This site describes diabetes mellitus and its management with antidiabetics. The oral drugs included in this chapter are classified in Table: Classification of oral antidiabetics. Insulin, which is given parenterally, is discussed on site. The adjunct pramlintide given subcutaneously, is described on site, and the incretin mimetic, exenatide, on site.
Table: Classification of oral antidiabetics.
| Aldose Reductase Inhibitors |
| Epalrestat |
| Alpha-glucosidase Inhibitors |
| Acarbose |
| Miglitol |
| Voglibose |
| Biguanides |
| Buformin |
| Metformin |
| Phenformin |
| Dipeptidylpeptidase-4 inhibitors |
| Sitagliptin |
| Vildagliptin |
| Meglitinides |
| Nateglinide |
| Repaglinide |
| Miscellaneous |
| Glybuzole |
| Guar Gum |
| Sulfonylureas |
| Acetohexamide |
| Carbutamide |
| Chlorpropamide |
| Glibenclamide |
| Glibornuride |
| Gliclazide |
| Glimepiride |
| Glipizide |
| Gliquidone |
| Glisentide |
| Glisolamide |
| Glisoxepide |
| Glycyclamide |
| Tolazamide |
| Tolbutamide |
| Thiazolidinediones |
| Pioglitazone |
| Rosiglitazone |
| Troglitazone |
Diabetes mellitus
Diabetes mellitus is a group of disorders of carbohydrate metabolism in which the action of insulin is diminished or absent through altered secretion, decreased insulin activity, or a combination of bom factors. It is characterised by hyperglycaemia. As the disease progresses tissue or vascular damage ensues leading to severe complications such as retinopathy, nephropamy, neuropathy, cardiovascular disease, and foot ulceration.
Diabetes mellitus may be categorised into several types but the two major types are type 1 (insulin-dependent diabetes mellitus DDDM) and type 2 (non-insulin-dependent diabetes mellitus NIDDM). The term juvenile-onset diabetes has sometimes been used for type 1 and maturity-onset diabetes for type 2. Malnutrition-related diabetes is no longer considered a separate entity (see Effects of Cassava, under Adverse Effects of Starch).
Type 1 diabetes mellitus is present in patients who have little or no endogenous insulin secretory capacity and who therefore require exogenous insulin therapy for survival. This form of the disease has an auto-immune basis in most cases, and usually develops before adulthood. The associated hypoinsulinaemia and hyperglucagonaemia put such patients at risk of ketosis and ketoacidosis.
In type 2 diabetes mellitus the disease typically develops in later life. Insulin secretion may appear normal or even excessive (and type 2 patients are thus less prone to ketosis) but it is insufficient to compensate for insulin resistance. Obesity is present in the majority of type 2 patients non-obese patients tend to have low insulin secretory capacity (although not as low as in type 1 diabetes) rather man appreciable insulin resistance. It is closely associated with cardiovascular disease, and the 2 may arise from a common antecedent described as the metabolic syndrome.
Diagnosis of diabetes mellitus
Diagnosis is based upon blood-glucose concentrations exceeding set values under specified conditions. Diagnostic values for measurements in venous whole blood are greater than or equal to 6.1 mmol/litre for the fasting state and 10.0 mmol/litre after a glucose load. The corresponding values for capillary whole blood are 6.1 and 11.1 mmol/litre, and for venous plasma 7.0 and 11.1 mmol/litre. If there are accompanying symptoms of increased thirst and urine volume, recurrent infections and weight loss, then a plasma-glucose concentration in excess of 11.1 mmol/litre in a single random sample is considered diagnostic. If symptoms are absent, a fasting plasma-glucose of 7.0 mmol/litre or more, repeated on a subsequent day, can be used to confirm the diagnosis. Alternatively, diagnosis can be confirmed with the oral glucose tolerance test (OGTT). This test consists of an overnight fast followed by measurement of the fasting blood-glucose concentration, men the administration of a 75-g oral glucose load (in children 1.75 g/kg up to a maximum of 75 g), and further measurement of the blood-glucose concentration two hours later. There has been some confusion at an international level as to whether the glucose load should be 75 g of the anhydrous form or the monohydrate. Sources at WHO have therefore suggested mat the form should be standardised as 75 g of anhydrous glucose (anhydrous dextrose), which would be equivalent to 82.5 g of the monohydrate (Glucose BP dextrose monohydrate). The threshold for the diagnosis of diabetes was lowered in the late 1990s from an earlier fasting plasma glucose concentration of 7.8 mmol/litre, to reflect an increased risk of microvascular disease in patients with concentrations of 7.0 mmol/litre ormore. Patients with abnormal blood sugar who do not reach the defined threshold for overt diabetes may be considered to have impaired fasting glucose or impaired glucose tolerance.Measurement of glycosylated haemoglobin (HbA1C) is not recommended for routine diagnosis. Similarly, other indicators, such as measurement of autoantibodies (to insulin or islet cells, for example) are not routinely used for diagnosis.
Once the presence of diabetes has been confirmed the distinction between type 1 and type 2 is made on clinical grounds.