type 1 diabetes

type 1 diabetesis an endocrine disorder characterized by insufficient insulin secretion and elevated blood glucose levels. As a result of prolonged high blood sugar, patients become thirsty, lose weight, and feel tired quickly. Characterized by muscle and headaches, cramps, itchy skin, increased appetite, frequent urination, insomnia, hot flashes. Diagnosis includes a clinical interview, blood and urine laboratory tests to reveal hyperglycemia, insulin deficiency, and metabolic disorders. Treatment is with insulin therapy and prescribed diet and physical exercise.

General information

The word "diabetes" comes from the Greek word meaning "to flow, to escape, " so the disease's name describes one of its main symptoms - polyuria, the excretion of large amounts of urine. Type 1 diabetes is also known as autoimmune diabetes, insulin-dependent diabetes, and juvenile diabetes. The disease can occur at any age, but is more common in children and adolescents. Epidemiological indicators have increased in recent decades. The prevalence of all forms of diabetes is 1-9%; insulin-dependent diabetes accounts for 5-10% of cases. The incidence depends on the patient's ethnicity, with the highest incidence among Scandinavians.

Causes of type 1 diabetes

The factors that contribute to the development of the disease continue to be studied. It is now well established that type 1 diabetes occurs as a result of a combination of biological predispositions and external adverse influences. The most likely causes of pancreatic damage and reduced insulin production include:

• genetics.The tendency to develop insulin-dependent diabetes is transmitted directly—from parent to child. Several gene combinations that induce the disease have been identified. They are most common among residents of Europe and North America. Children whose parents have the disease are at a 4-10% increased risk compared to the general population.
• unknown external factors.Certain environmental influences can trigger type 1 diabetes. This fact is supported by the fact that identical twins with identical genomes are affected at the same time in only 30-50% of cases. The study also found that people who moved from areas with low incidence to areas with higher epidemiology were more likely to develop diabetes than those who refused to move.
• Viral infection.Viral infections may trigger an autoimmune response against pancreatic cells. The most likely effects are coxsackievirus and rubella virus.
• Chemicals, pharmaceuticals.The beta cells of the gland that produce insulin can be damaged by certain chemicals. Examples of such compounds are rat poisons and drugs for cancer patients.

onset

Its pathology is based on insufficient production of the hormone insulin in the beta cells of the pancreatic islets. Insulin-dependent tissues include liver, fat, and muscle. When insulin secretion decreases, they stop getting glucose from the blood. Developing a state of hyperglycemia – a key symptom of diabetes. The blood becomes viscous and blood flow in the blood vessels is disturbed, manifesting as vision loss and trophic lesions in the limbs.Insulin deficiency stimulates the breakdown of fat and protein. They enter the bloodstream and are metabolized by the liver into ketones, which become a source of energy for non-insulin-dependent tissues, including brain tissue. When blood glucose concentrations exceed 7-10 mmol/l, an alternative pathway for glucose excretion is activated - via the kidneys. Glycosuria and polyuria occur, leading to an increased risk of dehydration and electrolyte deficiencies in the body. 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 is divided into autoimmune (caused by the production of antibodies by gland cells) and idiopathic (the glands have no organic changes and the pathological cause is unknown). The development of the disease is divided into several stages:

1. Identify tendencies.Get preventive screening to determine genetic burden. The level of future risk of contracting the disease is calculated, taking into account the average statistical indicators for the country.
2. The initial starting moment.Autoimmune processes are activated and beta cells are damaged. Antibodies are produced, but insulin production remains normal.
3. Active chronic autoimmune insulitis.The antibody titer becomes higher and the number of insulin-producing cells decreases. Determine the high risk of developing diabetes in the next 5 years.
4. Hyperglycemia occurs after carbohydrate loading.A large proportion of the cells that produce insulin are destroyed. Hormone secretion decreases. Fasting blood glucose remained normal, but hyperglycemia was detected within 2 hours of eating.
5. clinical manifestations of the disease.Symptoms specific to diabetes appear. Hormone secretion is drastically reduced, and 80-90% of gland cells are destroyed.
6. Absolute insulin deficiency.All cells responsible for insulin synthesis die. Hormones only enter the body in the form of drugs.

Symptoms of type 1 diabetes

The main clinical symptoms of the disease are polyuria, polydipsia, and weight loss. The urge to urinate becomes more frequent, the daily urine output reaches 3-4 liters, and bedwetting sometimes occurs. The patient feels thirsty and has a dry mouth, and drinks up to 8-10 liters of water per day. Appetite increases, but weight decreases by 5-12 kg within 2-3 months. Additionally, you may experience symptoms such as nighttime insomnia, daytime sleepiness, dizziness, irritability, and fatigue. The patient experiences persistent fatigue and difficulty performing daily tasks.Itching, rashes and ulcers of the skin and mucous membranes occur. The condition of hair and nails worsens, and wounds and other skin injuries fail to heal for a long time. Impaired blood flow in capillaries and blood vessels is called diabetic vasculopathy. Capillary damage manifests itself as decreased vision (diabetic retinopathy), decreased kidney function with edema, arterial hypertension (diabetic nephropathy), and uneven flushing of the cheeks and chin. In the case of macrovascular disease, when veins and arteries are involved in the pathological process, atherosclerosis of the heart and lower limb vessels begins to progress, and gangrene forms.Half of patients develop symptoms of diabetic neuropathy, which is the result of an imbalance of electrolytes, insufficient blood supply, and swelling of nerve tissue. The conductivity of nerve fibers decreases, causing convulsions. Patients with peripheral neuropathy complain of burning and pain in the legs (especially at night), "pins and needles, " numbness, and increased sensitivity to touch. Autonomic neuropathy is characterized by visceral dysfunction - symptoms of digestive disorders, bladder paralysis, genitourinary infections, erectile dysfunction and angina pectoris. Focal neuropathy causes pain that varies in location and intensity.

complication

Long-term disruption of carbohydrate metabolism leads to diabetic ketoacidosis, a disease characterized by the accumulation of ketones and glucose in the plasma and increased blood acidity. Acute onset: loss of appetite, nausea and vomiting, abdominal pain, and the smell of acetone in the exhaled air. Without medical care, delirium, coma, and death can occur. Patients with symptoms of ketoacidosis require emergency treatment. Other dangerous complications of diabetes include hyperosmolar coma, hypoglycemic coma (improper use of insulin), "diabetic foot" with risk of amputation, severe retinopathy leading to complete loss of vision.

diagnosis

The patient was examined by an endocrinologist. Adequate clinical criteria for the disease are polydipsia, polyuria, changes in weight and appetite - signs of hyperglycemia. During the investigation, doctors also clarified the existence of a genetic burden. Blood and urine laboratory test results confirmed the suspected diagnosis. Detection of hyperglycemia can differentiate diabetes from psychogenic polydipsia, hyperparathyroidism, chronic renal failure, and diabetes insipidus. In the second stage of diagnosis, various forms of diabetes are differentiated. A comprehensive laboratory examination includes the following tests:

• Glucose (blood).Glucose measurements were performed three times: in the morning on an empty stomach, 2 hours after carbohydrate loading, and before bed. Blood glucose readings were 7 mmol/l on an empty stomach and 11. 1 mmol/l after eating carbohydrate foods, indicating hyperglycemia.
• Glucose (urine).Glycosuria indicates persistent and severe hyperglycemia. The normal value of this test (in mmol/l) is up to 1. 7, the critical value - 1. 8-2. 7, the pathological value - more than 2. 8.
• Glycated hemoglobin.Unlike free glucose, which is not bound to proteins, the amount of glycosylated hemoglobin in the blood remains relatively constant throughout the day. The diagnosis rate of diabetes is 6. 5% and above.
• Hormone testing.Get insulin and C-peptide tests. Normal fasting blood concentrations of immunoreactive insulin range from 6 to 12. 5 µU/ml. The C-peptide indicator allows you to assess beta cell activity and insulin production. Normal results are 0. 78-1. 89 μg/l; in diabetes, the concentration of this marker is reduced.
• Protein metabolism.Perform creatinine and urea tests. The final data could shed light on the extent of changes in kidney function and protein metabolism. If the kidneys are damaged, their levels will be higher than normal.
• fat metabolisim.To detect ketoacidosis early, the levels of ketone bodies in the blood and urine need to be checked. To assess the risk of atherosclerosis, blood cholesterol (total cholesterol, low-density lipoprotein, high-density lipoprotein) levels are measured.

Type 1 diabetes treatment

Doctors' efforts are aimed at eliminating the clinical manifestations of diabetes, preventing complications, and teaching patients to independently maintain normal blood sugar. Patients are accompanied by a multi-specialty team of experts, including endocrinologists, nutritionists and exercise therapy coaches. Treatment includes counseling, the use of medications, and educational sessions. The main methods include:

• Insulin therapy.The use of insulin preparations is necessary to maximize compensation for metabolic disorders and prevent hyperglycemia. Injections are crucial. Dosing regimens are formulated individually.
• diet.Patients are placed on a low-carbohydrate diet, including a ketogenic diet (ketones replace glucose as a source of energy). The basis of the diet is vegetables, meat, fish and dairy products. Sources of complex carbohydrates - whole wheat breads, cereals - can be eaten in moderation.
• Personal physical activity dose.Physical activity is beneficial for most patients without serious complications. Sessions are individually selected and conducted systematically by physical therapy instructors. Experts determine the duration and intensity of training based on the patient's overall health and diabetes compensation level. Regular walks, athletics and athletic competitions are provided for. Strength sports and marathon running are contraindicated.
• Self-control training.The success of diabetes maintenance treatment depends largely on the patient's motivation level. In special courses, they are informed about the mechanisms of the disease, possible compensation methods, complications and the importance of regular monitoring of sugar levels and insulin use is emphasized. Patients learn the skills to independently administer injections, select food items, and create menus.
• Prevent complications.Medications are used to improve the enzyme function of glandular cells. These include drugs that promote tissue oxygenation and immunomodulatory drugs. Prompt treatment of infection, hemodialysis and detoxification therapy to remove compounds that accelerate the development of pathology (thiazides, corticosteroids).

Notable among experimental treatments is the development of special DNA vaccines to treat early-stage diabetes. Levels of C-peptide, a marker of islet cell activity, increased in patients who received intramuscular injections for 12 weeks. Another research direction is to convert stem cells into insulin-producing glandular cells. Experiments in rats yielded positive results, but using the method in clinical practice requires evidence of the safety of the procedure.

prognosis and prevention

Insulin-dependent diabetes is a chronic disease, but appropriate maintenance treatment can allow patients to maintain a high quality of life. Because the exact cause of the disease has not yet been determined, preventive measures have not yet been developed. Currently, it is recommended that all high-risk groups have annual check-ups so that the disease can be detected early and treatment can be started promptly. This measure slows the development of persistent high blood sugar and minimizes the possibility of complications.