About 8,000 years ago, Aretaeus, a Greek physician from Cappadocia, wrote a total of 8 books on medicine. In one of his books, he described a patient with<unk>  and called it 'koiliakos'. It came from Greek word of 'koelia' (abdomen), explaining diarrhea as the inability to retain  food and the passage of undigested material through the gastrointestinal tract. This later formed the basis of explanation of various diseases presenting as chronic malabsorptive diarrhea, including<unk> .<unk>  <unk>  may be classified according to the symptoms and laboratory findings into 5 sub groups as, classical, atypical, asymptomatic, latent, and potential<unk> . The etiology of the<unk>  is known to be multifactorial, both in that multiple factors can lead to the disease and that multiple factors are necessary for the disease to manifest in a patient. Gluten triggers autoimmunity and results in the inflammation of the gastrointestinal mucosa. Gluten in wheat, rye, and barley may trigger the autoimmunity to develop<unk> . Gluten peptides cross the epithelium into the lamina propria where they are deamidated by tissue transglutaminase. The peptides are then presented by DQ2+ or DQ8+ antigen-presenting cells to pathogenic<unk> 4+ T cells. The<unk> 4+ T cells trigger the T-helper-cell type 1 response which results in the infiltration of inflammatory cells into the lamina propria and epithelium. This inflammatory process ultimately leads to crypt hyperplasia and villous atrophy.<unk>  must be differentiated from other diseases presenting as chronic diarrhea. Common differentials of<unk>  include lactose intolerance, cystic fibrosis, Crohns disease,  laxative overuse, hyperthyroidism and irritable bowel syndrome. The prevalence of<unk>  in 2017 is estimated to be 500 to 1000 per 100,000 individuals worldwide. The incidence of<unk>  is approximately 10-13 per 100,000 individuals worldwide. The symptoms of<unk>  usually develop in the first decade of life, and start with symptoms suggestive of malabsorption such as abdominal pain and distension, diarrhea, malnutrition, and failure to thrive within the first few years of life. The diagnosis of<unk>  is made when at least four of the following five or three out of four (if the HLA genotype is not performed) diagnostic criteria are met: typical symptoms (chronic diarrhea, chronic abdominal pain, malabsorption, bloating, constipation, failure to thrive/weight loss, anorexia, vomiting, GERD), serum positivity for Ig A autoantibodies at high titer, HLA-DQ2 or HLA-DQ8 genotypes,<unk>  enteropathy at the small intestinal biopsy, and response to gluten-free diet. Laboratory findings consistent with the diagnosis of<unk>  include electrolyte abnormalities such as hypokalemia, hypocalcemia, hypomagnesemia, metabolic acidosis,hypoalbuminemia, hypoproteinemia, hypocholesterolemia and low serum carotene level. Hematologic findings include low folate and vitamin B-12 levels, low serum ironlevel and prothrombin time (PT) prolongation. Stool examination may show fat droplets on Sudan stain and a 72-hour fecal fat collection may be used for documentation of steatorrhea. Features present on CT enteroclysis consistent with the diagnosis of<unk>  may include, jejunoileal fold pattern reversal, ileal fold thickening, vascular engorgement, prominent mesenteric lymph nodes may cavitate with a fluid-fat level, submucosal fat deposition may be observed in long standing cases, and features suggestive of splenic atrophy may be present. Preferred therapy for<unk>  is dietary modification which includes gluten-free diet. Patients with<unk>  should be referred to a dietitian once the diagnosis of<unk>  is made. A minority of patients suffer from refractory disease, which means that they do not improve with a gluten-free diet. Pharmocotherapy is used if alternative causes are eliminated and dietary modification is not beneficial. Pharmacotherapy include steroids, azathioprine, cyclosporin, and monoclonal antibodies. Effective measures for the primary prevention of<unk>  include breastfeeding, delayed introduction of gluten-including diet, and preventing GI infections.
Celiac disease
Tropical sprue
Crohn's disease
Autoimmune enteropathy
Inflammatory bowel disease
Gastroesophageal reflux disease
Irritable bowel syndrome
Gastric lymphoma