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1 en associated with autoimmune conditions and sprue.
2 peutic potential for the treatment of celiac sprue.
3 oral peptidase supplement therapy for Celiac Sprue.
4 hly restricted diet for patients with celiac sprue.
5 ointestinal bleeding in patients with celiac sprue.
6 agents for the potential treatment of Celiac Sprue.
11 f the gastrointestinal tract, such as celiac sprue and scleroderma, and their relationship with Barre
12 tected in about half of patients with celiac sprue and should be added to the list of factors that ca
14 f response to a gluten-free diet (refractory sprue) and ulcerative jejunitis are complications of cel
15 critical role in the pathogenesis of Celiac Sprue by binding to epitopes derived from dietary gluten
16 HLA-DQ2 predisposes an individual to celiac sprue by presenting peptides from dietary gluten to inte
17 of various human disorders including celiac sprue, certain neurological diseases, and some types of
31 r understanding the role of tTGase in Celiac Sprue, our results lay the groundwork for the design of
32 oral therapeutic enzyme for treating celiac sprue, our results provide a strong foundation for furth
33 in all food grains that are toxic to Celiac Sprue patients but are absent from all nontoxic food gra
34 ion in the small intestinal mucosa of Celiac Sprue patients therefore represents a potentially attrac
35 ten in the small intestinal mucosa of celiac sprue patients, our findings reveal a new strategy for i
41 utenases (proposed oral therapies for celiac sprue) were proteolyzed in the absence or presence of a
42 atorrhea; and 7 patients with treated celiac sprue who had normal intestinal histologic features.
44 glutaminase, the major autoantigen in Celiac Sprue, with substantially greater selectivity than known
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