Diabetes insipidus - causes, symptoms and treatment. Idiopathic diabetes mellitus Idiopathic type 1 diabetes mellitus

– a chronic metabolic disease characterized by impaired insulin secretion and the development of hyperglycemia. Diabetes mellitus in children usually develops rapidly; is accompanied by rapid weight loss in the child with increased appetite, uncontrollable thirst and excessive urination. In order to identify diabetes mellitus in children, extensive laboratory diagnostics are carried out (determination of sugar, glucose tolerance, glycated hemoglobin, insulin, C-peptide, Ab to pancreatic β-cells in the blood, glucosuria, etc.). The main directions in the treatment of diabetes mellitus in children include diet and insulin therapy.

General information

Diabetes mellitus in children is a disorder of carbohydrate and other types of metabolism, which is based on insulin deficiency and/or insulin resistance, leading to chronic hyperglycemia. According to WHO, every 500th child and every 200th adolescent suffers from diabetes. Moreover, in the coming years, the incidence of diabetes mellitus among children and adolescents is predicted to increase by 70%. Considering the wide distribution, the tendency towards “rejuvenation” of the pathology, the progressive course and severity of complications, the problem of diabetes mellitus in children requires an interdisciplinary approach with the participation of specialists in the field of pediatrics, pediatric endocrinology, cardiology, neurology, ophthalmology, etc.

Classification of diabetes mellitus in children

In pediatric patients, diabetes doctors in most cases have to deal with type 1 diabetes mellitus (insulin-dependent), which is based on absolute insulin deficiency. Type 1 diabetes mellitus in children is usually autoimmune in nature; it is characterized by the presence of autoantibodies, destruction of β-cells, association with the genes of the major histocompatibility complex HLA, complete insulin dependence, a tendency to ketoacidosis, etc. Idiopathic diabetes mellitus type 1 has an unknown pathogenesis and is more often recorded in people of non-European race.

In addition to the dominant type 1 diabetes mellitus, rarer forms of the disease also occur in children: type 2 diabetes mellitus; diabetes mellitus associated with genetic syndromes; diabetes mellitus MODY type.

Causes of diabetes in children

The leading factor determining the development of type 1 diabetes mellitus in children is a hereditary predisposition, as evidenced by the high frequency of familial cases of the disease and the presence of pathology in close relatives (parents, siblings, grandparents).

However, to initiate the autoimmune process, exposure to a provoking environmental factor is necessary. The most likely triggers leading to chronic lymphocytic insulitis, subsequent destruction of β-cells and insulin deficiency are viral agents (Coxsackie B, ECHO, Epstein-Barr, mumps, rubella, herpes, measles, rotavirus, enterovirus, cytomegalovirus, etc.) viruses. .

In addition, the development of diabetes mellitus in children with a genetic predisposition can be facilitated by toxic effects, nutritional factors (artificial or mixed feeding, cow's milk, monotonous carbohydrate foods, etc.), stressful situations, and surgical interventions.

The risk group for the development of diabetes mellitus includes children with a birth weight of over 4.5 kg, those who are obese, who lead an inactive lifestyle, who suffer from diathesis, and who are often ill.

Secondary (symptomatic) forms of diabetes mellitus in children can develop with endocrinopathies (Itsenko-Cushing syndrome, diffuse toxic goiter, acromegaly, pheochromocytoma), diseases of the pancreas (pancreatitis, etc.). Type 1 diabetes mellitus in children is often accompanied by other immunopathological processes: systemic lupus erythematosus, scleroderma, rheumatoid arthritis, periarteritis nodosa, etc.

Diabetes mellitus in children can be associated with various genetic syndromes: Down syndrome, Klinefelter syndrome, Prader-Willi syndrome, Lawrence-Moon-Bardet-Biedl syndrome, Wolfram syndrome, Huntington's chorea, Friedreich's ataxia, porphyria, etc.

Symptoms of diabetes in children

Manifestations of diabetes mellitus in a child can develop at any age. There are two peaks of manifestation of diabetes mellitus in children - at 5-8 years and in the puberty period, i.e. during periods of increased growth and intensive metabolism.

In most cases, the development of insulin-dependent diabetes mellitus in children is preceded by a viral infection: mumps, measles, ARVI, enterovirus infection, rotavirus infection, viral hepatitis, etc. Type 1 diabetes mellitus in children is characterized by an acute rapid onset, often with the rapid development of ketoacidosis and diabetic coma. From the moment of the first symptoms to the development of a coma, it can take from 1 to 2-3 months.

Diabetes mellitus in children can be suspected based on pathognomonic signs: increased urination (polyuria), thirst (polydipsia), increased appetite (polyphagia), and weight loss.

The mechanism of polyuria is associated with osmotic diuresis, which occurs with hyperglycemia ≥9 mmol/L, exceeding the renal threshold, and the appearance of glucose in the urine. Urine becomes colorless, its specific gravity increases due to the high sugar content. Daytime polyuria may go unrecognized. More noticeable is nocturnal polyuria, which in diabetes mellitus in children is often accompanied by urinary incontinence. Sometimes parents pay attention to the fact that urine becomes sticky, and so-called “starch” stains remain on the child’s underwear.

Polydipsia is a consequence of increased urine output and dehydration of the body. Thirst and dry mouth can also plague your child at night, causing him to wake up and ask for something to drink.

Children with diabetes experience a constant feeling of hunger, but along with polyphagia, they experience a decrease in body weight. This is due to energy starvation of cells caused by the loss of glucose in the urine, impaired glucose utilization, and increased processes of proteolysis and lipolysis under conditions of insulin deficiency.

Already at the onset of diabetes mellitus, children may experience dry skin and mucous membranes, the appearance of dry seborrhea on the scalp, flaking of the skin on the palms and soles, seizures in the corners of the mouth, candidal stomatitis, etc. Pustular skin lesions, furunculosis, mycoses, diaper rash, etc. are typical. vulvitis in girls and balanoposthitis in boys. If the debut of diabetes mellitus in a girl occurs during puberty, this can lead to menstrual irregularities.

With decompensation of diabetes mellitus, children develop cardiovascular disorders (tachycardia, functional murmurs), hepatomegaly.

Complications of diabetes mellitus in children

The course of diabetes mellitus in children is extremely labile and is characterized by a tendency to develop dangerous conditions of hypoglycemia, ketoacidosis and ketoacidotic coma.

Hypoglycemia develops as a result of a sharp decrease in blood sugar caused by stress, excessive physical activity, insulin overdose, non-compliance with diet, etc. Hypoglycemic coma is usually preceded by lethargy, weakness, sweating, headache, feeling of extreme hunger, tremors in the limbs. If measures are not taken to increase blood sugar, the child develops convulsions, agitation, followed by depression of consciousness. In hypoglycemic coma, body temperature and blood pressure are normal, there is no smell of acetone from the mouth, the skin is moist, the blood glucose level

Diagnosis of diabetes mellitus in children

In identifying diabetes, an important role belongs to the local pediatrician, who regularly monitors the child. At the first stage, the presence of classic symptoms of the disease (polyuria, polydipsia, polyphagia, weight loss) and objective signs should be taken into account. When examining children, attention is drawn to the presence of diabetic blush on the cheeks, forehead and chin, a crimson tongue, and decreased skin turgor. Children with characteristic manifestations of diabetes mellitus should be referred for further management to a pediatric endocrinologist.

The final diagnosis is preceded by a thorough laboratory examination of the child. Basic studies for diabetes mellitus in children include determination of blood sugar levels (including through daily monitoring), insulin, C-peptide, proinsulin, glycosylated hemoglobin, glucose tolerance, blood CBS; in urine - glucose and ketone bodies. The most important diagnostic criteria for diabetes mellitus in children are hyperglycemia (above 5.5 mmol/l), glucosuria, ketonuria, acetonuria. For the purpose of preclinical detection of type 1 diabetes mellitus in groups with high genetic risk or for the differential diagnosis of type 1 and type 2 diabetes, determination of Abs to pancreatic β-cells and Abs to glutamate decarboxylase (GAD) is indicated. An ultrasound examination is performed to assess the structural condition of the pancreas.

Differential diagnosis of diabetes mellitus in children is carried out with acetone syndrome, diabetes insipidus, nephrogenic diabetes. Ketoacidosis and who needs to be distinguished from acute abdomen (appendicitis, peritonitis, intestinal obstruction), meningitis, encephalitis,.

Treatment of diabetes mellitus in children

The main components of treatment for type 1 diabetes mellitus in children are insulin therapy, diet, proper lifestyle and self-control. Dietary measures include excluding sugars from the diet, limiting carbohydrates and animal fats, split meals 5-6 times a day, taking into account individual energy needs. An important aspect of the treatment of diabetes mellitus in children is competent self-control: awareness of the seriousness of one’s disease, the ability to determine the level of glucose in the blood, and adjust the dose of insulin taking into account the level of glycemia, physical activity, and dietary errors. Self-control techniques are taught to parents and children with diabetes in “diabetes schools.”

Replacement therapy for children suffering from diabetes mellitus is carried out with drugs of human genetically engineered insulin and their analogues. The dose of insulin is selected individually, taking into account the degree of hyperglycemia and the age of the child. Basis-bolus insulin therapy has proven itself well in pediatric practice, providing for the administration of long-acting insulin in the morning and evening to correct baseline hyperglycemia and the additional use of short-acting insulin before each main meal to correct postprandial hyperglycemia.

A modern method of insulin therapy for diabetes mellitus in children is an insulin pump, which allows insulin to be administered in a continuous mode (imitation of basal secretion) and bolus mode (imitation of post-alimentary secretion).

The most important components of the treatment of type 2 diabetes mellitus in children are diet therapy, sufficient physical activity, and the use of oral hypoglycemic drugs.

With the development of diabetic ketoacidosis, infusion rehydration, administration of an additional dose of insulin taking into account the level of hyperglycemia, and correction of acidosis are necessary. If a hypoglycemic state develops, it is necessary to urgently give the child sugar-containing products (a lump of sugar, juice, sweet tea, caramel); if the child is unconscious, intravenous administration of glucose or intramuscular administration of glucagon is necessary.

Forecast and prevention of diabetes mellitus in children

The quality of life of children with diabetes mellitus is largely determined by the effectiveness of disease compensation. If you follow the recommended diet, regimen, and therapeutic measures, life expectancy corresponds to the average in the population. In case of gross violations of doctor's instructions, or decompensation of diabetes, specific diabetic complications develop early. Patients with diabetes mellitus are monitored for life by an endocrinologist-diabetologist.

Vaccination of children with diabetes mellitus is carried out during the period of clinical and metabolic compensation; in this case, it does not cause deterioration in the course of the underlying disease.

Specific prevention of diabetes mellitus in children has not been developed. It is possible to predict the risk of the disease and identify prediabetes based on an immunological examination. In children at risk for developing diabetes, it is important to maintain optimal weight, daily physical activity, increase immunoresistance, and treat concomitant pathologies.

Diabetes insipidus is a fairly rare endocrine disease that occurs as a result of relative or absolute deficiency of vasopressin (a non-hypophyseal hormone) and is manifested by debilitating urination (polyuria) and severe thirst (polydipsia).

Let's look at more details about what kind of disease this is, what causes, symptoms in men and women, as well as what is prescribed as treatment for adults.

What is diabetes insipidus?

Diabetes insipidus is a chronic disease of the hypothalamic-pituitary system, which develops due to a deficiency in the body of the hormone vasopressin, or antidiuretic hormone (ADH), the main manifestations of which are the release of large volumes of urine with low density.

Disease may start suddenly or develop gradually. The primary signs of diabetes insipidus are increased thirst and frequent urination.

Despite the fact that there are two types of diseases with similar names - diabetes mellitus and diabetes insipidus, these are two completely different diseases, but the symptoms overlap. They are united only by some similar signs, but the diseases are caused by completely different disorders in the body.

The body has a complex system for balancing the volume and composition of fluid. The kidneys, removing excess fluid from the body, form urine, which accumulates in the bladder. When water intake decreases or there is water loss (excessive sweating, diarrhea), the kidneys will produce less urine to conserve fluid in the body.

The hypothalamus, a part of the brain responsible for regulating the entire endocrine system of the body, produces antidiuretic hormone (ADH), also called vasopressin.

In diabetes insipidus, everything that is filtered excreted from the body. This results in liters and even tens of liters per day. Naturally, this process creates a strong thirst. A sick person is forced to drink a lot of fluid in order to somehow compensate for its deficiency in the body.

Diabetes insipidus is a rare endocrinopathy that develops regardless of the gender and age group of patients, most often in people 20-40 years old. In every 5th case, diabetes insipidus develops as a complication of neurosurgical intervention.

In children, diabetes insipidus usually has a congenital form, although its diagnosis can occur quite late - after 20 years. In adults, the acquired form of the disease is more often diagnosed.

Classification

Modern endocrinology classifies diabetes insipidus depending on the level at which disorders occur. There are central (neurogenic, hypothalamic-pituitary) and renal (nephrogenic) forms.

Neurogenic diabetes insipidus

Neurogenic diabetes insipidus (central). Develops as a result of pathological changes in the nervous system, in particular in the hypothalamus or posterior pituitary gland. As a rule, the cause of the disease in this case is surgery to completely or partially remove the pituitary gland, infiltrative pathology of this area (hemochromatosis, sarcoidosis), trauma or changes of an inflammatory nature.

In turn, the central type of diabetes insipidus is divided into:

• idiopathic - a hereditary type of disease, which is characterized by a decrease in ADH synthesis;
• symptomatic – develops against the background of other pathologies. It can be either acquired (develops throughout life), for example, as a result of a head injury or the development of a tumor. Or congenital (due to gene mutation).

With long-term central diabetes insipidus, the patient develops renal insensitivity to artificially administered antidiuretic hormone. Therefore, the sooner treatment for diabetes insipidus of this form is started, the more favorable the prognosis.

Renal diabetes insipidus

What it is? Renal or nephrogenic DI is associated with decreased sensitivity of kidney tissue to the influence of vasopressin. This type of disease is much less common. The cause of the pathology is either the structural inferiority of the nephrons or the resistance of the renal receptors to vasopressin. Renal diabetes can be congenital, or it can occur as a result of damage to kidney cells caused by medications.

Sometimes a third type of diabetes insipidus is also identified, affecting women during pregnancy. This is quite a rare occurrence. It occurs due to the destruction of hormones by enzymes of the resulting placenta. After the baby is born, this type goes away.

Acquired renal diabetes insipidus in adults develops as a result of renal failure of various etiologies, long-term therapy with lithium drugs, hypercalcemia, etc.

Causes

Diabetes insipidus develops when there is a deficiency of the antidiuretic hormone (ADH) vasopressin - relative or absolute. ADH is produced by the hypothalamus and it performs various functions, including influencing the normal functioning of the urinary system.

Diabetes insipidus is not a hereditary disease, but some autosomal recessive inherited syndromes (for example, Wolfram's disease, complete or incomplete diabetes insipidus) are part of the clinical picture, indicating a genetic mutation.

Factors predisposing to the development of this pathology are:

• diseases of an infectious nature, especially viral ones;
• brain tumors (meningioma, craniopharyngioma);
• metastases to the hypothalamus of cancer of extracerebral localization (usually bronchogenic - originating from bronchial tissue, and breast cancer);
• skull injuries;
• concussions;
• genetic predisposition.

In the idiopathic form of diabetes insipidus, the patient’s body, for no apparent reason, begins to produce antibodies that destroy the cells that produce antidiuretic hormone.

Renal diabetes insipidus (renal form) occurs as a result of intoxication of the body with chemicals, disorders or previous diseases of the kidneys and urinary system (renal failure, hypercalcinosis, amyloidosis, glomerulonephritis).

Symptoms of diabetes insipidus in adults

The disease occurs equally in men and women, at any age, most often between the ages of 20-40 years. The severity of the symptoms of this disease depends on the degree of vasopressin deficiency. With a slight deficiency of the hormone, clinical symptoms may be blurred and not clearly expressed. Sometimes the first symptoms of diabetes insipidus appear in people who have been in conditions of drinking deficiency - during travel, hiking, expeditions, and also when taking corticosteroids.

The main symptoms of diabetes insipidus include the following:

• excessive urination (up to 3–15 liters of urine per day);
• the main volume of urination occurs at night;
• thirst and increased fluid intake;
• dry skin, nausea and vomiting, convulsions;
• mental disorders (emotional lability, decreased mental activity).

Even if the patient is limited in fluid intake, urine will still be released in large quantities, which will lead to general dehydration of the body.

In addition to general symptoms, there are a number of individual symptoms that occur in patients of different genders and ages:

Complications

The danger of diabetes insipidus lies in the risk of developing dehydration of the body, which occurs in situations in which the loss of fluid from the body through urine is not adequately replenished. Characteristic manifestations of dehydration are:

• general weakness and
• vomit,
• mental disorders.

Blood thickening, neurological disorders and hypotension, which can reach a state of collapse, are also noted. It is noteworthy that even severe dehydration is accompanied by persistence of polyuria.

Diagnostics

A doctor who deals with such pathologies is an endocrinologist. If you feel most of the symptoms of this disease, then the first thing you should do is go to an endocrinologist.

At your first visit, the doctor will conduct an “interview”. It will allow you to find out how much water a woman drinks per day, whether she has problems with the menstrual cycle, urination, whether she has endocrine pathologies, tumors, etc.

In typical cases, the diagnosis of diabetes insipidus is not difficult and is based on:

• pronounced thirst
• daily urine volume is more than 3 liters per day
• plasma hyperosmolality (more than 290 mOsm/kg, depends on fluid intake)
• high sodium content
• hypoosmolality of urine (100–200 mOsm/kg)
• low relative density of urine (<1010).

Laboratory diagnosis of diabetes insipidus includes the following:

• conducting a Zimnitsky test - accurate calculation of daily fluid consumed and excreted;
• ultrasound examination of the kidneys;
• X-ray examination of the skull;
• computed tomography of the brain;
• echoencephalography;
• excretory urography;
• detailed biochemical blood test: determination of the amount of sodium, potassium, creatinine, urea, glucose ions.

The diagnosis of diabetes insipidus is confirmed based on laboratory data:

• low urine osmolarity;
• high level of blood plasma osmolarity;
• low relative density of urine;
• high sodium levels in the blood.

Treatment

After confirming the diagnosis and determining the type of diabetes insipidus, therapy is prescribed aimed at eliminating the cause that caused it - tumors are removed, the underlying disease is treated, and the consequences of brain injuries are eliminated.

To compensate for the required amount of antidiuretic hormone for all types of disease, desmopressin (a synthetic analogue of the hormone) is prescribed. It is applied by instillation into the nasal cavity.

Desmopressin drugs are now widely used to compensate for central diabetes insipidus. It is produced in 2 forms: drops for intranasal administration - Adiuretin and tablet form Minirin.

Clinical recommendations also include the use of drugs such as Carbamazepine and Chlorpropamide to stimulate the body’s production of the hormone. Since excessive urine production leads to dehydration of the body, saline solutions are administered to the patient to restore the water-salt balance.

When treating diabetes insipidus, drugs that affect the nervous system (for example, Valerian, Bromine) can also be prescribed. Nephrogenic diabetes requires the prescription of anti-inflammatory drugs and thiazide diuretics.

An important component of treatment diabetes insipidus is the correction of water-salt balance using infusion of a large volume of saline solutions. To effectively reduce diuresis, it is recommended to take sulfonamide diuretics.

Thus, diabetes insipidus is the result of a deficiency of antidiuretic hormone in the human body for various reasons. However, modern medicine makes it possible to compensate for this deficiency with the help of replacement therapy with a synthetic analogue of the hormone.

Competent therapy returns a sick person to the mainstream of a full life. This cannot be called a complete recovery in the literal sense of the word, however, in this case, the state of health is as close as possible to normal.

Nutrition and diet for diabetes insipidus

The main goal of diet therapy is to reduce urination, and in addition, to replenish the body with vitamins and minerals that they “lose” due to frequent urge to go to the toilet.

It is worth giving preference to cooking in these particular ways:

• boil;
• steamed;
• stew food in a saucepan with olive oil and water;
• bake in the oven, preferably in a sleeve, to preserve all the beneficial substances;
• in a slow cooker, except for the “fry” mode.

When a person has diabetes insipidus, the diet should exclude those categories of foods that increase thirst, for example, sweets, fried foods, spices and seasonings, and alcohol.

The diet is based on the following principles:

• reduce the amount of protein consumed, leaving the norm of carbohydrates and fats;
• reduce salt concentration by reducing its consumption to 5 g per day;
• food should consist mainly of vegetables and fruits;
• to quench your thirst, use natural juices, fruit drinks and compotes;
• eat only lean meat;
• include fish and seafood, egg yolks in the diet;
• take fish oil and phosphorus;
• eat small meals often.

Sample menu for the day:

• first breakfast – omelet (steamed) of 1.5 eggs, vinaigrette (with vegetable oil), tea with lemon;
• second breakfast – baked apples, jelly;
• lunch - vegetable soup, boiled meat, stewed beets, lemon drink;
• afternoon snack – rosehip decoction, jam;
• dinner - boiled fish, boiled potatoes, sour cream, tea with lemon.

Drinking plenty of fluids is necessary - after all, the body loses a lot of water during dehydration and needs to be compensated.

Folk remedies

Before using folk remedies for diabetes insipidus, be sure to consult an endocrinologist, because possible contraindications.

1. Twenty grams of dried elderberry blossoms pour a glass of very hot water, and the resulting broth is infused for one hour. The resulting composition is mixed with a spoon of honey and consumed three times daily.
2. To significantly get rid of thirst and reduce urine output, it is necessary to be treated with burdock infusion. To prepare the product, you will need 60 grams of the root of this plant, which must be crushed as much as possible, poured into a liter thermos and filled with boiling water until the volume is full. You need to infuse burdock root until the morning, after which the remedy is taken 3 times a day, half a glass.
3. Motherwort infusion for diabetes insipidus. Ingredients: motherwort (1 part), valerian root (1 part), hop cones (1 part), rose hips and mint (1 part), boiling water (250 ml.). All herbal ingredients are mixed and thoroughly crushed. Take 1 spoon of the mixture and pour boiling water over it. They insist for an hour. Take in an amount of 70 - 80 ml. before bedtime. Benefits: the infusion calms the body, relieves irritability, improves sleep.
4. To reduce thirst and restore balance in the body, you can use infused walnut leaves. The young leaves of this plant are collected, dried and crushed. After this, a teaspoon of the dry substance is brewed with a glass (250 milliliters) of boiling water. After just fifteen minutes, the resulting decoction can be consumed like regular tea.
5. A collection of different herbs will also help overcome the disease: fennel motherwort, valerian, fennel, caraway seeds. All ingredients must be taken in equal quantities and mixed well. After this, a tablespoon of the dry mixture is poured into a glass of boiling water and left until the liquid cools completely. You need to take half a glass before bed.

Forecast

Diabetes insipidus, which develops in the postoperative period or during pregnancy, is often transient (transient) in nature, while idiopathic diabetes is, on the contrary, persistent. With appropriate treatment there is no danger to life, although recovery is rarely recorded.

Recovery of patients is observed in cases of successful removal of tumors, specific treatment of diabetes insipidus of tuberculosis, malaria, and syphilitic origin. When hormone replacement therapy is prescribed correctly, the ability to work is often preserved.

Idiopathic (spontaneous) diabetes mellitus is a chronic multihormonal disorder of all types of metabolism with hyperglycemia, glycosuria and ketoacidosis.

Insulin-dependent diabetes mellitus (IDDM) is the most common endocrine disease in adolescents. It accounts for generally 10 to 20% of all cases of diabetes and is especially significant in adolescent medicine. Globally, 6-8% of people with diabetes are under the age of 14 years. After 14 years, the incidence drops. In 1991, adolescents aged 15-17 years old made up 0.36% of all patients with diabetes in Russia, and 2.2% of patients with IDDM.

Etiology and pathogenesis. A special contribution to the predisposition to diabetes mellitus is made by the genes of the major histocompatibility complex (MHC) in the short arm of chromosome 6, and viruses (enterovirus infection Coxsackie B, rubella, mumps, measles viruses). Diabetogens provoke cytolysis of insulin-secreting beta cells of the islets of Langerhans with autoallergic aggression in genetically predisposed individuals, especially adolescents. Smoking contributes to this. Cellular autoimmunity and humoral immunity play a role in the destruction of beta cells. The appearance of autoantibodies precedes insulitis. Spontaneous type I IDDM occurs suddenly, sometimes within 1 day (stress, acute illness, event with increased insulin demand). The insulin precursor C-peptide is still produced at first, but within 2 years its production decreases. Hyperglycemia induces the last reserves of beta cells, and a short period of decreased insulin requirements occurs. The extreme degree of metabolic disorders in IDDM leads to ketonemic coma. Glucose utilization is disrupted, counterinsular islet hormones increase, disturbances of all types of metabolism occur with complications caused by diabetic microangiopathy and neuropathy.

Insulin-dependent diabetes mellitus type II (NIDDM) is not significant in adolescents. This is a heterogeneous group of diseases in etiology and pathogenesis with a multifactorial hereditary predisposition, relative insulin deficiency and insulin resistance. For certain types of NIDDM, the exact type of inheritance has been established. These include NIDDM of adolescence, which is exclusively characteristic of adolescents - MODF syndrome ("maturity onset diabetes of the young" - "adult diabetes in youth"). It has a highly penetrant autosomal dominant inheritance of a defect in glucokinase, the gene of which is located on the short arm of chromosome 7.

With absolute and relative insulin deficiency, hyperglycemia and glycosuria occur. They cause polydipsia and polyuria. If immediate treatment with insulin is not started, Kussmaul ketoacidotic coma develops. The accumulation of ketone bodies (acetone, hydroxybutyric and acetoacetic acids) is associated both with the acceleration of their formation and with impaired utilization. This leads to endogenous intoxication. Extracellular and intracellular dehydration, hemoconcentration and peripheral circulatory failure increase. Decompensated acidosis causes Kussmaul breathing - shortness of breath with rare, noisy and deep breathing, the acidosis worsens. Excess lactate accumulates in the brain with increasing acidosis. Excessive hyperglycemia causes acute disturbance of water-salt metabolism and hyperglycemic (hyperosmolar) coma. The key link in its pathogenesis is hyperosmolality. Hyperosmolality leads to pronounced intracellular dehydration, the glucose content in brain cells increases slightly, but the concentration of this osmotically active substance in the blood plasma and intercellular fluid remains much higher than in the intracellular “compartment”. This leads to severe neurological symptoms and tissue hypoxia of the brain with loss of consciousness. The blood thickens, thrombohemorrhagic syndrome is formed with blockage of the glomeruli of the kidneys. Acute renal failure progresses. Oliguria and anuria develop, leading to death from acute renal failure.

With chronic exposure, hyperglycemia can cause dysfunction of capillary basement membranes, proliferation and hypertrophy of the vascular endothelium with occlusion of arterioles, venules and capillaries. Glycosylated hemoglobin, lipoproteins and other proteins are formed, giving impetus to the development of autoimmune and immune complex processes in blood vessels. Generalized diabetic microaigiopathy develops (a histological symptom complex of diabetes mellitus, especially IDDM). Damage to Schwann cells, degeneration of myelin and axons, and microaigiopathy of the vasa nervorum cause diabetic neuropathy.

Symptoms. In adolescents, diabetes mellitus is often diagnosed late, already in the stage of ketoacidosis. It manifests itself as abdominal pain, nausea, vomiting, and diarrhea. Thirst, dry skin and mucous membranes intensify, and a sour smell of acetone appears from the mouth. Polyuria reaches enuresis. Diabetes infections are provoked when teenagers are pampered with sweets, juices, and even prescribed glucose (“restorative”), which accelerates the development of ketoacidosis and coma. This is facilitated by the hyperproduction of counter-insular hormones characteristic of adolescents. There is anorexia, less often - a “wolfish” appetite, weight loss, despite bulimia. Itching of the skin appears (in girls - in the perineal area). Diabetic blush of the cheeks, forehead, brow ridges, and chin is often detected. The tongue is usually sticky or dry, covered with a white coating. Bleeding gums appear, frequent jams, gingivitis, stomatitis, periodontal disease, ecchymosis, caries. Nails are brittle.

Complications. Ketoacidosis is a manifestation of decompensated diabetes mellitus, which in adolescents is most often complicated by Kussmaul ketoacidotic coma. This is facilitated by their disorganization, non-compliance with diet and insulin therapy, refusal of self-control and visits to the endocrinologist, stressful situations, and labile course of IDDM. Ketoacidotic coma occurs more often in adolescents. It develops gradually (from 12-24 hours to several days). Brain swelling often occurs.

Non-ketogenic hyperglycemic (hyperosmolal) coma with acute renal failure rarely occurs in adolescence due to stress, trauma, illness, severe dehydration (vomiting, diarrhea, burns, frostbite, blood loss, excessive urination after diuretics). Hyperosmolal coma is a dangerous complication of diabetes mellitus, causing up to 50% mortality without proper treatment.
Hyperlactic acidemic coma is not observed in adolescents, since it is caused by biguanides, which are not used in IDDM.

With a labile course of IDDM, with an overdose of insulin or if its dose does not correspond to the diet, hypoglycemic states occur, including hypoglycemic coma. The prognosis is serious and unpredictable, especially regarding the future state of the adolescent’s intelligence. Encephalopathy with inappropriate behavior develops.

A severe complication of IDDM is systemic diabetic microangiopathy. Its development directly depends on the duration and degree of hyperglycemia. Intensive insulin therapy, keeping glycemia within normal limits, can sharply slow down the development and/or progression of microvascular complications of diabetes mellitus. They are the main cause of disability and mortality in young patients with IDDM. In early, severe diabetes mellitus, already in adolescence, the first signs of Kimmelstiel-Wilson syndrome (proteinuria, neuroretinopathy, arterial hypertension) may appear, which leads to uremia by the age of 25-35. It develops in all individuals with IDDM “experience” of more than 25 years. IDDM in adolescents is often complicated by chronic pyelonephritis, which in combination with diabetic glomerulosclerosis is called diabetic nephropathy. Diabetic neuroretinopathy is accompanied by hemorrhages, which can cause retinal detachment and blindness, especially if the “macula” is affected.

Diabetic neurovegetopathy leads to tachycardia and diarrhea. Adolescents with IDDM often develop polyneuritis. Peripheral neuropathy in combination with accelerated atherosclerosis of the arteries of the lower extremities are combined into an extremely unfavorable “pathogenic constellation”, leading to non-healing and infection of microdamages of the lower extremities. Neuropathic diabetic foot may develop with abscess, cellulitis and even gangrene. Occasionally, aseptic necrosis of the terminal phalanges of the toes develops. Peeling of the skin and scratching contribute to the development of pyoderma and mycoses.

A frequent complication of diabetes mellitus in adolescents is damage to the joints, especially the interphalangeal joints of the fourth and fifth fingers, and the cervical spine. May occur as part of an autoimmune process, Dupuytren's contracture.

Severe IDDM is often accompanied by fatty liver degeneration (hepatosteatosis), bacterial and giardiasis cholecystitis, and a tendency to cholelithiasis occur. With a long course of IDDM, a third of boys and half of girls experience a clear delay in sexual development with menstrual irregularities in 15-20% of cases. Boys have balanoposthitis, girls have vulvitis and vulvovaginitis. Sexual disorders in young men (erectile dysfunction) are explained by a decrease in the production of nitric oxide in microvessels and atherosclerosis of the arteries that bring blood to the genitals. Obvious nanism, subnanism and hypogenitalism may be observed, as the pace of development slows down. This is especially evident in IDDM from early childhood with a duration of 10 years or more. The sequence of development of secondary sexual characteristics is disrupted with simultaneous general exhaustion (Nobecourt syndrome). Adolescents with severe IDDM may develop Mauriac syndrome (delayed growth and sexual development, hepatomegaly, matronism with fat deposition on the chest, abdomen and in the area of ​​the VII cervical vertebra, sometimes with pink stretch marks, delayed bone age with osteoporosis, labile diabetes with prone to hypoglycemia).

Classification. The term “type I” is often used as a synonym for IDDM, and the term “type II” refers to any NIDDM. But the terms “IDDM” and “NIDDM” describe only the clinical course of a particular case (tendency to ketoacidosis and resistance to it), while the terms “type I” and “type II” refer to the pathogenetic mechanisms of the disease (the result of the dominance of the autoimmune process, or the result of the implementation of other mechanisms of pathogenesis).

The vast majority of cases of diabetes mellitus are spontaneous diabetes associated with malnutrition). Its other types make up only 6-8% of the total number of patients with diabetes. In Russia, there are traditionally 3 degrees of severity of diabetes mellitus (mild, moderate, severe), 3 types of compensation for metabolic disorders (compensation - with normoglycemia and aglucosuria; subcompensation - hyperglycemia, glucosuria, but without ketoacidosis; decompensation - hyperglycemia with ketoacidosis). There are acute complications of diabetes mellitus - coma (ketoacidotic Kussmaul coma, hyperosmolal, hypoglycemic, hyperlacticidemic), late complications of diabetes (microangiopathy, macroangiopathy - atherosclerosis of different localization, neuropathy), as well as damage to other organs and systems (enteropathy, osteoarthropathy, diabetic foot, hepatopathy , cataract, lipoid necrosis).

Diagnostics. The main laboratory sign of diabetes mellitus is fasting hyperglycemia. If it is higher than 6.7 mmol/l during repeated studies, and 10.0 mmol/l after meals, then glucosuria occurs in most people. With decompensation of diabetes mellitus, high glucosuria and ketone bodies (acetone) appear in the blood and urine. In the terminal stage of diabetic glomerulosclerosis, due to a spontaneous decrease in glycemic levels and a decrease in the need for exogenous insulin up to its complete withdrawal (Zubroda-Dan syndrome), aglucosuria occurs, and there is no acetone in the urine.

For IDDM, the typical content of C-peptide is below 300 pmol/l and its progressive drop over 2-3 years of illness to zero; after 3-4 years, IDDM becomes terminal with the absence of C-peptide production and with the formation of diabetic microangiopathies, the pathogenesis of which is also autoimmune . Moderate anemia is often detected in adolescents with IDDM. In diabetic glomerulosclerosis, it can be severe due to a deficiency of renal erythropoietin. With an advanced clinical picture of diabetic glomerulosclerosis, due to massive proteinuria, the level of total plasma protein falls, and globulins sharply increase (as in amyloidosis).

In the blood - moderate hypercholesterolemia, hypertriglyceridemia, the level of free fatty acids increases, especially when diabetes mellitus is combined with obesity and with hereditary diabetes mellitus. Signs of chronic pyelonephritis are often detected in urine. In diabetic glomerulosclerosis, the urine sediment often contains high proteinuria (up to 30-40 g/l), and the sediment is scanty. The development of renal failure is initially accompanied by a compensatory increase in renal blood flow and glomerular filtration, which then progressively decrease, and uremia occurs.

The ECG shows signs of myocardial dystrophy with rhythm disturbances, tachycardia. Tachooscillography often reveals an increase in mean blood pressure, especially during bicycle ergometry or during a cold test. EEG changes increase with the progression of cerebral microangiopathy.

Microangiopathies are detected by capillaroscopy of the nail bed of the fingers, conjunctiva, by ophthalmoscopy (microaneurysms of retinal vessels), and by thermal imaging examination of the lower extremities in the form of a symmetrical break in the infrared glow in the distal sections. A test for early diagnosis of microangiopathy - microalbumiuria (above 30 mcg/min), determined by radioimmunology. It correlates with blood pressure, the content of HbAlc and anti-insulin autoantibodies, diabetic retino- and nephropathy, and the duration of IDDM.

With latent diabetes mellitus, the level of glycemia on an empty stomach is normal, after meals - no more than 10 mmol/l. To detect diabetes, a glucose tolerance test (GTT) is performed. Glycemia is examined on an empty stomach, then the subject drinks 250 ml of glucose solution (with lemon juice to improve taste). Glucose is given at the rate of 50 g per 1 m2 of body surface (determined according to the nomogram). In prepuberty, glucose is given at the rate of 1.75 g per 1 kg of body weight. After taking glucose, every half hour for 2.5 hours the level of glycemia in the capillary blood of the finger is examined, and at the end of the test - urine for sugar and acetone. With impaired glucose tolerance, glycemia occurs within 2 hours, and after exercise it should range from 7.8 to 11.1 mmol/l (140-200 mg/dl); with obvious diabetes, it exceeds 6.7 mmol/l on an empty stomach, after 2 hours it exceeds 11.1 mmol/l, and glucosuria is almost always present in the urine. The sensitivity of GTT in case of a doubtful test can be increased by Conn's test (15 mg of prednisolone is given 8 and 2 hours before GTT). GTT is carried out only in the absence of symptoms of diabetes mellitus, otherwise decompensation of diabetes mellitus with ketoacidosis may develop. The diagnosis can be verified by studying anti-insulin antibodies, antibodies to the islets of Langerhans, as well as HbAlc (in diabetes it increases to 12% or more).

An example of a diagnosis. Insulin-dependent diabetes mellitus of an autoimmune nature, severe, decompensated. Ketoacidotic coma. Diabetic microangiopathy of the retina. Right lower lobe bronchopneumonia. Hepatosteatosis. Periodontal disease. Polyhypovitaminosis.

Differential diagnosis. Hyperglycemia is not always diabetic. It can be nutritional (with the rapid intake of excess carbohydrates into the body, for example, more than 150-200 g of sweets eaten in one sitting, while it does not exceed 200 mg/dl), stress (reflects the effect of stressors, often psycho-emotional), convulsive (with epileptic seizures, tetanus), endocrine (with hypersecretion of contrainsular hormones).

Thirst and polyuria raise suspicion for diabetes insipidus, but with diabetes the blood glucose level is normal, and the urine always has a low density (no more than 1005). Sometimes glucosuria is observed even with a normal diet, but the level of glycemia does not increase even after a glucose load (low threshold of renal permeability to glucose) - renal diabetes. Such persons often suffer from headaches and get tired easily. Renal diabetes may be a precursor to IDDM. With hyperparathyroidism, there is also thirst and polyuria, but with normoglycemia and hypercalcemia and hypersecretion of parathyroid hormone.

Disease outcomes and prognosis. Diabetes mellitus ranks third as a cause of death after cardiovascular disease and cancer. With timely detection and treatment, the prognosis is relatively favorable. Behavioral characteristics of a teenager can cause decompensation of diabetes, which contributes to the progression of microangiopathy, loss of vision, development of chronic renal failure, and polyneuritis. IDDM after puberty is calmer and more stable. Teenagers with diabetes are prone to tuberculosis.

80% of patients who develop diabetes in early childhood die within 20-30 years. For adolescents with diabetes, the main cause of death (from 0.5 to 15.4%) is ketoacidotic coma. Its outcome is favorable if the loss of consciousness lasted no more than 6 hours. As the time of the coma increases, deaths become more frequent.

The mortality rate for hyperosmolal coma is still 40-60%. With adequate insulin therapy, up to 60% of IDDM patients can maintain satisfactory renal function for many years, with minimal histological signs of diabetic glomerulosclerosis and microalbuminuria. Effective antihypertensive therapy can prolong life to 30-35 years. In diabetic glomerulosclerosis, hemodialysis and kidney transplantation prolong life.

Treatment. In the treatment of IDDM, the principle of strict dietary therapy is followed using a diet containing 15-20% proteins, 25-30% fats and 50-60% carbohydrates. The diet should ensure normal physical and sexual development.

With stable compensation for IDDM, no more than 20 g of sugar per day is allowed, which protects against hypoglycemia. Severe carbohydrate restriction leads to ketoacidosis due to lipolysis. The need for sweets is compensated by their substitutes. They are especially indicated for diabetes mellitus with obesity.

When taking sorbitol and xylitol, take into account their calorie content, which is equal to glucose. Saccharin and its analogues are undesirable for liver and kidney diseases, pregnancy and lactation; sorbitol and xylitol contribute to microangiopathy; fructose suppresses gastric secretion and causes lipidemia; aspartame - headaches, nausea, gastralgia, depression. Chewing gum with sweeteners helps with sweet cravings. When compensating for IDDM, honey is allowed (no more than 3 teaspoons per day). You can include rice and pasta in your diet. Ice cream is acceptable within reasonable limits. Cholesterol-rich foods and fats are limited to 30-40 g per day.

A teenager with newly diagnosed IDDM is immediately hospitalized in an endocrinology hospital. For catoacidosis, treatment begins in the intensive care unit. For decompensated diabetes (especially in coma), antibiotics are prescribed.

For patients with IDDM, even their own insulin is often immunogenic, not to mention foreign insulin. With the advent of genetically engineered (recombinant) insulin, the use of animal insulin is archaic. The International Society for the Control of IDDM in Adolescents recommends the use of recombinant insulin that is free from animal viruses. Short- and long-acting insulins have been obtained. The effect is achieved by their combination. From the long-acting ones, insulins with a smooth action are selected, and against their background, short-acting insulins are administered 30-60 minutes before the next meal, simulating the natural secretion of insulin. Injections of short-acting insulin can be made repeatedly using a Novopen-type syringe pen, which has an atraumatic needle and is refilled with Penfill-type insulin cartridges. Insulin is drawn by pressing a special button on the cap of the pen syringe (with 1 press, 2 IU of insulin is drawn). Such injections resemble physiological insulin secretion.

Systems have been developed equipped with timers to monitor the last dose administered and the time since the injection (Innovo from the Danish company Novo Nordix). Short-acting insulin analogs with faster peak efficacy and shorter duration of effect have been developed (NovoRapid) to better control postprandial glycemia and reduce the incidence of hypoglycemia at night. To achieve maximum effect, select the minimum dose of insulin. The level of glycemia at night and early morning hours is taken into account, since in most patients with IDDM the lowest glycemia occurs at 3-4 a.m., and the highest at 5-8 a.m. (due to high production of contrainsular hormones). Therefore, injections at 6 a.m. or administration of long-acting insulin at a later time, before bedtime, are more effective. The best effect is obtained with 1-2 injections per day of long-acting insulin and 3-4 injections of short-acting insulin.

Currently, devices are sold for rapid determination of glycemia by the patient himself, which facilitates treatment control. Aerosol and oral insulin preparations in liposomal form are being intensively developed. Biostator insulin dispensers are effective, but inconvenient to use. Pancreas transplantation is problematic due to tissue incompatibility. Hopes are placed on cell therapy with the implantation of genetically modified beta cells or stem cells that differentiate into beta cells. The prospects for treating IDDM as an autoallergic disease with immunosuppressants are of interest. Among the non-traditional methods of treating diabetes mellitus, oxygenation, hemosorption, plasmapheresis, enterosorption, electroacupuncture, blood irradiation with ultraviolet radiation and laser, and various herbal infusions are used. However, this in no way replaces insulin therapy. Such methods are effective only in latent diabetes mellitus or in rare cases NIDDM.

In the treatment of microangiopathy, trental, complamin, agapurin, and theonicol are used; anabolics such as retabolil; disaggregants, cardiotrophics, cardiac energizers, vitamins of all groups. But the most effective method is careful compensation of diabetes mellitus. With normoglycemia and aglucosuria, microangiopathy develops much later. For arterial hypertension, the effect is provided by Arifon (Indap), calcium channel blockers. Captopril and its analogues are widely used in the treatment of diabetic glomerulosclerosis.

Teenagers should take special care of the hygiene of the genitals and feet, wear comfortable, roomy shoes, avoid scuffs and calluses, inspect and wash their feet daily, and do not use too hot heating pads if they are cold.

Exercise therapy has a beneficial effect on the course of diabetes mellitus. Sanatorium-resort treatment of adolescents with diabetes is carried out only in the absence of ketoacidosis and severe vascular complications.

Prevention. The strategic goal is early detection of IDDM and preventive therapy. Diabetes mellitus is a medical and social problem. A group at risk for diabetes requires attention (those born with large body weight, those with relatives with diabetes, those suffering from obesity and arterial hypertension, persons with questionable GTT). The role of heredity makes the issue of preventing diabetes mellitus still problematic; it is important to prevent provoking factors: balanced nutrition, reasonable consumption of sweets, physical education, organization of work and rest, and stress prevention. It is necessary to monitor children from families with diabetes, those who have had enterovirus infection and mumps, children of mothers who suffered from rubella in the second half of pregnancy, and all carriers of the MHC haplotype D3 and D4. Dietary and medicinal diabetogens should be avoided.
For adolescents with diabetes mellitus who want to get married, medical genetic counseling is important, which is especially indicated for the so-called low-progressive NIDDM of adolescents with autosomal dominant inheritance (a congenital defect in insulin secretion that is inadequate to the level of glycemia).

Clinical examination. Dispensary group - D-3. Adolescents with IDDM are not removed from dispensary registration. The medical examination system should be based on data on the immunopathological nature of diabetes mellitus. It is necessary to register adolescents with IDDM as immunopathological individuals. Sensitizing interventions are contraindicated. This is the basis for medical withdrawal from vaccinations and for limiting the introduction of antigenic drugs. Chronic insulin treatment is a difficult task and requires the patience of the teenager and the doctor. Diabetes mellitus frightens a lot of restrictions and changes the way of life of a teenager. We need to teach a teenager to overcome his fear of insulin. Almost 95% of adolescents with IDDM do not have a correct understanding of diet and do not know how to change insulin doses when changing food intake or during physical activity that reduces glycemia. The most optimal thing is to attend classes at “Schools for Diabetes Patients” or “Health Universities for Diabetes Patients.” At least once a year, an inpatient examination with correction of insulin doses is necessary. Observation by an endocrinologist at the clinic - at least once a month. Permanent consultants should be an ophthalmologist, therapist, neurologist, and, if necessary, a urologist, gynecologist, nephrologist. Anthropometry is performed and blood pressure is measured. The levels of glycemia, glycosuria and acetonuria are regularly examined, and blood lipids and kidney function are periodically examined. All adolescents with diabetes need a phthisiological examination. In case of reduced glucose tolerance - dynamic observation once every 3 months, examination by an ophthalmologist once every 3 months, ECG - once every six months, and if glycemia levels are normal for 3 years - deregistration.

Expertise Questions. Health group - 5. Physical activity for IDDM is strictly dosed. Exercise therapy begins in the first months of the disease, before complications develop. All types of athletics, sports games, tennis are allowed, but strength sports, weightlifting, mountaineering and marathon running are prohibited. Excessive loads are fraught with retinal hemorrhages and hypoglycemic coma. Before physical education, you need to take carbohydrates (an apple, a glass of juice or milk, a sandwich). With glycemia above 15 mmol/l and with ketoacidosis, physical exercise is prohibited. Training with an increased teaching load is not indicated. Teenagers with diabetes are exempt from exams. Work is shown with minimal psychophysical overload, without business trips. It is prohibited to work on the night shift, in hot shops, at heights, with moving mechanisms, or to drive cars. For IDDM with complications, transfer to disability is indicated.

With compensated IDDM of moderate severity with an insulin dose of up to 60 IU per day and moderate dysfunction, adolescents are limitedly fit for military service; with severe diabetes mellitus, they are not suitable for military service. Military educational institutions are not accepted. The issue of military service under a contract is decided individually.

Diabetes mellitus is a very common disease. It affects 2 to 4% of the population. According to American statistics, 50% of patients with diabetes die from myocardial infarction, from blindness (2nd place), from atherosclerosis of the extremities, from pyelonephritis, from urolithiasis.

Acute complications of diabetes mellitus

1. Diabetic ketoacidosis.

2. Hyperosmolar coma.

3. Hyperglycemia.

Diabetes mellitus is a chronic polyetiological disease, which is characterized in terms of disorders by hyperglycemia, protein and fat catabolism, and regardless of the cause, these disorders are associated with a lack of insulin (absolute and relative). In diabetes mellitus, the fasting blood glucose level is more than 7.2 mmol/l in a double study (*18 mg%).

Types of diabetes

1. Primary (idiopathic).

2. Secondary (symptomatic).

Secondary symptomatic diabetes mellitus

Occurs in pathologies of the endocrine system:

1. Itsenko-Cushing disease or symptom (disease of chronic excess cortisone).

2. Acromegaly (excess growth hormone).

3. Pheochromocytoma (a tumor that produces catecholamines in excess).

4. Cohn's sign (primary hyperaldosteronism). Under the influence of aldosterone, potassium levels decrease, and it is necessary for the utilization of glucose.

5. Glucogonoma (tumor of L-cells of the islets of Langerhans). The patients are exhausted, with ulcers on the extremities.

Secondary pancreatic diabetes: after removal of the pancreas, with pancreatic cancer (body and tail).

Iron storage disease (hemachromatosis). Normally, the level of iron in the blood is regulated by a feedback mechanism. More iron is absorbed than needed, and it goes to the liver, pancreas, skin:

Triad: dark skin, gray color, enlarged liver, diabetes mellitus.

Primary diabetes mellitus

This is a polyetiological disease.

Highlight:

1. Insulin - dependent diabetes mellitus - absolute insulin deficiency - type 1.

2. Insulin - independent diabetes mellitus. Occurs with relative insulin deficiency. In the blood of such patients, insulin is normal or elevated. Can be obese or normal weight.

Insulin-dependent diabetes mellitus is an autoimmune disease. Its development is based on:

1. A defect in chromosome 6 - 1 associated with the NLA system - D 3, D 4. This defect is hereditary.

2. Mumps viruses, measles, coxsackie viruses, severe stressful situations, some chemicals. Many viruses are similar to beta cells. The normal immune system resists viruses. With a defect, the islets are infiltrated by lymphocytes. B lymphocytes produce cytotoxic antibodies. beta cells die, and insufficient insulin production develops - diabetes mellitus.

Insulin-independent diabetes mellitus has a genetic defect, but manifests itself without the influence of external factors.

1. Defect in the beta cells themselves and peripheral tissues. Insulin secretion can be basal and stimulated (at a blood glucose level of 6.5 mmol/l).

2. The sensitivity of peripheral tissues to the action of insulin decreases.

3. Changes in the structure of insulin.

Insulin-dependent diabetes is affected by obesity. At the same time, the cells need more insulin, but there are not enough of its receptors in the cells.

Clinical manifestations

4 groups of violations:

1. Metabolic disorders, carbohydrate metabolism disorders - hyperglycemia, protein catabolism, fat catabolism.

2. Polyneuropathy, peripheral and autonomic.

3. Microangiopathy.

4. Macroangiopathy (atherosclerosis).

Metabolic disorders

The functions of insulin are the utilization of amino acids and glucose from human food.

Tetraanabolic hormone lowers blood glucose levels. He is opposed by:

1. Glucagon. The stimulus for its secretion is a decrease in blood glucose levels. It acts through glycogenolysis. An increase in blood glucose stimulates the breakdown of protein, and glucose is formed from amino acids.

2. Cortisone - stimulates protein catabolism and gluconeogenesis.

3. Growth hormone - promotes protein synthesis, saves glucose for RNA synthesis.

4. Adrenaline - stimulates the breakdown of glycogen, inhibits insulin secretion.

Normal blood glucose concentration is less than 6.1 mmol/l. The maximum limit during the day is 8.9 mmol/l.

Action of insulin

With an increased amount of glucagon, little glucose is consumed in the cells, so permeability decreases.

The patient complains of thirst, polyuria (with type 1 diabetes), loss of body weight, increased appetite.

Polyuria is due to the fact that when the glucose concentration increases to more than 9 - 10 mmol/l, glucose appears in the urine. Osmotic diuresis - a lot of urine with a high specific gravity.

Thirst: blood osmolarity increases, the thirst center is stimulated. Reducing body weight: contrainsular factors have a lipolytic effect --> weight loss. Increased appetite: since the tissue does not utilize glucose efficiently, the hunger center is stimulated.

With type 2 diabetes mellitus, obesity develops. since insulin is enough to carry out lipogenesis, However, in 5% of patients it is difficult to decide what type of diabetes they have.

Diabetes insipidus is a syndrome caused by a lack of vasopressin in the body, which is also defined as antidiuretic hormone. Diabetes insipidus, the symptoms of which are impaired water metabolism and manifest as constant thirst with simultaneous increased polyuria (increased urine production), is, however, a rather rare disease.

general description

The development of diabetes insipidus occurs due to the relevance of pathologies of the pituitary gland, which, in turn, arise due to malignant or benign metastatic tumors. Among other possible causes of the formation of destructive processes, unsuccessful surgical interventions affecting the brain are also noted. Thus, in every fifth case, diabetes insipidus occurs precisely because of unsuccessful neurosurgical surgery.

Diabetes insipidus is not a hereditary disease, but some autosomal recessive inherited syndromes (for example, Wolfram's disease, complete diabetes insipidus or incomplete diabetes insipidus) are part of the clinical picture indicating a genetic mutation.

As we have already noted, diabetes insipidus is a fairly rare disease, which represents only about 0.7% of the total number of actual endocrine pathologies. There is an equal incidence rate among both sexes. As for childhood morbidity, in this case, diabetes insipidus often manifests itself in a congenital form, and its diagnosis can be made quite late - often this happens around or even after 20 years. Among adults, acquired diabetes mellitus is most often diagnosed.

Diabetes insipidus: classification

In addition to the above-mentioned congenital and acquired forms, there are such varieties of the disease as central diabetes insipidus, renal diabetes insipidus and idiopathic diabetes insipidus.

Central diabetes insipidus

The development of central or hypothalamic-pituitary diabetes insipidus occurs due to the inability of the kidneys to accumulate fluid. This pathology occurs due to disturbances that occur in the functions of the distal tubules of the nephron. As a result, a patient with this form of diabetes insipidus suffers from frequent urination in combination with polydipsia (that is, unquenchable thirst syndrome).

It should be noted that if the patient has the opportunity to consume unlimited water, then there are no threats to his condition. If for one reason or another there is no such opportunity, and the patient cannot quench his thirst in time, he rapidly begins to develop dehydration (or hyperosmolar dehydration). Reaching the extreme stage of this syndrome is life-threatening for the patient, because the next stage is the transition to hypersomolar coma.

The long-term course of central diabetes insipidus for the patient develops into renal insensitivity to the antidiuretic hormone artificially administered for therapeutic purposes. For this reason, the sooner treatment for this form of diabetes insipidus begins, the more favorable the prognosis for the patient’s subsequent condition becomes.

It should also be noted that significant volumes of fluid consumed by the patient can cause the appearance of conditions accompanying this disease, such as biliary dyskinesia, the development of irritable bowel syndrome or gastric prolapse.

Idiopathic diabetes insipidus

The incidence of diabetes insipidus in this form accounts for a third of cases. Here, in particular, we are talking about the absence of any types of organic pathologies of the organ during diagnostic imaging of the pituitary gland. In other words, the reported incidence of diabetes insipidus is unknown. In some cases, it can be passed on by inheritance.

Renal diabetes insipidus

Diabetes insipidus in this form is provoked by organic or receptor pathologies of the kidneys, including enzymatic enzymes. The form is quite rare, and if it is observed in children, then, as a rule, in this case it is congenital. It is caused by mutations in the aquaporin-2 gene or mutations in the vasopressin receptor. If we are talking about the acquired form of morbidity in adults, then it is advisable to note as the cause renal failure, which provokes this form of diabetes, regardless of the characteristics of its etiology. In addition, renal diabetes insipidus can also occur as a result of long-term therapy using lithium preparations and other specific analogues.

Symptoms of diabetes insipidus

The main symptoms of diabetes insipidus, as we have already highlighted, are polyuria (that is, frequent urination), as well as polydipsia (thirst syndrome). As for the severity of these manifestations, here we can talk about their different intensities.

Dwelling on the features of symptoms, it should be noted that polyuria manifests itself in an increase in the total volume of urine excreted per day (which is most often about 4-10 liters, and in some cases can reach up to 30 liters). The excreted urine is colorless, it contains a small amount of salts and other types of elements. All portions are characterized by low specific gravity.

An unquenchable feeling of thirst in the case of actual diabetes mellitus leads, accordingly, to polydipsia, in which significant volumes of fluid are consumed, in some cases they can be equal to the volume of urine lost.

The severity of diabetes insipidus itself in the complex is characterized by the degree of lack of antidiuretic hormone in the body.

The development of the idiopathic form of diabetes insipidus occurs extremely acutely and suddenly; in rare cases, the course of the process is determined by a gradual increase. Pregnancy can lead to the manifestation of the disease (that is, to the development of the severity of its characteristic clinical manifestations following an erased or asymptomatic form of the course).

Due to the frequent occurrence of the urge to urinate (which is defined as pollakiuria), sleep disturbances and (i.e., mental state disturbances) appear, and increased physical fatigue and emotional imbalance are also noted. The early manifestation of diabetes insipidus in children is expressed in, subsequently the manifestations of the disease are accompanied by delays in growth and puberty.

Late manifestations of the disease include dilations that occur in the renal pelvis, bladder and ureters. Due to significant water overload, overdistension of the stomach and its prolapse occurs; in addition, the development of biliary dyskinesia and chronic intestinal irritation are also noted.

Patients with diabetes insipidus experience significant dry skin and secretion of saliva and sweat. Appetite is reduced. Somewhat later, such manifestations as dehydration, headaches, vomiting, weight loss, and low blood pressure appear. Diabetes insipidus, caused by damage to parts of the brain, occurs with the development of neurological disorders, as well as with symptoms indicating pituitary insufficiency.

In addition to the listed symptoms, diabetes insipidus occurs in men and menstrual irregularities in women.

Complications of diabetes insipidus

The danger of diabetes insipidus lies in the risk of developing dehydration of the body, which occurs in situations in which the loss of fluid from the body through urine is not adequately replenished. For dehydration, characteristic manifestations are general weakness and tachycardia, vomiting, and mental disorders. Blood thickening, neurological disorders and hypotension, which can reach a state of collapse, are also noted. It is noteworthy that even severe dehydration is accompanied by persistence of polyuria.

Diagnosis of diabetes insipidus

Diagnosis of diabetes insipidus requires an appropriate test for polyuria. In a normal state of the body, the volume of urine excreted per day does not exceed three liters. Accordingly, patients with diabetes insipidus exceed this indicator; in addition, there is also a low degree of density of urine excreted.

Another test is used to diagnose diabetes insipidus, which is defined as a dry eating test. In this case, the patient must refrain from drinking for eight hours. With a sharp decrease in weight over a given period of time and a urine density of no more than 300 mOsm/liter, the diagnosis of “diabetes insipidus” is confirmed.

The differential diagnosis of diabetes insipidus involves excluding the insulin-dependent form of diabetes, as well as the presence of tumors in the hypothalamic-pituitary region, neurotic and mental disorders and kidney pathologies of an organic nature.

Treatment of diabetes insipidus

If we are talking about the need to treat a symptomatic type of diabetes insipidus, that is, diabetes insipidus that has arisen as one of the symptoms of a particular type of disease, then therapy focuses primarily on eliminating the root cause (for example, a tumor).

Regardless of the form of diabetes insipidus, patients are prescribed replacement therapy using a synthetic analogue of antidiuretic hormone (ADH). The use of this kind of drugs is carried out orally or by instillation of the nose. Long-acting medications are also used. The central form of diabetes insipidus involves the prescription of drugs whose action stimulates the secretion of ADH.

Additionally, a correction is carried out aimed at replenishing the water-salt balance, for which saline solutions are infused in significant volumes. The use of diuretics seriously reduces diuresis.

As for the nutritional features in the treatment of diabetes insipidus, it involves limiting protein intake, which helps reduce the load on the kidneys. In addition, the intake of fats and carbohydrates should be sufficient. Food should be taken frequently, and emphasis is placed on increasing the total amount of fruit and vegetable dishes consumed. To quench your thirst, it is recommended to consume compotes, fruit drinks and juices.

To diagnose diabetes insipidus, if characteristic warning symptoms appear, you must contact an endocrinologist.

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Diseases with similar symptoms:

Diabetes mellitus is a chronic disease in which the functioning of the endocrine system is affected. Diabetes mellitus, the symptoms of which are based on a prolonged increase in the concentration of glucose in the blood and on the processes accompanying an altered state of metabolism, develops in particular due to a deficiency of insulin, a hormone produced by the pancreas, due to which the body regulates the processing of glucose in the tissues of the body and in his cells.

Irritable bowel syndrome (IBS) is a series of functional disorders associated with the functioning of all lower parts of the digestive tract. It is otherwise called irritable bowel syndrome, but she is not the only one who suffers. This problem occurs in half of the world's population, and affects both the elderly and children. Irritable bowel syndrome most often occurs in women.

Renal failure means a syndrome in which all functions relevant to the kidneys are disrupted, resulting in a disorder of various types of metabolism in them (nitrogen, electrolyte, water, etc.). Renal failure, the symptoms of which depend on the course of this disorder, can be acute or chronic, each of the pathologies develops due to the influence of different circumstances.