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The aim of this retrospective study was to establish whether the distinctive intestinal fold pattern of celiac disease (CD), known by barium studies as jejunoileal fold pattern reversal (JFPR) may be recognized at CT. The number of intestinal folds per 2.5 cm, seen at CT, were counted in the jejunum and in the ileum of 22 adult patients with CD and compared with the folds of 30 consecutive subjects in whom an intestinal disease had been excluded. The results were submitted to statistical analysis by Student's t-test. In the control group the number of folds per 2.5 cm were 4.88 (SD +/- 0.78) in the jejunum and 2.84 ( +/- 0.62) in the ileum; in the CD group the number of folds were 2.42 ( +/- 1.61) in the jejunum and 5.11 ( +/- 1.24) in the ileum. There was a statistically significant difference in the number of jejunal and ileal folds between the CD patients and the control group (in both cases p < 0.001). The JFPR was seen in 15 patients with CD (68.2 %) but in none of the controls. Our study shows that JFPR is not a normal finding and can be demonstrated by CT in the majority of patients with CD.

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OBJECTIVE. The aim of thisstudywasto investigatewith Doppler sonography the vanations of resistance in the superior mesenteric artery, both at fasting and in the postprandial state, in patients with celiac disease.SUBJECTSAND METHODS. Twenty-fivepatientswith celiacdisease(20 women,five men; mean age, 30 ± 7 yeas) and 10 healthy volunteers (seven women, three men; mean age, ±6 yeas)were examined with Doppler sonography. Nineteen patients were untreated (no dietary restrictions) and six patients were treated with a gluten-free diet at the time of the ex amination. Imaging was performed at both fasting and 15 mm after an l890-kJ meal. We in

Angiotensin-converting enzyme (ACE) is a dipeptidylcarboxypeptidase that occurs in three types of cells: endothelial, epithelial, and neuroepithelial. ACE activity is present in plasma, urine, and vascular endothelium. High levels of ACE are found in the brush border of human small bowel. The aim of this study was to evaluate ACE activity in human stools and to find a correlation with the intestinal loss of epithelial cells. Fifteen healthy subjects (HS) (8 males, 7 females; age range 6-56 years), 20 patients with celiac disease (CD) (11 males, 9 females; age range 15-53 years), and 18 patients with CD in remission after a gluten-free diet (CD-GFD) (8 males, 10 females; age range 14-54 years) were enrolled in the study. The fecal ACE activity was measured in all groups. Fecal samples were kept at -20 degrees C for a subsequent test. In HS, fecal ACE activity was 21.03 +/- 16.17 nmol/min/100 g (mean +/- SD). In patients with CD with subtotal mucosa atrophy, ACE activity was significantly higher (113 +/- 88.94) than in HS and CD on GFD (36.65 +/- 23.9). We have demonstrated ACE activity in human stools. ACE activity in stools seems to derive from the microvilli of the intestinal mucosa, thus suggesting the potential usefulness of ACE determination as an index of enterocyte damage.