Corticosteroids, such as prednisone and dexamethasone, are powerful medications used to treat a wide range of conditions, from autoimmune disorders to severe asthma. When people ask if “steroids” cause diabetes, they are usually referring to these anti-inflammatory drugs, not anabolic steroids used to build muscle mass. Corticosteroids frequently disrupt the body’s ability to manage blood sugar, leading to a temporary or sometimes permanent condition known as steroid-induced diabetes. This side effect requires careful medical attention during treatment.
Corticosteroids and the Development of Hyperglycemia
The use of corticosteroids can lead to a specific clinical condition called Steroid-Induced Diabetes Mellitus (SIDM) or Steroid-Induced Hyperglycemia. This condition is characterized by an abnormal rise in blood glucose levels in a patient who did not previously have diabetes, or a severe worsening of control in someone with pre-existing diabetes. The severity of the blood sugar elevation is closely tied to the medication’s dose, potency, and duration of treatment. SIDM is often temporary, resolving once the steroid dose is reduced or stopped. However, the stress on the glucose-regulating system can unmask an underlying inability to use insulin effectively, accelerating the onset of permanent Type 2 Diabetes.
Biological Mechanism of Blood Sugar Disruption
Corticosteroids interfere with glucose metabolism through two primary actions that work together to raise the concentration of sugar in the blood. The first action occurs in the liver, where the steroids promote hepatic gluconeogenesis. This process involves the liver manufacturing and releasing a greater amount of glucose into the bloodstream.
The second mechanism is the induction of peripheral insulin resistance throughout the body, particularly in muscle and fat tissue. Corticosteroids make cells less receptive to insulin, meaning the body’s cells do not respond effectively to the insulin present. This leaves glucose trapped in the circulation.
This combination of increased glucose production and decreased glucose uptake rapidly drives blood sugar levels upward. Corticosteroids can also directly inhibit the production and release of insulin from the pancreatic beta-cells. The result is a post-meal surge in blood glucose that often peaks several hours after the steroid is taken.
Identifying Patient Risk Factors for Steroid-Induced Diabetes
While corticosteroids can affect anyone’s blood sugar, certain patient characteristics significantly increase the likelihood of developing steroid-induced diabetes. The two most direct factors are a higher corticosteroid dosage and a longer duration of therapy. Clinicians use these variables to identify those who require proactive blood sugar monitoring.
Risk factors for susceptibility include:
- Older age.
- High Body Mass Index (BMI).
- Family history of diabetes.
- Pre-existing impaired glucose tolerance (prediabetes).
- Concurrent medical conditions, such as chronic kidney disease or Hepatitis C virus infection.
- Simultaneous use of other immunosuppressive drugs, like tacrolimus.
Monitoring and Management
Managing steroid-induced hyperglycemia requires proactive monitoring and tailored clinical interventions to keep blood glucose within a safe range.
Monitoring Protocol
Patients should check their blood glucose, ideally once daily, when the steroid’s effect is likely to be highest. Following a morning dose, this peak typically occurs between lunchtime and the evening meal. This post-meal timing is important because the drug often causes a disproportionate rise in blood sugar after eating. Lifestyle measures are the starting point, including dietary adjustments that focus on limiting simple carbohydrates and increasing fiber intake.
Clinical Interventions
If blood sugar levels remain high—generally above 200 mg/dL (11.1 mmol/L)—medication is necessary. The choice of anti-diabetic medication depends on the severity and expected duration of the steroid course. For short-term use, a sulfonylurea medication, which increases insulin secretion, or mealtime insulin injections are often considered. For severe or prolonged hyperglycemia, insulin therapy is frequently required, with doses adjusted in anticipation of the steroid’s peak effect.
Reversal and Tapering
Monitoring must continue during the tapering phase of the steroid dose. Blood sugar levels usually return to normal shortly after the medication is stopped, necessitating a corresponding reduction in diabetes medication to prevent low blood sugar.