Morphologic, immunophenotypic, and cytogenetic characteristics.

<p>TCR: T-cell receptor β gene rearrangement; TVA: total villous atrophy; STVA: subtotal villous atrophy; SNP: single nucleotide polymorphism; LOH: loss of heterozygosity; LP: lamina propria; ND: not done; PC: polyclonal.</p

Duodenum as seen at endoscopy demonstrating nodular mucosa with scalloping of folds (Case 3).

<p>Duodenum as seen at endoscopy demonstrating nodular mucosa with scalloping of folds (Case 3).</p

Representative photomicrographs of duodenal biopsies.

<p>Severe villous atrophy is seen (A) without any increase in intraepithelial lymphocytes (B). The lamina propria is expanded by a dense infiltrate of predominantly small-sized lymphocytes with evidence of crypt destruction and a lymphoepithelial lesion (C). On IHC analysis, the lymphocytes are CD4+ (D), CD5− (E), and CD7− (F), and have a low Ki-67 proliferation index (<5%)(G).</p

Clinical characteristics at presentation.

<p>Clinical characteristics at presentation.</p

Association of persistent villous atrophy with IHD overall, and stratified by time after follow-up biopsy.

<p>HR, Hazard Ratio</p><p>†Adjusted for patient age at follow-up biopsy, gender, calendar period of follow-up biopsy, education, and duration of celiac disease at the time of follow-up biopsy</p><p>Association of persistent villous atrophy with IHD overall, and stratified by time after follow-up biopsy.</p

Section from a small intestinal resection specimen showing large cell transformation (Case 2).

<p>Transmural infiltrate of neoplastic lymphocytes is observed (A). The lamina propria shows admixtures of small and large atypical lymphocytes, including bizarre and multinucleated forms (B and C). The large lymphocytes express CD4 (D), CD30 (F) and granzyme B (G) and lack CD5 expression (E).</p

Association of persistent villous atrophy with IHD, stratified by gender, age, and year of CD diagnosis.

<p>HR, Hazard ratio</p><p>IHD. Ischemic heart disease</p><p>†Adjusted for patient age at follow-up biopsy, gender, calendar period of follow-up biopsy, education, and duration of celiac disease at the time of follow-up biopsy.</p><p>Association of persistent villous atrophy with IHD, stratified by gender, age, and year of CD diagnosis.</p

Risk of IHD type (myocardial infarction, stable angina, and unstable angina), and risk of death due to IHD in patients with CD who have persistent villous atrophy on follow-up biopsy, compared to those with mucosal healing.

<p>CD, celiac disease</p><p>HR, Hazard ratio</p><p>IHD. Ischemic heart disease</p><p>MI, Myocardial infarction</p><p>†Adjusted for patient age at follow-up biopsy, gender, calendar period of follow-up biopsy, education, and duration of celiac disease at the time of follow-up biopsy</p><p>Risk of IHD type (myocardial infarction, stable angina, and unstable angina), and risk of death due to IHD in patients with CD who have persistent villous atrophy on follow-up biopsy, compared to those with mucosal healing.</p

Clinical and pathological characteristics of published cases.

<p>TCR: T cell receptor β or γ gene rearrangement; LP: lamina propria; ND: not done; MACOP-B: methotrexate, ARA-C, cyclophosphamide, oncovin, prednisone, bleomycin; CVP: cyclophosphamide, vincristine, prednisone; ACVB-P: doxorubicin, cyclophosphamide, vindesine, bleomycin, prednisone.</p

Characteristics of the patient cohort with CD and follow-up biopsies.

<p>(Excludes patients with a diagnosis of IHD prior to follow-up biopsy, n = 208).</p><p>CD, celiac disease</p><p>IHD. Ischemic heart disease</p><p>MI, Myocardial infarction</p><p>*The sum of IHD subtypes is greater than the total number of patients with IHD because of patients who had more than one type of IHD event</p><p>†Among patients without a history of AF at the time of follow-up biopsy (n = 7,530).</p><p>Characteristics of the patient cohort with CD and follow-up biopsies.</p