| Abstrakt: |
Steroids are medications that have been widely utilized for a number of ailments, both acute and chronic. The action of endogenous steroids, nuclear hormones that penetrate cell membranes to bind to certain glucocorticoid receptors in the cytoplasm of target cells to form glucocorticoid-receptor (GR) complexes, is mimicked by synthetic glucocorticoids. The translocated activated GR complex regulates DNA transcription in the cell nucleus. The main factor for drug-induced hyperglycemia is steroids. They not only worsen hyperglycemia in those who already have diabetes mellitus (DM), but they can also lead to DM in people who've not previously experienced it. Their incidence can reach up to 46% of patients, and their glucose levels can rise by up to 68% over baseline. Steroid effects are often narrow and reversible. Drug-induced diabetes is supposed to go away as steroid doses are decreased because their impact on endocrine metabolism returns to normal; however, this is often not the case. The synthesis of lipolysis, proteolysis, and hepatic glucose is increased by glucocorticoids (GCs) because they act as a substrate for oxidative stress metabolism. A wide range of medical conditions has been treated with GCs. Although steroid-induced hyperglycemia has been proven to be medically effective, it is still a widespread and potentially dangerous issue that must be taken into consideration when administering any GC dose. The most common scenario requires the use of insulin, particularly when the serum glucose level is greater than 200 mg/dL. [ABSTRACT FROM AUTHOR] |
