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The current classification of diabetes is based on the aetiology of the disease. There are four categories:

 Type 1 diabetes (caused by pancreatic islet cell destruction);

 Type 2 diabetes (caused by a combination of insulin resistance and β‐cell insulin secretory dysfunction);

 Other specific types of diabetes (caused by conditions such as endocrinopathies, diseases of the exocrine pancreas, genetic syndromes, steroid induced etc., see below);

 Gestational diabetes (defined as diabetes that occurs for the first time in pregnancy).

Type 1 diabetes is subdivided into two main types: 1a or autoimmune (about 90% of type 1 patients in Europe and North America, in which immune markers, such as circulating islet cell antibodies, suggest autoimmune destruction of the β‐cells) and 1b or idiopathic (where there is no evidence of autoimmunity).

A steady increase (2.5–3% per annum) in the incidence of type 1 diabetes has been reported worldwide, especially among young children <4 years old. There are large differences between countries in the incidence of type 1 diabetes, e.g up to 10‐fold differences among European countries.

This classification has now replaced the earlier, clinical classification into ‘insulin‐dependent diabetes mellitus’ (IDDM) and ‘non‐insulin‐dependent diabetes mellitus’ (NIDDM), which was based on the need for insulin treatment at diagnosis. IDDM is broadly equivalent to type 1 diabetes and NIDDM to type 2 diabetes. One of the disadvantages of the old classification according to treatment was that subjects could change their type of diabetes – for example, some type 1a patients diagnosed after the age of 40 years masquerade as NIDDM, before eventually becoming truly insulin‐dependent (this is now classified as latent autoimmune diabetes in adults, LADA). Where diagnostic uncertainty exists between type 1 versus non type 1 diabetes, c‐peptide assessments can determine residual function beta cells (and insulin dependency to prevent ketoacidosis).

Various clinical and biochemical features can be used to decide whether the patient has type 1 or type 2 diabetes. The distinction may be difficult in individual cases.

A recent study have suggested a novel classification of adult onset diabetes according to patient characteristics (glutamate decarboxylase antibodies, age at diagnosis, BMI, HbA1c and homoeostatic model assessment 2 estimates of beta cell function and insulin resistance) and risk of diabetic complications.

1 Severe Autoimmune Diabetes (SAID)

2 Severe Insulin Deficient Diabetes (SIDD)

3 Severe Insulin Resistance Diabetes (SIRD)

4 Moderate Obesity Diabetes (MOD)

5 Moderate Age Related Diabetes (MARD)

Their study showed that individuals in cluster 3 (Most resistant to insulin) had significantly higher risk of diabetic kidney disease than individuals in cluster 4 and 5. Cluster 2 (insulin deficient) had the highest risk of diabetic eye disease. The largest cluster is cluster 5.

The category of ‘other specific types of diabetes’ is a large group of conditions, which includes genetic defects in insulin secretion [such as in maturity‐onset diabetes of the young (MODY) and insulinopathies], genetic defects in insulin action (e.g. syndromes of severe insulin resistance), pancreatitis, steroid induced and other exocrine disorders, hormone‐secreting tumours such as acromegaly (growth hormone) and Cushing’s syndrome (cortisol). Some cases are caused by the administration of drugs such as glucocorticoids. Some genetic syndromes are sometimes associated with diabetes (e.g. Down syndrome, Klinefelter’s syndrome and many more).