Celiac Disease and Sprue Spectrum

• Audio chapter
  Single-voice audio, listen on the commute.
• ABIM-format MCQs
  5-option vignettes with full wrong-answer teaching.
• Study guide
  Tables, decision trees, primary sources.
• AI tutor
  Chapter-grounded, answers the question you're stuck on.

What this chapter covers

• Section 10.1: Pathogenesis, genetics, and epidemiology

  Celiac disease is an HLA-restricted, gluten-driven enteropathy, and every fact in the chapter falls out of a single mechanistic sentence: gluten peptides resist gastrointestinal proteolysis, reach the lamina propria, are deamidated by tissue transglutaminase 2, and the deamidated peptides bind HLA-DQ2 or HLA-DQ8 on antigen-presenting cells where they activate gluten-specific CD4+ T cells that drive the cytokine cascade behind the villous atrophy.

• Section 10.2: Clinical presentations

  Modern celiac disease in adults rarely looks like the textbook malabsorption picture, and practice has moved with the literature.

• Section 10.3: Diagnosis

  Diagnosis of celiac disease is anchored on serology drawn on a gluten-containing diet, confirmed by upper endoscopy with multiple duodenal biopsies, and triangulated against HLA in selected scenarios.

• Section 10.4: Treatment, monitoring, and mucosal healing

  A strict, lifelong gluten-free diet is the entire treatment for celiac disease, and every other element of management is built around supporting and verifying that diet.

• Section 10.5: Refractory celiac disease

  Refractory celiac disease is the diagnosis to consider when a patient with biopsy-proven celiac disease has persistent or recurrent malabsorptive symptoms with histologic villous atrophy despite at least 12 months of strict gluten-free diet and no other explanation.

• Section 10.6: Complications

  The malignancy spectrum in celiac disease is the high-stakes downstream consequence, and the central fact is that risk is concentrated in patients with refractory disease (especially RCD2) and in patients with poorly controlled or unrecognized disease, while strict gluten-free diet attenuates but does not eliminate the risk.

Podcast episodes

1. 01

   Celiac Diagnosis and Treatment

   Celiac disease built from mechanism through monitoring: modified gluten peptides bind HLA-DQ2/DQ8, drive T-cell inflammation, and trigger lymphocyte-mediated villous atrophy. The modern adult presents like IBS, iron deficiency, or an extraintestinal finding, so the threshold to test is broad. Diagnosis is serology-anchored and biopsy-confirmed while the patient still eats gluten, treated by a strict lifelong gluten-free diet with structured monitoring.

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2. 02

   Refractory Celiac and Complications

   Most celiac patients failing a gluten-free diet are not refractory; they are eating hidden gluten or have a coexisting condition, so a structured non-responsive differential precedes any refractory workup. When refractory disease is genuine, the type one versus type two split on intraepithelial lymphocyte phenotype separates a steroid-responsive disease with good survival from a pre-lymphoma syndrome. The malignancy spectrum, enteropathy-associated T-cell lymphoma, ulcerative jejunitis, and small-bowel adenocarcinoma, is the payoff of getting that distinction right.

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Key topics

• ·Pathogenesis and HLA-DQ2/DQ8
• ·Extraintestinal and IBS-like presentations
• ·Silent, potential, and seronegative phenotypes
• ·Dermatitis herpetiformis
• ·tTG-IgA serology and total IgA
• ·Duodenal biopsy and Marsh classification
• ·Gluten-free diet and nutritional repletion
• ·Serologic and histologic monitoring
• ·Non-responsive celiac differential
• ·Refractory celiac type 1 vs type 2
• ·Intraepithelial lymphocyte phenotyping
• ·Enteropathy-associated T-cell lymphoma
• ·Ulcerative jejunitis
• ·Small-bowel adenocarcinoma
• ·Small-bowel imaging and surveillance