Steroid hyperglycemia: Prevalence, early detection and therapeutic recommendations: A narrative review

Table 1 Pathophysiology of corticosteroid-induced hyperglycemia

Increase in insulin resistance with increased glucose production and inhibition of the production and secretion of insulin by pancreatic β-cells
Corticosteroids increase endogenous glucose production, increment in gluconeogenesis and antagonizing the metabolic actions of insulin
Enhance the effects of other counterregulatory hormones, such as glucagon and epinephrine, which increase the endogenous synthesis of glucose
Also been shown that the expression of the nuclear receptor peroxisome proliferator-activated receptor α is necessary for the increment in endogenous glucose production induced by corticosteroids
Corticosteroids reduce peripheral glucose uptake at the level of the muscle and adipose tissue
Costicosteroids also inhibit the production and secretion of insulin from pancreatic β-cells and induce β-cell failure indirectly by lipotoxicity

Table 2 List of most commonly used drugs in glucocorticoids-induced hyperglycemia and their adverse effects

Drug	Adverse effects
Metformin	Gastrointestinal distress, lactic acidosis, B12 deficiency, contraindicated in renal failure and interactions with other drugs
Insulin	Hypoglycemia, weight gain, cancer-related
Sulfonylureas and Glinides	Hypoglycemia, weight gain, cardiovascular risk
Incretins (DPP-4 inhibitors and GLP-1 agonists)	Gastrointestinal distress, heightened pancreatitis risk, heightened risk of cardiac insufficiency
Thiazolinediones	Weight gain, liquid retention, heightened fracture risk

DPP-4: Dipeptidyl peptidase-4; GLP-1: Glucagon-like peptide-1.