Steroid diabetes | |
---|---|
Other names | Steroid-induced diabetes |
Specialty | Endocrinology |
Steroid diabetes or steroid-induced diabetes is characterized as an unusual rise in blood sugar that is linked to the use of glucocorticoids in a patient who may or may not have had diabetes mellitus in the past. [1]
Steroid diabetes is caused by the use of glucocorticoids. [1]
Traditional risk factors for type 2 diabetes, such as advanced age, a family history of the disease, a high body mass index, and impaired glucose tolerance, are also suggested risk factors for steroid-induced diabetes, in addition to cumulative dosage and length of steroid course. [2]
Glycemic control can be impacted by other immunosuppressive medications through different mechanisms, which could complicate the effects of glucocorticoid therapy. [1] By inhibiting the production of insulin, calcineurin inhibitors, especially tacrolimus, are used in transplant patients, which increases their risk of developing glucose intolerance. [2] Diabetes was linked to the concurrent use of mycophenalate mofetil in patients with lupus receiving high-dose steroid therapy; this could be explained by decreased insulin secretion due to elevated beta cell stress. [3] [4]
There is an inverse correlation between serum magnesium levels and glycemic control, according to several studies. [5]
Although chronic hepatitis C virus (HCV) infection is thought to be a separate risk factor for the development of diabetes in both the general population and liver transplant recipients, liver disease is known to exacerbate impaired glucose tolerance. [6] [7]
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). [8]
Like with all forms of diabetes, lifestyle modification, including exercise and dietary counseling to offer options that might lessen post-prandial hyperglycemia, is the first step toward improving glycemic control. [1]
Current guidelines may not adequately address this because the initiation of glucocorticoids can result in post-prandial hyperglycemia and the tapering of glucocorticoids can normalize glycemic control. The most accommodating option for patients is still basal bolus insulin therapy, which consists of three parts: basal insulin, prandial insulin, and supplemental correction factor insulin. [1]
Steroid diabetes | |
---|---|
Other names | Steroid-induced diabetes |
Specialty | Endocrinology |
Steroid diabetes or steroid-induced diabetes is characterized as an unusual rise in blood sugar that is linked to the use of glucocorticoids in a patient who may or may not have had diabetes mellitus in the past. [1]
Steroid diabetes is caused by the use of glucocorticoids. [1]
Traditional risk factors for type 2 diabetes, such as advanced age, a family history of the disease, a high body mass index, and impaired glucose tolerance, are also suggested risk factors for steroid-induced diabetes, in addition to cumulative dosage and length of steroid course. [2]
Glycemic control can be impacted by other immunosuppressive medications through different mechanisms, which could complicate the effects of glucocorticoid therapy. [1] By inhibiting the production of insulin, calcineurin inhibitors, especially tacrolimus, are used in transplant patients, which increases their risk of developing glucose intolerance. [2] Diabetes was linked to the concurrent use of mycophenalate mofetil in patients with lupus receiving high-dose steroid therapy; this could be explained by decreased insulin secretion due to elevated beta cell stress. [3] [4]
There is an inverse correlation between serum magnesium levels and glycemic control, according to several studies. [5]
Although chronic hepatitis C virus (HCV) infection is thought to be a separate risk factor for the development of diabetes in both the general population and liver transplant recipients, liver disease is known to exacerbate impaired glucose tolerance. [6] [7]
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). [8]
Like with all forms of diabetes, lifestyle modification, including exercise and dietary counseling to offer options that might lessen post-prandial hyperglycemia, is the first step toward improving glycemic control. [1]
Current guidelines may not adequately address this because the initiation of glucocorticoids can result in post-prandial hyperglycemia and the tapering of glucocorticoids can normalize glycemic control. The most accommodating option for patients is still basal bolus insulin therapy, which consists of three parts: basal insulin, prandial insulin, and supplemental correction factor insulin. [1]