Abstract
Celiac disease is gluten induced enteropathy and is a chronic inflammatory disorder of the small intestine characterized by malabsorption. It is a common immune mediated disorder which is triggered by consumption of wheat (gluten). It occurs in genetically predisposed individuals (carriers of HLA-DQ2 and DQ8 haplotypes). It is characterized by inflammation of the small-intestinal mucosa and myriad gastrointestinal and systemic manifestations. A duodenal biopsy with positive serology is the gold standard for the diagnosis of Celiac disease. As there are changing presentation for Celiac disease, communication of pathologist and gastroenterologists is essential for appropriate interpretation of duodenal biopsy.
Highlights
Celiac disease (CD) is a common disease, affecting 1% of the population and evidence suggests that prevalence is increasing.[1]
There are two groups of serological tests, autoantibodies- EMA, tTG antibody and antibodies targeting the offending agent (AGAs) which is considered obsolete for diagnostic purposes because of their lower sensitivity and specificity and antibodies against synthetic deamidated gliadin peptides (DGPs). These antibodies are based on immunoglobulin A (IgA) or immunoglobulin G (IgG)
Serologic testing is very useful for screening patients with suspected CD as early detection is essential to prevent the complications of Celiac disease.[19]
Summary
The clinical manifestations of CD are changeable in nature and vary markedly with the age of the patient, the duration and extent of disease and the presence of extra intestinal pathological conditions. Detection of specific auto antibodies (anti- transglutaminase type 2 IgA) and compatible findings at duodenal histology like surface enterocyte damage, increased intraepithelial lymphocytes (IELs), crypt hyperplasia and villous atrophy being considered the principal hallmark.[2,4,5]. Elimination of gliadin stops the direct mucosal injury and eliminates the substrate necessary to form the neopeptide that propagates immunologically mediated damage.[9,10] A diverse population of immune mediators contribute to CD including macrophages, plasma cells, CD4+T helper cells, CD8+ cytotoxic T cells and natural killer cells.[3] The inflammatory cascade produces inflammatory cytokine, proteinases and other tissue damaging mediators which damages the mucosa leading to characteristic histopathological findings.[10]
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