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 suffer from thirst, lose weight and get tired quickly. Characterized by muscle pain and headache, cramps, itchy skin, increased appetite, frequent urination, insomnia, hot flashes. Diagnosis includes a clinical interview, laboratory tests on blood and urine that reveal hyperglycemia, lack of insulin and metabolic disorders. Treatment is carried out using insulin therapy, diet and exercise are prescribed.

general informations

The term "diabetes" comes from Greek and means "to flow, 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. The disease can occur at any age, but most often occurs 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 disease represents 5-10% of cases. The incidence depends on the ethnicity of the patients and is higher among Scandinavian peoples.

Causes of type 1 diabetes

Factors that contribute to the development of the disease continue to be studied. It is now established that type 1 diabetes mellitus occurs based on a combination of biological predisposition and adverse external influences. The most likely causes of pancreatic damage and decreased insulin production include:

• Inheritance.The tendency to insulin-dependent diabetes is transmitted in a direct line, from parents to children. Several combinations of genes that predispose 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 some environmental factors that 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 in only 30-50% of cases. It was also found that people who emigrated from an area with a low incidence to an area with a higher epidemiology were more likely to develop diabetes than those who refused to emigrate.
• Viral infection.An autoimmune response to pancreatic cells can be triggered by a viral infection. The most likely influenza viruses are Coxsackie and rubella.
• 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 in glucose from the blood. A state of hyperglycemia occurs, a key sign of diabetes mellitus. 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 degradation 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, through the kidneys, is activated. 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 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 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 tests 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 moment of departure.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 the meal.
5. Clinical manifestation of the disease.Symptoms characteristic of diabetes mellitus appear. Hormone secretion is drastically 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 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 nocturnal enuresis sometimes occurs. Patients experience thirst, 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 suffer from insomnia at night and drowsiness during the day, dizziness, irritability and fatigue. Patients feel constant tiredness 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 deteriorates, wounds and other skin lesions do not heal for a long time. Impairment of blood flow in capillaries and vessels is called diabetic angiopathy. Damage to the capillaries is manifested by decreased vision (diabetic retinopathy), decreased renal function with edema, arterial hypertension (diabetic nephropathy), irregular 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, which is the result of 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, a sensation 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 acidity of the blood. 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 treatment, 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.

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 inspection the doctor also clarifies the presence of hereditary burdens. The suspected diagnosis is confirmed by the results of laboratory tests on blood and urine. Detection of hyperglycemia allows distinguishing diabetes mellitus from psychogenic polydipsia, hyperparathyroidism, chronic renal failure, and diabetes insipidus. In the second phase of diagnosis, the differentiation of the various forms of diabetes is carried out. A complete 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 values of 7 mmol/l on an empty stomach and 11. 1 mmol/l after eating foods containing carbohydrates.
• 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 - above 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 higher.
• Hormone tests.Insulin and C-peptide tests are performed. Normal fasting blood concentrations of immunoreactive insulin range from 6 to 12. 5 µU/ml. The C-peptide indicator allows you to evaluate beta cell activity 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 allow us 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 diagnosis of ketoacidosis, the content of ketone bodies in the blood and urine is examined. To assess the risk of atherosclerosis, the level of cholesterol in the blood (total cholesterol, LDL, HDL) is determined.

Treatment of type 1 diabetes

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, including endocrinologists, nutritionists and physical 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 the 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 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.
• Measured individual physical activity.Physical activity is beneficial for the majority of patients who do not have serious complications. Classes are individually selected by a physiotherapy instructor and conducted systematically. The specialist determines the duration and intensity of training taking into account the patient's general state of health and the level of diabetes compensation. Regular walks, 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 lectures they are informed about the mechanisms 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 of independently giving injections, choosing food items and creating menus.
• Prevention of complications.Medicines are used to improve the enzymatic function of glandular cells. These include agents that promote tissue oxygenation and immunomodulatory drugs. Timely treatment of infections, hemodialysis and antidotal therapy are carried out to remove compounds that accelerate the development of the pathology (thiazides, corticosteroids).

Among the 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 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 glandular cells that produce insulin. Experiments conducted on rats have given 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 as the exact causes of the disease have not been clarified. It is currently recommended that all people at risk undergo annual examinations to detect the disease at an early stage and start treatment promptly. This measure allows you to slow down the process of formation of persistent hyperglycemia and minimizes the likelihood of complications.