An increasingly common condition characterised by a raised concentration of glucose in the blood due to a deficiency in the production and/or action of INSULIN, a hormone made in beta cells in the pancreas. It is one of the world's most serious health problems. According to the World Health Organisation the disorder affects over 400 million individuals worldwide – four times its prevalence in 1994. The incidence of insulin-dependent diabetes is even rising in young children, who will be liable to develop late complications.
Also known as juvenile-onset diabetes or type 1 diabetes, this describes those with a severe deficiency or absence of insulin production. Insulin therapy is essential to prevent KETOSIS – a disturbance of the body's acid/base balance which leads to coma and can be fatal. The onset is most common during childhood, but can occur at any age.
Also known as maturity-onset diabetes or type 2 diabetes, this is where insulin production is reduced but not absent. This type usually occurs after the age of 40 years in overweight people. With increasing childhood obesity, it is now being seen in young persons, including adolescents. It comes on gradually, weight loss is uncommon and KETOSIS rarely develops.
(a) Due to pancreatic disease – for example, chronic pancreatitis (see PANCREAS, DISORDERS OF); (b) secondary to drugs – for example, GLUCOCORTICOIDS (see PANCREAS, DISORDERS OF); (c) excess hormone production – for example, growth hormone (ACROMEGALY); (d) insulin receptor abnormalities; (e) GENETIC syndromes (see GENETIC DISORDERS).
Diabetes occurring in pregnancy and resolving afterwards.
IDDM occurs as a result of autoimmune destruction of beta cells, the insulin producing cells in the PANCREAS. There is some genetic influence so that if one parent has IDDM, the risk of a child developing IDDM by the age of 25 years is 1.5–2.5 per cent, and the risk of a sibling of person with IDDM developing diabetes is about 3 per cent. NIDDM has a stronger genetic influence. For example, the risk of a sibling of a NIDDM subject developing NIDDM up to the age of 80 years is 30–40 per cent. Obesity and decreased exercise markedly increase the risk of disease development.
In IDDM, the main symptoms are THIRST, POLYURIA, GLYCOSURIA, weight loss despite eating and recurrent infections (e.g. BALANITIS and vulval infections). However, subjects with NIDDM may have the disease for several years without symptoms, and diagnosis is often made incidentally when a urine or blood sample happens to be tested or when presenting with a complication of the disease.
Complications
occurs when amounts of glucose in the blood become low, for example if a patient with IDDM misses a meal but takes their usual insulin dose. Symptoms usually develop when the glucose concentration falls below 2.5 mmol/l and include confusion, hunger and sweating, with coma developing if blood-sugar concentrations remain low. A dose of refined sugar followed by complex carbohydrate will return the glucose concentration to normal. If the person is unable to swallow, GLUCAGON may be given intramuscularly or glucose intravenously, followed by oral carbohydrate once the subject is able to swallow.
occurs when there is insufficient insulin present to prevent KETONE production. This may occur before the diagnosis of IDDM or when insufficient insulin is being given. It is recognised by the usually rapid onset of the acute symptoms described above with a raised blood sugar, a low blood pH and large amounts of ketones in the urine. Treatment is urgent as coma and death may result if the condition is left untreated.
(a) retinopathy (b) cataract. Regular examination of the eyes enables any developing abnormalities to be detected and treatment given when appropriate, to preserve eyesight.
People with diabetes may develop kidney damage which can result in renal failure.
(a) Symmetrical sensory polyneuropathy – damage to the sensory nerves that commonly presents with tingling, numbness or pain in the feet or hands; (b) asymmetrical motor diabetic neuropathy, presenting as progressive weakness and wasting of the proximal muscles of legs; (c) mononeuropathy; individual motor or sensory nerves may be affected; (d) autonomic neuropathy, which affects the autonomic nervous system and has many presentations including IMPOTENCE, diarrhoea or constipation and postural HYPOTENSION.
There are several skin disorders associated with diabetes, including: (a) necrobiosis lipoidica diabeticorum, characterised by one or more yellow atrophic lesions on the legs; (b) ulcers, which most commonly occur on the feet due to peripheral vascular disease, neuropathy and infection. Foot care is very important.
of diabetes aims to prevent symptoms, restore carbohydrate metabolism to as near normal as possible, and to minimise complications. Concentration of glucose, and Glycosylated Haemoglobin (HbA1c) in the blood are used variously to give an indication of blood-glucose control.
Insulin-dependent diabetes requires insulin for treatment. Non-insulin-dependent diabetes may be treated with diet, oral HYPOGLYCAEMIC AGENTS or insulin.
Many NIDDM diabetics may be treated with diet alone. For those who are overweight, weight loss is important so a diet high in complex carbohydrate, high in fibre, low in fat and aiming towards ideal body weight is prescribed. Subjects taking insulin need to eat at regular intervals in relation to their insulin regime.
are used in the treatment of NIDDM in addition to diet, when diet alone fails to control blood-sugar levels. (a) SULPHONYLUREAS act mainly by increasing the production of insulin; (b) BIGUANIDES, of which only metformin is available, may be used alone or in addition to sulphonylureas. Metformin's main actions are to lower the production of glucose by the liver and improve its uptake in the peripheral tissues.
Insulin-dependent diabetes requires insulin for treatment. Insulin is injected under the skin – mainly by syringe but sometimes by insulin pump. There are three main types of insulin preparation: (a) short action (approximately six hours), with rapid onset; (b) intermediate action (approximately 12 hours); (c) long action, with slow onset and lasting for up to 36 hours. There are many regimens of insulin treatment involving different combinations of insulin; regimens vary depending on the requirements of the patients, most of whom administer the insulin themselves. Carbohydrate intake, energy expenditure and the presence of infection are important determinants of insulin requirements on a day-to-day basis.