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Celiac disease (celiac disease): treatment

 
, medical expert
Last reviewed: 23.04.2024
 
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One of the main methods of celiac disease is a diet with the total exclusion of gluten. The toxicity of wheat protein in children with gluten enteropathy and the need to eliminate gluten from the diet have been established more than 30 years ago. Later it was proved that the introduction of flour from wheat, barley and rye into the histologically-apparent normal small intestine of patients with cured gluten enteropathy quickly elicited the corresponding symptoms, which were accompanied by the development of lesions typical of gluten enteropathy. Despite the fact that all the cereals containing gluten (wheat, barley, rye and, possibly, oats) are completely removed from food, it is quite simple, it is really very difficult to observe such a diet. This is due to the fact that wheat is the most common component of many food products (confectionery, sauces, canned food, instant coffee, etc.), so it is necessary to persistently advocate by a doctor and a dietician the need for constant compliance with a gluten-free diet for all patients with gluten enteropathy and persons with suspicion on her from the so-called risk group, especially since this diet has a protective effect on the development of malignant tumors in this disease.

A diet that does not contain wheat, rye, barley or oat gluten should be balanced and contain a normal amount of fat, protein (initially 100 grams per day) and carbohydrates.

Since some patients, very sensitive to ingesting even a small amount of wheat flour, tolerate oats painlessly, it can be tried with caution in the diet, but only during remission. At the stage of exacerbation of the disease, oats are best excluded from the diet.

Rice, soy beans, corn flour, potatoes, vegetables, fruits, berries, animal products are completely non-toxic and should be included in the diet. Treatment with gluten-free diet is a lifelong necessity for patients with this disease. Adherence to a gluten-free diet requires the implementation of two rules: initially prescribe treatment and, if clinical improvement follows, confirm the diagnosis histologically. The most common reason for the unsuccessful treatment of the gluten-free diet is the incomplete removal of gluten from it.

In the absence of severe metabolic disorders, the patient's discipline, awareness of the need for constant compliance with the gluten-free diet for hospitalization of the grounds is not enough. Hospitalization is necessary for severe metabolic disorders, no response to gluten exclusion, insufficient awareness of patients about the high effectiveness of the permanent exclusion of gluten from the diet. If the patient has an enteropathy resistant to the treatment with the aglutene diet, then another causative food agent should be tried, although its identification is not always possible.

With celiac disease, the ability of patients to tolerate varying amounts of gluten is not the same. These differences are most pronounced in those of them that respond to gluten exclusion by restoring intestinal absorption function to normal or close to normal. In such cases, patients suffer a small amount of gluten, still retaining remission, and from time to time may not comply with the diet, which does not contribute to exacerbation of the disease. Other patients are extremely sensitive to digesting even the slightest amount of toxic gluten. Within hours after digesting products containing a little bit of gluten, for example two pieces of baked bread, they have massive watery diarrhea resembling cholera. Acute dehydration due to severe diarrhea can cause a shock that threatens the patient's life - a "gliadin shock".

Treatment with a gluten-free diet leads to a faster reverse development of less severe damage to the distal intestine compared with pronounced lesions of its proximal part. Clinical improvement is more clearly correlated with the length of the histological improvement of the intestine than with the severity of the lesion of its proximal part. This explains the earlier occurrence of clinical remission compared with the morphological, which may be absent for many months. Ultimately, the mucosa of the proximal small intestine on the background of the gluten-free diet becomes normal in about 50% of patients; in the remaining patients is partially restored, approaching the norm; a few remain damaged, despite a good clinical effect. With prolonged hospitalization, you can determine which of the patients does not digest gluten. A number of patients with untreated gluten enteropathy poorly tolerate milk and dairy products, since after their use, bloating, diarrhea, and abdominal pain are of a spastic nature. However, milk and dairy products are completely excluded from the diet only if they cause unpleasant symptoms. These foods are an excellent source of protein, calcium, calories for a depleted diet of patients. The results of the observations indicate that even many seriously ill at the beginning of the treatment with the gluten-free diet tolerate a small amount of milk; As the structure and function of the intestine are normalized, the milk is tolerated even better by the sick.

Additional treatment. In severe cases, in addition to the gluten-free diet, patients should receive appropriate substitution therapy, which helps to correct abnormalities caused by insufficiency of absorption. So, with anemia, iron, folic acid and / or vitamin B12 are additionally prescribed, depending on the deficiency of a particular substance. With hemorrhages, signs of bleeding, a significant elongation of prothrombin time, parenteral administration of vitamin K or one of its analogues is indicated.

In patients with dehydration and depletion of electrolytes due to severe diarrhea, a substantially intensive intravenous replacement of fluid and electrolytes. Hypokalemia is quickly eliminated by parenteral administration of potassium chloride with severe insufficiency and oral administration - with mildly expressed. When seizures occur, which is rare, an urgent intravenous injection of 1-2 g of calcium gluconate is indicated. If there is no effect from its administration, convulsions can be caused by hypomagnesemia. In such a situation, 0.5 g of magnesium sulfate in a diluted solution or oral magnesium chloride (100 milliequivalents per day by fractional doses) can be introduced very slowly, which is safer and usually sufficient. When hypocalcemia, clinical or radiographic signs of osteoporosis and osteomalacia, calcium preparations in the form of gluconate or calcium lactate (6-8 g per day) and vitamin D. Are mandatory. It is advisable to introduce additional calcium and vitamin D to all gluten patients before the normalization of intestinal absorption under the influence of the gluten-free diet Enteropathy with significant steatorrhea to prevent the mobilization of calcium from the bones. To avoid side effects due to an overdose of vitamin D and calcium, control of serum calcium is necessary. If hypercalcemia occurs, stop taking the medication immediately.

Patients with gluten enteropathy with impaired absorption are shown the administration of vitamin A, thiamine, riboflavin, nicotinic acid, pyridoxine, vitamin C and E in the form of multivitamin preparations in the therapeutic dose, although some researchers doubt the need for additional administration of these vitamins.

Corticosteroid therapy should be carried out only as an emergency aid in secondary adrenal insufficiency of the adrenal gland, which can accompany a severe course. Usually treatment with gluten-free diet leads to a fairly rapid and persistent improvement, even in seriously ill patients.

It should be emphasized that in connection with the absorption disorder, when absorption of not only food substances, but also drugs, is disrupted, medications should be administered parenterally until the absorption process improves under the influence of the gluten-free diet.

The prognosis for patients with precisely diagnosed and treated disease is excellent. With gluten enteropathy not recognized in time, a lethal outcome is possible due to increasing depletion, bleeding, intercurrent infections, or secondary adrenal insufficiency.

trusted-source[1], [2], [3], [4], [5], [6], [7]

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