Steroid-induced diabetes mellitus: symptoms, diagnosis, treatment

Steroid-induced diabetes or steroid diabetes mellitus is an endocrine disorder affiliated with excess adrenal cortex hormones in the blood and impaired carbohydrate metabolism. How the pathology manifests itself, is diagnosed and treated, you will learn from the article.


  1. Causes.
  2. Pathogenesis.
  3. Symptoms.
  4. Complications.
  5. Diagnosis.
  6. Treatment.
  7. Prognosis and prevention.


Steroid-induced diabetes mellitus most often occurs as a result of prolonged use of hormonal drugs or increased secretion of corticosteroids. If medication administration is the trigger, the disease is called drug diabetes. This pathology is not a priori related to the potential of the pancreas, it develops and passes depending on the self-administration and withdrawal of drugs for the treatment of steroid diabetes.

If the pathology is provoked by an increase in natural hormones, the symptomatology of Icenko-Cushing’s disease is most often observed. Statistically, this group includes up to 12% of all cases of this disease. There is no accurate data on the prevalence of steroid diabetes. The disease has no gender coloring, age range, seasonality, or racial preference.


Depending on the trigger of the pathology, steroid diabetes may be endogenous or exogenous. In the first case, pancreatic failure is caused by hypercorticism, either primary or secondary. The triggers of this condition include:

  1. Cushing’s syndrome against a background of high levels of ACTH, which causes the risk of pancreatic dysfunction.
  2. Adrenal tumors.

In the second option, the high-risk group includes patients with autoimmune diseases, CKD, hypertension. Diabetes may be provoked by long-term use of glucocorticoids, thiazide diuretics, hormonal contraceptives.


The essence of the formation of steroid diabetes is that the high concentration of glucocorticoids on the internal organs and metabolic processes block the synthesis and increase the breakdown of proteins. Consequently, the excretion of amino acids from tissues increases, accelerating their re- and deamination in the liver, which automatically increases glucogenesis – the synthesis of glucose from non-carbohydrate compounds. Glycogen is deposited in hepatocytes at an accelerated rate.

Corticoids affect carbohydrate metabolism by increasing the activity of glucose-6-phosphatase, which controls the formation of glucose and the phosphate group, and by blocking glucokinase activity inhibits the conversion of glucose to glycogen. The periphery stops utilization of sugar by the tissues. Lipid metabolism stimulates lipogenesis, involves leptin and ghrelin, which control human eating behavior, so there is no loss of extra pounds. But in type 1 and type 2 diabetes, this would definitely happen.

Steroids affect the formation of ketone bodies, preventing the oxidation of pyruvic acid, and the level of lactic acid in the blood increases. The nature of the course of the pathology resembles type 1 diabetes at first, because β-cells are affected and insulin synthesis is reduced. But over time, insulin resistance grows, affiliated with leptin resistance, which is typical for diabetes mellitus 2.


The diabetic triad is typical for steroid diabetes: polydipsia, polyuria and polyphagia against a background of rapid fatigue. However, the symptomatology is subdued compared to type 1 diabetes. Patients are disturbed by a feeling of thirst and dry mouth. A large role in changes in eating behavior is played by leptin, a hormone of adipose tissue. A person drinks up to 8 liters of water a day, but thirst doesn’t weaken even at night.

Urination becomes more frequent, up to 3 liters of urine are excreted per day, and nocturnal enuresis may progress. Many suffer from insomnia, so they feel drowsy during the day, are tired and cannot cope with their usual duties.

At first, symptoms increase rapidly, resembling the course of type 1 diabetes: malaise, fatigue, cephalgia, irritability, flushes of hyperthermia. The prolonged course of the pathology provokes itching of the skin and mucous membranes, pyoderma, and long non-healing wounds. Hair is dry and brittle, nails break, break. Blood supply and innervation of tissues are disturbed, numbness, tingling, burning sensations occur, thermoregulation is impaired.


Prolonged hyperglycemia provokes diabetic angiopathy, retinopathy. If the vascular network of the kidneys is affected, their filtration deteriorates, pastosity occurs, blood pressure rises, diabetic nephropathy is formed.

Atherosclerosis develops in the large-caliber vessels, which gives the most dangerous complications, damaging the arteries of the heart and legs. The imbalance of water-salt metabolism and blockage of nourishment of nervous tissue provoke diabetic neuropathy. This is manifested by cramps, anemia of the feet, fingers, internal organ disorders, and pain syndromes.


At risk for steroid diabetes are patients with hypercorticism, both exogenous and endogenous. Glucose monitoring to detect hyperglycemia is necessary for Cushing’s disease, adrenal tumors, glucocorticoids, diuretics, and hormonal contraceptives.

A complete examination is performed by an endocrinologist, specific techniques include:

  1. Fasting blood tests show normal or minimal glucose elevations ranging from 5-5.5 to 6 mmol/l, sometimes from 6.1 to 6.5 mmol/l or higher.
  2. Glucose tolerance test a couple of hours after a sugar load provides information about predisposition and the presence of diabetes. Glucose resistance is indicated by a level of 7.8 to 11.0 mmol/L, and diabetes is indicated by a level greater than 11.1 mmol/L.
  3. Urinalysis for the presence of 17-CS, 17-OX gives an opportunity to assess the hormone-secreting activity of the adrenal cortex. Increased excretion rates are typical for pathology.
  4. Hormonal profile gives information about the preservation of pituitary and cortical adrenal gland potential. Depending on the root cause of the pathology, the concentration of cortisol, aldosterone, ACTH is determined.


The goal of etiotropic correction is to eliminate the triggers of hypercorticism with simultaneous restoration and maintenance of normal blood glucose levels, increased tissue sensitivity to insulin by activation of preserved β-cells. In case of complex therapy, help is provided in the following directions:

  1. Minimization of corticosteroid concentrations up to operative correction in the absence of drug results.
  2. Drug correction of hyperglycemia with individually selected drugs: insulin therapy or sulfo-urea drugs, and sometimes a combination of drugs.
  3. Anti-diabetic diet – therapeutic table № 9, taking into account the glycemic index of products and fractional meals.

Prognosis and prevention

Steroid diabetes runs and corrects more easily in Diabetes 1 and 2. The prognosis is correlated with the trigger of the pathology and is almost always favorable. Prevention consists in the timely and adequate correction of Cushing’s disease, adrenal tumors, glucocorticoids, diuretics and oral contraceptives. This provides an opportunity to see metabolic abnormalities at the pre-diabetes stage and to start basic treatment.


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