gluten intolerance|impaired small intestine function|celiac disease | Gesundheit-Aktuell.de

In those affected, this disease causes symptoms such as diarrhoea, a feeling of fullness, nausea, weight loss, anemia, vitamin and protein deficiency. In childhood, the impaired function of the small intestine resulting from celiac disease can lead to malnutrition and thus growth and development disorders.

Celiac disease is distributed worldwide, but occurs more frequently in Europe and populations of European origin in North America and Australia. The incidence (frequency) ranges from 1/300 (e.g. western Ireland) to 1/6,500 (Sweden) and affects more women than men. In Germany, the frequency is about 1:1,000. The disease usually manifests in infancy with a first peak in age between 9 months and 3 years and a second in the 4th decade of life.

Sprue is caused by a constant intolerance reaction to gluten. Circulating antibodies against gluten and its components are mostly detectable in the serum of the patients, and increased levels of sensitized immune defense cells (T lymphocytes and plasma cells) are detectable in the wall of the small intestine. This attacks and reduces the surface of the mucous membrane in the small intestine. The consequence of the reduced surface area of ​​the small intestine is impaired absorption (malabsorption) of glucose, amino acids, fat, vitamins, calcium and iron. Furthermore, there are disturbances in the electrolyte and water transport, which promote diarrhea (diarrhea). In addition, there is a genetic disposition (hereditary predisposition) with familial accumulation of the disease. The structural changes are reversible on a gluten-free diet.

The clinical picture of sprue is extremely variable. In children, the focus is on failure to thrive, which in most cases occurs 3 – 6 months after the start of a gluten-containing diet (semolina porridge, whole-grain porridge, etc.). In adult full-on sprue, the patient experiences severe weight loss, muscle wasting, and protein deficiency edema due to malabsorption. In addition, diarrhea, flatulence and other symptoms such as iron deficiency anemia (anemia) occur.

Celiac disease can be unequivocally proven by means of an endoscopic assessment of the small intestinal mucosa with evidence of small intestinal villous atrophy, i.e. destruction of the normal mucosal relief, as well as by examining removed tissue particles.

A second form of clear proof is the determination of antibodies in the blood. Antiendomyseal antibodies are specific to celiac disease, and antigliadin antibodies are specific to the degree of severity. The value of the measured antibodies correlates with the severity of the disease and can be used as a progress parameter in addition to clinical symptoms.

The decisive factor in therapy is a consistent, lifelong gluten-free diet. Gluten-free grains are rice, corn and millet. Due to the lack of declaration regulations for gluten in finished products or medicines, strict adherence to the diet often causes problems. The vast majority of patients respond to a gluten-free diet within a week. In severe cases, substitution of vitamins and trace elements and/or artificial nutrition may be necessary initially. At the beginning, the diet should always be lactose-free, as there is almost always an initial lactose intolerance (intolerance to milk sugar) due to villous atrophy.

Life expectancy is not restricted if a consistent gluten-free diet is adhered to. The untreated increased tendency to develop malignant diseases of the gastrointestinal tract equals the risk of the normal population after several years of dieting, so that a lifelong diet is recommended.