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Celiac disease (gluten enteropathy) - Treatment
Last reviewed: 06.07.2025

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One of the main treatments for celiac disease is a diet that completely eliminates gluten. Wheat protein toxicity in children with celiac disease and the need to eliminate gluten from the diet were established more than 30 years ago. It was later shown that the introduction of wheat, barley, and rye flour into the histologically normal small intestine of patients with treated celiac disease quickly caused the corresponding symptoms, which were accompanied by the development of lesions typical of celiac disease. Although it is relatively easy to completely eliminate all cereals containing gluten (wheat, barley, rye, and possibly oats) from the diet, it is very difficult to actually follow such a diet. This is due to the fact that wheat is the most common component of many food products (confectionery, sauces, canned goods, instant coffee, etc.), therefore, persistent propaganda by a doctor and nutritionist is required for the need for constant adherence to a gluten-free diet for all patients with celiac disease and persons suspected of it from the so-called risk group, especially since this diet has a protective effect on the development of malignant neoplasms in this disease.
A diet that does not contain gluten from wheat, rye, barley or oats should be balanced and contain normal amounts of fat, protein (initially 100 g per day) and carbohydrates.
Since some patients who are very sensitive to the ingestion of even a small amount of wheat flour tolerate oats painlessly, it can be tried to be carefully introduced into the diet, but only during the period of remission. During the acute stage of the disease, oats are best excluded from the diet.
Rice, soybeans, corn flour, potatoes, vegetables, fruits, berries, animal products are completely non-toxic and should be included in the diet. Treatment with a gluten-free diet is a lifelong necessity for patients with this disease. Compliance with a gluten-free diet requires two rules: initially prescribe treatment and, if clinical improvement follows, confirm the diagnosis histologically. The most common reason for unsuccessful treatment with a gluten-free diet is incomplete removal of gluten from it.
In the absence of severe metabolic disorders, patient discipline, and awareness of the need for constant adherence to a gluten-free diet, there are few grounds for hospitalization. Hospitalization is necessary in the case of severe metabolic disorders, lack of response to the exclusion of gluten, and insufficient patient awareness of the high effectiveness of constant exclusion of gluten from the diet. If the patient has enteropathy resistant to treatment with a gluten-free diet, then an attempt should be made to identify another causative food agent, although its identification is not always possible.
In celiac disease, patients' ability to tolerate different amounts of gluten varies. These differences are most pronounced in those who respond to the elimination of gluten by restoring intestinal absorptive function to normal or close to normal. In such cases, patients tolerate small amounts of gluten, still maintain remission, and may occasionally not follow a diet, which does not contribute to an exacerbation of the disease. Other patients are extremely sensitive to the digestion of even the smallest amount of toxic gluten. Within a few hours of digesting foods containing a small amount of gluten, such as two slices of baked bread, they develop massive watery diarrhea resembling cholera. Acute dehydration due to severe diarrhea can cause life-threatening shock - "gliadin shock".
Treatment with a gluten-free diet results in a more rapid regression of less severe lesions of the distal intestine compared to severe lesions of the proximal intestine. Clinical improvement correlates more clearly with the extent of histological improvement of the intestine than with the severity of the lesion of its proximal section. This explains the earlier onset of clinical remission compared with morphological remission, which may be absent for many months. Ultimately, the mucous membrane of the proximal small intestine becomes normal in about 50% of patients on a gluten-free diet; in the remaining patients, it is partially restored, approaching normal; in a few, it remains damaged, despite a good clinical effect. With prolonged hospitalization, it is possible to determine which of the patients does not digest gluten. A number of patients with untreated celiac enteropathy do not tolerate milk and dairy products well, since after their consumption, bloating, diarrhea, and abdominal pain of a spastic nature occur. However, milk and dairy products are completely excluded from the diet only if they cause unpleasant symptoms. These products are an excellent source of protein, calcium, and calories for the poor diet of patients. Observations show that even many seriously ill patients tolerate a small amount of milk at the beginning of treatment with a gluten-free diet; as the structure and function of the intestine normalizes, milk is tolerated even better by patients.
Additional treatment. In severe cases of the disease, in addition to the gluten-free diet, patients should receive appropriate replacement therapy, which helps correct the disorders caused by insufficient absorption. Thus, in case of anemia, iron, folic acid and/or vitamin B12 are additionally prescribed, depending on the deficiency of a particular substance. In case of hemorrhages, signs of bleeding, significant prolongation of prothrombin time, parenteral administration of vitamin K or one of its analogues is indicated.
In patients with dehydration and electrolyte depletion due to severe diarrhea, intensive intravenous fluid and electrolyte replacement is essential. Hypokalemia is rapidly corrected by parenteral administration of potassium chloride in severe cases and by oral administration in mild cases. If convulsions occur, which is rare, urgent intravenous administration of 1-2 g of calcium gluconate is indicated. If there is no effect from its administration, the convulsions may be due to hypomagnesemia. In such a situation, 0.5 g of dilute magnesium sulfate can be administered very slowly or magnesium chloride orally (100 milliequivalents per day in divided doses), which is safer and usually sufficient. In case of hypocalcemia, clinical or radiographic signs of osteoporosis and osteomalacia, calcium preparations in the form of calcium gluconate or lactate (6-8 g per day) and vitamin D are mandatory. It is advisable to administer additional calcium and vitamin D to all patients with gluten enteropathy with significant steatorrhea until intestinal absorption is normalized under the influence of a gluten diet to prevent calcium mobilization from bones. To avoid side effects due to an overdose of vitamin D and calcium, it is necessary to monitor serum calcium. If hypercalcemia occurs, the administration of the preparations should be stopped immediately.
For patients with celiac enteropathy with impaired absorption, it is recommended to administer therapeutic doses of vitamin A, thiamine, riboflavin, nicotinic acid, pyridoxine, vitamin C and E in the form of multivitamin preparations, although some researchers doubt the need for additional administration of these vitamins.
Corticosteroid therapy should be used only as an emergency treatment for secondary transient adrenal insufficiency, which may accompany severe disease. Usually, treatment with a gluten-free diet leads to fairly rapid and lasting improvement even in severely ill patients.
It should be emphasized that due to malabsorption, when the absorption of not only nutrients but also drugs is disrupted, medications must be administered parenterally until the absorption process improves under the influence of a gluten-free diet.
The prognosis for patients with accurately diagnosed and treated disease is excellent. If gluten enteropathy is not recognized in time, a fatal outcome is possible due to increasing exhaustion, bleeding, intercurrent infections or secondary adrenal insufficiency.