Article

Histology of the terminal ileum in coeliac disease.

Depts. of Gastroenterology and Histopathology, Altnagelvin Hospital, Londonderry, Northern Ireland BT47 6SB, UK.
Scandinavian Journal of Gastroenterology (Impact Factor: 2.16). 07/2004; 39(7):665-7. DOI: 10.1080/00365520410004901
Source: PubMed

ABSTRACT The histological lesion of gluten sensitivity primarily affects the proximal small bowel. The purpose of this study was to assess whether there were features of gluten-sensitive enteropathy in biopsies taken from the terminal ileum during colonoscopy/ileoscopy. Specific and sensitive abnormalities might facilitate diagnosis of coeliac disease in patients undergoing colonoscopy as their initial procedure or help select those who should proceed to upper gastrointestinal endoscopy and duodenal biopsy.
Terminal ileal biopsies, taken from 30 patients with duodenal villous atrophy consistent with coeliac disease and from 60 control patients with no evidence of coeliac or inflammatory bowel disease, were reviewed blindly and compared. Biopsies were assessed for the presence or absence of villous atrophy and crypt hyperplasia, and counts were made of intraepithelial lymphocytes (IELs).
One patient only, in the coeliac group, had partial villous atrophy with crypt hyperplasia in the terminal ileum. IEL counts were significantly higher (P< 0.005) in the coeliac group than among controls (mean per 100 enterocytes 26 versus 10). An ileal IEL count > or =25 had a sensitivity for duodenal villous atrophy (VA) of 60% and specificity of 100%.
Coeliac disease may affect the entire small bowel. Increased IEL density in the terminal ileum is associated with duodenal VA and should prompt a search for coeliac disease by serology and duodenal biopsy. Conversely, a normal IEL count does not allow the exclusion of coeliac disease with confidence.

0 Bookmarks
 · 
182 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: The initial development and maintenance of tolerance to dietary antigens is a complex process that, when prevented or interrupted, can lead to human disease. Understanding the mechanisms by which tolerance to specific dietary antigens is attained and maintained is crucial to our understanding of the pathogenesis of diseases related to intolerance of specific dietary antigens. Two diseases that are the result of intolerance to a dietary antigen are celiac disease (CD) and dermatitis herpetiformis (DH). Both of these diseases are dependent upon the ingestion of gluten (the protein fraction of wheat, rye, and barley) and manifest in the gastrointestinal tract and skin, respectively. These gluten-sensitive diseases are two examples of how devastating abnormal immune responses to a ubiquitous food can be. The well-recognized risk genotype for both is conferred by either of the HLA class II molecules DQ2 or DQ8. However, only a minority of individuals who carry these molecules will develop either disease. Also of interest is that the age at diagnosis can range from infancy to 70-80 years of age. This would indicate that intolerance to gluten may potentially be the result of two different phenomena. The first would be that, for various reasons, tolerance to gluten never developed in certain individuals, but that for other individuals, prior tolerance to gluten was lost at some point after childhood. Of recent interest is the concept of non-celiac gluten sensitivity, which manifests as chronic digestive or neurologic symptoms due to gluten, but through mechanisms that remain to be elucidated. This review will address how animal models of gluten-sensitive disorders have substantially contributed to a better understanding of how gluten intolerance can arise and cause disease.
    Seminars in Immunopathology 05/2012; 34(4):497-511. · 5.38 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Celiac disease (CD) is an autoimmune inflammatory disease of the small intestine as a result of reaction to wheat protein, gluten. Exclusion of dietary gluten is the mainstay of the treatment that necessitates a precise diagnosis of the disease. Serological screening may aid in identifying patients with suspected CD, which should be confirmed by intestinal biopsy. It has been shown that duodenal biopsies are good for detection of the disease in most patients. However, there is a group of patients with positive serology and inconclusive pathology. As a result of the widespread use of serology, many patients with equivocal findings grow quickly. Unfortunately current endoscopic methods can only diagnose villous atrophy, which can be present in the later grades of disease (i.e., Marsh III). To diagnose CD correctly, going deeper in the intestine may be necessary. Enteroscopy can reveal changes in CD in the intestinal mucosa in 10%-17% of cases that have negative histology at initial workup. Invasiveness of the method limits its use. Capsule endoscopy may be a good substitute for enteroscopy. However, both techniques should be reserved for patients with suspected diagnosis of complications. This paper reviews the current literature in terms of the value of enteroscopy for diagnosis of CD.
    World Journal of Gastroenterology 08/2012; 18(31):4095-101. · 2.55 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Tropical sprue is an acquired chronic diarrheal disorder of unclear etiology affecting residents of and visitors to tropical regions. Patients usually present with profuse diarrhea, weight loss, and malabsorption, notably of vitamin B12 and folate. The histologic changes typically resemble that of gluten-sensitive enteropathy. Reports of tropical sprue have become infrequent in the literature, and the diagnosis is often not considered either clinically or pathologically. This disease may, however, cause significant morbidity, although it is eminently treatable with broad-spectrum antibiotics. In this study, we report the clinical presentation of 12 tropical sprue patients along with the histologic changes of the intestinal mucosa and compare it with those of a series of 150 cases of gluten-sensitive enteropathy, the condition with which it is most frequently misdiagnosed. The cohort comprised 6 men and 6 women with a median age of 59 years (range, 38 to 78 y) with a history of residence or visitation in South Asia or Papua New Guinea. Partial villous blunting in the duodenal mucosa was present in 75% of cases, and a marked intraepithelial lymphocytosis was observed in all cases (mean per 100 epithelial cells 77.3; range, 42 to 124). A villous tip accentuation of intraepithelial lymphocytosis was not appreciable in most cases. No case of complete villous blunting (Marsh stage 3c) was identified in tropical sprue, contrasting with 25% in gluten-sensitive enteropathy cases. A duodenal mucosa eosinophil infiltrate was present in all cases with significantly higher counts compared with untreated gluten-sensitive enteropathy patients (26.6/HPF vs. 14.6/HPF; P=0.009). The ileal mucosa displayed more severe villous blunting with higher Marsh stages than in the corresponding duodenum from 5 patients. There was a mild intraepithelial lymphocytosis and eosinophil infiltrate in the colonic mucosa of half of the cases. Follow-up biopsies in 6 patients demonstrated a histologic response after oral folates and doxycycline treatment. In summary, tropical sprue is a pan-enteric inflammatory process often mistaken for gluten-sensitive enteropathy. Histologic findings suggesting tropical sprue in the appropriate clinical context include incomplete duodenal villous blunting without development of flat mucosa, frequent involvement of the terminal ileum with more marked inflammation and villous blunting than in the duodenum, and a conspicuous eosinophil infiltrate in the lamina propria. With the expansion of tourism and increasing employment opportunities in tropical regions, pathologists in the West are increasingly likely to encounter cases of tropical sprue and should be aware of this diagnosis.
    The American journal of surgical pathology 01/2014; · 4.06 Impact Factor