Type 1 diabetes mellitus

Type 1 diabetes mellitusis an endocrine disease characterized by insufficient insulin production and increased blood glucose levels. Due to prolonged hyperglycemia, patients feel thirsty, lose weight and get tired quickly. Characterized by muscle and headache pain, cramps, itchy skin, increased appetite, frequent urination, insomnia, hot flashes. Diagnosis includes a clinical interview, laboratory blood and urine tests that reveal hyperglycemia, lack of insulin and metabolic disorders. Treatment is with insulin therapy, with a prescribed diet and physical exercise.

General information

The term "diabetes" comes from the Greek and means "to flow, escape", which is why the name of the disease describes one of its main symptoms – polyuria, the passage of large amounts of urine. Type 1 diabetes is also called autoimmune, insulin-dependent and juvenile. The disease can appear at any age, but it appears more frequently 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 higher among Scandinavian people.

Causes of type 1 diabetes

The factors that contribute 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 a 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 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 medicine for cancer patients.

Pathogenesis

The pathology is based on insufficient production of the hormone insulin in the beta cells of the islets of Langerhans in the pancreas. Insulin-dependent tissues include liver, fat, and muscle. When insulin secretion decreases, they stop removing glucose from the blood. A state of hyperglycemia occurs - a key sign of diabetes mellitus. The blood thickens, blood flow 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 sources of energy for non-insulin-dependent tissues, including brain tissue. When the blood sugar concentration exceeds 7-10 mmol/l, the alternative pathway for glucose excretion is activated – through the kidneys. Glycosuria and polyuria develop, resulting in an increased risk of body dehydration and electrolyte deficiency. To compensate for the loss of water, the sensation of thirst increases (polydipsia).

Classification

According to recommendations from the World Health Organization, type I diabetes mellitus is divided into autoimmune (caused by the production of antibodies against glandular 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 exams are carried out and the genetic load is determined. Taking into account the country's average statistical indicators, the level of risk of developing the disease in the future is calculated.
2. Initial moment of departure.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 increases 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 the insulin-producing cells are destroyed. Hormone production decreases. Normal fasting glucose levels are maintained, but hyperglycemia is detected 2 hours after ingestion.
5. Clinical manifestation of the disease.Symptoms characteristic of diabetes mellitus appear. Hormone secretion is sharply reduced, 80-90% of glandular 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 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 daily urine volume reaches 3-4 liters, and nocturnal enuresis sometimes occurs. Patients feel thirsty, dry mouth and drink 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 drowsiness during the day, dizziness, irritability and fatigue. Patients feel constant fatigue and have difficulty carrying out their usual work.

Itching of the skin and mucous membranes, rashes and ulcerations occur. The condition of hair and nails worsens, wounds and other skin injuries take a long time to heal. Impaired blood flow in capillaries and vessels is called diabetic angiopathy. Damage to capillaries is manifested by decreased vision (diabetic retinopathy), decreased kidney function with edema, high blood pressure (diabetic nephropathy), irregular flushing of 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. In peripheral neuropathy, patients complain of burning and pain in the legs, especially at night, a "pins and needles" sensation, 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 occur. With focal neuropathy, pain of varying location and intensity is formed.

Complications

Prolonged interruption of carbohydrate metabolism can lead to diabetic ketoacidosis, a condition characterized by the accumulation of ketones and glucose in plasma and increased blood acidity. It occurs acutely: appetite disappears, nausea and vomiting appear, abdominal pain and the smell of acetone in the exhaled air. 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 insulin misuse), "diabetic foot" with risk of limb amputation, severe retinopathy with complete loss of vision.

Diagnosis

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 clarifies the presence of hereditary burden. The suspected diagnosis is confirmed by the results of laboratory blood and urine tests. Detection of hyperglycemia makes it possible to distinguish diabetes mellitus from psychogenic polydipsia, hyperparathyroidism, chronic renal failure and diabetes insipidus. In the second stage of diagnosis, the different forms of diabetes are differentiated. 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 carbohydrate loading and before bed. Hyperglycemia is indicated by readings of 7 mmol/l on an empty stomach and 11. 1 mmol/l after eating carbohydrate foods.
• Glucose (urine).Glycosuria 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. Diagnosis of diabetes is confirmed at rates of 6. 5% and above.
• Hormone tests.Insulin and C-peptide tests are performed. The normal concentration of immunoreactive insulin in fasting blood 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.Creatinine and urea tests are performed. The final data make it possible to clarify the functionality of the kidneys and the degree of change in protein metabolism. If the kidneys are damaged, the levels will be 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 cholesterol in the blood (total cholesterol, LDL, HDL) is determined.

Type 1 diabetes treatment

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

• Insulin therapy.The use of insulin preparations is necessary for the maximum possible compensation of metabolic disorders and prevention of hyperglycemia. Injections are vital. The administration regime is drawn up individually.
• Diet.Patients are prescribed a low-carb diet, including ketogenic (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 experience serious complications. Classes are individually selected by a physical therapy instructor and conducted systematically. The specialist determines the duration and intensity of training taking into account the patient's general health status 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 patients' level of motivation. During special classes, they are informed about the mechanisms of the disease, possible compensation methods, complications and emphasize the importance of regularly monitoring the amount of sugar and the use of insulin. Patients learn the skill of independently giving injections, choosing food products and creating menus.
• Prevention of complications.Medications are used to improve the enzyme function of glandular cells. These include agents that promote tissue oxygenation and immunomodulatory medications. 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 highlighting the development of special DNA vaccines for the treatment of diabetes mellitus at an early stage of development. In patients who received 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 insulin-producing glandular cells. Experiments carried out on rats gave positive results, but to use the method in clinical practice, proof of the safety of the procedure is necessary.

Prognosis and prevention

The insulin-dependent form of diabetes mellitus is a chronic disease, but adequate 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, it is recommended that all people at risk undergo annual exams 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.