[Histopathological changes of duodenal salami ulcer in children].

OBJECTIVE: Duodenal salami ulcer is a common disease found on routine endoscopic examination in children. The purpose of the study was to explore the characteristics and the clinicopathological features of duodenal salami ulcer in children and to deepen the understanding of duodenal salami ulcer. METHODS: The endoscopic results of 117 cases with the duodenal salami ulcer were analyzed. The specimens of gastric antrum and duodenal bulb were subjected to HE and Giemsa staining and were examined for any alteration in histopathology and infection with Helicobacter pylori (Hp). The duodenal mucosa was stained with AB (pH 2.5)/PAS in order to diagnose the duodenal metaplasia. RESULTS: The major endoscopic finding was a kind of hoarfrost, which was dotty or flaky, covered on the hyperemic and edematous mucosa. The detection rate of this change was 2.29% (117/5 106) of all the endoscopic examinations in children and the rate among cases with duodenal ulcer was 49.2% (117/238). The histopathology was characterized by a heavy infiltration of mainly lymphocytes, plasmocytes and neutrophilic granulocytes, frequently accompanied by superficial erosion. Sixty-one cases were pathologically diagnosed as chronic active duodenitis, superficial erosion in 45; chronic duodenitis in 50; eosinophilic duodenitis in 6. Detection rate of Hp in gastric antrum was 58% (68/117) of all cases. Detection rate of Hp infection and gastric epithelium metaplasia in duodenal bulb was 11.1% (13/117) and 31.1% (37/117), respectively. However, detection rate of Hp in gastric antrum was 25.0% (1 203/4 810) in 4 810 cases of normal duodenal bulb and chronic duodenitis in the same period. Detection rate of Hp in duodenal bulb was 0% and the detection rate of gastric epithelium metaplasia in duodenal bulb was 2.7% (128/4 810). All these detection rates were much higher than those of the specimens collected during the same period with normal duodenal bulb and chronic duodenitis (P < 0.001). Twenty-one cases were reexamined by endoscopy after having been treated with antacids or antacids and antimicrobial agents for 4 weeks. The lesions were healed up and no scars were found. CONCLUSION: Duodenal salami ulcer in children had a special manifestation of duodenal inflammation or erosion but not a real ulcer. It was caused by the Hp infection in gastric antrum or duodenal bulb and the increase of gastric acids. The therapeutic principles were antacid and antimicrobial agents. The prognosis was good.

[Expression of tumor necrosis factor-alpha and nuclear factor-kappa B in childhood ulcerative colitis].

OBJECTIVE: It has been proposed that aberrant immunity of local bowel mucosa may cause ulcerative colitis (UC) and the tumor necrosis factor-alpha (TNF-alpha) and nuclear factor-kappa B (NF-kappa B) may play a role in the development of this disease. To investigate the role of TNF-alpha and NF-kappa B in childhood UC, the expression of TNF-alpha and NF-kappa B in the bowel mucosa and their relationship were studied. METHODS: Using anti-CD68, anti-TNF-alpha and anti-NF-kappa Bp65 antibodies, the cytokine immunoreactivities in the bowel mucosa of 39 cases of childhood UC (active UC: n = 21, non-active UC: n = 18) were detected by immunohistochemistry. The control specimens of normal bowel mucosa were collected from 7 cases with colorectal polyp or abdominal pain by sigmoidoscopy. RESULTS: The numbers (median: interquartile range) of CD68(+) cells, TNF-alpha(+) cells and NF-kappa Bp65(+) cells were 44.0 (31.5 - 48.2), 42.7 (19.5 - 65.0) and 50.7 (30.0 - 58.0) in the active UC mucosa, and were 9.2 (7.9 - 16.6), 5.5 (2.5 - 9.1) and 4.2 (3.0 - 8.4) in non-active UC mucosa, and 5.3 (4.3 - 8.7), 3.0 (0.0 - 6.3) and 3.3 (0.0 - 4.0) in the control mucosa, respectively. The levels of CD68, TNF-alpha and NF-kappa Bp65 expressions in the active UC were significantly higher than those in the non-active UC (P < 0.001) and the controls (P < 0.001). The expression level of CD68 in non-active UC was much higher than that in the controls (P = 0.008). Using the correlation analysis, a positive correlation between TNF-alpha and NF-kappa B activation was found (r = 0.885, P < 0.001). CONCLUSIONS: Macrophages TNF-alpha and NF-kappa B may play an important role in the pathophysiologic mechanism of childhood active UC. The activation of NF-kappa B may be associated with the release of TNF-alpha.