• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.8 no.1
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• pp.21-30
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• 2005

Purpose: The aim of this study was to identify the clinical features and natural history of dietary protein induced proctocolitis (DPIPC) and to detect the causative foods of DPIPC, and to evaluate the effect of elimination of the foods on the course of the disease. Methods: Between March 2003 and July 2004, data from 30 consecutive patients with DPIPC who were followed for over 6 months, was reviewed. The diagnostic criterion used for DPIPC was an increase in the number of eosinophils in the lamina propria (${\geq}60per$ 10 high-power fields). In breast feeding mothers, 5 highly allergenic foods were eliminated from the maternal diet for 7 days, namely, allergenic food groups such as dairy products, eggs, nuts and soybean, fish and shellfish, and wheat and buckwheat. We observed the disappearance or appearance of hematochezia after elimination or challenge with the offending foods. Results: Before diagnosis infants were breast-fed (93.3%) or formula-fed (6.7%). Mean age at symptom onset was $11.5{\pm}5.1$ (5~24) weeks, and mean age at diagnosis was $17.8{\pm}9.5$ (8~56) weeks. Duration from symptom onset to diagnosis was $6.3{\pm}6.7$ (0~36) weeks. Mean peripheral blood eosinophil count was $478{\pm}320$ (40~1,790)/$mm^3$ and eosinophilia (> $250/mm^3$) was observedin 90.0% of patients. None of patients were found to have an increased serum IgE level. Of 15 patients that received sigmoidoscopy, nodular hyperplasia with erosion was observed in 93.3%. Of 27 patients whose mother ate the diet eliminated the 5 food groups, hematochezia diappeared in 74.1% of patients. Offending foods were identified as dairy products (37.5%), wheat and buckwheat (27.5%), fish and shellfish (20.0%), nuts and soybean (7.5%) and eggs (7.5%). A free maternal diet without patient's clinical symptoms was achieved at $29.4{\pm}8.7$ (9~44) weeks of patient's age, and a free baby diet without blood in stools was achieved at $37.5{\pm}9.7$ (12~56) weeks of age. Conclusion: DPIPC commonly occurs in exclusively breast-fed babies. Elimination of the above-mentioned 5 hyper-allergenic food groups from the maternal diet for 7days enables the detection of the offending foods. DPIPC is a transient disorder and 96.0% of patients can tolerate the offending foods at 12 months of age.

• 한국유가공학회:학술대회논문집
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• 2007.09a
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• pp.49-58
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• 2007

Inflammatory process leads to the well-known mucosal damage and therefore a further disturbance of the epithelial barrier function, resulting abnormal intestinal wall function, even further accelerating the inflammatory process[1]. Despite of the records, etiology and pathogenesis of IBD remain rather unclear. There are many studies over the past couple of years have led to great advanced in understanding the inflammatory bowel disease(IBD) and their underlying pathophysiologic mechanisms. From the current understanding, it is likely that chronic inflammation in IBD is due to aggressive cellular immune responses including increased serum concentrations of different cytokines. Therefore, targeted molecules can be specifically eliminated in their expression directly on the transcriptional level. Interesting therapeutic trials are expected against adhesion molecules and pro-inflammatory cytokines such as TNF-${\alpha}$. The future development of immune therapies in IBD therefore holds great promises for better treatment modalities of IBD but will also open important new insights into a further understanding of inflammation pathophysiology. Treatment of cytokine inhibitors such as Immunex(Enbrel) and J&J/Centocor(Remicade) which are mouse-derived monoclonal antibodies have been shown in several studies to modulate the symptoms of patients, however, theses TNF inhibitors also have an adverse effect immune-related problems and also are costly and must be administered by injection. Because of the eventual development of unwanted side effects, these two products are used in only a select patient population. The present study was performed to elucidate the ability of TNF-${\alpha}$ antibodies produced in sheep colostrums to neutralize TNF-${\alpha}$ action in a cell-based bioassay and in a small animal model of intestinal inflammation. In vitro study, inhibitory effect of anti-TNF-${\alpha}$ antibody from the sheep was determined by cell bioassay. The antibody from the sheep at 1 in 10,000 dilution was able to completely inhibit TNF-${\alpha}$ activity in the cell bioassay. The antibodies from the same sheep, but different milkings, exhibited some variability in inhibition of TNF-${\alpha}$ activity, but were all greater than the control sample. In vivo study, the degree of inflammation was severe to experiment, despite of the initial pilot trial, main trial 1 was unable to figure out of any effect of antibody to reduce the impact of PAF and LPS. Main rat trial 2 resulted no significant symptoms like characteristic acute diarrhea and weight loss of colitis. This study suggested that colostrums from sheep immunized against TNF-${\alpha}$ significantly inhibited TNF-${\alpha}$ bioactivity in the cell based assay. And the higher than anticipated variability in the two animal models precluded assessment of the ability of antibody to prevent TNF-${\alpha}$ induced intestinal damage in the intact animal. Further study will require to find out an alternative animal model, which is more acceptable to test anti-TNF-${\alpha}$ IgA therapy for reducing the impact of inflammation on gut dysfunction. And subsequent pre-clinical and clinical testing also need generation of more antibody as current supplies are low.