risk of type-2 diabetes.
A positive family history confers a 2.4-fold increased risk of type-2 diabetes, but the genetics are complex. As already mentioned, ethnicity is important.
Morbidity and mortality
Mortality is two to three times higher in patients with type-2 diabetes. About 75 per cent of patients will die of heart disease and 15 per cent of stroke.
The HbA1c level is a useful indicator of risk, because for every 1 per cent increase, the risk of death from a diabetes-related cause increases by 21 per cent. About 50 per cent of patients who are not controlled by diet alone will need more than one hypoglycaemic drug by the third year after diagnosis.
Type-2 diabetes may present with typical symptoms such as thirst, polyuria, blurred vision, weight loss and recurrent infections, but these are usually mild or absent. Ketoacidosis and hyperosmolar, hyperglycaemic non-ketotic coma (HONK) is rare, and usually associated with intercurrent illness such as a severe infection.
Type-2 diabetes may be discovered while investigating a secondary complication in a previously undiagnosed patient. General population screening is not undertaken, but people with the risk factors already described should be screened, as should all patients who have heart disease, cerebrovascular disease, peripheral vascular disease or hypertension.
Once diagnosis has been confirmed, much of the management of type-2 diabetes may be carried out in dedicated clinics by trained diabetes specialist nurses. After diagnosis, the patient should be taught to carry out their own blood glucose measurement.
The management of glucose control is of great importance, and includes essential dietary measures and advice about alcohol and exercise.
If patients cannot achieve good glucose control with diet alone, they must be considered for hypoglycaemic drug monotherapy or combinations of drugs if necessary.
If the patient is overweight (BMI>25), metformin should be used, but if this is not tolerated or is contraindicated, a sulphonylurea such as gliclazide, glimepiride or glipizide may be considered.
Newer agents (DPP-4 inhibitors and the glitazones, pioglitazone and rosiglitazone) may be considered for use instead of a sulphonylurea as second-line therapy to first-line metformin, if blood glucose control is inadequate.
These options, which have not been met with universal acceptance, are discussed in NICE guideline CG87 'Type 2 Diabetes: newer agents', published in May 2009.
The HbA1c should be checked within two to six months to assess blood glucose control. The management of hypoglycaemic episodes will also need explanation and advice.
BP management is another essential component of type-2 diabetes management. If the patient has kidney, eye or cerebrovascular damage, the target BP should be <130/80mmHg. For others, the target BP is <140/80mmHg. In primary care, type-2 diabetes evaluation should be based on the systolic value.
The ACE inhibitors enalapril, lisinopril, perindopril, ramipril or trandolapril are suitable choices for type-2 diabetics with hypertension, but renal function and electrolytes should be checked first.
In those intolerant of an ACE inhibitor, an angiotensin-II receptor antagonist such as candesartan, irbesartan, losartan or valsartan may be considered.
Lipid control also needs careful consideration, and the question of whether all type-2 diabetics should receive a statin is much debated.
It is agreed that a patient of any age at high risk of or with evidence of CVD should receive a statin, but in the latest NICE guidelines (CG66, 2008) it is suggested that all type-2 diabetics over the age of 40 should receive a statin.
However, NICE does not seem wholehearted in its support and says: 'The evidence of effectiveness and safety of generic statins, and in particular simvastatin seemed clear, and at current prices probably costsaving in the population with type-2 diabetes over the age of 40 years (irrespective of experience of CVD).'
Perhaps the use of the word 'probably' explains why this has not been universally implemented, and NHS Clinical Knowledge Summaries state that over-40s with no risk factors should not receive a statin.
Part of any management plan for type-2 diabetics must include checking for specific complications.
A separate article will deal with the question of complications in diabetes, but in brief these include foot problems, eye complications, renal disease, neuropathy and cardiovascular disease.
- Dr Barnard is a former GP in Fareham, Hampshire