Description
Synonyms (rus): Fat fraction of feces
Synonyms (eng): Steatocrit, fecal fat excretion
Biomaterial: Feces
Indicator(s): Percentage of fat in stool
Method(s): Quantitative fat analysis method
Container type and preanalytical features: Sterile stool container with spoon
Normally, the absorption of fats in the digestive tract occurs in the small intestine after the food bolus is processed by a number of enzymes. The most important components in this process are the components of bile, which emulsify lipids, and pancreatic juice, which directly contains lipase enzymes that break down the internal bonds of fat molecules. Steatocrit is the ratio of the fat fraction of feces to its total mass. Normally, this value should not exceed 10%. An increase in steatocrit levels indicates steatorrhea (excessive loss of fats in feces) and is observed in various pathological conditions of the gastrointestinal tract. The most common cause is exocrine pancreatic insufficiency, whose enzymes directly break down lipids. Such conditions include chronic and autoimmune pancreatitis, type 1 diabetes mellitus, cystic fibrosis and others. Another common cause of increased steatocrit is impaired absorption of fats in the intestines, for example, with inflammatory bowel diseases, celiac disease, and autoimmune enteropathy. Determination of fecal steatocrit is recommended as part of a comprehensive assessment of exocrine pancreatic insufficiency in conjunction with the study of chymotrypsin and pancreatic elastase in the stool. It must be taken into account that the physiological cause of an increase in steatocrit may be age under 1 year, prematurity and excessive intake of fats from food.
Differential diagnosis of chronic diarrhea in children
Diarrhea is one of the leading causes of child mortality, killing approximately 2.5 million children worldwide each year. A significant proportion of these patients are children with prolonged and chronic diarrhea.
Rice. 1. Causes of chronic diarrhea
Rice. 2. Character of the stool
Table 1. Differential diagnosis of osmotic and secretory diarrhea
Table 2. Characteristics of different types of congenital diarrhea
Rice. 3. Morphological picture of celiac disease
Rice. 4. Morphological picture of allergic enteropathy
Rice. 5. Algorithm for diagnosing diseases of the small intestine based on morphological data
Table 3. Differential diagnosis of celiac disease and autoimmune enteropathy
Rice. 6. Morphological picture of autoimmune enteropathy
Table 4. Morphological features of intractable infant diarrhea
Rice. 7. Clinical diagnosis of intractable infantile diarrhea
Diarrhea lasting more than 3 weeks with a bowel movement frequency of three or more times a day is considered chronic. Considering that such a frequency of stool may be the norm for children in the first months of life, it is also necessary to pay attention to the nature of the stool and its volume. Normally, in a healthy child, the volume of stool usually does not exceed 10 g/kg body weight per day. Watery or greasy stools, the presence of greens, mucus, blood, and undigested food debris are signs of pathology.
The causes of chronic diarrhea (CD) are very diverse (Fig. 1), the most common of them are: intestinal infections (usually viral, less often bacterial, caused by opportunistic microflora), as well as parasitic infestations (giardiasis, sometimes cryptosporidiosis, amebiasis, etc.) . The transformation of acute diarrhea into chronic may be due to the unfavorable background against which the infection occurs (hypotrophy, micronutrient deficiency, immunodeficiency), as well as inadequate therapy. As a consequence of prolonged inflammation, atrophy of the small intestinal mucosa (SIMU) develops with a secondary impairment of its functions.
Along with infectious and parasitic causes, HD can be caused by congenital genetically determined defects of digestion (lactase deficiency, sucrase-isomaltase deficiency) and absorption (glucose-galactose malabsorption, chloride, sodium diarrhea, malabsorption of bile acids, acrodermatitis enteropathica, etc. .), congenital anomalies of the structure of enterocytes (microvillous atrophy, intestinal epithelial dysplasia) and immunopathological diseases accompanied by chronic inflammation of the somatic tissue (allergic enteropathy, celiac disease, autoimmune enteropathy, Crohn's disease). The most severe form of HD is the so-called intractable infantile diarrhea, caused by enterocyte abnormalities or autoimmune enteropathy.
Diagnosis of diseases manifested by HD should be based on a thorough assessment of the nature of the intestinal syndrome, symptoms from other organs and systems, medical history and additional studies. Due to the widespread prevalence of intestinal infections and parasitoses in children, the first stage of diagnosis is the establishment or exclusion of these diseases. To do this, each child with HD needs to:
- clinical blood test;
- stool cultures;
- examination of stool for worm eggs and Giardia cysts using microscopy, ELISA and PCR;
- microscopy of a stool smear for cryptosporidiosis (with Ziehl-Neelsen staining or treatment with 1% HCl solution);
- stool examination for
Clostridium difficile
A
and using ELISA; - scatological examination (at least 3 coprograms);
- stool examination for occult blood.
Even in the case of a negative result of bacteriological examination, if an infectious origin of diarrhea is suspected, a course of antibacterial therapy ex juvantibus is indicated. Usually in these cases, nitrofurans (nifural 15 mg/kg or nifuroxazide 100 mg 2 times a day), aminoglycosides (gentamicin 3–5 mg/kg, amikacin 10 mg/kg) or third generation cephalosporins (cefotaxime 50 mg/kg, ceftriaxone) are prescribed 50 mg/kg). Since diarrhea in childhood has a predominantly viral etiology and is characterized by watery stools with significant loss of fluid and salts, it is important to carry out adequate rehydration and correction of electrolyte metabolism from the very first days of illness. It is equally important to provide adequate nutrition to the child, taking into account reduced digestive capabilities.
To correct intestinal microbiocenosis in post-infectious diarrhea, probiotic preparations are used. When prescribing a probiotic drug, you must ensure that it contains no lactose. For children of the early neonatal period, a lactose-free probiotic Primadophilus Children is produced, which contains strains of lacto- and bifidobacteria selected according to age in an age-specific dosage of 2 x 10 9 CFU per daily dose.
If the child is breastfed, it can be continued, but it is recommended to add the Lactase Baby enzyme to each feeding.
When artificial feeding, taking into account the likely development of secondary lactase deficiency against the background of an intestinal infection, it is advisable to use lactose-free or fermented milk mixtures: NAN fermented milk, NAN lactose-free, Enfamil Lactofri.
Lactase deficiency
in young children it can be not only secondary, but also primary: congenital or transient. Congenital lactase deficiency is an extremely rare pathology in which, as a result of genetic mutations, lactase is not transported from the Golgi apparatus to the surface of the enterocyte membrane. Symptoms of congenital lactase deficiency manifest themselves very clearly from the first days of life in the form of repeated watery diarrhea, accompanied by bloating, weight loss and dehydration. In the vast majority of cases, lactase deficiency in a newborn or premature baby is transient in nature and is caused by immaturity of the intestinal villi and insufficient activity of the lactase enzyme on the surface of the epithelium (hypolactasia).
Transient lactase deficiency can cause mild “sour” watery diarrhea in the first months of life, which is often accompanied by intestinal colic and restlessness of the child, but does not affect his physical development. Symptoms gradually improve as breastfeeding continues. This is because human milk contains numerous growth factors (EGF, IGF-1, TGF-β, spermine, spermidine, nucleotides, short-chain fatty acids, etc.) that promote the growth and maturation of the intestinal epithelium and increase lactase activity.
Therefore, with symptoms of hypolactasia, breastfeeding should be continued, but to eliminate the symptoms, it is advisable to use the Lactase Baby enzyme
700 units each at the beginning of each feeding. Children from birth are prescribed the contents of 1 capsule of Lactase Baby per 100 ml of milk. Before feeding, you should express 20 ml of milk and pour out the contents of the capsules. Start feeding after 10 minutes with this portion. If the child receives only expressed breast milk, Lactase Baby is added to the full amount of food. When artificial feeding, the required amount of enzyme is also added to the full volume of milk nutrition. The fermentation time is 10 minutes.
To confirm lactase deficiency of any origin in a child, you can use various tests: fecal pH test (below 5.5), glycemic curve with lactose load at the rate of 2 g/kg (increase in glucose level no more than 25% of the original), hydrogen test (increase level of hydrogen in exhaled air above 20 ppm).
If intestinal infection and lactase deficiency (the most common causes of chronic diarrhea) are excluded, and diarrhea continues despite antibacterial therapy and a lactose-free diet, it is necessary to continue the examination, providing adequate nutritional support through a combination of parenteral and enteral nutrition with mixtures of lactose-free protein hydrolysates: Alfare, Nutrilon Pepti TSC, Nutramigen, Frisopep AS, Pregestimil.
A further algorithm for diagnosing CD is based on assessing the nature of the stool (Fig. 2). A distinction must be made between watery diarrhea, diarrhea with steatorrhea, and diarrhea with colitic syndrome (blood and mucus in the stool).
Watery diarrhea
If, despite the abolition of lactose, watery “acidic” diarrhea persists (fecal pH), malabsorption of glucose-galactose is confirmed by examining the excretion of sugars in feces and testing for tolerance to glucose and fructose. Since the functioning of the glucose-galactose transporter is impaired in this disease, while the functions of the fructose transporter in SOTC are preserved, the child’s body perceives the load of these monosaccharides differently. After taking glucose, diarrhea intensifies, and the glycemic curve has a flat appearance. Fructose is the only carbohydrate that is well tolerated by children with glucose-galactose malabsorption, therefore, when the diagnosis is confirmed, feeding should be carried out with an artificial mixture prepared from calcium caseinate, vegetable oil and fructose.
All disorders of the breakdown and absorption of carbohydrates - lactase, sucrase-isomaltase deficiency, glucose-galactose malabsorption, fructose malabsorption - are manifested by osmotic diarrhea
, which develops as a result of the formation of osmotically active products of bacterial fermentation from unabsorbed carbohydrates. Temporarily transferring the child to parenteral nutrition or eliminating the carbohydrate that caused diarrhea from the diet is accompanied by relief of symptoms.
Diarrhea that persists after the child is switched to total parenteral nutrition indicates its secretory nature
. The main difference between secretory diarrhea and osmotic diarrhea is the lack of effect from “starvation,” that is, from canceling normal nutrition and transferring the child to parenteral nutrition (Table 1). To confirm the secretory nature of diarrhea, it is necessary to study the level of electrolytes in the blood and their excretion in feces. In secretory diarrhea, stool osmolality depends mainly on its electrolyte content and is the sum of the concentrations of Na+ and K+ ions (or Na+, K+ and Cl-) multiplied by two. In osmotic diarrhea, stool osmolality is due to undigested or unabsorbed food particles, while the concentration of electrolytes in it remains low, which explains the large osmotic difference, so the sum of fecal electrolytes (Na++K++Cl-) is significantly less than osmolality. Secretory diarrhea is more often observed with acute (so-called watery) diarrhea, but its long-term persistent course can be observed with such rare diseases as congenital chloride or sodium diarrhea, as well as with malabsorption of bile acids. Chloride diarrhea is characterized by a predominance of chlorine ions in the feces over other electrolytes, while sodium diarrhea is characterized by a predominance of sodium ions. If selective loss of the appropriate electrolyte is confirmed, replacement therapy in the form of saline solutions is indicated, first intravenously, then orally.
Severe mixed diarrhea with a secretory component, loss of a large amount of fluid (more than 300 ml per day), combined with loss of plasma protein, observed from birth is characteristic of congenital anomalies of enterocytes
(Table 2). This type of diarrhea is characterized by a lack of effect from transferring the child to parenteral nutrition and increased diarrhea after eating. There is no osmotic difference in stool, as with secretory diarrhea. This type of diarrhea is an indication for a biopsy of the somatic tissue and electron microscopic examination of biopsy specimens. The detection of the phenomenon of “included microvilli” or “tufted dysplasia” of enterocytes confirms the fact of a congenital anomaly of their structure. The only treatment for these congenital anomalies is a small intestine transplant.
Diarrhea with steatorrhea
Steatorrhea is accompanied not so much by frequent stools as by fatty-looking, bulky and foul-smelling stools, which usually have a mushy character and are difficult to wash out of the potty. During a scatological examination, it is important to distinguish between two types of steatorrhea: steatorrhea with neutral fat, which is a symptom of pancreatic insufficiency, and steatorrhea with fatty acids, which is characteristic of pathology of the small intestine.
Pancreatic type steatorrhea
(neutral fat) is possible with cystic fibrosis, Shwachman-Diamond syndrome, Pearson syndrome, isolated lipase deficiency (Sheldon-Reay syndrome). If it is detected in a series of coprograms, a more accurate assessment of exocrine pancreatic function is indicated using a fecal elastase-1 test. A decrease in elastase-1 levels below 200 mg/g confirms the likelihood of pancreatic insufficiency. The subsequent diagnostic algorithm is aimed at identifying a specific pancreatic disease. The diagnosis of cystic fibrosis is confirmed by elevated sweat chloride levels and the detection of CFTR gene mutations.
Shwachman-Diamond syndrome is characterized by a combination of pancreatic insufficiency and hematological disorders (neutropenia, less commonly thrombocytopenia and anemia), as well as growth retardation and the presence of some bone abnormalities (dyschondroplasia of the hip joints, non-union of the ribs, wedge-shaped fingers, etc.).
Pearson syndrome is also manifested by hematological disorders, but they are usually more severe, and a persistent course of anemia and thrombocytopenia is characteristic. There are no bone abnormalities in Pearson syndrome.
Sheldon-Reay syndrome is characterized by the absence of lipase in the blood and urine, pronounced steatorrhea; There are no growth disturbances.
The basis of treatment for all these genetically determined diseases is pancreatic enzyme replacement therapy. The dose of enzymes is selected individually, usually starting with 2,000 IU/kg of lipase per day, increasing the dose if necessary. Preferred are preparations with microspherical enzymes (Creon, Pancitrate), which should be given to the child at the beginning of each meal and distributed according to its quantity. In case of severe malnutrition, mixtures with medium chain triglycerides (MCTs ) are used in the diet of patients: Alfare, Nutrilon Pepti TSC, Pregestimil, Peptamen, Portagen
. Additionally, fat-soluble vitamins are prescribed: A, E, D, K.
Intestinal type steatorrhea
(fatty acids) is not a specific sign of certain diseases, but is quite often observed in diseases of the small intestine. To clarify the nature of the intestinal pathology, a morphological study of biopsy specimens of the somatic tissue taken during an endoscopic examination from the distal duodenum or proximal jejunum is necessary.
The presence of lymphoplasmacytic infiltration of the lamina propria of the STC indicates chronic inflammation, which in most cases is accompanied by mucosal atrophy, manifested by shortening of the villi and thinning of the epithelium. Assessment of the degree of atrophy of the atrophy is carried out in accordance with the Marsh classification; 3 degrees are distinguished. If atrophy of the 2nd or 3rd degree is detected (shortening of the villi, deepening of the crypts, dense uniform lymphoplasmacytic infiltration of the lamina propria, increase in interepithelial lymphocytes - IEL) (Fig. 3) in a child who has already received gluten, it is necessary to conduct a study of the level of antigliadin antibodies (IgA, IgG), antibodies to tissue transglutaminase (IgA, IgG) and endomysium. When the level of these immunoglobulins is elevated, a diagnosis of celiac disease
, the child is prescribed a lifelong strict gluten-free diet. Classic signs of celiac disease at an early age are insufficient weight gain with the development of malnutrition and an enlarged abdomen.
Enteral syndrome, similar to celiac disease, is often observed in children with food allergies. Symptoms of allergic enteropathy
may manifest themselves already in the first months of life in the form of anxiety, intestinal colic, regurgitation, and later iron deficiency anemia may occur. However, in some cases, in children under 2 years of age, symptoms of allergic colitis may dominate with the appearance of blood and mucus in the stool. Intestinal symptoms in most children are combined with the picture of atopic dermatitis. The morphological picture of allergic enteropathy is characterized by signs of chronic inflammation of the villi with normal height (or slight shortening) and depth of the villi and the presence of eosinophils in the infiltrate (Fig. 4). The diagnosis can be confirmed by an increase in general and specific IgE in the blood, but since gastrointestinal allergies are more often realized through cellular mechanisms of sensitization, a normal IgE level in a child does not at all exclude the possibility of allergic damage to the intestines. A similar morphological picture is also characteristic of giardiasis. The diagnostic algorithm based on morphological characteristics is presented in Fig. 5.
The combination of chronic diarrhea with skin lesions is also characteristic of enteropathic acrodermatitis
caused by zinc deficiency. Since zinc is part of more than 40 metal-containing enzymes and is involved in providing immunological protection, diarrhea in this disease can be supported by endogenous microflora, in particular, secondary candidiasis often develops. Morphological changes in STC are characterized by a combination of inflammation and moderate atrophy against the background of a reduced number of MEL, plasma cells in the lamina propria and reduced regenerative capacity of the epithelium. Skin manifestations of the disease are characterized by clearly demarcated zones of hyperemia, infiltration and excoriation from normal skin, usually localized on the buttocks, around the mouth, on the chin and cheeks. Enteropathic acrodermatitis manifests itself after stopping breastfeeding, since human milk contains a zinc-absorbing ligand that prevents the development of deficiency of this microelement. Sometimes the disease begins against the background of an acute intestinal infection, which is associated with significant enteral loss of zinc. Thus, a vicious circle is formed: acute diarrhea causes zinc deficiency, which in turn maintains and aggravates diarrhea, contributing to its transition to chronic. Blood zinc levels usually fall below 8 mmol/L. Oral administration of zinc preparations in high doses (zinc sulfate 50–100 mg/day) quickly relieves diarrhea and skin symptoms.
Diarrhea with blood and mucus in the stool
The appearance of blood and mucus in the stool is characteristic of colitic syndrome. After excluding infections (dysentery, salmonellosis, yersiniosis, campylobacteriosis), establishing the causes of diarrhea primarily involves morphological and immunological verification. In any case, diarrhea with mucus and blood in the stool indicates high activity of inflammation in the intestines and the presence of defects in the mucous membrane. An indirect proof of the activity of the inflammatory process can be an assessment of the level of calprotectin in the feces, the level of which normally does not exceed 50, and with inflammation in the intestines increases several times.
For morphological verification of the disease, a patient with chronic colitic syndrome is advised to undergo colonoscopy with ileoscopy. Endoscopic examination may reveal specific changes characteristic of Crohn's disease
or
ulcerative colitis.
The combination of severe enteropathy with colitic syndrome is characteristic of autoimmune enteropathy.
The disease most often develops in children in the first two years (sometimes the first months) of life; intestinal symptoms are combined with signs of damage to other organs (kidneys, liver, lungs, skin, joints, etc.). Autoimmune enteropathy in boys can be combined with polyendocrinopathy (IPEX) or be a manifestation of severe immunodeficiency diseases.
Morphological changes in SOTK in autoimmune enteropathy (Fig. 6) are characterized by moderate or severe villous atrophy, which is always associated with pronounced mononuclear infiltration of the lamina propria. Crypt hyperplasia can be variable. In most cases, severe or total villous atrophy is combined with crypt deepening. Severe atrophy in combination with mononuclear infiltration can be initially regarded as signs of celiac disease (Table 3), however, it is characterized by an increase in the mitotic activity of the epithelium and an increase in the number of MEL, while with autoimmune enteropathy, mitotic activity is reduced, and the infiltrate is localized in the lamina propria without increasing or with a slight increase in the number of MEL. MEL have mainly αβ receptors, while in celiac disease the number of MEL carrying γδ receptors increases. In some patients, total villous atrophy is associated with necrosis of epithelial cells and the formation of crypt abscesses. The surface epithelium is flattened and degenerated. The number of goblet cells is reduced. Mononuclear cells are mainly represented by CD4+ T lymphocytes and macrophages. Morphological changes are most pronounced in the mucous membrane of the small intestine, but can also be found in other parts of the digestive tract - the stomach or large intestine. Extensive damage to the gastrointestinal tract has the most severe manifestations and a poor prognosis.
Autoantibodies (mainly IgG class) to the intestinal epithelium are detected in the blood, directed against the components of the brush border or the cytoplasm of enterocytes of the normal intestinal mucosa. Antigoblet cell antibodies may be present. Nonspecific autoantibodies may also be directed against nuclei, DNA, smooth muscle, or mitochondria, usually associated with extraintestinal manifestations. In cases of association of autoimmune enteropathy with kidney damage, the circulation of autoantibodies against renal tissue, in particular against the 75 kDa antigen, has been described. After a diagnosis of autoimmune enteropathy has been established, the patient is prescribed therapy with glucocorticosteroids in combination with cytostatics.
Autoimmune diarrhea, along with congenital anomalies of enterocytes, belongs to the group of so-called intractable infant diarrhea
. It is necessary to emphasize once again the main features of diseases of this group: genetic predisposition;
- early onset;
- absence of connection with any infectious agent or food substrate;
- persistent nature of watery diarrhea of the secretory type, which does not stop when the child is transferred to parenteral nutrition;
- pronounced atrophy of the cellular tissue.
The algorithm for the clinical diagnosis of intractable infant diarrhea is presented in Figure 7, the histological features of STD are in Table 4.
Thus, chronic diarrhea in children can be due to many different causes. Success in the treatment of this syndrome, which is extremely difficult in terms of differential diagnosis, largely depends on the knowledge of the doctor and his desire to find the truth.
Establishing the correct diagnosis is known to be the key to choosing the right therapy. As mentioned above, in the treatment of chronic diarrhea, primarily various dietary approaches are used. As for drug therapy, the general strategy for the treatment of all diarrheal diseases is the correction of water-electrolyte imbalances and strengthening of the intestinal barrier. The latter is achieved by prescribing cytoprotectors and adsorbents.
Interpretation
The reasons for a positive test result may be: 1. Exocrine pancreatic insufficiency (chronic and autoimmune pancreatitis, type 1 diabetes mellitus, cystic fibrosis, etc.); 2. Impaired absorption of fats in the intestines (Crohn's disease, ulcerative colitis, celiac disease, autoimmune enteropathy, etc.) 3. Other gastrointestinal diseases; 4. Excessive intake of fats from food; 5. Age up to 1 year, prematurity. Normal fecal steatocrit values significantly reduce the likelihood of disruption of exocrine pancreatic function and intestinal lipid absorption.
