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The American Diabetes Association defines the following criteria for the diagnosis of diabetes: a HbA1c of 6.5%, an 8-hour fasting blood glucose of 7.0 mmol/L (126 mg/dL), a 2-hour oral glucose tolerance test (OGTT) of ≥ 11.1 mmol/L (200 mg/dL), or in patients exhibiting hyperglycemic symptoms, a random plasma glucose of ≥ 11.1 mmol/L (200 mg/dL).
Endocrine: By increasing the production of glucose from amino-acid breakdown and opposing the action of insulin, corticosteroids can cause hyperglycemia, [26] insulin resistance and diabetes mellitus. [27] Skeletal: Steroid-induced osteoporosis may be a side-effect of long-term corticosteroid use.
Steroid diabetes is a specific and prolonged form of stress hyperglycemia. [citation needed] People who have experienced stress hyperglycemia during severe illness have a threefold risk of developing diabetes in subsequent years, and it may be appropriate to screen for diabetes in survivors of critical illness. [2]
Weight gain due to increased visceral and truncal fat deposition (central obesity) and appetite stimulation; see corticosteroid-induced lipodystrophy; Hypercortisolemia with prolonged or excessive use (also known as, exogenous Cushing's syndrome) Impaired memory and attention deficits [50] See steroid dementia syndrome.
Steroid hormones are synthesized from cholesterol within the adrenal cortex. Aldosterone and corticosterone share the first part of their biosynthetic pathway. The last part is either mediated by the aldosterone synthase (for aldosterone) or by the 11β-hydroxylase (for corticosterone). [citation needed]
11β-Hydroxysteroid dehydrogenase (HSD-11β or 11β-HSD) enzymes catalyze the conversion of inert 11 keto-products to active cortisol, or vice versa, [1] thus regulating the access of glucocorticoids to the steroid receptors. The human genome encodes two distinct HSD-11β isozymes (HSD-11β Type 1 and HSD-11β Type 2) on distinct genes.