Introduction
The use of glucocorticoids is widespread in practically all medical subspecialties. Exacerbation of chronic obstructive pulmonary disease, acute gout, chemotherapy regimens, bacterial meningitis, and fetal lung maturation in pregnant women are indications of short-term acute steroid therapy. Chronic glucocorticoid use is beneficial for the following disease processes: inflammatory bowel diseases, autoimmune conditions, neurologic diseases like multiple sclerosis and myasthenia gravis, and pulmonary illnesses like idiopathic interstitial pneumonia, hypersensitivity pneumonitis, and sarcoidosis.
More recently, the immune system has been modulated after solid organ donation with the help of prolonged glucocorticoid medication. Although glucocorticoids are frequently given for their ability to reduce inflammation and the immune system, they also have a number of typical metabolic adverse effects, such as diabetes, hypertension, and osteoporosis. The complication known as steroid-induced diabetes mellitus (SIDM) has been identified. A patient with or without a history of diabetes mellitus who uses glucocorticoids may develop steroid-induced diabetes mellitus, which is characterized by an abnormal rise in blood glucose.
What Are Steroids?
Corticosteroids are another name for steroids. They are synthetic versions of hormones that the body naturally produces. They assist in treating a variety of illnesses by reducing inflammation in the body, such as:
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Severe cystic fibrosis.
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Asthma.
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Inflammatory intestinal disease.
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Cancer.
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Arthritis.
Steroids come in a wide variety of forms and many different dosages. High doses of steroids are frequently ingested or administered intravenously and are more likely to have an impact on blood sugar levels.
What Causes Steroid Diabetes?
Prednisolone and Dexamethasone are the two glucocorticoids that cause steroid diabetes most frequently. They are administered systemically over days or weeks in pharmacologic dosages. Severe asthma, organ transplantation, cystic fibrosis, inflammatory bowel disease, and induction chemotherapy for leukemia or other cancers are common medical diseases where steroid diabetes develops after high-dose glucocorticoid therapy.
A net increase in hepatic glucose output results from the antagonistic effects of glucocorticoids on insulin action and the stimulation of gluconeogenesis, particularly in the liver. Most people can create enough extra insulin to counteract this impact and keep blood sugar levels within normal ranges, but those unable to develop steroid diabetes.
What Is the Etiology of Steroid Induced Diabetes Mellitus?
Glucocorticoids have a significant and reciprocal impact on glyceroneogenesis in the liver and adipose tissue, which is one of the etiologies of steroid-induced diabetes mellitus. Glyceroneogenesis regulates the rate of fatty acid release into the blood in adipose (fat) tissue, while it also produces triacylglycerol in the liver from fatty acids and glycerol 3-phosphate. This process is controlled in the liver and adipose tissue through the action of the enzyme phosphoenolpyruvate carboxykinase (PEPCK).
Glucocorticoids limit glyceroneogenesis by suppressing PEPCK gene expression in adipose tissue. As a result of lipoprotein lipase's action, PEPCK in the liver stimulates the formation of glycerol and raises the blood's concentration of fatty acids. Glucocorticoids, therefore, enhance the number of fatty acids released into the circulation as their overall effect. Particularly in skeletal muscle, an increase in fatty acids causes insulin resistance and impairs the body's ability to use glucose. Thiazolidinediones decrease serum fatty acid levels, which decreases insulin resistance while increasing the expression of PEPCK in adipose and skeletal muscle.
What Are the Risk Factors for Steroid Induced Diabetes Mellitus?
Traditional type 2 diabetes risk variables, such as advanced age, family history, a high body mass index, and impaired glucose tolerance, also play a role in steroid-induced diabetes risk factors beyond cumulative dose and longer steroid course duration are:
1. Concurrent Immunosuppression
The impact of glucocorticoid therapy can be complicated by the effects of other immunosuppressive drugs, which can potentially influence glycemic control through different pathways. The use of calcineurin inhibitors, especially tacrolimus, in transplant patients reduces the synthesis of insulin, which exacerbates glucose intolerance. Mycophenolate mofetil use was linked to the development of diabetes in persons with systemic lupus erythematosus who were receiving high-dose steroid therapy; this association may be explained by reduced insulin production due to increased beta cell stress.
2. Hepatitis C Virus
Impaired glucose tolerance is a result of liver disease, but there is evidence that chronic hepatitis C virus (HCV) infection itself is a separate risk factor for the development of diabetes in both the general population and in people who had liver transplants.
3. Hypomagnesemia
The glycemic control and blood magnesium levels have an antagonistic connection.
What Are the Signs and Symptoms of Steroid Induced Diabetes?
The patient might not even exhibit signs of steroid-induced diabetes if blood sugar levels are slightly higher than normal. However, when blood sugar levels rise, the following indications and symptoms may occur:
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Frequently urinate, particularly at night.
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Increased thirst.
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Greater than usual fatigue.
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Weight loss.
The doctor might advise the patient to monitor blood sugar levels when taking steroids.
What Are the Treatment Modalities for Treating Steroid Induced Diabetes?
Steroid-induced diabetes mellitus requires a different management approach than non-steroid-induced diabetes for optimal therapy. For instance, due to its numerous relative or absolute contraindications, such as nausea or vomiting, hypoxia, and liver or kidney disease, metformin which is frequently prescribed as the first-line medication for type 2 diabetes, is not advised for steroid-induced diabetes mellitus.
1. Non Pharmacological Interventions
As with all types of diabetes, lifestyle changes that include exercise and nutritional counseling are the first steps to improving glycemic control. These changes may help to reduce post-prandial hyperglycemia.
2. Insulin Therapy
Glucocorticoid administration can result in postprandial hyperglycemia, and glucocorticoid reduction can normalize glycemic control. The three parts of basal-bolus insulin therapy - basal insulin, prandial insulin, and a supplemental correction factor insulin - remain the most adaptable choice for patients. Nocturnal hypoglycemia may result from the conventional administration of long-acting basal insulin with a conventional weight-based dose. However, it is generally advisable to administer intermediate-acting insulin and glucocorticoids at a midday or evening meal.
3. Oral Secretagogues
Long-acting medications may be associated with hypoglycemia if the patient skips meals frequently since oral secretagogues, such as sulfonylurea treatment, do not explicitly target post-prandial hyperglycemia. Short-acting secretagogues like Nateglinide or Repaglinide administered before meals might be tried on patients with mild hyperglycemia that are unable or reluctant to administer insulin injections.
Conclusion
The prevalence of steroid-induced or steroid-exacerbated diabetes will keep rising as the therapeutic advantages of glucocorticoids spread across medical disciplines. The concepts of early identification and risk factor reduction are applicable, just like in diabetes not caused by steroids. Prior to the start of chronic glucocorticoids, diagnosing impaired fasting glucose or impaired glucose tolerance will help identify patients who would benefit from steroid-sparing treatment. If this is not possible, blood glucose monitoring will be used to monitor patients' blood sugar levels while they begin medication. A deeper understanding of the precise mechanism underlying steroid-induced insulin resistance will aid in the development of particular treatments and diabetes prevention strategies in the future.
