Etiology
• Gluten is due to intestinal inflammation and cell damage caused by an immunological reaction against the gliadin metabolite.
• Gluten; It is found in rye, wheat, barley, but absent from corn and rice. It is found in small amounts in oats.
• The role of immunological, genetic (HLA-DQ2 or HLA-DQS) and environmental factors (adenovirus type 12) in etiology is emphasized.
Clinic
• Subtypes according to clinical signs/signs, histology (mucosal damage) and serology:
Form with classical intestinal malabsorption: Typical malabsorption findings are seen. There is mucosal damage. Serology and HLA positive.
Form with atypical symptoms: There are no typical signs of malabsorption. It is characterized by one or more of the clinical pictures such as anemia, osteopenia, infertility, neurological etc. There is mucosal damage. Serology and HLA positive.
Asymptomatic (silent - subclinical) form: There is no obvious clinical sign/finding. There is mucosal damage. Serology and HLA positive.
Latent form: There are no obvious clinical signs/signs. There is no mucosal damage.
Serology and HLA positive.
• Typical frothy, oily, odorous diarrhea is the most important clinical sign.
The proximal small intestine is predominantly affected.
Iron malabsorption may occur first. Unexplained iron deficiency should be considered when investigating.
• May be associated with dermatitis herpetiformis.
• Hyposplenism may be seen.
• It has also been shown that there is a relationship between celiac disease and Type I diabetes, IgA deficiency, Down and Turner syndrome.
• The risk of developing T-cell lymphoma and intestinal adenocarcinoma is increased in celiac disease.
Diagnosis
• Especially serum carotene level and D-Xylose tests, which reflect the mucosal integrity of the small intestine, are defective.
Serological tests
Anti-gliadin IgA (low sensitivity and specificity)
Anti-endomysium IgA and anti-tissue transglutaminase IgA
They are 90-95% sensitive and specific.
It is very valuable for diagnosis. They are also used for scanning purposes.
Serological tests are expected to become negative with treatment.
• The combined sensitivity of HLA-DQ2 or HLA-DQS is 95-100%, but they do not have specificity. They can also be found positive in healthy people. Both negatives largely rule out gluten enteropathy.
• Small intestine biopsy findings
Intraepithelial lymphocyte increase
Villous atrophy, mucosal blunting
crypt hyperplasia
• biopsy; shows the pathology conclusively, but does not specifically indicate its relationship with gluten-sensitive enteropathy.
• diagnosis; clinical findings, serology and pathology are combined. Histological improvement with treatment establishes the definitive diagnosis.
Treatment
Diet: All gluten-containing grain products are excluded from the diet. 90% of cases respond to a gluten-free diet.
• Steroid: It is used in cases that do not respond to treatment despite diet.
• Peptidase: Inactivates toxic gluten peptides in the stomach.
• Dietary non-compliance should be considered first in patients presenting with increased complaints. Despite diet, abdominal symptoms and increased sedimentation should be warning signs for lymphoma development.
• Things to consider in gluten enteropathy that does not respond to treatment:
Non-compliance with the diet (the most common and the first reason to come to mind)
Other accompanying diseases (Lactase deficiency, infection, etc.)
refractory sprue
Complication development (collagenous sprue, lymphoma)