Malignant complications of celiac disease

Department of Pathology, Service d'Anatomie et de Cytologie Pathologiques, Hôpital Necker-Enfants Malades, 149, rue de Sèvres 75743, Paris Cedex 15, France.
Baillière&#x027 s Best Practice and Research in Clinical Gastroenterology (Impact Factor: 3.48). 07/2005; 19(3):401-12. DOI: 10.1016/j.bpg.2005.02.002
Source: PubMed


Patients with coeliac disease (CD), particularly those who are undiagnosed or do not adhere to a strict gluten free diet (GFD), are prone to develop complications. Malignant complications are the most serious and should be suspected when expected responses to GFD are not achieved or sustained. Lymphomas, mostly T-cell type, and other malignant tumours, particularly carcinoma of the small bowel, less frequently of stomach and oesophagus, are associated with CD. Loss of response to a gluten free diet (refractory coeliac disease) and ulcerative jejunitis are two recently described complications of CD that may progress to an Enteropathy-Associated T-cell Lymphoma (EATL). Coeliac disease-related lymphoma most often appears at extra-nodal sites, essentially the small bowel, although one have to realise that T-cell lymphomas arising in sites outside the small bowel could be related to coeliac disease. Workup of an EATL must include immunehistology and if necessary T-cell flow cytometry and T-cell rearrangement. Adequate imaging with CT and PET-scanning is mandatory.

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    • "Celiac disease occurs in genetically predisposed people and affects approximately 1% of the population in Western countries [13] [14] [15]. Many pathological conditions such as malignancy have been reported as a possible association with CD [16] [17] [18] [19] [20] [21] [22]. Hepatic disorders are common in CD [23] [24] and include steatosis, cryptogenic hypertransaminasemia [25], and autoimmune liver diseases [26]. "
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    ABSTRACT: Background and Aims. Hepatic hemangioma (HH) has a widely ranging prevalence. The etiology is unclear; however, associations with autoimmune disorders have been described. We aimed at evaluating the prevalence of HH in celiac disease. Methods. Ninety-seven consecutive patients with celiac disease (18 M, 79 F, median age 41, and range 17-84 years) underwent liver ultrasound between January 2011 and 2012. The findings were compared with those of 1352 nonceliac patients (581 M, 771 F, median age 50, and range 16-94 years), without liver disease or previously detected HH, who underwent US in the same period. Results. Ultrasonographic findings consistent with HH were observed in 14 celiac patients (14.4%), a prevalence significantly higher than in controls (69 cases, 5.1%) (P = 0.0006). Subgroup analysis showed that, among women, the prevalence of HH was 16.4% in the celiac disease group (13/79) compared with 5.9% in controls (46/771) (P = 0.002). In celiac setting, HH had a median diameter of 1.3 cm and presented as a single lesion in 12 cases (86%). Conclusions. Our findings are consistent with a significantly higher prevalence of HH in celiac patients. Although mechanisms underlying this association remain unclear, autoimmune and metabolic processes, as well as alterations of gut-liver axis equilibrium, could play a role.
    Gastroenterology Research and Practice 01/2015; 2015:1-6. DOI:10.1155/2015/749235 · 1.75 Impact Factor
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    • "Usually, SBA is most commonly located in the duodenum (55%), followed by the jejunum (30%) and the ileum (15%) [8]. However,; in coeliac patients these carcinomas tend to develop in the jejunum and are more likely to develop as an adenoma-carcinoma sequence than as dysplasia in flat mucosa [6]. Development of carcinoma is well recognized in association with long-standing gluten enteropathy; nevertheless, it can occur in patients with no history suggestive of a malabsorption syndrome, and the CD is diagnosed until "
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    ABSTRACT: Coeliac disease is associated with an increased risk of malignancy, not only of intestinal lymphoma but also of small intestinal adenocarcinoma which is 82 times more common in patients with celiac disease than in the normal population. We report three additional cases of a small bowel adenocarcinoma in the setting of coeliac disease in order to underline the epidemiological features, clinicopathological findings, and therapeutic approaches of this entity based on a review of the literature. The three patients underwent a surgical treatment followed by adjuvant chemotherapy based on capecitabine/oxaliplatin regimen, and they have well recovered.
    Case Reports in Oncological Medicine 12/2012; 2012(1):935183. DOI:10.1155/2012/935183
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    • "The development of serious or even fatal complications (autoimmunity, cancers) requires the earliest possible diagnosis of CD [22]. This also explains the importance of a strict gluten-free diet for celiac patients who seem to be protected against long-term complications [23, 24]. "
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    ABSTRACT: Celiac disease (CD) is an autoimmune disorder that can be divided into typical and atypical forms. Atypical forms can show extraintestinal manifestations among which oral signs are very frequent. Considering that the pathogenesis of CD is related to a positivity to specific HLA-DQB1 haplotypes, we tested whether the presence of the HLA-DQB1*02 allele could be a hypothetical cause of the development of oral manifestations. For this study was been examined the oral condition of 98 Sardinian patients, all affected by CD and all on a gluten-free diet for at least 1 year. Then was been determined each patient's HLA-DQB1 haplotype and compared these results with clinical information. The statistical analysis evidenced that the absence of the HLA-DQB1*02 allele predisposes to oral manifestations such as dental enamel defects (DED) and recurrent aphthous stomatitis (RAS) (Pvalue=5.98x10(-05), OR = 0.23, CI: (0.10 - 0.45) per each copy of the HLA allele). These results showed that the presence of the HLA-DQB1*02 allele influences the development of oral signs in a dose-dependent manner and also how the HLA haplotype connected to oral signs could have a fundamental role for the diagnosis of atypical forms of CD.
    The Open Dentistry Journal 11/2011; 5(1):174-8. DOI:10.2174/1874210601105010174
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