Indication
Type 2 diabetes adjunct in Cushing's syndrome
Type 2 diabetes adjunct in Cushing's syndrome refers to the management of glucocorticoid-induced hyperglycemia occurring as a secondary complication in patients with endogenous Cushing's syndrome, particularly those who have failed surgical resection or are not candidates for surgery. Read more about Type 2 diabetes adjunct in Cushing's syndrome
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Coming soonType 2 diabetes adjunct in Cushing's syndrome refers to the management of glucocorticoid-induced hyperglycemia occurring as a secondary complication in patients with endogenous Cushing's syndrome, particularly those who have failed surgical resection or are not candidates for surgery.
The endocrine and metabolic systems are primarily affected, resulting from chronic, autonomous hypercortisolism.
Pathophysiologically, sustained cortisol excess promotes hepatic gluconeogenesis, impairs insulin sensitivity in skeletal muscle and adipose tissue, and diminishes pancreatic beta-cell insulin secretory capacity.
Clinically, affected adults present with persistent hyperglycemia, glucose intolerance, and elevated hemoglobin A1c refractory to conventional glycemic therapies, often accompanied by classic signs of hypercortisolism such as central adiposity, proximal muscle weakness, and hypertension.
- nih.gov
Type 2 diabetes adjunct in Cushing's syndrome refers to the management of glucocorticoid-induced hyperglycemia occurring as a secondary complication in patients with endogenous Cushing's syndrome, particularly those who have failed surgical resection or are not candidates for surgery The endocrine and metabolic systems are primarily affected, resulting from chronic, autonomous hypercortisolism Clinically, affected adults present with persistent hyperglycemia, glucose intolerance, and elevated he...
- myamericannurse.com
Type 2 diabetes adjunct in Cushing's syndrome refers to the management of glucocorticoid-induced hyperglycemia occurring as a secondary complication in patients with endogenous Cushing's syndrome, particularly those who have failed surgical resection or are not candidates for surgery
- fda.gov
The endocrine and metabolic systems are primarily affected, resulting from chronic, autonomous hypercortisolism
- nih.gov
Pathophysiologically, sustained cortisol excess promotes hepatic gluconeogenesis, impairs insulin sensitivity in skeletal muscle and adipose tissue, and diminishes pancreatic beta-cell insulin secretory capacity Clinically, affected adults present with persistent hyperglycemia, glucose intolerance, and elevated hemoglobin A1c refractory to conventional glycemic therapies, often accompanied by classic signs of hypercortisolism such as central adiposity, proximal muscle weakness, and hypertension
- adces.org
Pathophysiologically, sustained cortisol excess promotes hepatic gluconeogenesis, impairs insulin sensitivity in skeletal muscle and adipose tissue, and diminishes pancreatic beta-cell insulin secretory capacity
- endocrine.org
Clinically, affected adults present with persistent hyperglycemia, glucose intolerance, and elevated hemoglobin A1c refractory to conventional glycemic therapies, often accompanied by classic signs of hypercortisolism such as central adiposity, proximal muscle weakness, and hypertension
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