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 experience thirst, lose weight, and quickly tire. Characterized by muscle and headache, cramps, itchy skin, increased appetite, frequent urination, insomnia, hot flashes. Diagnosis includes a clinical interview, blood and urine laboratory tests that reveal hyperglycemia, insulin deficiency and metabolic disorders. Treatment is carried out using insulin therapy, prescribed diet and physical exercise.

General information

The term "diabetes" comes from the Greek language and means "flowing, running away, " so the name of the disease describes one of its main symptoms - polyuria, an abundant passage of urine. Type 1 diabetes is also called autoimmune, insulin dependent and juvenile. The disease can manifest itself 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 pathological variant accounts for 5-10% of cases. The incidence depends on the ethnicity of the patient, and is highest among Scandinavian communities.

Causes of type 1 diabetes

Factors that contribute to the development of this 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:

• Ancestry.The tendency for insulin-dependent diabetes is transmitted in a direct line - from parents to children. Several gene combinations that predispose to this disease have been identified. They are most common among the population 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 trigger type 1 diabetes. This fact is confirmed by the fact that identical twins, who have the same set of genes, get sick together in only 30-50% of cases. It was also found that people who migrated from areas with low incidence to areas with higher epidemiology were more likely to develop diabetes than those who refused to migrate.
• Viral infection.An autoimmune response against pancreatic cells can be triggered by a viral infection. The most likely influences are Coxsackie virus and rubella.
• Chemicals, drugs.The beta cells of the gland that produce insulin can be damaged by certain chemicals. Examples of such compounds are rat poison and drugs 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 - the main sign of diabetes mellitus. The blood thickens, the blood flow in the vessels is disturbed, which is shown by the deterioration of vision and trophic lesions on the legs.

Lack of insulin stimulates the breakdown of fats and proteins. They enter the bloodstream and are then metabolized by the liver into ketones, which become a source of energy for non-insulin-dependent tissues, including brain tissue. When the blood sugar concentration exceeds 7-10 mmol/l, an alternative 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 water loss, thirst increases (polydipsia).

Classification

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

1. Identification of tendencies.Preventive screening is carried out, genetic load 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. Early start moment.Autoimmune processes are activated and β cells are damaged. Antibodies are already produced, but insulin production remains normal.
3. Active chronic autoimmune insulitis.Antibody titers become 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.Most of the insulin-producing cells are destroyed. Hormone production decreases. Normal fasting glucose levels are maintained, but hyperglycemia is detected within 2 hours after a meal.
5. Clinical manifestations of the disease.Symptoms of diabetes mellitus appear. Hormone secretion decreases dramatically, 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 medicine.

Symptoms of type 1 diabetes

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

Itching of the skin and mucous membranes, rashes, and ulcers 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 shown by decreased vision (diabetic retinopathy), decreased kidney function with edema, arterial hypertension (diabetic nephropathy), blushing and uneven chin. With macroangiopathy, when veins and arteries are involved in the pathological process, atherosclerosis of the heart vessels and the lower part of the legs begins to develop, and gangrene develops.

Half of the patients experience symptoms of diabetic neuropathy, which is caused by an 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, "pins and needles" feeling, numbness, and increased sensitivity to touch. Autonomic neuropathy is characterized by disturbances in the function of internal organs - symptoms of indigestion, bladder paresis, genitourinary infections, erectile dysfunction, and angina occur. With focal neuropathy, pain with varying localization and intensity is formed.

Complications

Prolonged disruption of carbohydrate metabolism can cause diabetic ketoacidosis, a condition characterized by the accumulation of ketones and glucose in the plasma and increased blood acidity. It occurs acutely: loss of appetite, nausea and vomiting, abdominal pain, and the smell of acetone in exhaled air appears. In the absence of medical treatment, confusion, coma and death occur. Patients with signs of ketoacidosis require immediate 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

The patient was examined by an endocrinologist. Adequate clinical criteria for this disease are polydipsia, polyuria, changes in body weight and appetite - signs of hyperglycemia. During the survey, the doctor also explained the presence of hereditary burden. The suspected diagnosis is confirmed by the results of blood and urine laboratory tests. Detection of hyperglycemia allows 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 done three times: in the morning on an empty stomach, 2 hours after a carbohydrate load and before going to bed. Hyperglycemia is indicated by a reading of 7 mmol/l on an empty stomach and 11. 1 mmol/l after eating a carbohydrate meal.
• Glucose (urine).Glucosuria indicates persistent and severe hyperglycemia. The normal value for this test (in mmol/l) is up to 1. 7, border - 1. 8-2. 7, pathology - more than 2. 8.
• Glycated hemoglobin.Unlike free glucose that is 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 a rate of 6. 5% and above.
• Hormone test.Insulin and C-peptide tests were performed. The normal concentration of immunoreactive insulin in fasting blood is between 6 and 12. 5 µU/ml. The C-peptide indicator allows you to evaluate the activity of beta cells and the amount of insulin production. A normal yield is 0. 78-1. 89 μg/l; in diabetes mellitus, the concentration of markers is reduced.
• Protein metabolism.Creatinine and urea tests were performed. The final data make it possible to clarify kidney function and the extent of changes in protein metabolism. If the kidneys are damaged, the level is higher than normal.
• Lipid metabolism.For the early detection of ketoacidosis, the content of ketone bodies in the bloodstream and urine is checked. To assess the risk of atherosclerosis, blood cholesterol levels (total cholesterol, LDL, HDL) are determined.

Treatment of type 1 diabetes

The doctor's efforts 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 multi-professional team of experts, including endocrinologists, nutritionists and exercise therapy instructors. Treatment includes counseling, the use of medications, and educational sessions. The main methods include:

• Insulin therapy.The use of insulin preparations is necessary for maximum achievable compensation of metabolic disorders and prevention of hyperglycemia. Injections are important. The administration regimen is prepared individually.
• Diet.Patients are prescribed a low-carbohydrate diet, including a ketogenic diet (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 - whole grain bread, cereals - are allowed in moderation.
• Individual physical activity is dosed.Physical activity is beneficial for most patients who do not experience severe complications. Classes are individually selected by physical therapy instructors and conducted systematically. Specialists determine the duration and intensity of training taking into account the general health of the patient and the level of diabetes compensation. Walking, athletics, and sports games are fixed. Strength sports and marathon running are contraindicated.
• Self control training.The success of maintenance treatment for diabetes largely depends on the patient's level of motivation. During a special class, they are told about the mechanism of the disease, possible compensation methods, complications, and the importance of regular monitoring of the amount of sugar and the use of insulin is emphasized. Patients learn the skills to independently administer injections, select food products, and create menus.
• Prevention of complications.Medicines are used to increase the enzyme function of glandular cells. These include agents that promote tissue oxygenation and immunomodulatory drugs. Treatment of infection, hemodialysis, and timely curative 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 a special DNA vaccine for the treatment of diabetes mellitus in the early stages of development. In patients who received intramuscular injections for 12 weeks, the level of C-peptide, a marker of pancreatic islet cell activity, increased. Another direction of research is the transformation of stem cells into insulin-producing gland cells. Experiments carried out on mice gave positive results, but to use the method in clinical practice, proof 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 been developed, because the exact cause of the disease has not been explained. At present, all people at risk are recommended to undergo an annual examination to detect the disease at an early stage and immediately start treatment. This step allows you to delay the process of formation of persistent hyperglycemia and minimize the possibility of complications.