Childhood diseases. Diabetes

Type 1 diabetes mellitus – idiopathic

Type 2 diabetes mellitus – from predominant insulin resistance, with relative insulin deficiency, to a predominantly secretory defect with insulin resistance.

Sugar Diadet Type 3 – Other specific types: 

? genetic defect in b-cell function     

? genetic defect in insulin action     

? endocrinopathies       

? diseases of the exocrine pancreas       

? drug-induced diabetes     

? infection     

4. Gestational diabetes

T1DM is more common in children, unlike T2DM, which is dominant in adulthood (rarely in children). Most often detected in Japanese, Native Americans, Australians. 3 types of mono-egg concordant twins on this basis in 100% of cases. Delayed fetal development of the fetus (IUGR) and weight loss in the first months of life, if the child subsequently begins to eat intensely, then insulin resistance occurs. 

To genetic defects: type A insulin resistance, atrophic diabetes, leprechaunism, Robson-Mendelhon syndrome, they appear at an early age. 

Diseases of the exocrine part of the pancreas: fibrosis, pancreatic cystic fibrosis, pancreatitis. 

Endocrinopathies: Ytsenko-Kushengo syndrome, pheochromocytoma, hyperthyroidism. With these diseases , the concentration of hormones increases. 

Diabetes can be induced by a number of drugs: thyroid hormones, thiazides, bentamidine. The mechanism of their action may be different: a decrease in the action of insulin on the periphery or an increase in insulin resistance. In childhood, the use of a-interferon is important. With virus-induced diabetes mellitus, the toxic effect of viral infection on b-cells occurs, followed by their destruction. With immobility syndrome, diabetes mellitus is observed in 50% of cases (autoimmune disease of the central nervous system + autoantibody to insulin). Diabetes mellitus can occur with genetic diseases: Shereshevsky-Turner syndrome, Goettington chorea, Down syndrome. Gestational diabetes mellitus occurs during pregnancy in the form of impaired carbohydrate metabolism, is fraught with the development of defects.

Diagnostic criteria:

1. On an empty stomach glycemia level:

up to 6.1 μmol / l – normal glucose 

6.1-7.0 μmol / L – impaired glycemia 

more than 7.0 μmol / l – a preliminary diagnosis of diabetes mellitus, for the formulation it is necessary to re-register the increased glucose level.

2. Determination of glucose tolerance:

2 hours after carbohydrate loading glucose level

? less than 7.8 μmol / l – normal tolerance     

? 7.8 – 11.1 μmol / L – reduced glucose tolerance     

? more than 11.1 μmol / l – diabetes mellitus.     

In patients without a clinic, a diagnosis can be made only after a second determination of increased blood sugar. In Russia, in the age range from 0 to 14 years, there are more than 15,000 patients with diabetes.  


Type 1 diabetes – autoimmune disease in which long current insulitis leads to degradation in the cell, produces cellular and humoral immunity in cells that and leads to insulin deficiency. The percentage of association with other autoimmune diseases is high. Sometimes an examination of relatives reveals a latently long-lasting disease. In development , 6 stages are distinguished:    

  1. Genetic predisposition. Diabetes is detected in 50% of genetically identical twins. 
  2. Hypothetical trigger
  3. Active autoimmunization, but the level of insulin secretion is still normal.
  4. Decreased insulin secretion in response to a decrease in glucose, but insulin levels remain normal 
  5. Clinical manifestation, with the death of more than 50% of b-cells, but residual insulin secretion. 
  6. Complete destruction of b-cells.

The factors initiating autoaggression to b-cells:

? viral infection: Coxsackie, rubella, chickenpox, measles, mumps, cytomegalovirus. (mumps virus directly lyses b cells).      

? Nutrition – early conversion to artificial feeding, nutritional supplements     

? Some other factors.     


T1DM is an autoimmune disease that is triggered by the factors listed above. In response to changes in the surface structure of b cells, an autoimmune process (insulin) develops. In 70-90% of b-cells, antibodies to insulin-producing cells appear, the death of 70% of the cells leads to a decrease in glucose tolerance (can occur in a stressful situation), 80-90% – to the manifestation of diabetes mellitus. If during pregnancy a woman suffered rubella, then in 25% of the child in the first 10 years type 1 diabetes develops. On the one hand, there is a close association of diabetes with HLA antigens. 5% of children with diabetes have a grandfather and grandmother, if the father is 5%, the mother is 2.5%, and both parents are 20%. It is believed that genetic predisposition does not play a decisive role, but with antigenic compatibility there is (HLA, …) a high risk of developing diabetes.  

Insulin function:

  1. Participation in the regulation of carbohydrate metabolism 
  2. Glycemia reduction due to transport to muscle and fat cells
  3. Promotes c. Krebs
  4. Promotes the formation of glycogen in the liver and muscles, inhibits neoglucogenesis
  5. It affects fat metabolism: reduces glycolysis, activates fat synthesis.
  6. It activates the transport of amino acids into the cell, promotes the synthesis of protein.
  7. Participates in supporting the intracellular ionic environment (Na, K, Mg, P),
  8. Increases the concentration of free Ca ions

Insulin deficiency causes metabolic disorders. An increase in glycogen activity leads to an increased breakdown of glycogen in the liver, an increase in gluconeogenesis, hyperglycemia does not depend on the amount of glucose supplied with food, in patients with diabetes mellitus against the background of hunger high blood sugar values ​​due to gluconeogenesis can be observed. With an increase in glucose to 8.88 μmol / L (renal threshold), it begins to be excreted in the urine. Glucose is an osmotic diuretic, therefore, an increase in glucose concentration leads to the release of water from the cells and the development of hypertonic cell dehydration, polyuria, cell starvation develops. Signs of dehydration are a decrease in skin turgor, a decrease in the tone and movement of the eyeballs.  

As a result of dehydration, electrolyte losses increase. In a place with water, potassium, magnesium, calcium are lost, in response, the activity of aldesterone and adrenal cortex increases, which leads to an increase in calcium yield – weakness, lethargy in patients with diabetes develops. In response to cell starvation, polyphagy appears, an increase in gluconeogenesis, since the main source for the production of endogenous glucose amino acids is the depletion of protein reserves, a decrease in protein synthesis, the reserves of potassium, phosphorus, magnesium are depleted, an increase in the level of residual nitrogen is a negative nitrogen balance. The balance between lipogenesis and lipolysis is disturbed, fatty acids and glycerol are mobilized, the breakdown of fats and proteins of muscle tissue increases, which leads to weight loss. Fatty acids enter the liver, where they are etrified – fatty degeneration of the liver develops. Ketone bodies cannot be fully used in the Krebs cycle – ketonemia and ketonuria develop (the smell of acetone in exhaled air). Hyperlactatemia develops, exacerbating ketoacidosis, resulting in severe metabolic acidosis. With ongoing ketoneemia, the body tries to neutralize it, which is spent on NaHCO3, which leads to its deficiency. A decrease in plasma pH stimulates the respiratory center, which is manifested by Kussmaul breathing, as a result of which fluid loss from the lungs increases, absolute deficiency of Na, water, NaHCO3, chlorine and magnesium develop.  

The concentration of gamma-ketobutyric acid is increasing, its toxic effect on nerve cells is increasing, severe hypovolemia and a decrease in myocardial contractility along with an increase in vascular tone are developing . 


T1DM can develop in children of any age, the risk increases after 9 months, gradually increasing to puberty. Clinical manifestations depend on age, stage of the disease. Acute manifest onset is observed in most patients. The clinical picture in older children in the presence of manifest symptoms:

? Polyuria – urine is colorless with an increased specific gravity; enuresis corresponds to massive polyuria     

? Enuresis (urinary incontinence)     

? Polydipsia – a sharp dehydration of the body, at night, dry mouth, healthy children do not drink water at night.     

? Polyphagy – a constant feeling of hunger, due to impaired glucose utilization, a characteristic loss of body weight.     

? Pseudo-abdominal syndrome – nausea, vomiting due to ketoacidosis (leading to erroneous laparotomy).     

? The growth of sick children is less than that of healthy     

An objective examination reveals dry skin and mucous membranes, dry seborrhea, seizures in the corners of the mouth, thrush of the oral cavity, diabetic blush on the cheeks, forehead – with severe ketoacidosis. Sometimes icteric staining of the palms and soles, which is associated with the deposition of carotene, in young children, the skin hangs in layers. Respiratory organs are rarely affected. Cardiovascular system: at the onset of the disease is characterized by tachycardia, muffling of heart sounds, on the ECG – metabolic changes. An increase in the liver due to concomitant diseases or is a manifestation of fatty liver. At puberty in girls – menstrual irregularities in the form of oligo- or amenorrhea, menarche delays of 0.8-2 years. Mariak’s syndrome (with prolonged decompensation): Cushingoid-type obesity, enlarged liver, ketoacidosis, hypoglycemia, decreased growth up to dwarfism, impaired puberty, osteoporosis.     

Young children (up to 3 years old) have a more acute onset with a small prodrome, often with ketosis. Thirst and polyuria can be viewed.

2 variants of the course of diabetes: 

  1. acute onset as a toxic-septic state
  2. The severity increases gradually, dystrophy progresses, children are restless, secondary infection, diaper rash, sticky spots of urine develop.

Children from 3 to 5 years of age have a more acute course and severe manifestations. The course of the disease is characterized by extreme instability, ease of development of ketosis, and increased sensitivity to insulin.

Laboratory diagnostics:

The diagnosis is made on the basis of the clinical picture, confirmed by the presence of hyperglycemia, glucosuria.

Hyperglycemia – 6.7 mmol / L on an empty stomach or up to 11.1 mmol / L (twice), if below 6.7 mmol / L, then a standardized glucose tolerance test (twice) is performed.

Glycosuria is normally absent if the blood glucose level is higher than the renal threshold (8.88 mmol / L) – glucosuria, the absence of glucosuria does not yet indicate the absence of the disease. The presence of glucose with normal blood sugar indicates hereditary syndromes (renal diabetes, Fanconi syndrome). Autoantibodies to b-cells and / or insulin in the blood are observed in 85-90% of patients. C-reactive peptide is a protein fragment that is cleaved from insulin during its activation. The level of C-reactive peptide is used for the differential diagnosis of type 1 and type 2 diabetes. In the first type, it does not increase, in the second it increases after glucose loading. 


  1. Diet
  2. Insulin therapy
  3. Physical exercise
  4. Patient training on self-monitoring of blood glucose
  5. Psychological training

The goal of diabetes treatment:

? achieving normal child development     

? normal psycho-social adaptation of the child       

? development of independence, motivation for self-preservation       

? prevention of diabetes complications       

The diet should fully satisfy the costs of vitamins, minerals, not differ from the rest (can be recommended for all family members), should cover the daily needs. Daily calorie can be calculated by the formula:

Daily calories = 1000 + 100 * N (number of years of a child’s life)

If the mass does not correspond to age, then the daily calorie content is calculated for the proper mass.

1g of fats – 9 kcal Proteins: fats: carbohydrates = 1: 1: 4

A set of products is taken in special tables. Mass distribution:

First breakfast7-9 hours20-25%
Dinner12-14 hours25-30%
Dinner19-21 hours20-25%
2 breakfast10-15%
Snack, 2 dinner5-10%

Fats should provide 30-35% of calories.

Insulin therapy:

Hormone replacement therapy.

Semi-synthetic – in porcine insulin they replace the amino acid alanine in the 30th position with tyrosine, it is recommended to use only human insulin.

According to the duration of action, they distinguish:

Type of insulinAction startPeak in bloodTime of actionDrug Names
Ultra short actionafter 10-20 minutes1-3 hours3-5 hours“Novorobit” “humalogue”.
Short actionin 30 minutespeak 1-3 hours6-8 hours“Actropid” “humulin-regular” “insuman-rapid”
Extended insulins1-2 hours4-12 hours17-22 h“ProtofanNM”Humulin NPH, insulin-vazan
Mixed insulinAtchildrennotapply


The first 2 years of the disease are 0.5-0.6 U / kg. In 40-50% of cases in the first months there is a partial remission prescribed – 0.1-0.2 U / kg (for 3 months in rare cases –2 years). After remission 1U / kg, during puberty, 1.5-2.0 IU / kg, then the dose is reduced to 1 IU / kg.u Ratio of prolonged and short insulin: prolonged use at an early age is more used in children during puberty short-acting insulins are used more.

In young children, from 0.1-1.3 IU / kg is used, the ratio of short to prolonged 1:12 and 1: 4, (the need for prolonged prevails). Pupils are prescribed 1-1.2 IU / kg short-acting 1: 6, prolonged – 1: 3. In adolescence, 0.5-2.0 U / kg short 1: 1 prolonged 1: 2. When the manifestation begins with the introduction of short-acting insulin, the first dose depends on the age of the child: the first years of life 0.5-1 ED / kg, school 2-4 U / kg, teenage 4-6 U / kg, re-analysis every 36 hours. If the blood sugar is unchanged, the dose is increased by 50%, if the reduced dose is reduced by 25-50%. Additional injection at 24 and 6 hours, and when expressed at 3 a.m. After one two days, they switch to fractional administration of a short one, then prolonged, in the daytime.

Intensified Scheme.

The introduction of short insulin before each meal and prolonged 1-2 times a day, the effectiveness criteria – fasting level of 4.7 μmol / l, after eating 5-11 mmol / l, the beginning of at least 3-6 mmol / l (tendency to hypoglycemia), the absence of severe hypoglycemia, the content of glycated hemoglobin should be less than 7-6% (normal 4-6%). 

Clinical examination.

Purpose: to create conditions for the patient for an able-bodied life, a clinic – targeted training for children and parents to correct the condition, classes for patients with diabetes mellitus (they must know the role of insulin, duration of action, knowledge of diet).

Complications: diabetic enzymopathy, nephropathy, pyelonephritis, coma. Perform vitamin therapy massage, physiotherapy, exercise therapy.

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