Diabetes mellitus type 1

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

General information

The term "diabetes" comes from the Greek and means "flowing, escaping, " so the name of the disease describes one of its key symptoms – polyuria, the passage of large amounts of urine. Type 1 diabetes is also called autoimmune, insulin-dependent and juvenile. The disease can manifest at any age, but more often manifests itself in children and adolescents. In recent decades, there has been an increase in epidemiological indicators. The prevalence of all forms of diabetes mellitus is 1-9%; the insulin-dependent variant of the pathology accounts for 5-10% 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 has now been established that type 1 diabetes mellitus occurs based on a combination of biological predisposition 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 transmitted in a direct line - from parents to children. Several combinations of genes predisposing to the disease have been identified. They are most common among residents of Europe and North America. Having an affected parent increases the child's risk by 4-10% compared to the general population.
• Unknown external factors.There are certain environmental influences that provoke 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 a low incidence to an area with a 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 the Coxsackie and rubella viruses.
• Chemicals, medicines.The beta cells of 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 flow in the vessels is disrupted, 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 7-10 mmol/l, the alternate pathway for glucose excretion is activated - through the kidneys. Glucosuria and polyuria develop, resulting in 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 to gland cells) and idiopathic (there are no organic changes in the gland, the causes of the pathology remain unknown). The development of the disease occurs in several stages:

1. Identification of predisposition.Preventive examinations are carried out, genetic burden is determined. Taking into account the average statistical indicators for the country, the level of risk of developing the disease in the future is calculated.
2. Initial starting moment.Autoimmune processes are activated and β-cells are damaged. Antibodies are already produced, but insulin production remains normal.
3. Active chronic 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 portion of insulin-producing cells are destroyed. Hormone production decreases. Normal fasting glucose levels are maintained, but hyperglycemia is detected within 2 hours after eating.
5. Clinical manifestation of the disease.Symptoms characteristic of diabetes mellitus appear. Hormone secretion is sharply reduced, 80-90% of gland cells are subject to destruction.
6. Absolute insulin deficiency.All cells responsible for insulin synthesis die. The hormone enters the body only in the form of a drug.

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 bedwetting occurs. Patients feel thirsty, feel dry mouth, and drink up to 8-10 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 drowsiness 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 occurs. 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, arterial hypertension (diabetic nephropathy), uneven blush 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, which is the result of electrolyte imbalance, insufficient blood supply and swelling of nerve tissue. The conductivity of nerve fibers deteriorates, convulsions are provoked. With peripheral neuropathy, patients complain of burning and pain in the legs, especially at night, a feeling of "pins and needles", numbness, and increased sensitivity to touch. Autonomic neuropathy is characterized by disruptions in the functions of internal organs - symptoms of digestive disorders, bladder paresis, genitourinary infections, erectile dysfunction, and angina occur. 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 the exhaled air appear. In the absence of medical care, 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 the risk of limb amputation, severe retinopathy with complete loss of vision.

Diagnostics

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 survey, the doctor also clarifies the presence of hereditary burden. The suspected diagnosis is confirmed by the results of laboratory tests of blood and urine. Detection of hyperglycemia makes it possible to distinguish diabetes mellitus from psychogenic polydipsia, hyperparathyroidism, chronic renal failure, and diabetes insipidus. At the second stage of diagnosis, differentiation of various forms of diabetes is carried out. A comprehensive laboratory examination includes the following tests:

• Glucose (blood).Sugar determination is performed 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 carbohydrate foods.
• 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 glucose not bound to protein, 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.
• Hormonal 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 evaluate the activity of beta cells and the volume of insulin production. The normal result is 0. 78-1. 89 μg/l; in diabetes mellitus, the concentration of the marker is reduced.
• Protein metabolism.Tests for creatinine and urea are performed. The final data makes it possible to clarify the functionality of the kidneys and the degree of change in protein metabolism. If the kidneys are damaged, the levels are higher than normal.
• Lipid metabolism.For early detection of ketoacidosis, the content of ketone bodies in the bloodstream and urine is examined. To assess the risk of atherosclerosis, the level of blood cholesterol (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 accompanied by a multiprofessional team of specialists, which includes endocrinologists, nutritionists, and exercise therapy instructors. Treatment includes consultations, the use of medications, and educational sessions. The main methods include:

• Insulin therapy.The use of insulin preparations is necessary for the maximum achievable compensation of metabolic disorders and prevention of hyperglycemia. Injections are vital. The administration regimen is drawn up individually.
• Diet.Patients are prescribed a low-carbohydrate diet, including a ketogenic one (ketones serve as a source of energy instead of glucose). The basis of the diet is vegetables, meat, fish, and dairy products. Sources of complex carbohydrates - whole grain bread, cereals - are allowed in moderation.
• Dosed individual physical activity.Physical activity is beneficial for most patients who do not have severe complications. Classes are selected individually by a physical therapy instructor and conducted systematically. The specialist determines the duration and intensity of 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 marathon running are contraindicated.
• Self-control training.The success of maintenance treatment for diabetes largely depends on the level of motivation of patients. During special classes, they are told about the mechanisms of the disease, possible methods of compensation, complications, and the importance of regular monitoring of the amount of sugar and the use of insulin is emphasized. Patients learn the skill of independently performing injections, choosing food products, and creating menus.
• Prevention of complications.Medicines are used to improve the enzyme function of glandular cells. These include agents that promote tissue oxygenation and immunomodulatory drugs. Timely treatment of infections, hemodialysis, and antidote therapy are carried out to remove compounds that accelerate the development of pathology (thiazides, corticosteroids).

Among experimental treatment methods, 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 required.

Prognosis and prevention

The insulin-dependent form of diabetes mellitus is a chronic disease, but proper 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 to detect the disease at an early stage and promptly begin treatment. This measure allows you to slow down the process of formation of persistent hyperglycemia and minimizes the likelihood of complications.