Type 1 diabetes mellitus

Type 1 diabetes mellitusis an endocrine disease characterized by insufficient insulin production and increased blood sugar levels. Due to prolonged hyperglycemia, patients suffer from thirst, lose weight and quickly get tired. Characterized by headaches and muscle aches, cramps, itchy skin, increased appetite, frequent urination, insomnia, hot flashes. Diagnosis includes a clinical interview, laboratory blood and urine tests that reveal hyperglycemia, insulin deficiency, and metabolic disorders. Treatment is carried out with insulin therapy, diet and exercise are prescribed.

general informations

The term "diabetes" comes from the Greek and means "to flow, to escape", so the name of the disease describes one of its main symptoms: polyuria, the passage of large quantities of urine. Type 1 diabetes is also called autoimmune, insulin-dependent and juvenile-onset. The disease can appear at any age, but it occurs more often in children and adolescents. Over the past decades, epidemiological indicators have increased. The prevalence of all forms of diabetes mellitus is 1-9%; the insulin-dependent variant of the pathology represents 5 to 10% of cases. The incidence depends on the ethnicity of the patients and is highest among Scandinavian peoples.

Causes of type 1 diabetes

Factors contributing to the development of the disease continue to be studied. It is now established that type 1 diabetes mellitus results from a combination of biological predispositions and external adverse influences. The most likely causes of damage to the pancreas and decreased insulin production include:

• Heredity.The tendency to insulin-dependent diabetes is passed down through a direct line – from parents to children. Several combinations of genes predisposing to the disease have been identified. They are more common among residents of Europe and North America. Having an affected parent increases the risk for the child by 4 to 10% compared to the general population.
• Unknown external factors.Certain environmental influences cause type 1 diabetes. This fact is confirmed by the fact that identical twins, who have exactly the same set of genes, get sick together only in 30-50% of cases. It was also found that people who migrated from an area with low incidence to an area with higher epidemiology are more likely to develop diabetes than those who refused to migrate.
• Viral infection.An autoimmune response to pancreatic cells can be triggered by a viral infection. The most likely influence is Coxsackie and rubella viruses.
• Chemicals, medicines.The beta cells in the gland that produces insulin can be damaged by certain chemicals. Examples of such compounds are rat poison and a drug for cancer patients.

Pathogenesis

The pathology is based on insufficient production of the hormone insulin in the beta cells of the islets of Langerhans of the pancreas. Insulin-dependent tissues include liver, fat and muscle. When insulin secretion decreases, they stop taking glucose from the blood. A state of hyperglycemia occurs - a key sign of diabetes mellitus. The blood thickens, blood circulation in the vessels is disturbed, which is manifested by deterioration of vision and trophic lesions of the extremities.

Insulin deficiency stimulates the breakdown of fats and proteins. They enter the bloodstream and are then metabolized by the liver into ketones, which become energy sources for non-insulin-dependent tissues, including brain tissue. When the blood sugar concentration exceeds 7 to 10 mmol/l, the alternative pathway of glucose excretion is activated: by the kidneys. Glycosuria and polyuria develop, leading to an increased risk of body dehydration and electrolyte deficiency. To compensate for the loss of water, the feeling of thirst increases (polydipsia).

Classification

According to the recommendations of the World Health Organization, type I diabetes mellitus is divided into autoimmune (provoked by the production of antibodies against the cells of the gland) and idiopathic (there are no changesorganic in the gland, the causes of the pathology remain unknown). The development of the disease occurs in several stages:

1. Identification of the predisposition.Preventive examinations are carried out, the genetic load is determined. Taking into account the average statistical indicators of the country, the level of risk of developing the disease in the future is calculated.
2. Initial departure time.Autoimmune processes are activated and β cells are damaged. Antibodies are already produced, but insulin production remains normal.
3. Chronic active autoimmune insulitis.The antibody titer becomes high and the number of insulin-producing cells decreases. A high risk of developing diabetes in the next 5 years is determined.
4. Hyperglycemia after carbohydrate loading.A significant part of the insulin-producing cells is destroyed. Hormone production decreases. Normal fasting glucose levels are maintained, but hyperglycemia is detected within 2 hours after a meal.
5. Clinical manifestation of the disease.Symptoms characteristic of diabetes mellitus appear. Hormonal secretion is greatly reduced, 80 to 90% of gland cells are destroyed.
6. Absolute insulin deficiency.All the cells responsible for insulin synthesis die. The hormone enters the body only in the form of medicine.

Symptoms of type 1 diabetes

The main clinical signs of the disease are polyuria, polydipsia and weight loss. The urge to urinate becomes more frequent, the volume of daily urine reaches 3-4 liters, and sometimes nocturnal enuresis occurs. Patients are thirsty, have dry mouth and drink up to 8 to 10 liters of water per day. Appetite increases, but body weight decreases by 5-12 kg in 2-3 months. Additionally, you may experience insomnia at night and sleepiness during the day, dizziness, irritability and fatigue. Patients feel constant fatigue and have difficulty performing their usual work.

Itching of the skin and mucous membranes, rashes and ulcerations occur. The condition of hair and nails deteriorates, wounds and other skin lesions do not heal for a long time. Impaired blood flow in capillaries and vessels is called diabetic angiopathy. Damage to the capillaries is manifested by decreased vision (diabetic retinopathy), decreased kidney function with edema, high blood pressure (diabetic nephropathy), patchy redness on the cheeks and chin. With macroangiopathy, when veins and arteries are involved in the pathological process, atherosclerosis of the vessels of the heart and lower extremities begins to progress and gangrene develops.

Half of patients develop symptoms of diabetic neuropathy, the result of electrolyte imbalance, insufficient blood supply and swelling of nerve tissue. The conductivity of nerve fibers deteriorates, convulsions are caused. With peripheral neuropathy, patients complain of burning and pain in the legs, especially at night, a feeling of "tingling", numbness and increased sensitivity to touch. Autonomic neuropathy is characterized by disturbances in the functions of internal organs - symptoms of digestive disorders, bladder paresis, genitourinary infections, erectile dysfunction and angina appear. With focal neuropathy, pain of varying localization and intensity is formed.

Complications

Prolonged disruption of carbohydrate metabolism can lead to diabetic ketoacidosis, a condition characterized by the accumulation of ketones and glucose in the plasma and increased blood acidity. It occurs acutely: appetite disappears, nausea and vomiting, abdominal pain and the smell of acetone in exhaled air appear. Without medical attention, confusion, coma and death occur. Patients with signs of ketoacidosis require urgent treatment. Other dangerous complications of diabetes include hyperosmolar coma, hypoglycemic coma (with improper use of insulin), "diabetic foot" with risk of limb amputation, severe retinopathy with complete loss of vision.

Diagnostic

Patients are examined by an endocrinologist. Sufficient clinical criteria for the disease are polydipsia, polyuria, changes in weight and appetite - signs of hyperglycemia. During the examination, the doctor also specifies the presence of a hereditary burden. The suspected diagnosis is confirmed by the results of blood and urine laboratory tests. Detection of hyperglycemia helps distinguish diabetes mellitus from psychogenic polydipsia, hyperparathyroidism, chronic renal failure and diabetes insipidus. At the second stage of diagnosis, differentiation of different forms of diabetes is carried out. A comprehensive laboratory examination includes the following tests:

• Glucose (blood).Sugar determination is carried out three times: in the morning on an empty stomach, 2 hours after a carbohydrate load and before bedtime. Hyperglycemia is indicated by readings of 7 mmol/l on an empty stomach and 11. 1 mmol/l after eating foods rich in carbohydrates.
• Glucose (urine).Glucosuria indicates persistent and severe hyperglycemia. Normal values for this test (in mmol/l) are up to 1. 7, borderline - 1. 8-2. 7, pathological - more than 2. 8.
• Glycated hemoglobin.Unlike free, non-protein-bound glucose, the amount of glycosylated hemoglobin in the blood remains relatively constant throughout the day. The diagnosis of diabetes is confirmed at rates of 6. 5% and above.
• Hormone tests.Insulin and C-peptide tests are performed. The normal fasting blood concentration of immunoreactive insulin ranges from 6 to 12. 5 µU/ml. The C-peptide indicator allows you to assess the activity of beta cells and the volume of insulin production. The normal result is 0. 78 to 1. 89 µg/l; in diabetes mellitus, the concentration of the marker is reduced.
• Protein metabolism.Creatinine and urea tests are performed. The final data helps clarify the functionality of the kidneys and the degree of change in protein metabolism. If the kidneys are damaged, levels are higher than normal.
• Lipid metabolism.For early detection of ketoacidosis, the content of ketone bodies in blood and urine is examined. To assess the risk of atherosclerosis, the blood cholesterol level (total cholesterol, LDL, HDL) is determined.

Treatment of type 1 diabetes

The efforts of doctors are aimed at eliminating the clinical manifestations of diabetes, as well as preventing complications, teaching patients to independently maintain normoglycemia. Patients are supported by a multiprofessional team of specialists, which includes endocrinologists, nutritionists and exercise therapy instructors. Treatment includes consultations, use of medications, and educational sessions. The main methods include:

• Insulin therapy.The use of insulin preparations is necessary to maximally compensate for metabolic disorders and prevent hyperglycemia. The injections are vital. The administration schedule is established individually.
• Diet.Patients are prescribed a low-carb diet, especially ketogenic (ketones serve as an energy source instead of glucose). The basis of the diet is vegetables, meat, fish and dairy products. Sources of complex carbohydrates - wholemeal bread, cereals - are allowed in moderation.
• Dosed individual physical activity.Physical activity is beneficial for most patients who do not have serious complications. Classes are individually selected by a physiotherapy instructor and delivered systematically. The specialist determines the duration and intensity of the training taking into account the general health of the patient and the level of diabetes compensation. Regular walking, athletics and sports games are prescribed. Strength sports and marathons are contraindicated.
• Self-control training.The success of diabetes maintenance treatment largely depends on the level of motivation of patients. During special courses, they are informed about the mechanisms of the disease, possible methods of compensation, complications and the importance of regular control of the amount of sugar and the use of insulin is emphasized. Patients learn to independently perform injections, choose food products and create menus.
• Prevention of complications.The drugs are used to improve the enzyme function of glandular cells. These include agents that promote tissue oxygenation and immunomodulatory drugs. Prompt treatment of infections, hemodialysis and antidote therapy are carried out to eliminate compounds that accelerate the development of pathology (thiazides, corticosteroids).

Among the experimental methods of treatment, it is worth noting the development of special DNA vaccines for the treatment of diabetes mellitus at an early stage of development. In patients receiving intramuscular injections for 12 weeks, levels of C-peptide, a marker of pancreatic islet cell activity, increased. Another direction of research is the transformation of stem cells into glandular cells that produce insulin. Experiments carried out on rats gave positive results, but to use the method in clinical practice, evidence of the safety of the procedure is needed.

Prognosis and prevention

The insulin-dependent form of diabetes mellitus is a chronic disease, but appropriate maintenance therapy allows patients to maintain a high quality of life. Preventive measures have not yet been developed, since the exact causes of the disease have not been clarified. Currently, all people at risk are recommended to undergo annual examinations in order to detect the disease at an early stage and begin treatment promptly. This measure allows you to slow down the process of formation of persistent hyperglycemia and minimize the risk of complications.