sprue

Celiac sprue (celiac disease) is an autoimmune reaction to gliadin (a gluten component) in genetically susceptible individuals (HLA-DQ2/DQ8), causing T-cell mediated damage to small intestinal villi, primarily in the duodenum and proximal jejunum. This leads to villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis, resulting in malabsorption of fats, vitamins (especially fat-soluble A,D,E,K), iron, and folate. Clinical features include diarrhea, steatorrhea, weight loss, bloating, dermatitis herpetiformis, and in children, failure to thrive. Diagnosis involves serology (anti-tissue transglutaminase IgA, anti-endomysial antibodies) and confirmatory duodenal biopsy showing villous blunting; symptoms improve on gluten-free diet. Associated with increased risk of enteropathy-associated T-cell lymphoma and other autoimmune diseases (type 1 diabetes, thyroiditis).

Tropical sprue occurs in residents of or travelers to tropical regions (Caribbean, Southeast Asia, India) and is thought to result from chronic bacterial infection/overgrowth causing diffuse mucosal damage throughout the small intestine (unlike celiac's proximal predominance). It presents similarly with malabsorption, diarrhea, and megaloblastic anemia due to folate and B12 deficiency. Treatment includes antibiotics (tetracycline) plus folic acid supplementation, distinguishing it from celiac disease which requires dietary gluten elimination.

Both conditions are high-yield for boards due to their classic presentations, distinct pathophysiology, and management differences. Key distinguishing features: celiac is autoimmune/genetic with proximal small bowel involvement and dermatitis herpetiformis association; tropical sprue is infectious/environmental with diffuse small bowel involvement and response to antibiotics.