T1DM is characterised by complete, or near-complete, deficiency of insulin production from the pancreatic beta cells due to auto-immune destruction of pancreatic islets. Diagnosis is usually clinical but is supported by finding high titres of anti-islet cell, or anti-glutamic acid decarboxylase antibodies, and low levels of C-peptide in the face of hyperglycaemia. Treatment is mandatory insulin therapy.
Polyuria and polydipsia are the cardinal symptoms of diabetes and occur when the blood glucose level exceeds the renal threshold for glucose excretion - usually approximately 10 mmol/L.
Difficulty with focussing - that has been present for only a short period and may be fluctuating - is due to osmotically driven swelling of the lens and varies as the degree of hyperglycaemia varies.
Weight loss is a cardinal symptom of insulin deficiency and arises due to a combination of lack of anabolic effects of insulin, negative caloric balance due to glycosuria and some contribution from dehydration.
Documenting an estimate of the pre-morbid weight helps to assess the severity of weight loss - and thus how ill the patient is - and also gives an idea of target weight that the patient should aim to return to.
Pruritis is a classical symptom of hyperglycaemia although not seen as commonly as the osmotic symptoms.
T1DM is less heritable than T2DM. A family history will also help to detect rare monogenic causes of diabetes such as MODY (maturity onset diabetes of youth), mitochondrial diabetes or APECED (autoimmune polyendocrinopathy, candidiasis and ectodermal dystrophy) that might otherwise be missed.
Steroid induced diabetes and post transplant diabetes are distinct from T1DM and are not usually insulinopaenic diabetes but usually arise due to insulin-resistance.
Any of these conditions may pre-dispose to loss of beta cell mass. If so, this would indicate a cause of diabetes other than auto-immune islet destruction.
The coexistence of auto-immune thyroid disease, auto-immune adrenal cortical failure or auto-immune premature ovarian failure suggests the diagnosis of Schmidt’s syndrome and raises the likelihood that the patient may develop further auto-immune conditions. A low threshold should therefore be used for testing for other auto-immune conditions.
The coexistence of diabetes with auto-immune hypoparathyroidism, adrenal cortical failure, recurrent mucocutaenous candidiasis and the presence of ectodermal dystrophic features (e.g. hypoplastic nails, alopecia, lens opacities) means that the very rare APECED (Autoimmune poly-endocrinopathy, candidiasis and ectodermal dystrophy) syndrome is likely to be the diagnosis.
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