Steroid induced diabetes

Glucocorticoids are potent inducers of insulin resistance. Steroid induced diabetes is therefore an iatrogenic form of T2DM. The mainstay of treatment is insulin therapy.

Diet

Standard dietary advice is to aim for a negative caloric balance if the BMI is greater than 25 kg/m2, avoid refined sugars and avoid foods high in saturated animal fats.

However, dietary management alone is rarely if ever adequate to control steroid induced diabetes and only provides the right dietary background for other modalities of treatment.

Oral hypoglycaemics

All the major classes of OHAs (metformin, sulphonylureas and thiazoledinediones) can be used in steroid induced diabetes but unless the dose of glucocorticoid used is relatively low (e.g. 5-10 mg od of prednisolone), these alone are rarely adequate. 

Insulin therapy

Insulin therapy is the mainstay of treatment of steroid induced diabetes and has the great advantages of being almost infinitely titratable and significantly more potent than any other currently available hypoglycaemic.

A typical regimen would be twice daily biphasic human sequence insulin such as Humulin M3 used with metformin 500-1,000 mg bd (if there are no metformin contraindications and the patient is able to tolerate it). Starting doses in the region of 10-20 units am and 6-12 units pm depending on the dose of steroid, BMI of the patient and starting blood glucose level would be usual.

However, these are only starting doses and the patient will need to keep in close contact with a specialist nurse or doctor to seek advice of titrating insulin doses depending on response to treatment. Furthermore, as the dose of steroid is altered, so the doses of insulin will normally need to be changed in parallel.

Twice daily biphasic insulin is, however, not the only treatment strategy and basal insulin plus sulphonylurea, full blown basal-bolus insulin regimen, and combinations of the above are all reasonable alternatives.

How long will the patient need to be treated for?

Usually for only as long as the course of steroids. However, in some cases, treatment can be stepped-down to oral hypoglycaemics-only or even just diet-only as the dose of steroid comes down.

In a proportion of cases, glucose tolerance will not return to normal after cessation of steroid therapy, and in these cases it is presumed that the patient was already developing T2DM and the onset of steroid therapy merely precipitated a worsening of glucose intolerance.

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