Nutrition for carbohydrate intolerance. National strategy for feeding infants in their first year of life

T.E. Borovik, E.A. Roslavtseva, G.V. Yatsyk, V.A. Skvortsova, N.N. Semyonova,
State Institution Scientific Center for Children's Health of the Russian Academy of Medical Sciences

Intolerance to carbohydrates

Disorders of hydrolysis and absorption of carbohydrates are manifested by similar symptoms - the so-called fermentative, acidic or osmotic diarrhea, which is explained by the same development mechanisms.

In the absence or insufficient activity of the enzyme involved in the hydrolysis of one or another carbohydrate, disaccharides and / or monosaccharides, not absorbed and remaining in the intestinal lumen, having high osmotic activity, promote the release of water and electrolytes into the intestinal lumen (osmotic diarrhea), stimulate motility upper gastrointestinal tract. As a result, excess carbohydrates enter the colon. In the large intestine, they are actively fermented by the intestinal microflora with the formation of organic acids, hydrogen gas, methane, carbon dioxide and water, which causes flatulence, colic, increased peristalsis and accelerates the passage of the chyme through the intestine. The child develops frequent (8-10 times a day or more) liquid, frothy stools with a sour odor, leaving a large watery spot on the diaper. In this case, the pH of the intestinal contents changes to the acidic side (pH less than 5.5). In children of the first year of life, carbohydrates are found in feces - more than 0.25 g%. In some cases, dehydration may develop, rarely - the development of severe malnutrition.

Lactase deficiency (LN) is the most common form of disaccharidase deficiency, which develops as a result of a decrease or complete absence of the enzyme lactase-phlorizin-hydrolase in enterocytes of the mucous membrane of the small intestine. This enzyme is one of the most vulnerable enzymes in the small intestine. It is superficially located, and its concentration is much lower than that of other enzymes of parietal digestion. Lactase activity in premature babies (from 28th to 34th week of gestation) is only 30% of its level in full-term babies. The maximum activity of the enzyme is reached by 2-4 months of age.

The severity of clinical symptoms in FN is determined by the total degree of decrease in the enzyme activity, the amount of lactose ingested with food, the nature of the intestinal microflora, as well as individual pain sensitivity to intestinal distension by gases.

Distinguish between primary LN associated with congenital enzymatic insufficiency, and secondary LN, which develops as a result of damage to the enterocyte in infectious, inflammatory, autoimmune bowel diseases, as well as lactose intolerance in the syndrome of "short bowel".

Most often, pediatricians meet with hypolactasia in children during the first months of life. Clinical symptoms (flatulence, colic, diarrhea) usually appear in a child at 3-6 weeks of life, which is apparently associated with an increase in the volume of milk or formula. In the anamnesis of such children, as a rule, there are indications of a complicated course of pregnancy and childbirth (hypoxia), and symptoms of adult-type FN are often detected in the closest relatives. In infants with signs of hypoxic lesions of the central nervous system, the so-called "locking" form of lactase deficiency is sometimes observed, which is characterized by the absence of independent stool in the presence of liquid feces and the other symptoms listed above. Usually, the symptoms in most children stop at 5-6 months (by the time of the introduction of complementary foods) and are not traced in the future, so this type of lactose intolerance can hardly be attributed to primary.

Diet therapy

The approach to treatment should be differentiated depending on the nature of feeding (natural or artificial), the degree of enzymatic deficiency (alactasia, hypolactasia), the genesis of fermentopathy (Table 1).

Table 1
The scheme of correction of lactase deficiency in children of the first year of life With natural feeding With artificial feeding

Maximum complete and long-term preservation of mother's milk in the baby's nutrition
Purpose of the enzyme: Lactase or Lactase Baby
Only if the enzyme is ineffective (while maintaining pronounced anxiety, colic, the appearance of symptoms of dehydration, insufficient weight gain) is it possible to partially replace breast milk with a lactose-free milk mixture by 1 / 3-2 / 3 of the volume of each feeding Partial or complete replacement of milk mixtures with low-lactose or lactose-free mixtures depending on lactose tolerance and the nature of concomitant pathology

With primary alactasia of newborns (it is extremely rare), the child is immediately and completely transferred to feeding with a lactose-free milk formula.

With hypolactasia, if the child is breastfed, a decrease in the amount of human milk is undesirable. The best option is to use lactase preparations. Lactase Baby (700 units) is prescribed 1 capsule per feeding. The dose of the enzyme preparation is mixed with 20-30 ml (1/3 of the feeding volume) of expressed milk and the baby is given this mixture before breastfeeding. The effectiveness of the preparations increases if expressed milk with lactase is left for fermentation for 15 minutes, as well as when the entire volume of milk is treated with lactase. It is possible to use the drug Lactase (3450 units), starting with 1/4 of the capsule per feeding.

If the use of the enzyme is ineffective (which is usually observed with a pronounced decrease in lactase activity), they resort to reducing the lactose load by replacing from 1/3 to 2/3 of the volume of each feeding with a lactose-free milk mixture, after which the child is supplemented with human milk (Table 2). The lactose-free mixture is introduced into the diet gradually, at each feeding, bringing within 3-5 days to the required amount, which is judged by a decrease in flatulence, restoration of the normal consistency of feces and stool frequency, a decrease in the excretion of carbohydrates with feces, and an increase in fecal pH. Typically, the volume of the lactose-free product is 30-60 ml for each feeding.

table 2
Chemical composition and the energy value low-lactose and lactose-free milk mixtures (in 100 ml of ready-made formula)
Name of the mixture Chemical composition, g Energy
value,
kcal
Proteins fats carbohydrates
total lactose

Lactose-free mixtures
Babushkino Lukoshko
(mixture without lactose; Russia) 1.69 3.38 7.56 0 67.37
NAN *, ** Lactose-free
(Switzerland) 1.4 3.3 7.8 0 67
Nutrilak Lactose-free (Russia) 1.4 3.45 7.4 0 66
Nutrilak Lactose Free Plus *
(Russia) 1.6 3.5 7.3 0 66.3
Enfamil Lactofree (USA) 1.42 3.7 7.2< 0,1 68

Low-lactose mixtures
Nutrilak Low-lactose (Russia) 1.6 3.5 7.3 0.9 66.3
Nutrilon Low-lactose
(Holland) 1.4 3.6 7.1 1.33 66
Humana PL (Germany) 1.8 2.0 9.2 1.1 62
Humana LP + SCT (Germany) 1.9 2.0 8.9 0.5 61

Introduced:
* nucleotides;
** arachidonic and docosahexaenoic acids.
In case of hypolactasia, if the child is bottle-fed, a low-lactose mixture should be selected with as much lactose as the patient can tolerate, preventing the appearance of clinical symptoms and an increase in the excretion of carbohydrates in the feces. A low-lactose formula is introduced into each feeding, gradually replacing the infant formula with it. Small amounts of lactose entering the colon are a natural prebiotic necessary for the proper formation of microflora. Lactose is also the only source of galactose, which is produced when it breaks down. Galactose is used for the synthesis of galactolipids, including cerebrosides, which are necessary for the formation of central nervous system and myelination of nerve fibers, as well as for the synthesis of mucopolysaccharides (hyaluronic acid), which are part of the vitreous body and synovial fluid. Complementary foods for children of the first year of life with FN are prepared not with milk, but with the low- or lactose-free formula that the child receives. From 4-4.5 months of age, industrial fruit purees or a baked apple are prescribed. It is advisable to prescribe porridge (rice, corn, buckwheat) or mashed vegetables with coarse vegetable fiber (cauliflower, zucchini, pumpkin, carrots) with the addition of vegetable oil as the first main food (from 5 months). After 2 weeks, meat puree is introduced. Fruit juices (diluted with water 1: 1) are introduced into the diet of these children later, usually after 6 months. In children of the second half of life, it is possible to use dairy products, where the lactose content is insignificant: cottage cheese washed from whey, butter, hard cheese.

In primary (constitutional) lactase deficiency, a low-lactose diet is prescribed for life.

With secondary hypolactasia, the symptoms of lactase deficiency are transient. Therefore, upon reaching remission of the underlying disease after 1-3 months, the diet should be gradually expanded by introducing milk mixtures containing lactose, under the control of clinical symptoms (diarrhea, flatulence) and the excretion of carbohydrates in the feces.

Congenital sucrase-isomaltase deficiency is a relatively rare disease among Europeans, inherited in an autosomal recessive manner. Enzyme deficiency is not a life-threatening condition. It appears for the first time when sucrose is introduced into the child's diet ( fruit juices, mashed potatoes, sweetened water or tea), less often - starch and dextrins (porridge, mashed potatoes) in the form of severe "carbohydrate" diarrhea with crises of dehydration. With age, children often acquire the ability to tolerate increasing amounts of dextrins, starch and sucrose without increasing the activity of the enzyme, which is associated with an increase in the absorption surface of the mucous membrane. Often, patients develop an aversion to sweet foods, fruits, starchy foods, that is, self-regulation of the flow of sucrose into the child's body occurs.

Any damage to the intestinal epithelium can lead to secondary deficiency of sucrase-isomaltase (infectious enteritis, giardiasis, celiac disease, radiation enteritis), but the activity of the enzyme does not drop to that extremely low level, as is the case with primary insufficiency.

Diet therapy

The mainstay of dietary therapy is the elimination of sucrose and, sometimes, a reduction in the amount of starch and dextrins in the diet. With primary (congenital) sucrase-isomaltase deficiency, children usually tolerate lactose well. Therefore, when choosing a formula for such a child, it is preferable to preserve breastfeeding for the longest possible time, and in its absence, it is necessary to prescribe an infant milk formula with a lactose carbohydrate component. With secondary (post-infectious) sucrase-isomaltase deficiency, lactase deficiency occurs and combined disaccharidase deficiency is formed.

Children with sucrase-isomaltase deficiency cannot tolerate fruits, berries, vegetables, juices with a high sucrose content (peaches, apricots, tangerines, oranges, melons, onion, beets, carrots), as well as foods rich in starch (cereals, potatoes, bread, jelly). It is recommended to start the introduction of complementary foods with vegetable puree, practically free of sucrose and starch (Table 3). You can sweeten your food with glucose or fructose. In the second year of life, it is usually possible to expand the diet by introducing a small amount of starch-containing foods (vegetables, cereals, potatoes).

Table 3
Vegetables and fruits containing minimal amounts of sucrose and starch
Basic carbohydrate -
fructose Main carbohydrate -
glucose
cauliflower tomato
broccoli lemons
brussels sprouts cherry
spinach cranberry
sea buckthorn salad
green beans
sorrel
green pea

With secondary intolerance to sucrose, the duration of its exclusion depends on the severity of the underlying disease and the success of treatment. It is recommended to compensate for the carbohydrate deficiency by parenteral and / or enteral administration of glucose solutions. The elimination period for sucrose, in contrast to lactose, is shorter and can be limited to 10-15 days.

Starch intolerance can occur in premature babies and children of the first half of life, in whom the activity of pancreatic amylase is physiologically reduced, as well as with exocrine pancreatic insufficiency, therefore, they are not shown the appointment of mixtures containing starch in the carbohydrate component.

In congenital (primary) malabsorption of glucose-galactose, there is a defect in the transport systems of the brush border of enterocytes, while the activity of disaccharidases and hydrolysis of carbohydrates are not impaired. This rare pathology is inherited in an autosomal recessive manner; manifests itself as profuse diarrhea and dehydration after the first feeding of the newborn. Replacing milk with lactose-free and dairy-free mixtures has no effect. The only monosaccharide that can be absorbed in the small intestine is fructose. The means of choice is to switch the child to full parenteral nutrition. Against the background of parenteral nutrition, feeding begins with a dosed administration of a 2.5% fructose solution, the concentration of which, in the absence of diarrhea, is increased to 7-8%. Next, a source of protein (protein preparation or meat puree), fat (vegetable oil or fat emulsion, starting with 1-2 drops) is introduced. In the future, the expansion of the diet is carried out at the expense of fructose vegetable puree. The prognosis of the disease with total glucose-galactose malabsorption is very serious. Surviving children with a partial defect in the glucose-galactose transport system suffer from chronic diarrhea and lag behind in physical development.

Acquired monosaccharide intolerance manifests as severe chronic delayed diarrhea physical development... It can accompany the course of severe intestinal infections in children of the first months of life with an unfavorable premorbid background, occur as a result of atrophy of the villi of the intestinal mucosa in celiac disease, intolerance to cow's milk proteins, protein-energy deficiency. The baby's diarrhea diminishes when he is fasting and returns when the amount of oral feeding increases. Low pH and high concentration of glucose and galactose in feces are characteristic. Therapy with lactose-free and dairy-free formulas is ineffective.

Acquired intolerance to monosaccharides is a transient state, however, it has a total character: glucose, galactose, fructose are not absorbed, the hydrolysis of di- and polysaccharides is also impaired. Oral rehydration with standard solutions is ineffective because of the glucose they contain. The patient's condition requires transfer to full parenteral nutrition. The introduction of glucose orally begins cautiously, with a 2.5% solution against the background of a stable state and the absence of diarrhea, with a gradual increase in the concentration of the solution. When the 5% glucose mixture is well tolerated, parenteral nutrition can be discontinued. The introduction of higher concentrations of glucose, starch can provoke diarrhea again, which requires repeated unloading. When a good tolerance of glucose, dextrins, starch is achieved, sucrose solutions are gradually introduced, starting with a 3-5% concentration, fruit puree, juices diluted with water 1: 1; and no earlier than in 1-2 months, you can try to introduce infant formula with a moderately reduced concentration of lactose.

CELLIACIA (GLUTEN ENTEROPATHY)

This autoimmune disease is characterized by damage to the mucous membrane of the small intestine - T-cell-mediated atrophic enteropathy in genetically predisposed individuals under the influence of proteins (prolamins) of the grain of some cereals: wheat gliadin, rye secalin, barley chordin, oat avenin. In the medical literature, proteins of cereals that are toxic to celiac disease are usually combined with the term "gluten". Celiac disease is characterized by persistent, lifelong gluten intolerance.

Symptoms of typical celiac disease develop in children, as a rule, 4-8 weeks after the introduction of gluten-containing complementary foods (semolina, wheat, oatmeal, biscuits, crackers, dryers, noodles) into the diet, usually at the age of 6-8 months to 1, 5-2 years old, however, they can first appear at any age.

Diet therapy

The only method of treating the disease and preventing complications of celiac disease is a strict and lifelong gluten-free diet. All foods and dishes containing wheat, rye, barley and oats, as well as industrial products, in which gluten-containing components are included in the form of additives - thickeners, shapers, stabilizers, are excluded from the diet (Table 4). Rice, buckwheat, corn, millet are considered non-toxic cereals for celiac disease. The question of the safety of oats for children early age is under discussion, needs further study. Flour and starches made from potatoes, tapioca, cassava, sweet potatoes, beans, peas, soybeans, and various nuts are safe.

Table 4
Gluten-free foods and meals excluded from the children's diet for celiac disease
Food Wheat Rye Barley Oats
Cereals, porridge Semolina, wheat, Artek, Poltavskaya, 4 cereals, 7 cereals, spelled Porridge Nordic with rye flakes Barley, pearl barley, barley Oatmeal, Hercules, Sports, oatmeal
Flour and bran Wheat flour and bran Rye flour and bran Oat flour
Baby milk formula Malyutka plus 2 with oat flour
Children's cereals Based on wheat, semolina and flakes, mixed cereal porridge, 7 cereals 7 cereals, mixed cereal Gerber barley
porridge, Beech Nut
barley
7 cereals, porridge
from mixed
cereals All ready-made cereals with oat flour and cereals, welling multi-cereal and oatmeal, 7 cereals, mixed cereal porridge
Canned food for children Canned food for baby food with meat, fish, vegetables, fruits, yoghurt, cream, etc. with additives wheat flour, semolina, pasta (see the composition on the package) Children's meat and vegetables, fish, fruit canned food with oatmeal (see the composition on the package)
Bread and bakery products, confectionery Bread, dryers, rusks, cookies, bagels, bagels, straws, crispbread, muffins Rye bread,
tortillas,
rusks Barley cakes breakfast cereals with barley syrup Bread, Hercules
Pasta Pasta, noodles, horns, spaghetti, noodles, curly products

The composition of the diet of a patient with celiac disease depends on the age, severity of the condition and the period of the disease and is based on general principles: the carbohydrate component is made up of portable cereals, potatoes, legumes, vegetables, fruits and berries; protein and fat - due to meat, eggs, fish, dairy products, vegetable and butter.

The acute period of celiac disease in early childhood is characterized by severe dyspeptic disorders and nutritional disorders up to dystrophy and the development of secondary transient food intolerance. Most often this is lactase deficiency, which requires the exclusion of lactose-containing dairy products in almost all patients in the acute period of the disease. Two-thirds of young children have an intolerance to cow's milk proteins, which requires the temporary elimination of all dairy products from the diet. Sensitization to other food proteins is often observed - rice, bananas, proteins chicken eggs etc. The lack of protein in such patients is compensated for with the help of meat-based products - canned meat for children of domestic and foreign production, as well as mixtures based on soy protein isolate.

In children with severe dystrophy, a high degree of polyvalent sensitization, specialized mixtures based on highly hydrolyzed protein can serve as an important source of protein, but their use is limited due to the specific organoleptic properties of these products (children with reduced appetite often refuse them).

In severe malnutrition, factors such as severe anorexia, reduced tolerance to food loads must be taken into account, therefore, children are prescribed a diet containing no more than 3-4 g of protein and 120-130 kcal per 1 kg of actual body weight.

The first signs of the effectiveness of treatment in the period of manifestation of celiac disease are an improvement in emotional tone, appetite and the beginning of weight gain, which should be expected after 1-2 weeks of treatment. Unstable stools, abdominal enlargement can persist for quite a long time.

During the period of clinical and morphological remission, the diet is gradually expanded by including products previously eliminated due to transient intolerance. Dairy products are introduced starting with low-lactose ones: cheese, butter, cottage cheese washed from whey, low-lactose milk mixtures. Gradually (taking into account tolerance), fermented milk products (kefir, yogurt) are prescribed, and then (after a year), kashi with diluted milk and whole milk. Just as carefully, under the control of individual tolerance, other previously excluded products, except those containing gluten, are introduced.

Tatiana Eduardovna Borovik, Head of the Department of Nutrition for a Healthy and Sick Child, State Institution SCCH RAMS, Professor, dr honey... sciences
Elena Aleksandrovna Roslavtseva, Senior Researcher, GU SCCH RAMS, Cand. honey. sciences
Galina Viktorovna Yatsyk, Chief Researcher, State Institution SCCH RAMS, Professor, Dr. med. sciences
Vera Alekseevna Skvortsova, Leading Researcher, State Institution SCCH RAMS, Dr. med. sciences
Natalia Nikolaevna Semyonova, doctor of the GU SCCH RAMS, Ph.D. honey. sciences

How interested are you in raising your life and health by new level? If you are really interested in this, we suggest you take a tolerance test. complex carbohydrates.

Carbohydrates in the diet

The problem is that all organisms are individual and tolerate the same foods in completely different ways. For some, it's completely normal to drink milk every morning with a large butter and cheese sandwich. And for some, such a breakfast will provide a terrible bloating and uncomfortable flatulence throughout the day.

You've probably heard a lot about lactose and gluten intolerance. There is also an intolerance to complex carbohydrates. Why is this happening?

The fact is that some people have a deficiency of one or more essential enzymes in the intestines. It is their absence that prevents complex carbohydrates from being absorbed normally. Fats and carbohydrates in the diet need special enzymes for complete assimilation.

The consequences for the body from such a deficiency are not catastrophic. However, if you constantly consume foods that will not be digested normally, then life will be very uncomfortable. The main side effects will be bloating, abdominal pain, and severe gas, from which colic can occur.

To determine if you have a complex carbohydrate intolerance, use this short list of simple questions:

Do you have excess weight?
Do you often feel tired, especially after a meal high in carbohydrates?
Are you sedentary?
Do you feel like you can't control your appetite?
Do you often crave sweets or starchy foods like bread, pasta, potatoes, or legumes?
Do you feel dizzy when you are hungry?
Sugar level is higher than normal in your blood?
Do you suffer anxiety, depression, skin problems? Do you have hormonal problems or sleep disorders?

If you answered yes to one or more questions, try cutting out all grains, legumes, starchy vegetables (carrots, corn, potatoes) and fruits from your diet.

Two weeks later, again answer questions 2, 5, 6 and 8. If you see a significant change, most likely you have intolerance to complex carbohydrates.

If, nevertheless, you find that you have this intolerance, it’s not a problem at all! Healthy low carb diet can help normalize blood pressure as well as significantly reduce sugar cravings. The feeling of constant hunger will go away, and the skin and digestion will noticeably improve.

How exactly should you change your diet?

Intolerance to complex carbohydrates is an unpleasant thing, but there is nothing really terrible about it. Try to follow these simple guidelines and replace the foods on the list with lower-carb options.

Remember, it's not just carbohydrate intolerance that can cause gas! You can find out more about the causes of flatulence on our website.

But what to do if your body lets you down at the most awkward moments? We will tell you!

Disorders of hydrolysis and absorption of carbohydrates are manifested by similar symptoms of the so-called "fermentative", "acidic" or "osmotic" diarrhea, which is explained by the same mechanisms of development.

Clinical symptoms of carbohydrate intolerance

frequent (8-10 times a day or more) liquid, frothy stools with a large water spot and a sour odor;
acidic stool (pH less than 5.5);

In the absence or insufficient activity of the enzyme involved in the hydrolysis of one or another carbohydrate, disaccharides and / or monosaccharides not absorbed and remaining in the intestinal lumen, having high osmotic activity, promote the release of water and electrolytes into the intestinal lumen (osmotic diarrhea), stimulate the motility of the upper parts of the gastrointestinal tract, as a result of which excess carbohydrates enters the large intestine. In the large intestine, they are actively fermented by the intestinal microflora with the formation of organic acids, hydrogen gas, methane, carbon dioxide and water, which causes flatulence, colic, increased peristalsis and accelerates the passage of the chyme through the intestine. In this case, the pH of the intestinal contents changes to the acidic side. Violation of the normal chemical composition of intestinal contents can contribute to the development of dysbiosis.

Lactase deficiency (ICD-10 E73) is the most common form of disaccharidase deficiency, which develops as a result of a decrease or complete absence of the enzyme lactase-phlorizin-hydrolase in enterocytes of the mucous membrane of the small intestine. This enzyme is one of the most vulnerable enzymes in the small intestine. It is superficially located, and its concentration is much lower than that of other enzymes of parietal digestion. In premature infants (from 28 to 34 weeks of gestation), lactase activity is only 30% of its level in term infants. The maximum activity of the enzyme is observed at the age of 2-4 months.

Most often, pediatricians meet with hypolactasia in children during the first months of life.

Clinical symptoms (flatulence, colic, diarrhea) usually appear in a child at 3-6 weeks of age, which, apparently, is associated with an increase in the volume of milk or milk formula. In the anamnesis of such children, as a rule, there are indications of a complicated course of pregnancy and childbirth (hypoxia), and symptoms of adult-type FN are often detected in the closest relatives. In infants with signs of hypoxic lesions of the central nervous system, the so-called "locking" form of lactase deficiency is sometimes observed, which is characterized by the absence of independent stool in the presence of liquid feces and the other symptoms listed above. Usually, the symptoms in most children stop at 5-6 months (by the time of the introduction of complementary foods) and are not traced in the future, so this type of lactose intolerance can hardly be attributed to primary.

The approach to treatment should be differentiated depending on the nature

feeding (natural or artificial), the degree of enzymatic deficiency (alactasia, hypolactasia), the genesis of fermentopathy (primary or secondary) table. 35.

Table 35. Scheme of correction of lactase deficiency in children of the first year of life

With breastfeeding

With artificial feeding

the most complete and long-term preservation of mother's milk in the baby's nutrition

partial or complete replacement of milk formulas with low-lactose or lactose-free formulas, depending on lactose tolerance and the nature of the concomitant pathology

enzyme purpose: lactase or baby lactase

in case of ineffectiveness (persistence of pronounced anxiety, colic, symptoms of dehydration, insufficient weight gain) - partial replacement of breast milk lactose-free milk mixture for 1/3 2/3 of the volume of each feeding

With primary alactasia of newborns, which is extremely rare, the child is immediately and completely transferred to feeding with a lactose-free milk formula.

With hypolactasia, when the child is breastfed a decrease in the amount of breast milk is undesirable. The best option is to use lactase preparations ("Lactase baby" (National Enzyme Company, USA, in 1 capsule 700 units (7 mg), 1 capsule per feeding). drink to the baby before breastfeeding.

The effectiveness of the preparations increases if expressed milk with lactase is left for fermentation for 15 minutes, as well as when the entire volume of milk is treated with lactase. It is possible to use "Lactase" (Enzyme Lactase from Nature's Way Products, Inc., USA, in 1 capsule 3450 units, starting from 1/4 capsule per feeding).

If the use of the enzyme is ineffective (which is usually observed with a pronounced decrease in lactase activity), they resort to reducing the lactose load by replacing from 1/3 to 2/3 of the volume of each feeding with a lactose-free milk mixture (Table 36), after which the child is supplemented with human milk. The lactose-free mixture is introduced into the diet gradually, at each feeding, bringing within 3-5 days to the required amount, as judged by the decrease in flatulence, the restoration of the normal consistency of feces and stool frequency, a decrease in the excretion of carbohydrates in the feces, and an increase in the pH of the feces. Typically, the volume of lactose-free product is ml for each feeding.

Table 36. Chemical composition and energy value of low-lactose and lactose-free milk mixtures (in 100 ml of ready-made formula)

Firm, country of origin

Energy value, kcal

Nutritek Group, Russia

Mead Johnson, USA

At artificial feeding a low-lactose mixture should be selected with such an amount of lactose that the patient will tolerate, preventing the appearance of clinical symptoms and an increase in the excretion of carbohydrates in the feces. A low-lactose formula, by introducing it into each feeding, is gradually replaced with infant formula. Small amounts of lactose entering the colon are a natural prebiotic necessary for the proper formation of microflora. Lactose is also the only source of galactose, which is produced when it breaks down. Galactose is used for the synthesis of galactolipids, including cerebrosides, which are necessary for the formation of the central nervous system and myelination of nerve fibers, as well as for the synthesis of mucopolysaccharides (hyaluronic acid) that make up the vitreous humor and synovial fluid.

Complementary foods for children of the first year of life with FN are prepared not with milk, but with the low- or lactose-free formula that the child receives. From 4-4.5 months of age, industrial fruit purees or a baked apple are prescribed. It is advisable to prescribe porridge (rice, corn, buckwheat) or mashed vegetables with coarse vegetable fiber (cauliflower, zucchini, pumpkin, carrots) with the addition of vegetable oil as the first main complementary food (from 4.5 to 5 months). After 2 weeks, meat puree is introduced. Fruit juices (diluted with water 1: 1) are introduced into the diet of such children later, as a rule, in the second half of their life. In children of the second half of the year, it is possible to use dairy products, where the lactose content is insignificant - cottage cheese washed from whey, butter, hard cheese.

In primary (constitutional) lactase deficiency, a low-lactose diet is prescribed for life.

With secondary hypolactasia, the symptoms of lactase deficiency are transient. Therefore, after reaching remission of the underlying disease after 1 to 3 months, the diet should be gradually expanded by introducing lactose-containing milk formulas, under the control of clinical symptoms (diarrhea, flatulence) and the excretion of carbohydrates in the feces.

Congenital sucrase-isomaltase deficiency is a rare disease among Europeans and is inherited in an autosomal recessive manner. Enzyme deficiency is not a life-threatening condition. It manifests itself for the first time when sucrose (fruit juices, mashed potatoes, sweetened water or tea) is introduced into the child's diet, less often starch and dextrins (porridge, mashed potatoes) in the form of severe "carbohydrate" diarrhea with dehydration crises. With age, children often acquire the ability to tolerate increasing amounts of dextrins, starch and sucrose without increasing the activity of the enzyme, which is associated with an increase in the absorption surface of the mucous membrane. Often, patients develop an aversion to sweet foods, fruits, starchy foods, that is, self-regulation of the flow of sucrose into the child's body occurs.

Any damage to the intestinal epithelium can lead to secondary deficiency of this enzyme (infectious enteritis, giardiasis, celiac disease, radiation enteritis), but the activity of the enzyme does not drop to that extremely low level, as is the case with primary failure.

The mainstay of diet therapy in this condition is the elimination of sucrose and, sometimes, a decrease in the amount of starch and dextrins in the diet. With primary (congenital) sucrase-isomaltase deficiency, children, as a rule, tolerate lactose well, with secondary (post-infectious) they cannot, i.e. they develop a combined disaccharidase deficiency. Therefore, when choosing a mixture for a child with primary sucrose-isomaltase deficiency, it is preferable to preserve breastfeeding for the longest possible time, and in its absence, it is necessary to prescribe an infant milk formula with a lactose carbohydrate component.

Children with sucrase-isomaltase deficiency cannot tolerate fruits, berries, vegetables, juices with a high sucrose content (peaches, apricots, tangerines, oranges, melons, onions, beets, carrots, etc.), as well as foods rich in starch (cereals, potatoes, bread, jelly, etc.). It is recommended to start the introduction of complementary foods with mashed vegetables, which practically do not contain sucrose and starch (Table 37).

Table 37. Vegetables and fruits containing the minimum amount of sucrose and starch

The main carbohydrate is fructose

Basic carbohydrate glucose

You can sweeten your food with glucose or fructose. In the second year of life, it is usually possible to expand the diet by introducing a small amount of starch-containing foods (vegetables, cereals, potatoes).

At secondary intolerance to sucrose, the duration of its exclusion depends on the severity of the underlying disease and the success of treatment. It is recommended to compensate for the carbohydrate deficiency by parenteral and / or enteral administration of glucose solutions. The elimination period for sucrose, in contrast to lactose, is shorter and may be limited to days.

Starch intolerance can occur in premature babies and children of the first six months of life, in whom the activity of pancreatic amylase is physiologically reduced, as well as with exocrine pancreatic insufficiency, therefore they are not shown

the appointment of mixtures including starch in the composition of the carbohydrate component.

At congenital (primary) malabsorption of glucose - galactose there is a defect in the transport systems of the brush border of enterocytes, while the activity of disaccharidases and hydrolysis of carbohydrates are not impaired. This rare pathology is inherited in an autosomal recessive manner; manifests itself as profuse diarrhea and dehydration after the first feeding of the newborn. Replacing milk with lactose-free and dairy-free mixtures has no effect.

The only monosaccharide that can be absorbed in the small intestine is fructose.

The means of choice is to switch the child to full parenteral nutrition. Against the background of parenteral nutrition, feeding begins with dosed administration of a 2.5% fructose solution, the concentration of which, in the absence of diarrhea, is increased to 7 8%. Next, a source of protein (protein preparation or meat puree), fat (vegetable oil or fat emulsion, starting with 1 2 drops) is introduced. In the future, the expansion of the diet is carried out at the expense of mashed potatoes from fructose-containing vegetables. The prognosis of the disease with total glucose-galactose malabsorption is very serious. Surviving children with a partial defect in the glucose-galactose transport system suffer from chronic diarrhea and lag behind in physical development.

Acquired intolerance to monosaccharides is manifested by severe chronic diarrhea with delayed physical development. It can accompany the course of severe intestinal infections in children of the first months of life with an unfavorable premorbid background, occur as a result of atrophy of the villi of the intestinal mucosa in celiac disease, intolerance to cow's milk proteins, protein-energy deficiency. The baby's diarrhea diminishes when he is fasting and returns when the amount of oral feeding increases. Low pH and high concentration of glucose and galactose in feces are characteristic. Therapy with lactose-free and dairy-free formulas is ineffective.

The introduction of oral glucose is started cautiously, with a 2.5% solution against the background of a stable state and the absence of diarrhea, with a gradual increase in the concentration of the solution. When the 5% glucose mixture is well tolerated, parenteral nutrition can be discontinued. The introduction of higher concentrations of glucose, starch can provoke diarrhea again, which requires repeated unloading. When good tolerance of glucose, dextrins, starch is achieved, sucrose solutions are gradually introduced, starting with 3-5% concentration, fruit puree, juices diluted with water 1: 1, and no earlier than 1-2 months later, you can try to introduce infant milk mixture with moderately reduced concentration of lactose.

Materials for this chapter are also provided by: Ph.D. E.A. Roslavtseva

Diagnosis by symptoms

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Carbohydrate intolerance in adults and children: symptoms, causes, treatment, diagnosis

Carbohydrate intolerance is the inability to assimilate certain types of carbohydrates due to a deficiency of one or more intestinal enzymes.

Clinical manifestations include diarrhea, bloating, and gas. Diagnosis is clinical and H2-breath test results. Treatment consists in excluding the use of the "guilty" disaccharide.

Pathophysiology of carbohydrate intolerance

Normally, disaccharides are broken down to monosaccharides by disaccharidases (in particular, lactase, maltase, isomaltase, sucrase [invertase]) located on the brush border of enterocytes. Unsplanted disaccharides have a high osmolarity, which attracts water and electrolytes to the intestinal lumen, resulting in watery diarrhea. Due to the processing of carbohydrates by the microflora, gases (H 2, CO 2, methane) are formed in the colon, which is accompanied by excess gas, bloating and distension of the abdomen, and the appearance of abdominal pain.

Causes of carbohydrate intolerance

Disaccharidase deficiency in origin can be congenital, acquired (primary) and secondary. Congenital failure (in particular, sucrase isomaltase deficiency) is rare.

Primary lactase deficiency (primary hypolactasia in adults) is the most common form of carbohydrate intolerance. Lactase activity is high in newborns, which promotes the absorption of milk; in most ethnic groups (80% of blacks and Hispanics,> 90% of Asian peoples), its content decreases after weaning, so adolescents and adults sometimes do not tolerate large amounts of lactose. However, 80% of the whites of the Northern European countries produce lactase throughout their lives, so they can tolerate dairy products well. It remains unclear why lactase deficiency in> 75% of the world's population can be considered normal.

Secondary lactase deficiency develops in conditions of damage to the mucous membrane of the small intestine. In young children, transient secondary disaccharidase deficiency complicates intestinal infections or surgery. Resolution of the underlying disease is accompanied by an increase in enzyme activity.

Symptoms and signs of carbohydrate intolerance

The clinical manifestations of all types of disaccharidase deficiency are similar. A child suffering from lactase intolerance, after consuming a significant amount of milk, develops diarrhea, and there may be a lack of weight gain. For adults, after consuming lactose, the development of watery diarrhea, bloating, excess gas, nausea, rumbling in the abdomen, and cramping pain is characteristic. Patients usually recognize the connection between the onset of symptoms and the use of dairy products as early as childhood and try to avoid them. Symptoms usually require dairy products containing 8-12 ounces of milk. Diarrhea can be quite severe and be accompanied by the excretion of others. nutrients that did not have time to be absorbed.

Clinical data.
H 2 breath test for confirmation.

Lactose intolerance can usually be recognized through careful history analysis and the results of a trial elimination diet. Patients usually report diarrhea and / or bloating after consuming dairy products; other symptoms such as rash, wheezing, and other signs of anaphylaxis (especially in infants and older children) indicate an allergy to cow's milk. Milk allergy is rare in adults and may be accompanied by vomiting and signs of gastroesophageal reflux, which do not fit into the picture of disaccharidase deficiency. Disaccharidase deficiency is also indicated by the acidic reaction of feces (pH<6); диагноз можно подтвердить с помощью Н 2 -дыхательного теста или теста переносимости лактозы.

When carrying out the H2-breath test, the patient takes 50 glactose internally, after 2.3 and 4 hours after that, using a special device in the exhaled air, the content of H2 produced by bacteria from the undigested disaccharide is measured. In most patients with lactase deficiency, the H2 content in the exhaled air is> 20 ppm compared to the baseline. Test sensitivity and specificity> 95%.

The lactose tolerance test is less sensitive (about 75%), but its specificity is> 95%. The patient is taking lactose. Determine the glucose content in serum before lactose intake and after 60 and 120 minutes. With lactose intolerance, diarrhea, bloating, discomfort and no increase in blood glucose> 20 mg / dL compared to baseline develop during the course of the mine.

Carbohydrate Intolerance Treatment

Diet restrictions.

Manifestations of malabsorption of carbohydrates respond well to treatment by excluding the use of carbohydrates, the absorption of which is impaired (for example, adherence to a lactose-free diet in cases of lactase deficiency). But due to the large variability in the degree of lactose malabsorption, many patients can tolerate drinking up to 375 ml of milk (18 glactose) or dairy products well. Usually yoghurt is better tolerated because contains a sufficient amount of lactase produced by the Lactobacilli culture. The lactose content of cheese is less than that of milk, and cheese is often well tolerated depending on the amount of food consumed.

If a patient suffering from manifestations of lactase deficiency wants to consume milk, it is advisable to add lactase preparations to it for the preliminary processing of lactose; milk already processed with lactase is commercially available. Enzyme preparations act as an adjunct to dietary restrictions, but not as replacement therapy. Patients with lactase deficiency should take calcium supplements (0 mg / day).

Basic Provisions

Disaccharidase deficiency (usually lactase deficiency) can be acquired, less often congenital.
Undigested disaccharides such as lactose create an osmotic load and cause diarrhea.
Intestinal bacteria metabolize some of the undigested disaccharides, which is accompanied by excess gas and bloating.
The clinical diagnosis is confirmed by the data of the H2-breath test.
Typically, treatment consists of prescribing dietary restrictions.

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Intolerance to carbohydrates

(Lactose intolerance; lactase deficiency; disaccharidase deficiency; glucose-galactose malabsorption; alactasia)

Carbohydrate intolerance - diarrhea and flatulence associated with impaired digestion of carbohydrates due to a lack of one or more intestinal enzymes.

Pathophysiology

Disaccharides are normally broken down into monosaccharides by lactase, maltase, isomaltase, or sucrase (invertase) in the small intestine. Lactase breaks down lactose into glucose and galactose. Undigested disaccharides remain in the intestinal lumen and osmotically retain fluid, contributing to diarrhea. The fermentation of sugar by bacteria in the colon leads to large amounts of gas and acidification of the stool. Since enzymes are located in the brush border of mucosal cells, their secondary deficiency occurs in diseases accompanied by morphological changes in the jejunal mucosa (for example, in celiac disease, tropical sprue, acute intestinal infections, toxic effects of neomycin). In infants, temporary secondary disaccharidase deficiency can be a complication of an intestinal infection or abdominal surgery.

Monosaccharides glucose and galactose are absorbed by active transport in the small intestine (fructose is absorbed passively). In glucose-galactose malabsorption, this transport system is defective, and most sugars cause characteristic symptoms.

Prevalence

Lactase deficiency is normal in about 75% of adults in all ethnic groups, except those from northwestern Europe, where the prevalence of the condition is less than 20%. In the majority of the colored population of North America, lactase deficiency gradually develops with age; however, the statistics are unreliable here. This condition occurs in 90% of the natives of Eastern countries, 75% of American blacks and Indians; it is also very common among the inhabitants of the Mediterranean.

Glucose-galactose intolerance is an extremely rare congenital disorder, as is the deficiency of other enzymes in the intestinal mucosa (eg sucrase, isomaltase).

"Carbohydrate Intolerance" - an article from the Gastroenterology section

Nutrition for carbohydrate intolerance

Clinical symptoms of carbohydrate intolerance

Frequent (8 - 10 times a day or more) liquid, frothy stools with a large water spot and a sour odor;

Bloating, rumbling (flatulence), abdominal pain (colic);

The presence of carbohydrates in feces (more than 0.25 g% in children of the 1st year of life);

Acid reaction of feces (pH less than 5.5);

Development of dehydration is possible;

Rarely - the development of severe malnutrition

LACTASE INSUFFICIENCY (ICD-10 E73)

Lactase deficiency (LN) is the most common form of disaccharidase deficiency, which develops as a result of a decrease in the activity of the enzyme lactase-phlorizin-hydrolase in enterocytes of the mucous membrane of the small intestine. This enzyme is one of the most vulnerable enzymes in the small intestine. It is superficially located, and its concentration is much lower than that of other enzymes of parietal digestion. In premature infants (from 28 to 34 weeks of gestation), lactase activity is only 30% of its level in term infants. The maximum activity of the enzyme is observed in the first year of life.

The severity of clinical symptoms in FN is due to the total degree of decrease in activity

enzyme, the amount of lactose ingested with food, the nature of the intestinal microflora, as well as individual pain sensitivity to stretching of the intestine with gases.

In the anamnesis of such children, as a rule, there are indications of a complicated course of pregnancy and childbirth (hypoxia), and symptoms of adult-type FN are often detected in the closest relatives. In infants with signs of hypoxic lesions of the central nervous system, the so-called "locking" form of lactase deficiency is sometimes observed, which is characterized by the absence of independent stool in the presence of liquid feces and the remaining 43 symptoms listed above. Usually, the symptoms in most children stop at 5-6 months (by the time of the introduction of complementary foods) and are not traced in the future, so this type of lactose intolerance can hardly be attributed to primary.

The approach to treatment should be differentiated depending on the nature of feeding (natural or artificial), the degree of enzymatic insufficiency (alactasia, hypolactasia), the genesis of fermentopathy (primary or secondary) - tab. 38

With primary alactasia of newborns, which is extremely rare, the child is immediately and completely transferred to feeding with a lactose-free milk formula.

With hypolactasia, when the child is breastfed, a decrease in the amount of breast milk is undesirable. The best option is to use the lactase enzyme, for example "Lactase Baby" (USA), in 1 capsule of 700 units, 1 capsule per feeding, in the absence of an effect, the amount of the enzyme is increased to 2-5 capsules per intake. It is possible to use the enzyme "Lactase Enzyme" (USA), in 1 capsule 3450 units, starting with 1/4 of the capsule for feeding, the maximum dose is 5 capsules per day. A dose of the enzyme preparation is mixed with 20-30 ml of expressed milk and fed to the child before breastfeeding. The effectiveness of the preparations increases if expressed milk with lactase is left for fermentation for 15-20 minutes, as well as when the entire volume of milk is treated with lactase.

Tab. 38. The scheme of correction of lactase deficiency in children of the first year of life

Purpose of enzyme: Lactase Enzyme or Lactase Baby

Only in case of ineffectiveness (persistence of pronounced anxiety, colic, symptoms of dehydration, insufficient weight gain) - it is possible to partially replace breast milk with a lactose-free milk formula by 1 / 3-2 / 3 of the volume of each feeding

With artificial feeding, a low-lactose mixture should be selected with such an amount of lactose that the patient will tolerate, preventing the appearance of clinical symptoms and an increase in the excretion of carbohydrates in the feces. A low-lactose formula, by introducing it into each feeding, is gradually replaced with infant formula. Small amounts of lactose entering the colon are a natural prebiotic necessary for the proper formation of microflora. Lactose is the source of galactose, which is formed when it is broken down. Galactose is used for the synthesis of galactolipids, including cerebrosides, which are necessary for the myelination of nerve fibers and the formation of the central nervous system, as well as for the synthesis of mucopolysaccharides (hyaluronic acid) that make up the vitreous humor and synovial fluid.

Complementary foods for children of the first year of life with FN are prepared not with milk, but with the low- or lactose-free formula that the child receives. From 4-4.5 months of age, industrial fruit purees or a baked apple are prescribed. It is advisable to prescribe porridge (rice, corn, buckwheat) or mashed vegetables with coarse vegetable fiber (cauliflower, zucchini, pumpkin, carrots) with the addition of vegetable oil as the first main complementary food (from 4.5-5 months). After 2 weeks, meat puree is introduced. Fruit juices (diluted with water 1: 1) are introduced into the diet of such children later, as a rule, in the second half of their life. In children of the second half of the year, it is possible to use dairy products, where the lactose content is insignificant - cottage cheese (washed from whey), butter, hard cheese.

In primary (constitutional) lactase deficiency, a low-lactose diet is prescribed for life.

With secondary hypolactasia, the symptoms of lactase deficiency are transient. Therefore, upon reaching remission of the underlying disease after 1-3 months, the diet should be gradually expanded by introducing milk formulas containing lactose, under the control of clinical symptoms (diarrhea, flatulence) and the excretion of carbohydrates in the feces.

CONNECTED INSUFFICIENCY OF SUGARASE-ISOMALTASE

Congenital sucrase-isomaltase deficiency is a rare disorder among Europeans and is inherited in an autosomal recessive manner. Enzyme deficiency is not a life-threatening condition. It manifests itself for the first time when sucrose (fruit juices, mashed potatoes, sweetened water or tea) is introduced into the child's diet, less often starch and dextrins (porridge, mashed potatoes) in the form of severe "carbohydrate" diarrhea with dehydration crises. With age, children often acquire the ability to tolerate increasing amounts of dextrins, starch and sucrose without increasing the specific activity of the enzyme, which is associated with an increase in the absorption surface of the mucous membrane. Often, patients develop an aversion to sweet foods, fruits, starchy foods, that is, self-regulation of the flow of sucrose into the child's body occurs.

Any damage to the intestinal epithelium can lead to a secondary deficiency of this enzyme (infectious enteritis, giardiasis, celiac disease), but the activity of the enzyme does not fall to such an extremely low level as in the case of primary deficiency.

Tab. 38. Chemical composition and energy value of low-lactose and lactose-free milk mixtures (in 100 ml of ready-made formula)

Intolerance to carbohydrates

Carbohydrate intolerance (carbohydrate intolerance) is the inability to digest certain carbohydrates due to a lack of one or more intestinal enzymes. Symptoms of carbohydrate intolerance include diarrhea, bloating, and flatulence. Diagnosis is based on clinical signs and an H2 breath test. Treatment for carbohydrate intolerance is to eliminate disaccharides from food.

ICD-10 code

What causes carbohydrate intolerance?

Enzyme deficiency can be congenital, acquired (primary), or secondary. Congenital deficiency is rare.

Acquired lactase deficiency (primary hypolactasia in adults) is the most common form of carbohydrate intolerance. High lactase levels are seen in newborns due to the need to digest milk; in most ethnic groups (80% of blacks and Hispanics, almost 100% of Asians) lactase levels decrease after breastfeeding, preventing older children and adults from digesting significant amounts of lactose. At the same time, 80-85% of the inhabitants of northwestern Europe have a good production of lactase throughout their life, which allows them to digest milk and dairy products. It remains unclear why more than 75% of the world's population is deficient in this enzyme.

Secondary lactase deficiency is associated with conditions that damage the lining of the small intestine (eg, celiac disease, tropical sprue, acute intestinal infections). In infants, temporary secondary disaccharidase deficiency can complicate the course of intestinal infections or abdominal surgery. The exit from the state of the disease is accompanied by an increase in the activity of the enzyme.

What happens if you have a carbohydrate intolerance?

Disaccharides are normally broken down to monosaccharides from disaccharides [eg, lactase, maltase, isomaltase, sucrase (invertase)], localized on the brush border of the enterocytes of the small intestine. Undigested disaccharides cause an increase in osmotic pressure, which attracts water and electrolytes into the intestinal lumen, causing watery diarrhea. Bacterial fermentation of carbohydrates in the colon causes gas (hydrogen, carbon dioxide, and methane), resulting in severe bloating, flatulence, and abdominal pain.

Symptoms of carbohydrate intolerance

Symptoms of carbohydrate intolerance are similar for all disaccharidase deficiency states. A child with lactose intolerance develops diarrhea after drinking significant amounts of milk and may not gain weight. Adults may have watery diarrhea, bloating, excessive flatulence, nausea, stomach rumbling, and bowel cramps after taking lactose. Patients notice this early enough and avoid dairy products. Symptoms of carbohydrate intolerance usually appear after eating the equivalent of 8-12 ounces of milk. Diarrhea can be severe enough, causing other nutrients to be excreted before they are absorbed. Symptoms may be similar to irritable bowel syndrome, requiring differential diagnosis.

Where does it hurt?

What's worried about?

Diagnosis of carbohydrate intolerance

Lactose intolerance is usually diagnosed by a careful history taking supported by a diet. Usually, patients have a history of milk and dairy intolerance. The diagnosis can be assumed if the stool in the form of chronic or intermittent diarrhea is acidic (pH

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Clinical manifestations include diarrhea, bloating, and gas. Diagnosis is clinical and H2-breath test results. Treatment consists in excluding the use of the "guilty" disaccharide.

Pathophysiology of carbohydrate intolerance

Causes of carbohydrate intolerance

Disaccharidase deficiency in origin can be congenital, acquired (primary) and secondary. Congenital failure (in particular, sucrase isomaltase deficiency) is rare.

Symptoms and signs of carbohydrate intolerance

The clinical manifestations of all types of disaccharidase deficiency are similar. A child suffering from lactase intolerance, after consuming a significant amount of milk, develops diarrhea, and there may be a lack of weight gain. For adults, after consuming lactose, the development of watery diarrhea, bloating, excess gas, nausea, rumbling in the abdomen, and cramping pain is characteristic. Patients usually recognize the connection between the onset of symptoms and the use of dairy products as early as childhood and try to avoid them. Symptoms usually require dairy products containing 250-375 ml of milk (8-12 ounces) for symptoms to appear. Diarrhea can be quite severe and be accompanied by the excretion of other nutrients that have not had time to be absorbed.

Diagnosis of carbohydrate intolerance

Clinical data.
H 2 breath test for confirmation.

The lactose tolerance test is less sensitive (about 75%), but its specificity is> 95%. The patient is taking lactose. Determine the glucose content in serum before lactose intake and after 60 and 120 minutes. With lactose intolerance, diarrhea, bloating, discomfort develops within 20-30 minutes and there is no increase in blood glucose> 20 mg / dL compared to baseline.

Carbohydrate Intolerance Treatment

Diet restrictions.

Basic Provisions

Disaccharidase deficiency (usually lactase deficiency) can be acquired, less often congenital.
Undigested disaccharides such as lactose create an osmotic load and cause diarrhea.
Intestinal bacteria metabolize some of the undigested disaccharides, which is accompanied by excess gas and bloating.
The clinical diagnosis is confirmed by the data of the H2-breath test.
Typically, treatment consists of prescribing dietary restrictions.

NATIONAL PROGRAM FOR THE OPTIMIZATION OF FEEDING IN THE FIRST YEAR OF CHILDREN IN THE RUSSIAN FEDERATION

Approved at the XVI Congress of Russian Pediatricians
(February 2009)

Moscow
Union of Pediatricians of Russia
2011

EXCERPT

11. NUTRITION WITH CARBON Intolerance

Clinical symptoms of carbohydrate intolerance

frequent (8-10 times a day or more) liquid, frothy stools with a large water spot and a sour odor;
bloating, rumbling (flatulence), abdominal pain (colic);
the presence of carbohydrates in feces (more than 0.25 g% in children of the 1st year of life);
acidic stool (pH less than 5.5);
the development of dehydration is possible;
rarely - the development of severe malnutrition

Lactase deficiency(ICD-10 E73) the most common form of disaccharidase deficiency, which develops as a result of a decrease or complete absence of the enzyme lactase-phlorizin-hydrolase in the enterocytes of the mucous membrane of the small intestine. This enzyme is one of the most vulnerable enzymes in the small intestine. It is superficially located, and its concentration is much lower than that of other enzymes of parietal digestion. In premature infants (from 28 to 34 weeks of gestation), lactase activity is only 30% of its level in term infants. The maximum activity of the enzyme is observed at the age of 2-4 months.

Clinic

Most often, pediatricians meet with hypolactasia in children during the first months of life.

Clinical symptoms (flatulence, colic, diarrhea) appear in a child usually at 3-6 weeks of age, which, apparently, is associated with an increase in the volume of milk or milk formula. In the anamnesis of such children, as a rule, there are indications of a complicated course of pregnancy and childbirth (hypoxia), and symptoms of adult-type FN are often detected in the closest relatives. In infants with signs of hypoxic lesions of the central nervous system, the so-called "locking" form of lactase deficiency is sometimes observed, which is characterized by the absence of independent stool in the presence of liquid feces and the other symptoms listed above. Usually, the symptoms in most children stop at 5-6 months (by the time of the introduction of complementary foods) and are not traced in the future, so this type of lactose intolerance can hardly be attributed to primary.

Diet therapy

The approach to treatment should be differentiated depending on the nature

feeding (natural or artificial), the degree of enzymatic deficiency (alactasia, hypolactasia), the genesis of fermentopathy (primary or secondary) table. 35.

Table 35. Scheme of correction of lactase deficiency in children of the first year of life

With primary alactasia of newborns, which is extremely rare, the child is immediately and completely transferred to feeding with a lactose-free milk formula.

With hypolactasia, when the child is breastfed a decrease in the amount of breast milk is undesirable. The best option is to use lactase preparations (Lactase baby (National Enzyme Company, USA, in 1 capsule 700 units (7 mg), 1 capsule per feeding) is prescribed. The dose of the enzyme preparation is mixed with 20 30 ml (1/3 of the feeding volume) expressed milk and drink to the baby before breastfeeding.

If the use of the enzyme is ineffective (which is usually observed with a pronounced decrease in lactase activity), they resort to reducing the lactose load by replacing from 1/3 to 2/3 of the volume of each feeding with a lactose-free milk formula (Table 36), after which the child is supplemented with human milk. The lactose-free mixture is introduced into the diet gradually, at each feeding, bringing within 3 to 5 days to the required amount, as judged by a decrease in flatulence, restoration of the normal consistency of feces and stool frequency, a decrease in the excretion of carbohydrates with feces, and an increase in fecal pH. Typically, the volume of lactose-free product is 30-60 ml for each feeding.

Table 36. Chemical composition and energy value of low-lactose and lactose-free milk mixtures (in 100 ml of ready-made formula)

The product's name	Firm, country of origin	Ingredients		Energy value, kcal
			carbohydrates

lactose-free mixtures
Nutrilak lactose-free	Nutritek Group, Russia
NAS lactose-free	Nestlé, Switzerland
Enfamil Lactofree	Mead Johnson, USA
low-lactose mixtures
Low-lactose nutrilak	Nutritek, Russia
Low-lactose nutrilon	Nutricia, Holland
Humana-LP	Humana, Germany
Humana-LP + MCT	Humana, Germany

Complementary foods For children in the first year of life with FN, they are prepared not with milk, but with the low- or lactose-free formula that the child receives. From 4-4.5 months of age, industrial fruit purees or a baked apple are prescribed. It is advisable to prescribe porridge (rice, corn, buckwheat) or mashed vegetables with coarse vegetable fiber (cauliflower, zucchini, pumpkin, carrots) with the addition of vegetable oil as the first main complementary food (from 4.5 to 5 months). After 2 weeks, meat puree is introduced. Fruit juices (diluted with water 1: 1) are introduced into the diet of such children later, as a rule, in the second half of their life. In children of the second half of the year, it is possible to use dairy products, where the lactose content is insignificant - cottage cheese washed from whey, butter, hard cheese.

With primary (constitutional) lactase deficiency a low-lactose diet is prescribed for life.

With secondary hypolactasia symptoms of lactase deficiency are transient. Therefore, after reaching remission of the underlying disease after 1 to 3 months, the diet should be gradually expanded by introducing lactose-containing milk formulas, under the control of clinical symptoms (diarrhea, flatulence) and the excretion of carbohydrates in the feces.

Congenital sucrase-isomaltase deficiency is a fairly rare disease among Europeans and is inherited in an autosomal recessive manner. Enzyme deficiency is not a life-threatening condition. It manifests itself for the first time when sucrose (fruit juices, mashed potatoes, sweetened water or tea) is introduced into the child's diet, less often starch and dextrins (porridge, mashed potatoes) in the form of severe "carbohydrate" diarrhea with dehydration crises. With age, children often acquire the ability to tolerate increasing amounts of dextrins, starch and sucrose without increasing the activity of the enzyme, which is associated with an increase in the absorption surface of the mucous membrane. Often, patients develop an aversion to sweet foods, fruits, starchy foods, that is, self-regulation of the flow of sucrose into the child's body occurs.

Diet therapy

Children with sucrase-isomaltase deficiency cannot tolerate fruits, berries, vegetables, juices with a high sucrose content (peaches, apricots, tangerines, oranges, melons, onions, beets, carrots, etc.), as well as foods rich in starch (cereals, potatoes, bread, jelly, etc.). It is recommended to start the introduction of complementary foods with mashed vegetables, which practically do not contain sucrose and starch (Table 37).

Table 37. Vegetables and fruits containing the minimum amount of sucrose and starch

Starch intolerance can occur in premature babies and children of the first half of life, in whom the activity of pancreatic amylase is physiologically reduced, as well as with exocrine pancreatic insufficiency, therefore they are not shown

the appointment of mixtures including starch in the composition of the carbohydrate component.

At congenital (primary) malabsorption of glucose - galactose there is a defect in the transport systems of the brush border of enterocytes, while the activity of disaccharidases and hydrolysis of carbohydrates are not disturbed. This rare pathology is inherited in an autosomal recessive manner; manifests itself as profuse diarrhea and dehydration after the first feeding of the newborn. Replacing milk with lactose-free and dairy-free mixtures has no effect.

The only monosaccharide that can be absorbed in the small intestine is fructose.

Acquired intolerance to monosaccharides manifested by severe chronic diarrhea with delayed physical development. It can accompany the course of severe intestinal infections in children of the first months of life with an unfavorable premorbid background, occur as a result of atrophy of the villi of the intestinal mucosa in celiac disease, intolerance to cow's milk proteins, protein-energy deficiency. The baby's diarrhea diminishes when he is fasting and returns when the amount of oral feeding increases. Low pH and high concentration of glucose and galactose in feces are characteristic. Therapy with lactose-free and dairy-free formulas is ineffective.

Materials for this chapter are also provided by: Ph.D. E.A. Roslavtseva