（idiopathic steatorrhea）。
The patient is thin, malnourished, has diarrhea, and has fatty stool. The etiology of this disease may be related to genetic metabolic abnormalities and immune factors. It is reported that about 80% of the patients with this disease have human leukocyte antigens HLA-B8 and HLA-DW3. After people eat cereals, the gliadin peptides contained in their gluten need related peptidase to hydrolyze in the intestine. If the intestinal mucosa epithelium of the patient lacks this enzyme, the intestinal mucosa will be stimulated by the hydrolyzed gliadin peptides to cause this disease. Others believe that the disease is gluten allergic enteropathy, and the allergen is glutenin. The addition of gliadin to the jejunal mucosa in vitro can cause the proliferation of T cells in the tissue.
The villi and microvilli of jejunum mucosa epithelium in this patient were obviously atrophied, and the mucosal surface was flat. Mucosal lamina propria showed chronic inflammatory changes, including lymphocytes, plasma cells, and sometimes eosinophils. If the patient's diet does not contain gluten food, the above intestinal mucosal lesions can be recovered.
