Diabetes mellitus is a group of diseases characterised by hyperglycaemia. This can arise either from lack of secretion of insulin from the β islets of the pancreas or due to resistance to the action of insulin. They are commonly referred to as Type 1 and Type 2. A further type of diabetes mellitus is called Secondary Diabetes.
Strict control of blood sugar is an important part of the management. Poor control has been shown to increase the chances of developing heart, kidney and eye problems. In recent years it has become clear that control of blood pressure is also critical, indeed the benefits to be had from control of blood pressure may be similar in magnitude to those from glucostasis. Diabetes, however, is a progressive condition.
In addition to diabetes mellitus we now recognise impaired glucose tolerance and IFG impaired fasting glucose; DM, IGT and IFG are manifestations of defects of insulin action e.g.insulin resistance, insulin production beta-cell failure or both.
- Seen in younger individuals - usually under 40 years of age
- North european predominance
- Human lymphocyte antigen DR3/DR4 very common
- Destruction of the islets of Langerhans - insulitis
- Possibly viral triggered autoimmune disease
- May be other autoimmune diseases - thyroid failure, ovarian failure, Addison's disease
- Antibodies found
- Seems to present more when viral illnesses more prevalent
- Suggested viruses are coxsackie B
- Prone to ketoacidosis
- Presentation is polyuria, polydipsia, weight loss, balanitis and sometimes with diabetic ketoacidosis
- All patients will require Insulin as well as dietary measures
- Older individuals but now beginning to present in younger patients due to dietary excess
- Presentation is polyuria, polydipsia, polyphagia, and are usually overweight.
- Diabetic ketoacidosis does not occur
- All races especially Pima indians, polynesians, African, Asians.
- Insulin resistance i.e. Insulin is present but for various reasons its effectiveness is diminished
- Patients are treated by weight reduction, exercises, diet and medications. Some cases may require Insulin.
- Insulin is not vital but can improve control and reduce complications long term
Ketosis prone diabetes
Usually all the phenotypic features of type 2 diabetes but prone to ketoacidosis at times of severe stress or infection; there is reversible glucose toxicity at the beta cell. Seems to be relatively confined to black patients.
A single gene failure could knock out the ability to produce functional insulin, or the control mechanisms for its secretion. One class of monogenic diabetes is MODY - maturity onset diabetes of the young - which differs from type 2 diabetes in that patients may appears to be doing relatively well, and by the considerable response to sulphonylurea drugs of some variants. Genetic testing in the UK is centred on Exeter. See genetics of diabetes.
Type 1 diabetes is caused by hereditary and environmental factors. A hypothesis is that there is a window of time for an infection with a coxsackie virus to trigger an auto-immune process destroying the insulin producing cells of the islets.
The genetics of diabetes is not fully understood.
Exclusion, screening and case finding
In the UK there is a de facto screening program with random urine testing on joining general practice lists. Previously there was a general policy of testing urine on attendance at hospital, but this is less common now. Severe diabetes, but not early diabetes can be excluded with reasonable certainty by a urine test, which is easy, cheap and generally acceptable. Random capillary glucose, fasting capillary glucose, fasting venous blood glucose and a 2 hour glucose challenge exclude diabetes with increasing reliability, cost and pain.
Much diabetes is discovered by case-finding - a somewhat targetted testing of people with conditions suggesting diabetes may have been present for some time.
- Onset is usually insidious with malaise and polydipsia
- May progress rapidly to diabetic ketoacidosis in type 1 diabetes
The primary test for diabetes is a measurement of sugar level. Urine sugar levels can rule in diabetes, but not wholly rule it out in its early stages. They are simple and cheap.
In an asymptomatic patient any diagnostic test for diabetes must be repeated on a separate occasion. In a symptomatic patient, or a patient with specific complications of diabetes mellitus, one diagnostic test will suffice.
- Fasting plasma glucose: >6.9 mmol/L
- Random plasma glusose:>11 mmol/L
- 2 hours after a 75 g glucose load >11 mmol/L
- Renal profile including bicarbonate and chloride
- Thyroid function test: TSH, T4 +/- T3
- Lipid profile
- HbA1c (not used for diagnosis, only for follow up).
C-peptide may be measured as a proxy for endogenous insulin secretion. Antibodies to islet cells may indicate whether diabetes is early type 1 or is type 2, in the minority of cases where this is not clinically evident.
- Lifestyle change: This is the first and most crucial part of management of diabetes;
- Diet. The most significant diet modification in type two diabetes is a reduction in energy content sufficient to cause a reduction in body weight (except in the rare type two diabetic who is not fat). Diet modifications include: sugar free, foods with high glycaemic index, fruit and vegetables,low fat and salt diet.
- Weight reduction
- Regular exercise. Aerobic and resistance training improves glycaemic control in type 2 diabetes
- Management of hypertension to a lower target than non-diabetics
- Management of hypercholesterolaemia - or indeed normal levels of cholesterol.
In patients undergoing bariatric surgery, exclusion of the duodenum appears to improve glycaemic control after several weeks, which is faster than would be expected from weight loss alone. This phenomenon has been reproduced in a rat model. A case series of 11 patients shows that this phenomenon may be potentially exploited in treating diabetes in non-obese patients through surgical partial duodenal bypass (duodeno-jejunal bypass).
Progression and complications
We should be able to cure Type 1 diabetes.
- ↑ Sigal RJ, Kenny GP, Boulé NG, Wells GA, Prud'homme D, Fortier M, Reid RD, Tulloch H, Coyle D, Phillips P, Jennings A, Jaffey J. Effects of aerobic training, resistance training, or both on glycemic control in type 2 diabetes: a randomized trial. Annals of internal medicine. 2007 Sep 18; 147(6):357-69.
- ↑ http://bmj.bmjjournals.com/cgi/content/full/332/7550/1103 Reckless' BMJ Leader on lipids and Diabetes, 2006
- ↑ http://www.gnn.gov.uk/content/detail.asp?ReleaseID=351617&NewsAreaID=2
- ↑ Rubino F, Marescaux J. Effect of duodenal-jejunal exclusion in a non-obese animal model of type 2 diabetes: a new perspective for an old disease. Annals of surgery. 2004 Jan; 239(1):1-11.(Link to article – subscription may be required.)
- ↑ Ramos AC, Galvão Neto MP, de Souza YM, Galvão M, Murakami AH, Silva AC, Canseco EG, Santamaría R, Zambrano TA. Laparoscopic duodenal-jejunal exclusion in the treatment of type 2 diabetes mellitus in patients with BMI<30 kg/m2 (LBMI). Obesity surgery. 2009 Mar; 19(3):307-12.(Link to article – subscription may be required.)