1.
Plasma citrulline is a marker of absorptive small bowel length in patients with transient enterostomy and acute intestinal failure.
Picot, D, Garin, L, Trivin, F, Kossovsky, MP, Darmaun, D, Thibault, R
Clinical nutrition (Edinburgh, Scotland). 2010;(2):235-42
Abstract
BACKGROUND & AIMS Small bowel disruption is often complicated by acute intestinal failure and can be corrected by chyme reinfusion (CR). Plasma citrulline ([Cit]) is a biomarker of the enterocyte mass. Our aim was to determine whether [Cit] could be a marker of absorptive intestinal mass or function by assessing whether CR could affect intestinal absorptive function and [Cit]. METHODS Twenty-six patients with small bowel disruption and double enterostomy were treated with CR. Fecal wet weight, nitrogen and fat absorption, parenteral nutrition delivery and [Cit] were measured before and after the initiation of CR with a median follow-up of 30 days. RESULTS CR decreased the intestinal wet weight output (median+/-IQ, 2384+/-969 vs. 216+/-242mLd(-1), P<0.0001) and parenteral nutrition dependence (65% vs. 8%, P<0.01). CR was associated with a rise in net nitrogen and fat digestive absorption and [Cit] (17.0+/-10.0 vs. 31.0+/-12.0micromolL(-1), P=0.0001). Before the initiation of CR, [Cit] correlated positively with the absorptive post-duodenal small bowel length (r=0.39, P=0.04), but not with the total post-duodenal small bowel length (r=0.11, P=0.60). CONCLUSION CR allows for a dramatic improvement of intestinal absorptive function and a near doubling in [Cit] level. [Cit] is not a marker of overall intestinal mass, but of the absorptive small bowel function.
2.
Antiendomysial antibody detection in fecal supernatants: in vivo proof that small bowel mucosa is the site of antiendomysial antibody production.
Picarelli, A, Sabbatella, L, Di, TM, Di, CT, Vetrano, S, Anania, MC
The American journal of gastroenterology. 2002;(1):95-8
Abstract
OBJECTIVES Serum antiendomysial antibodies (EMAs), highly sensitive and specific serological markers of celiac disease (CD), are detectable in culture media of biopsy samples from CD patients. This finding can be considered an in vitro evidence that intestinal mucosa is a site of EMA production. To confirm this finding, we investigated the presence of EMAs and of anti-tissue transglutaminase (anti-tTG), recently identified as the autoantigen of the EMA, in fecal supernatants of CD patients. METHODS Twenty-one newly diagnosed CD patients, 10 treated CD patients on a gluten-free diet, and 14 control disease patients on a gluten-containing diet were enrolled. Twenty-four-hour stool collections and fecal supernatants were obtained from all patients in the study. Biopsy cultures were also performed. IgA EMAs were detected in sera, culture media, and fecal supernatants. IgA, IgG, IgM, and IgE anti-gliadin antibodies (AGAs) and IgA anti-tTG antibodies were measured in fecal supernatants. The weights, water content, and pHs of the 24-h stool collections were also measured. RESULTS In all untreated CD patients EMAs were detectable in sera, culture media, and fecal supernatants. In treated CD patients, EMAs were detected only in culture media after in vitro gliadin challenge. No EMAs were detected in controls. Anti-tTG levels were higher in untreated CD patients than in treated CD patients and controls. IgA AGA levels were higher in untreated CD patients than in treated CD and control patients, whereas IgM AGAs were higher in both untreated and treated CD patients than in controls. No statistically significant differences were observed for IgG and IgE AGAs among the above-mentioned populations. Fecal weights, water content, and pHs were higher in untreated CD than in control patients. CONCLUSIONS The presence of EMAs in fecal supernatants represents the in vivo proof that intestinal mucosa is a site of EMA production. Furthermore, EMA detection in the stools could be a simple and useful additional tool to clarify diagnosis in the patchy conditions of CD.