Medications known as glucocorticoids, such as prednisone and cortisone, are mainly used as anti-inflammatories or as anti-rejection drugs. They are prescribed, for example, for an arthritis attack or after an organ transplant.
One of their side effects is to increase blood glucose (sugar) since these drugs promote glucose production in the liver and reduce the sensitivity of the cells to insulin. Consequently, glucose accumulates in the blood and can cause a rise in blood sugar levels. The side-effects vary from person to person based on the prescribed dose of glucocorticoids, the way it is administered (cream, tablets or injection), and the length of time a person takes the drug.
Gluco-corticoids induced diabetes mellitus is a common and potentially harmful problem in clinical practice, affecting almost all medical specialties. However, its diagnosis and treatment are surprisingly undervalued by most healthcare professionals. The knowledge that hyperglycemia leads to longer hospital stays, delayed wound healing, increased infections, and higher mortality rates should encourage health-care providers to monitor its occurrence and to manage it appropriately. Similarly to T2DM in general, the principles of early detection and risk factor modification apply. Screening for GIDM should be considered in all patients (especially in those with risk factors) treated with medium to high doses of glucocorticoids. Diagnosing impaired fasting glucose or impaired glucose tolerance prior to the initiation of chronic glucocorticoids will better identify those who would benefit from glucocorticoid-sparing treatment, or if this is not an option, blood glucose monitoring while starting therapy. Together with, or after, lifestyle measures, hypoglycemic drugs with important insulin-sensitizing effects are indicated. Other oral hypoglycemic drugs or insulin therapy can be considered to be the drug of choice. Treatment, in most cases with insulin, should take into account the degree and pattern of hyperglycemia and the type, dose, and schedule of glucocorticoid used. Treatment should then be adjusted based on capillary glycemia and on changes in the dose of glucocorticoids. Moreover, it is essential to instruct the patient and/or the patient's family about how to perform these adjustments. Further investigation into the precise mechanism of glucocorticoid-induced insulin resistance will provide insights for future diabetes prevention efforts and targeted therapies.
Glucocorticoids promote gluconeogenesis in the liver, but in skeletal muscle and white adipose tissue they decrease glucose uptake and utilization by counteracring insulin response thereby causing hyperglycemia and insulin resistance, and thus diabetes mellitus
Dr. Emmanuel Adebayo's explanation of metabolic processes leading to my views of enhancement of blood glucose and associated diabetes by glucocorticoid administration seems to be correct and ofcourse logical.
In hand dermatitis, integrity of epidermal barrier is compromised, so there is a chance of enhanced absorption after topical use of glucocorticoids though circulating levels might be very low. Again this absorbed amount will be metabolized. Chance of development of diabetes mellitus is a worth consideration. We should be more rational regarding topical use of glucocorticoids.
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I do believe strongly the positive implication of glucocorticoids with diabetes and hence glucocorticoid administration be avoided until necessary to raise glucose level through gluconeogenesis.
For topical steroids , I fully endorse the views of Dr. Abbas Abd. In addition prolong usage of topical glucocorticoids would not cause Diabetes mellitus as the amount absorbed would be really small. Unfortunately to my knowledge , published papers pertaining to this are not available .