Apoptotic Epithelial Cells in Biopsy Specimens from Infants with Streaked Rectal Bleeding

Kumagai, Hideki; Masuda, Tomoyuki; Maisawa, Shun-ichi; Chida, Shoichi

doi:10.1097/00005176-200104000-00007

Cited by 11 publications

(14 citation statements)

References 21 publications

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“…We have already reported that nuclear dust within the lamina propria beneath the basement membrane of the epithelium in colonic mucosal biopsies of patients with colitis is a form of apoptotic epithelial cells in pathological situations and that its expression correlates with clinical severity of colitis [7]. Kumagai et al [8] described apoptotic epithelial cells in biopsy specimens from infants with streaked rectal bleeding. They showed that the presence of high numbers of apoptotic epithelial cells in the lamina propria in sections of rectosigmoid biopsy specimens of young infants who presented with allergic proctocolitis characterized by eosinophilic infiltration.…”

Section: Discussionmentioning

confidence: 98%

“…Recently, we postulated that nuclear dust within the lamina propria beneath the basement membrane of the epithelium in colonic mucosal biopsies of patients with colitis is a form of apoptotic epithelial cells in pathological situations and that its expression correlates with clinical severity of colitis [7]. Kumagai et al [8] described apoptotic epithelial cells in biopsy specimens from infants with streaked rectal bleeding.…”

Section: Introductionmentioning

confidence: 99%

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Expression of Apoptotic Epithelial Cells Within Lamina Propria Beneath the Basement Membrane Triggers Dextran Sulfate Sodium-Induced Colitis

et al. 2008

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We postulated that nuclear dust within the lamina propria beneath the basement membrane of the epithelium in colonic mucosa is a form of apoptotic epithelial cells and that its expression triggers dextran sulfate sodium-induced colitis. The aim was to determine the origin of nuclear dust and to explore the correlation between nuclear dust expression and clinicopathologic parameters of colitis. Rats were treated with 3% dextran sulfate sodium. Cells showing double positive staining with cytokeratin and TdT-mediated uUTP-biotin nick-end labeling technique were apoptotic cells derived from epithelial cells. Nuclear dust expression on day 5 correlated with bloody stools and a decrease of mitotic colonic cells just before ulceration. Examination of cultures under light and fluorescent microscopy showed that dextran sulfate sodium caused early apoptosis and late apoptosis or necrosis. Our results suggest that interventions directed toward the apoptotic process may be beneficial in the treatment of ulcerative colitis.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Expression of Apoptotic Epithelial Cells Within Lamina Propria Beneath the Basement Membrane Triggers Dextran Sulfate Sodium-Induced Colitis

et al. 2008

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“…For a definitive diagnosis, elimination and challenge of allergens are recommended [7]. As a distinctive approach, the histological findings associated with eosinophil infiltrations – for example, >20 eosinophils/HPF (87 and 130 eosinophils/HPF in cases 3 and 4, respectively) – are also reported to be good criteria for the diagnosis of AC [6,18,19]. A cluster of eosinophils in mucous and bloody stool may be of diagnostic value.…”

Section: Discussionmentioning

confidence: 99%

Eosinophilic Gastrointestinal Disorders in Infants: A Japanese Case Series

Yamada

Nishi²,

Ebara³

et al. 2011

Int Arch Allergy Immunol

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Background: Eosinophilic gastrointestinal disorders (EGIDs) are disorders characterized by primary eosinophil inflammation in the gastrointestinal tract. There are a small number of reports of eosinophil infiltration in gastrointestinal tracts presenting as EGIDs in infants. In this study, we present Japanese cases of EGIDs in infants. Methods: Five patients diagnosed with or strongly suspected to have EGIDs in our hospital from 2008 to 2010 were reviewed. Radiographic contrast enema examinations and/or endoscopies were performed in 4 and 3 patients, respectively. Results: There were patients with eosinophilic colitis (1 suspected and 2 biopsy-proven), a patient who was suspected of having allergic eosinophilic enterocolitis, and a patient with eosinophilic gastroenteritis associated with pediatric hypereosinophilic syndrome. Conclusions: The causes and clinical findings of patients with intestinal eosinophil inflammation vary. Therefore, deliberate examination and observation are important for patients with infantile EGID.

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“…The differential diagnosis of FPIAP in an infant with increased numbers of eosinophils in the lamina propria is relatively straightforward after exclusion of anal fissures and enteric infections, which usually obviates the need for food challenges after an elimination diet [19,20,21]. In our study, the diagnosis of FPIAP was made when the following 3 criteria were satisfied in the presence of consistent endoscopic and histological findings [21]: (i) small and bright red-colored rectal bleeding with or without mucus in a healthy neonate or infant (age ≤6 months), (ii) no other cause of rectal bleeding (anal fissure, polyp, bleeding diathesis, infection, necrotizing enterocolitis, pseudomembranous colitis, or any other surgical abdominal condition) or systemic symptoms, and (iii) disappearance of rectal blood after elimination of the offending food protein from the infant's or the lactating mother's diet. The elimination diet was continued for at least 6 months, until a cure challenge was carried out to test whether the infants had developed immunological tolerance.…”

Section: Methodsmentioning

confidence: 99%

Food Protein-Induced Non-Immunoglobulin E-Mediated Allergic Colitis in Infants and Older Children: What Cytokines Are Involved?

Ozen

Gülcan²,

Ercan

et al. 2015

Int Arch Allergy Immunol

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Background: Food protein-induced allergic proctocolitis (FPIAP) is mostly a non-immunoglobulin E-mediated disease where a T-cell-mediated reaction to cow's milk protein has been suggested. We determined the expression of transforming growth factor (TGF)-β, TGF-β receptor-1, tumor necrosis factor (TNF)-α, CD86, and CD23 on the colon mucosa to investigate their roles in the pathogenesis of the two subtypes of FPIAP, i.e. infantile FPIAP and FPIAP in older children. Methods: Group 1 comprised children with infantile FPIAP (age <6 months, n = 21), group 2 referred to FPIAP in older children (age >1.5 years, n = 7), and group 3 included children with juvenile hyperplastic polyps (n = 22). Immunohistochemical staining of colonic biopsy specimens was performed. Results: The expression of TNF-α was signiﬁcantly higher in groups 1 and 2 compared to group 3. Group 2 patients had a signiﬁcantly lower TGF-β expression compared to the other groups. The expression of CD86 was higher in group 1 than in group 3 (p = 0.012). Eosinophil counts per high-power field in the lamina propria were signiﬁcantly correlated with CD86 expression (p = 0.026, r = 0.388). Conclusion: Our results suggest that TNF-α is implicated in the pathogenesis of both types of FPIAP. The decreased activity of TGF-β receptor-1 accompanied by the increased expression of CD86 in infants and the decreased activity of TGF-β in older children appear to play a role in the development of FPIAP.

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Apoptotic Epithelial Cells in Biopsy Specimens from Infants with Streaked Rectal Bleeding

Abstract: The high number of apoptotic epithelial cells in rectosigmoidal mucosal biopsies of infants with streaked rectal bleeding is probably caused by accelerated epithelial cell turnover and apoptosis.

Cited by 11 publications

References 21 publications

Expression of Apoptotic Epithelial Cells Within Lamina Propria Beneath the Basement Membrane Triggers Dextran Sulfate Sodium-Induced Colitis

Expression of Apoptotic Epithelial Cells Within Lamina Propria Beneath the Basement Membrane Triggers Dextran Sulfate Sodium-Induced Colitis

Eosinophilic Gastrointestinal Disorders in Infants: A Japanese Case Series

Food Protein-Induced Non-Immunoglobulin E-Mediated Allergic Colitis in Infants and Older Children: What Cytokines Are Involved?

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