Steroid diabetes is an endocrine pathology that develops as a result of a high content of adrenal cortex hormones in the blood plasma and a violation of carbohydrate metabolism. It is manifested by symptoms of hyperglycemia: fatigue, increased thirst, frequent profuse urination, dehydration, increased appetite. Specific diagnostics is based on laboratory detection of hyperglycemia, assessment of the level of steroids and their metabolites (urine, blood). Treatment of steroid diabetes includes the abolition or reduction of the dosage of glucocorticoids, surgical operations that reduce the production of corticosteroid hormones, and antidiabetic therapy.
E13 Other specified forms of diabetes mellitus
Steroid diabetes (SD) can be triggered by a prolonged increase in the secretion of corticosteroids or their intake in the form of drugs. In the second case, the disease has a synonymous name – medicinal diabetes. Initially, it is not associated with the functional state of the pancreas, develops against the background of hormonal treatment and can take place independently after the withdrawal of medications. SD, provoked by an increase in natural hormones, is most often observed in Cushing’s disease. In this group of patients, epidemiological indicators reach 10-12%. There is no accurate information about the prevalence of SD among the general population.
According to the etiological feature, steroid diabetes is divided into endogenous and exogenous. In the endogenous form, disorders of the pancreas are caused by primary or secondary hypercorticism. The reasons for this group include:
- Secondary hypercorticism. Cushing syndrome occurs when the level of ACTH, a hormone produced by the pituitary gland and regulating the activity of the adrenal glands, increases. Corticoid secretion increases, there is a high risk of pancreatic dysfunction.
- Neoplasms of the adrenal glands. In primary hypercorticism, the production of corticosteroids is stimulated by a growing tumor of the adrenal gland. SD is often diagnosed with corticosteroma, aldosteroma, corticoestroma, androsteroma.
The second variant of the origin of steroid diabetes is exogenous. The high-risk group includes patients with autoimmune pathologies, chronic renal failure, arterial hypertension. Diabetes develops with prolonged therapy with drugs that inhibit insulin secretion by beta cells in the pancreas. Such drugs are glucocorticoids, thiazide diuretics, hormonal contraceptives.
The basis for the development of SD is the prolonged effect of increased concentrations of glucocorticoids on internal organs and metabolic processes. Steroid hormones inhibit the synthesis and enhance the breakdown of proteins. The release of amino acids from tissues increases, the reactions of their transamination and deamination in the liver accelerate, which causes an increase in the rate of gluconeogenesis – the synthesis of glucose from non-carbohydrate compounds. Glycogen is deposited more actively in liver cells. The effect of corticoids on carbohydrate metabolism is manifested through an increase in the activity of glucose-6-phosphatase, responsible for the reactions of glucose and phosphate group formation, and through inhibition of glucokinase activity, that is, slowing down the process of glucose processing into glycogen.
On the periphery, the utilization of sugar by tissues is reduced. The change in fat metabolism is represented by stimulation of lipogenesis, therefore, there is no loss of body weight characteristic of type 1 and type 2 diabetes. The antiketogenic effect of steroids is an obstacle to the oxidation of pyruvic acid, an increase in lactic acid in the bloodstream. By the nature of the course of SD in the first stages is similar to type I diabetes: β-cells are affected, insulin production is reduced. Over time, insulin resistance of tissues increases, which is typical for type II diabetes.
The clinical picture is represented by a diabetic triad – polydipsia, polyuria and fatigue. In general, the symptoms are less pronounced than in type 1 diabetes. Patients notice an increased feeling of thirst, constant dry mouth. The volume of liquid consumed increases several times, up to 4-8 liters per day. Thirst does not weaken even at night. Appetite is increased, weight remains the same or increases. The urge to urinate is becoming more frequent. 3-4 liters of urine are excreted per day, children and the elderly develop nocturnal enuresis. Many patients suffer from insomnia, feel tired during the day, do not cope with their usual tasks, experience drowsiness.
At the beginning of the disease, symptoms increase rapidly, as with type 1 diabetes: general well-being worsens, headache, irritability, hot flashes appear. The long course of the disease is accompanied by the appearance of itching of the skin and mucous membranes. More often there are pustular lesions, rashes, wounds do not heal for a long time. Hair becomes dry, nails become stratified and break off. Deterioration of blood flow and nervous transmission is manifested by a violation of thermoregulation in the extremities, a feeling of tingling, numbness and burning in the feet, less often in the fingers.
Prolonged hyperglycemia leads to diabetic angiopathy – damage to large and small vessels. Violation of blood circulation in the retinal capillaries is manifested by a decrease in vision – diabetic retinopathy. If the vascular network of the kidneys suffers, then their filtering function worsens, edema occurs, blood pressure rises – diabetic nephropathy develops. Changes in large vessels are represented by atherosclerosis. The most dangerous are atherosclerotic lesions of the arteries of the heart and lower extremities. Electrolyte imbalance and insufficient blood supply to the nervous tissue provoke the development of diabetic neuropathy. It can manifest itself as cramps, numbness of the feet and fingers, malfunctions of internal organs, pain of various localization.
Individuals with endogenous and exogenous hypercorticism are at risk for the development of the steroid form of diabetes. Periodic studies of glucose levels in order to detect hyperglycemia are indicated for patients with Cushing’s disease, adrenal tumors, people taking glucocorticoid medications, thiazide group diuretics, hormonal contraceptives. A full examination is carried out by an endocrinologist. Specific research methods include:
- Fasting glucose test. In most patients, normal or slightly elevated blood glucose levels are determined. The final values are more often in the range from 5-5.5 to 6 mmol/l, sometimes they are 6.1-6.5 mmol/l and higher.
- Glucose tolerance test. Measuring glucose two hours after a carbohydrate load gives more accurate information about the presence of diabetes and predisposition to it. Glucose tolerance disorders are indicated by indicators from 7.8 to 11.0 mmol/l, diabetes – more than 11.1 mmol /l.
- Test for 17-KS, 17-OKS. The result allows us to evaluate the hormone-secreting activity of the adrenal cortex. The biomaterial for the study is urine. An increase in the excretion of 17-ketosteroids and 17-oxycorticosteroids is characteristic.
- Hormone research. For additional data on the functions of the pituitary gland and the cortical layer of the adrenal glands, hormonal tests can be performed. Depending on the underlying disease, the level of cortisol, aldosterone, ACTH is determined.
Etiotropic therapy is to eliminate the causes of hypercorticism. At the same time, measures aimed at restoring and maintaining normoglycemia, increasing the sensitivity of tissues to the action of insulin, stimulating the activity of preserved beta cells are carried out. With an integrated approach, medical care for patients is carried out in the following directions:
- Decreased corticosteroid levels. In case of endogenous hypercorticism, the methods of treatment of the underlying disease are reviewed first of all. If the correction of the dosage of drugs is not effective, the issue of surgical intervention is resolved – removal of the adrenal glands, the cortical part of the adrenal glands, tumors. The concentration of steroid hormones decreases, the blood sugar level normalizes. With exogenous hypercorticism, drugs that provoke steroid diabetes are canceled or replaced. If it is impossible to cancel glucocorticoids, for example, with severe bronchial asthma, anabolic hormones are prescribed to neutralize their effects.
- Drug correction of hyperglycemia. The drugs are selected individually, taking into account the etiology of diabetes, its stage, and the severity of the course. If the pancreas is affected, beta cells are partially or completely atrophied, then insulin therapy is prescribed. In mild forms of the disease, the preservation of glandular tissue and reversible resistance of cells to insulin, oral hypoglycemic agents are prescribed, for example, preparations of the sulfonylurea group. Sometimes patients are shown the combined use of insulin and hypoglycemic drugs.
- Antidiabetic diet. Most patients are shown a therapeutic diet No. 9. The diet is compiled in such a way that the chemical composition of the dishes is balanced, does not provoke hyperglycemia and contains all the necessary nutrients. The principles of low–carb nutrition are used: sources of light carbohydrates are excluded – sweets, pastries, sugary drinks. The diet is dominated by protein products and foods with a high fiber content. The glycemic index is taken into account. Meals are taken in small portions, 5-6 times a day.
Prognosis and prevention
Steroid DM, as a rule, proceeds in a milder form and is easier to treat than DM of the first and second types. The prognosis depends on the cause of hypercorticism, in most cases it is favorable. Prevention involves timely and adequate therapy of Cushing’s disease and adrenal tumor diseases, proper use of glucocorticoid preparations, thiazide diuretics and oral contraceptives. Individuals from risk groups should regularly perform blood glucose screening tests. This allows you to identify disorders of carbohydrate metabolism at the stage of prediabetes, adjust the main treatment, and begin to comply with the principles of dietary nutrition.
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