Adult Celiac Disease and Its Malignant Complications

Department of Medicine (Gastroenterology), University of British Columbia, Vancouver, Canada.
Gut and liver (Impact Factor: 1.49). 12/2009; 3(4):237-46. DOI: 10.5009/gnl.2009.3.4.237
Source: PubMed

ABSTRACT Adult celiac disease is a chronic intestinal disorder that has been estimated to affect up to 1-2% of the population in some nations. Awareness of the disease has increased, but still it remains markedly underdiagnosed. Celiac disease is a pathologically defined condition with several characteristic clinical scenarios that should lead the clinician to suspect its presence. Critical to diagnosis is a documented responsiveness to a gluten-free diet. After diagnosis and treatment, symptoms and biopsy-proven changes may recur and appear refractory to a gluten-free diet. Recurrent symptoms are most often due to poor diet compliance, a ubiquitous and unrecognized gluten source, an initially incorrect diagnosis, or an associated disease or complication of celiac disease. Some patients with persistent symptoms and biopsy-proven changes may not have celiac disease at all, instead suffering from a sprue-like intestinal disease, so-called unclassified sprue, which is a specific entity that does not appear to respond to a gluten-free diet. Some of these patients eventually prove to have an underlying malignant cause, particularly lymphoma. The risk of developing lymphoma and other malignancies is increased in celiac disease, especially if initially diagnosed in the elderly, or late in the clinical course of the disease. However, recent studies suggest that the risk of gastric and colon cancer is low. This has led to the hypothesis that untreated celiac disease may be protective, possibly due to impaired absorption and more rapid excretion of fat or fat-soluble agents, including hydrocarbons and other putative cocarcinogens, which are implicated in the pathogenesis of colorectal cancer.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Although many groups have attempted to develop an automated computerized method to detect pathology of the small intestinal mucosa caused by celiac disease, the efforts have thus far failed. This is due in part to the occult presence of the disease. When pathological evidence of celiac disease exists in the small bowel it is visually often patchy and subtle. Due to presence of extraneous substances such as air bubbles and opaque fluids, the use of computerized automation methods have only been partially successful in detecting the hallmarks of the disease in the small intestine – villous atrophy, fissuring, and a mottled appearance. By using a variety of computerized techniques and assigning a weight or vote to each technique, it is possible to improve the detection of abnormal regions which are indicative of celiac disease, and of treatment progress in diagnosed patients. Herein a paradigm is suggested for improving the efficacy of automated methods for measuring celiac disease manifestation in the small intestinal mucosa. The suggestions are applicable to both standard and videocapsule endoscopic imaging, since both methods could potentially benefit from computerized quantitation to improve celiac disease diagnosis.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Celiac disease is a chronic genetically based gluten-sensitive immune-mediated enteropathic process primarily affecting the small intestinal mucosa. The disorder classically presents with diarrhea and weight loss; however, more recently, it has been characterized by subclinical occult or latent disease associated with few or no intestinal symptoms. Diagnosis depends on the detection of typical histopathological biopsy changes followed by a gluten-free diet response. A broad range of clinical disorders may mimic celiac disease, along with a wide range of drugs and other therapeutic agents. Recent and intriguing archeological data, largely from the Gobleki Tepe region of the Fertile Crescent, indicate that ce-liac disease probably emerged as humans transitioned from hunter-gatherer groups to societies dependent on agriculture to secure a stable food supply. Longitudinal studies per-formed over several decades have suggested that changes in the prevalence of the disease, even apparent epidemic disease, may be due to superimposed or novel environmen-tal factors that may precipitate its appearance. Recent thera-peutic approaches are being explored that may supplement, rather than replace, gluten-free diet therapy and permit more nutritional options for future management. (Gut Liver 2015;9:28-37).
    Gut and liver 01/2015; 9(1):28-37. DOI:10.5009/gnl14288 · 1.49 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Ghrelin is a gut hormone shown to have protective effects throughout the gastrointestinal tract. This study aims to investigate its protective effect in celiac disease induced in rats. Twenty-four rat pups were divided into 4 groups as follows: control, disease (1.5 mg/g intragastric gliadin), co-treatment (50 ng/g intraperitoneal ghrelin after gliadin gavage) and pretreatment (50 ng/g intraperitoneal ghrelin before gliadin gavage). Animals' weight gain was charted. Histological features assessed include villus length, villus width, crypt depth and number of intraepithelial lymphocytes. Tissue interferon-gamma was quantified by ELISA. ANOVA was used to compare results statistically. Results showed that villi were shortened in the diseased group, but were as long as the control in pretreatment and co-treatment groups. Crypt depth had increased in disease group, but turned to normal in co-treatment group. Number of intraepithelial lymphocytes was significantly higher in disease group than the control, while no difference was observed between co-treatment and control groups. Disease and control animals weighed equally at the end of the experiment, but ghrelin-treated animals had significantly gained more weight than these two. Interferon-gamma measurement revealed no significant difference among groups. We concluded administration of ghrelin led to histological improvement of celiac disease which was more obvious if administered after exposure to gliadin.
    Acta Physiologica Hungarica 12/2014; 101(4):438-47. DOI:10.1556/APhysiol.101.2014.4.5 · 0.75 Impact Factor


Available from