Celiac disease (celiac disease): diagnosis

Despite the absence of specific clinical signs pathognomonic for gluten enteropathy, it is necessary to take into account all the listed symptoms, the analysis of which together with the data of other research methods and the results of treatment will allow to correctly diagnose.

The laboratory features of celiac disease, like clinical, differ depending on the extent and severity of the bowel and are also nonspecific.

Laboratory and instrumental data

1. General blood test: hypochromic iron deficiency or B _12- deficiency macrocytic hyperchromic anemia.
2. Biochemical blood test: a decrease in the total protein and albumin, prothrombin, iron, sodium, chloride, glucose, calcium, magnesium in the blood, a slight increase in the bilirubin content. With gluten enteropathy, a number of organs and systems are involved in the pathological process, in connection with this many biochemical indicators deviate from the norm. With severe diarrhea, the body is depleted of electrolytes with a decrease in the content of sodium, potassium, chlorides and bicarbonates in the blood serum. Sometimes there is a significant metabolic acidosis due to loss of bicarbonates with feces. In patients with diarrhea and steatoria, the content of serum calcium, magnesium, and zinc decreases. When osteomalacia, the serum phosphorus level can be lowered, and alkaline phosphatase - increased. The serum albumin and, to a lesser extent, serum globulin content may decrease as a result of a significant release of the serum protein into the intestinal lumen. With severe lesion of the small intestine that caused steatorrhea, the serum cholesterol and carotene levels are usually reduced. The content of cholesterol in the serum of less than 150 mg / ml in adults should alert the clinician regarding the possible violation of gastrointestinal absorption.
3. General analysis of urine: without significant changes, in severe cases - albuminuria, microhematuria.
4. Koprologichesky the analysis: polifepalija is characteristic. Cal is watery, semi-formal, yellowish-brown or greyish, greasy (shiny). When a microscopic examination determines a large amount of fat (steatorrhea). During the day, much more than 7 g of fat is secreted (normally, the daily release of fat with feces does not exceed 2-7 g). With limited lesion of the proximal small intestine, steatorrhoea is slightly or even absent.
5. Investigation of the small intestinal absorption function: D-xylose, glucose samples are used (after an oral glucose load, a flat glycemic curve is determined), lactose (after an oral lactose application, an increase in the concentration of exhaled hydrogen is ascertained). The samples indicate a decrease in the intestinal absorption function.
6. Immunological analysis of blood: the most typical appearance in the blood of antibodies to gluten, which are detected by the express method, applying blood serum to the patient's blood. Circulating antibodies in the blood can also be detected by an indirect fluorescence reaction. Characteristic is also the detection of autoantibodies to reticulin and epitheliocytes of the small intestine. It is possible to reduce the content of immunoglobulin A in the blood.
7. Hormonal blood test. In the blood, the content of T ₃, T ₄, cortisol, testosterone, estradiol is reduced . These changes are observed with the development of hypofunction of the corresponding endocrine glands.
8. X-ray examination of the gastrointestinal tract. There is an expansion of the loops of the small intestine, the disappearance of its folds, a change in the relief of the intestinal mucosa. Sometimes in the proximal part of the small intestine an excessive amount of fluid is observed (due to a violation of the absorption capacity of the intestine), which leads to dilution of the contrast medium and as a result, in the distal parts of the small intestine the mucosal pattern appears to be indistinct.
9. A variety of diagnostic tests. With the syndrome of inadequate absorption, the exchange of tryptophan is disrupted, which may be due to a deficiency of pyridoxine and nicotinic acid; while urinary excretion of 5-hydroxyindol-butyacetic acid and an indicator increases. With severe digestive disturbances that caused pituitary or adrenal insufficiency, daily urinary excretion of 17-CS and 17-ACS decreases. As a diagnostic test, it is suggested to use the LIF factor, which is formed due to the interaction of lymphocytes from patients with gluten enteropathy with gluten fractions and suppresses increased migration of leukocytes. A certain diagnostic value is the secretion of IgA and IgM in vitro by isolated lymphocytes from the duodenum and jejunum using an enzyme-like immunosorbent assay.
10. For the rapid diagnosis of gluten enteropathy in the serum, antibodies to gluten are detected, applying whole or diluted buffered isotonic sodium chloride solution (pH 7.4) to the wheat grain medium at a ratio of 1:11 of the patient's serum. Circulating antibodies in the blood to gluten, as well as autoantibodies to reticulin and epitheliocytes of the small intestine, were found by an indirect immunofluorescence reaction.
11. Biopsy of the small intestine mucosa. Bioptate is most expedient to take from the duodenal joint near the Treitz ligament. In this place the gut is fixed and therefore it is easier to take biopsies here. Characteristic signs of gluten enteropathy are:
    • an increase in the number of goblet cells in the intestinal mucosa;
    • increase in the number of interepithelial lymphocytes (more than 40 per 100 epitheliocytes of intestinal villi);
    • atrophy of villi;
    • infiltration of the surface and pit epithelium with lymphocytes, and of the own plate with lymphocytes and plasmocytes.

Diagnostic criteria for celiac disease

1. The appearance of diarrhea, malabsorption syndrome in early childhood, lag in growth and physical development in childhood and adolescence.
2. Typical results of a study of biopsy specimens of the mucosa of the duodenum or jejunum.
3. Detection of circulating antibodies to gluten in the blood, as well as autoantibodies to reticulin and epitheliocytes of the small intestine.
4. Clear clinical and morphological (by results of repeated biopsy) improvement after exclusion from the diet of gluten (products from wheat, barley, rye, oats).
5. Positive load results with gliadin (rapid increase in glogamine in the blood after ingestion of 350 mg gliadin per 1 kg of body weight).

Differential diagnosis of celiac disease. The first stage of diagnosis is the establishment of a violation of intestinal absorption and the cause underlying it. Steatorrhea and lowering serum cholesterol, carotene, calcium and prothrombin by themselves do not allow differentiating gluten enteropathy from other diseases that may be due to insufficient absorption. They are also observed when there is a violation of the cavity digestion caused by a preliminary resection of the stomach and ileum or pancreatic insufficiency.

In the differential diagnosis of the primary disease of the small intestine mucosa, a test for tolerance to xylose is of particular importance, since its normal absorption with disturbed cavity digestion persists for a long time - until the mucosal structure changes. Radiographs of the small intestine after receiving the contrast medium also help differentiate the absorption disorders due to either mucosal lesions or other causes. "Abnormal" mucosal relief, dilatation of the intestine, dilution of barium sulfate suspension are very suspicious of mucosal disease.

Reliably exclude the diagnosis of clinically expressed untreated gluten enteropathy normal biopsies obtained from the proximal small intestine. At the same time, biopsy specimens showing a typical lesion for gluten enteropathy reliably confirm this diagnosis. Exclude its detection in the study of the biopsy of histological signs characteristic of Whipple's disease and Crohn's disease. For hypogammaglobulinemia, in which the change in the mucous membrane of the small intestine resembles the picture observed with gluten enteropathy, the absence or significant decrease in the number of plasma cells is characteristic.

Absence of absolutely specific histological signs, pathognomonic for gluten enteropathy, indicates the need to consider the results of biopsy in combination with other manifestations of the disease.

Mucosal lesion, identical or similar to that observed with gluten enteropathy, occurs in tropical sprue, diffuse small bowel lymphoma, Zollinger-Ellison syndrome with significant hypersecretion, unclassified sprue, viral gastroenteritis in young children.

The detection in the blood of circulating antibodies to gluten as well as autoantibodies to reticulin and epitheliocytes of the small intestine simultaneously with the evaluation of the histological structure of the mucous membrane of its initial department makes diagnosis and differential diagnosis reliable.

Clinical and morphological improvement after treatment with a diet completely free of toxic gluten, confirms the diagnosis of gluten enteropathy. It should be noted that clinical improvement occurs in a few weeks, and the normalization of the histological pattern requires adherence to the gluten-free diet for several months and even years, although some morphological improvement can be observed in the early stages of clinical remission.

In young children suffering from gastroenteritis, diagnosis complicates not only the similarity of histological changes in the small intestine mucosa with gluten enteropathy, but also a positive reaction to a gluten-free diet.

Differentiate gluten enteropathy from other diseases of the small intestine, in particular chronic enteritis, with a gliadin load (rapid increase in glutamine in the blood after oral administration of 350 mg gliadin per 1 kg of body weight); long, beginning with childhood, anamnesis of the disease; exacerbation of the disease due to the use of products from wheat, rye, barley, oats; good effect of gluten-free diet.

The diagnosis of celiac disease is based on the following signs: a malfunction of the mucosa of the small intestine; documented the most characteristic signs of its damage; the presence of circulating antibodies to gluten; clear clinical and morphological improvement after exclusion from the diet of toxic gluten.

[1], [2], [3], [4]