Disease Knowledge Centres

  • Gastroenterology - Disease Topic Overview

    Gastroenterology is the medical specialty that involves the study of the digestive system and its associated glands. It also encompasses the treatment of many diseases that affect the organs or glands of the digestive system.

    The role of the digestive system is to ensure the ingestion and digestion of food in order to extract energy and nutrients necessary for survival of the organism and excrete what can not be absorbed.1 The digestive system is made up of a series of hollow organs linked together to form a tube that connects the mouth to the anus, and includes; the oral cavity, oesophagus, stomach, duodenum, small intestine, large intestine or colon, and rectum.1 The digestive system also includes organs that lie outside the digestive tract; salivary glands, liver, gallbladder and pancreas, but they secrete enzymes and juices necessary to digest food chemicals.1

    Many diseases can interfere with the functioning of the digestive system.1 They can be genetic, caused by infections, or induced by environmental factors, nutritional deficiencies or secondary to other diseases.1 The diseases most commonly supported are stomach or duodenal ulcers, liver cirrhosis, hepatitis and digestive cancers.

    Ulcers are a relatively common disease of the stomach and can be greatly exacerbated by stress.1 The most common causes of erosion of the stomach lining are: the long-term use of non steroidal anti-inflammatory drugs such as aspirin, and infection with the Helicobacter pylori bacterium.2

    Liver cancer ranks fifth among the most prevalent cancers in the world, and is the third most common cause of cancer related mortality.3 The main risk factors for developing liver cancer are; metabolic syndrome, diabetes and excessive alcohol consumption.3 Many diseases of the digestive system are strongly associated with behavioral choices, such as alcohol or tobacco consumption, and major prevention and education campaigns are implemented in European countries to reduce the impact of these risk factors.3

    1. Kara Rogers et al. The Digestive System. Britannica Educational Publishing, 2010 ; 288 pages.
    2. Ramsoekh D.et al. Outcome of peptic ulcer bleeding, nonsteroidal anti-inflammatory drug use, and Helicobacter pylori infection. Clinical Gastroenterology and Hepatology. September 2005 ; 3 (9) : 859-64.
    3. Livraghi T. et al. Treatment options in hepatocellular carcinoma today. Scandinavian Journal of Surgery. 2011 ; 100 : 22-29.

  • Gastrointestinal Stromal Tumours

    Gastrointestinal stromal tumours (GISTs) are the most common mesenchymal tumours of the gastrointestinal (GI) tract. Before the current definition of GIST evolved, GISTs were classified as benign or malignant smooth muscle tumours including true smooth muscle tumours (leiomyomas, leiomyoblastomas, leiomyosarcomas) and neuronal tumours (schwannomas)1,2.

    Patients with GIST may be asymptomatic (31%) or symptomatic.3 Asymptomatic GISTs can be discovered incidentally during endoscopy or laparoscopy as well as during computed tomography (CT)4. Symptomatic GIST patients may present with a range of symptoms associated with the location of the tumour, growth pattern, and size.

    The diagnosis of GIST relies on standard histologic examination and immunohistochemical analysis of several markers, including KIT. Equivocal cases should be submitted to a central review by an expert in sarcoma pathology, experienced in the diagnosis of GIST.

    Before the availability of Glivec, the only treatments for GIST other than surgery were conventional chemotherapy and radiation therapy5,6. The role of chemotherapy and radiation therapy has been limited by a lack of efficacy and intolerable toxicity, currently surgery is Standard of Care for Resectable Primary GIST.

    GIST is now recognised as having a much higher incidence than previously thought. Under the current, widely accepted definition of GIST as a distinct molecular and pathologic entity, the incidence of GIST is in the range of 10-20 cases per million persons per year 7-11. The prevalence of GIST in a population-based study was estimated to be 129 cases per million persons11. GIST tumours occur at a median age of 60 years and are slightly more predominant in men than women9. 

    Enter the Gastrointestinal Stromal Tumours (GIST) Knowledge Centre

    What’s in the Gastrointestinal Stromal Tumours (GIST) Knowledge Centre?

    References

    1. Fletcher CDM, Berman JJ, Gorstein F, et al. Diagnosis of gastrointestinal stromal tumors: a consensus approach. Hum Pathol. 2002;33:459-465.
    2. Connolly EM, Gaffney E, Reynolds JV. Gastrointestinal stromal tumours,Br J Surg. 2003;90:1178-1186.
    3. Kindblom LG. Gastrointestinal stromal tumors: diagnosis, epidemiology, prognosis. Available at: www.asco.org. Accessed July 13, 2007.
    4. Joensuu H, Fletcher C, Dimitrijevic S, Silberman S, Roberts P, Demetri G. Management of malignant gastrointestinal stromal tumours. Lancet Oncol. 2002;3:655-664.
    5. Eisenberg BL, Judson I. Surgery and imatinib in the management of GIST: emerging approaches to adjuvant and neoadjuvant therapy. Ann Surg Oncol. 2004;11:464-475.
    6. Dematteo RP, Heinrich MC, El-Rifai WM, Demetri G. Clinical management of gastrointestinal stromal tumors: before and after STI-571. Hum Pathol. 2002;33:466-477.
    7. Goettsch WG, Bos SD, Breekveldt-Postma N, Casparie M, Herings RM, Hogendoorn PC. Incidence of gastrointestinal stromal tumours is underestimated: results of a nation-wide study. Eur J Cancer. 2005;41:2868-2872.
    8. Joensuu H. Current perspectives on the epidemiology of gastrointestinal stromal tumours. Eur J Cancer. 2006;4(suppl 1):4-9.
    9.  Blay JY, Bonvalot S, Casali P, et al. Consensus meeting for the management of gastrointestinal stromal tumors. Report of the GIST Consensus Conference of 20-21 March 2004, under the auspices of European Society for Medical Oncology. Ann Oncol. 2005;16:566-578.
    10. Miettinen M, Lasota J. Gastrointestinal stromal tumors--definition, clinical, histological, immunohistochemical, and molecular genetic features and differential diagnosis. Virchows Arch. 2001;438:1-12.
    11. Nilsson B, Bumming P, Meis-Kindblom JM, et al. Gastrointestinal stromal tumors: The incidence, prevalence, clinical course, and prognostication in the preimatinib mesylate era. Cancer. 2005;103:821-829

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• Treatment of duodenal and gastric ulcer • Treatment of reflux oesophagitis • Prophylaxis of reflux oesophagitis • Eradication of Helicobacter pylori (H.

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Napo Pharma has terminated its agreement with Salix Pharma for failure of Salix Pharma to proceed with an application to the FDA for crofelemer for chronic diarrhoea in people living with HIV/AIDS, despite a successful Phase III result. Napo has filed a lawsuit against Salix seeking $150 million for breach of contract.

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International Journal of Cancer
In the majority of colorectal cancers (CRCs) under clinical suspicion for a hereditary cause, the disease-causing genetic factors are still to be discovered. To identify such genetic factors we stringently selected a discovery cohort of 41 CRC index patients with microsatellite-stable tumors. All patients were below 40 years of age at diagnosis and/or exhibited an overt family history. We employed genome-wide copy number profiling using high-resolution SNP arrays on germline DNA, which resulted in the identification of novel copy number variants (CNVs) in six patients (15%) encompassing, among others, the cadherin gene CDH18, the bone morphogenetic protein antagonist family gene GREM1, and the breakpoint cluster region gene BCR. In addition, two genomic deletions were encountered encompassing two microRNA genes, hsa-mir-491/KIAA1797 and hsa-mir-646/AK309218. None of these CNVs has previously been reported in relation to CRC predisposition in humans, nor were they encountered in large control cohorts (>1,600 unaffected individuals). Since several of these newly identified candidate genes may be functionally linked to CRC development, our results illustrate the potential of this approach for the identification of novel candidate genes involved in CRC predisposition.
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Epidemiologic studies of pancreatic cancer risk have reported null or nonsignificant positive associations for obesity, while associations for height have been null. Waist and hip circumference have been evaluated infrequently. A pooled analysis of 14 cohort studies on 846,340 individuals was conducted; 2,135 individuals were diagnosed with pancreatic cancer during follow-up. Study-specific relative risks (RRs) and 95% confidence intervals (CIs) were calculated by Cox proportional hazards models, and then pooled using a random effects model. Compared to individuals with a body mass index (BMI) at baseline between 21–22.9 kg/m2, pancreatic cancer risk was 47% higher (95%CI:23–75%) among obese (BMI ≥ 30 kg/m2) individuals. A positive association was observed for BMI in early adulthood (pooled multivariate [MV]RR = 1.30, 95%CI = 1.09–1.56 comparing BMI ≥ 25 kg/m2 to a BMI between 21 and 22.9 kg/m2). Compared to individuals who were not overweight in early adulthood (BMI < 25 kg/m2) and not obese at baseline (BMI < 30 kg/m2), pancreatic cancer risk was 54% higher (95%CI = 24–93%) for those who were overweight in early adulthood and obese at baseline. We observed a 40% higher risk among individuals who had gained BMI ≥ 10 kg/m2 between BMI at baseline and younger ages compared to individuals whose BMI remained stable. Results were either similar or slightly stronger among never smokers. A positive association was observed between waist to hip ratio (WHR) and pancreatic cancer risk (pooled MVRR = 1.35 comparing the highest versus lowest quartile, 95%CI = 1.03–1.78). BMI and WHR were positively associated with pancreatic cancer risk. Maintaining normal body weight may offer a feasible approach to reducing morbidity and mortality from pancreatic cancer.

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Gastroenterology