Diabetes mellitus in children

In the structure of endocrine pathologists, diabetes is one of the leading places. According to the association of West European pediatricians, the last 10 years are characterized by a distinct increase in this pathology. This applies to the Scandinavian countries, Belgium, Poland, St. Petersburg. Moscow data:

In the 70s, the incidence of 5.5%, in the 80s – 9.5%, in the 90s – 11.5%.

The prevalence of diabetes in children is 55 per 100 thousand. Population. In St. Petersburg there are approximately 500 children with diabetes. A child with diabetes is a tragedy for the family. Today, our country does not have the ability to reliably monitor these patients. 

There are several options for diabetes.

1. 1. Primary (not related to other diseases). It is found in the vast majority of cases – insulin-dependent.  
2. 2. Secondary (forms of diabetes – a consequence of any pancreatic disease: chronic pancreatitis, insulitis, tumors, pancreatic resection – non-insulin-dependent.  
3. 3. Diabetes caused by increased production of hormones by an insulin antagonist (STH, for example, with acromegaly, there are symptoms of diabetes, cortisol with Itenko-Cushing’s syndrome, catecholamines with pheochromocytoma, thyroid hormones with thyrotoxicosis).  

Further in the lecture the problem of only primary, insulin-dependent diabetes will be considered.

PATHOGENESIS.

The development of autoimmune insulin (i.e., the production of antibodies to beta cells of islets of Langerhans). Apparently, there is a base, the background for the development of this process is a genetically determined disease. In 11-60% of cases of diabetes, heredity can be traced. There may be a monogenic inheritance variant transmitted in an autosomal recessive fashion. But more often it is a polygenic type of inheritance (there is a certain anomaly of the constitution at the molecular cellular level, which is realized under the influence of external factors and leads to the development of autoimmune insulin).

Risk factors:

1. 1. Obesity (exogenous-constitutional, excessive intake of easily digestible carbohydrates leads to an increase in the volume of islets of Langerhans and hyperplasia.  
2. 2. Mental trauma (a child’s life in a state of chronic stress, while the activity of the sympathetic nervous system increases, accompanied by an increase in the level of catecholamines and a second negative effect on the synthesis of insulin).  
3. 3. Infections (viral: rubella, enterovirus infection, chickenpox, cytomegalovirus infection, mumps, viral hepatitis).  

The combination of hereditary factors with risk factors, in some way affects homeostasis with the development of autoimmune insulin. There is a latent period of development of insulin before the onset of clinical and laboratory manifestations of the disease (signs of insulin deficiency). The clinic appears only when 80-90% of beta cells are affected. 

The pathogenesis of autoimmune insulin.

Autoimmune inflammation develops in the area of ​​islets of Langerhans with mononuclear cell infiltration. Cells involved in inflammation acquire cytotoxic properties and damage the tissue of the islets. Also, cytotoxic effects are possessed by CECs, which have a killer effect. As a result, we see the defeat of 80-90% beta cells. At this level, the first signs of the disease appear , when it is still possible to control glycemia (the “honey period” of diabetes mellitus). Further, as a result of a continuous process, all beta cells are affected and absolute insulin deficiency develops. The next stage in the development of the lesion is damage to other endocrine cells of the pancreas: alpha (produce glucagon), D-cells (somatostatin), that is, impaired synthesis, the production of contrainsular hormones, which leads to the development of difficultly controlled hypoglycemia. 

CLINIC.

1. 1. The early stages  

• prediabetes
• latent diabetes
• mild manifest diabetes
• forms of diabetes in which the reverse development and use of diet alone is possible

1. 2. Late  

• medium and heavy forms
• diabetic ketoacidosis
• diabetic coma

The concept of potential diabetes. We are talking about children at risk:

• close diabetes
• mothers have a history of miscarriages, stillbirths
• birth weight more than 4000 g,
• children who develop symptoms of paratrophy and subsequently obesity
• children with unmotivated symptoms of hypoglycemia
• with symptoms of a carbohydrate metabolism disorder (enzymatic deficiency)

these children should be closely monitored.

Stage of diabetes.

Prediabetes. Changes in fasting sugar during the day are not detected, and when the sugar curve is drawn, its type is not diagnostic. This stage can be detected in one of the identical twins, if the second one suffers from diabetes.

Latent diabetes mellitus.

n Fasting sugar and glycemia during the day are normal

n diabetic type of sugar curve during glucose tolerance test

n lack of glucosuria

n the clinic is characterized by the presence of poorly healing wounds, cuts, a tendency to furunculosis.

n Mild symptoms of retinopathy (in 4.5% of cases).

Obvious diabetes.

n Fasting hyperglycemia

n change in glycemia during the day

n glucosuria, polyuria

n polydipsia

n weight loss

By severity.

1. 1. Lightweight  
2. 2. Moderate to severe form  
3. 3. Severe   

The clinical picture.

The triad of symptoms comes first.

n Polydipsia (thirst). Its cause is hyperglycemia and polyuria is compensatory in nature for the dilution of blood sugar. Up to 6 liters of fluid per day.

n Polyuria (compensatory adaptive reaction).

n Weight loss. Due to dehydration, metabolic disorders – increased glycolysis, impaired protein and fat metabolism – proteins and fats are actively broken down, and decreased appetite.

n Dry pale skin with reddish spots on the cheeks and cheekbones (manifestation of dystrophic changes associated with a change in the microvasculature) – diabetic rubeosis

n on the skin of the palms of the hands, feet, yellowish elements appear – xanthomatosis, which is based on the deposition of carotene in the surface layers of the skin, since it is poorly absorbed

n recurrent pyoderma (since local skin resistance decreases).

n Lipoid necrobiosis (plaques protrude above the surface of the skin with point necrosis in the center) at the heart of a violation of lipid metabolism.

n Girls – symptoms of vulvovaginitis 

n changes in the muscle system: symptoms of hypotension, decreased physical strength, in the subsequent development of muscle atrophy; gradual growth lag. However, in the early stages of the development of diabetes, growth advances are different (since there is a compensatory increase in the secretion of antagonists – insulin, including somatostatin).

n Microangiopathies are at the heart of the cardiovascular syndrome, therefore, muffled heart sounds, systolic murmur, rhythm disturbance, sometimes expanding the borders to the left, sometimes lowering blood pressure. In severe cases of diabetes, the development of symptoms of heart failure is observed. Microangiopathies also underlie eye damage in diabetes, leading to neuroretinopathy (a change in the microvasculature of the retina leads to the development of cataracts).

n Intracapillary glomerulosclerosis. Renal permeability threshold for glucose: glucosuria develops when the blood sugar level is more than 5.6 -11.1 mmol / l. It is interesting that in diabetes mellitus there is no correlation of glucosuria and hyperglycemia, and, apparently, this is due to intercapillary glomerulosclerosis. Symptoms of glomerulonephritis are manifested: edema, proteinuria, hypercholesterolemia, hyperazotemia – up to the development of uremia, severe renal failure. At the heart of this symptomatology are violations of the microvasculature of the kidneys and trophic changes due to which nephron function is impaired 

n diabetic encephalopathy is manifested by symptoms of a violation of the central and autonomic nervous system, peripheral nervous structures (development of paresis, paralysis, polyradiculitis).

n Symptoms of involvement in the pathological process of the digestive system (damage to the parathyroid and salivary glands, the development of periodontal disease, erosive-ulcerative conditions, inflammatory changes, liver involvement up to the development of cirrhosis.

Manifestations of diabetes in infants.

• Thirst
• stopping weight gain or weight loss, flattening weight curves
• unusual anxiety that goes away after drinking
• the phenomenon of starched diapers (due to glucosuria).
• Dry skin, pyoderma, persistent diaper rash
• the debut of diabetes can be different: gradual or acute, with the development of symptoms of intoxication and dehydration.
• In severe cases, fasting hyperglycemia may be absent. 

Laboratory diagnostics.

1. 1. Examination of fasting blood sugar  
2. 2. The study of fluctuations in blood sugar during the day  
3. 3. glucose tolerance test  
4. 4. urine quality response to sugar  
5. 5. prednisone glucose tolerance test  

TREATMENT.

Therapy is based on 2 provisions: normalization of the diet, an attempt to compensate for insulin deficiency. At some stage, you can do only diet. This is possible in cases of latent diabetes, with the level of glycemia in the dynamics of the glucose tolerance test (one hour after exercise 10-10.8, after 2 hours – 7.2-8.3 mmol / l; in the period of persistent remission (aglycosuria).

The principles of diet therapy.

1. 1. The caloric value and the ratio of proteins, fats, carbohydrates should be close to physiological for preschoolers: 1: 0.7-0.8: 3-4 (approximately the norm is 1: 1: 5-6)   
2. 2. the first 3-6 months. From the beginning of treatment, a significant limitation of products containing rapidly absorbed carbohydrates, or their complete exclusion (sugar, confectionery, semolina, rice, pasta, white flour noodles, etc.) is necessary. They are replaced by potatoes, brown bread, cereals, buckwheat (their composition is difficult to digest carbohydrates). It is recommended that the diet include up to 300-400 g of fruit, excluding grapes, figs, sweet pears, bananas, cherries. In order to somehow diversify the diet, you can replace the products with equivalent ones: 25 g of brown bread = 70 g of potato = 15 g of cereal (wheat, rye, oats).  
3. 3. Normalization of lipid metabolism. You can use food additives (polyene, omega-3 fats).  
4. 4. When normoglycemia and aglycosuria are achieved, an expansion of the diet begins, through training introductions of new products.  
5. 5. It is necessary to adapt the introduction of food to the time of administration of insulin.  
6. 6. If hyperglycemia reappears during the expansion of the diet, it is necessary to connect insulin preparations.  

Insulin therapy.

1. 1. Short-acting insulins (up to 8 hours). – Pork insulin, huinsulin, etc.  
2. 2. Preparations of semi-prolonged action (from 10 to 16 hours): semilent, insulin B,  
3. 3. Long-acting drugs (22-24 hours): insulin monotard.  

In the debut of the disease, the dose of insulin is 0.5 units. per kg per day. Then 0.7 – 1 unit. per kg per day. An individual approach is required in accordance with the level of glycemia: 1 unit. insulin reduces blood glucose by 2.3 mmol / L. 1% hyperglycemia corresponds to the introduction of 2-4 units. Insulin. Control of insulin administration is more reliable in terms of glycemia rather than glucosuria. 

Insulin preparations are administered 3 times a day:

1. 1. before breakfast  
2. 2. before lunch  
3. 3. before dinner in 30 minutes.  

In the morning, long and short-acting insulin is administered in different syringes. Before lunch and dinner, short-acting insulin is administered. Long-acting insulin is 50% of the daily dose of insulin. Intensive insulin therapy tactics are recommended. Patients and their parents are taught to determine the level of glycemia and calculate the dose of insulin. A sick child needs psychological support, the organization of an optimal regime of the day, nutrition, and sanitation of foci of infection