Endoscopy and Histopathology

Endoscopy and histopathology are two morphological diagnostic procedures which allow direct examination of organs with optical methods. They can detect abnormalities of the normal anatomy and histology and provide a precise diagnosis. Based on the information derived from these investigations an adequate treatment, either medical or surgical can be proposed. The optical resolution of both methods is different. Classical endoscopy is using essentially the naked eye observation of the tissue which allows a diagnosis of an ulcer or a raised lesion for instance, while histopathology is reaching the cellular and sub-cellular level. The new endoscopic techniques however do increase the optical resolution. The major contributions of histopathology to endoscopy are situated in inflammatory and neoplastic diseases. Histopathology allows a more precise diagnosis of the type of inflammation and a better classification of tumours. This has again an impact upon treatment. For the diagnosis, histopathology can be an essential element, as illustrated by gluten sensitive enteropathy (although serology is also an essential element) or by identification of specific pathogens such as Giardia lamblia, Mycobacterium avium, cryptosporidia.... Histopathology can further be important for the confirmation of a diagnosis but very often it will provide a more precise diagnosis by determining the aetiology of inflammation as illustrated by autoimmune gastritis, or by typing a tumour (adenocarcinoma or lymphoma). In addition, histopathology can provide essential elements for further therapy strategy by demonstrating the presence or absence of risk factors for residual tumour in polypectomy or endoscopic mucosal resection. Indirectly, it offers the possibility of using additional techniques such as biomarkers for dysplasia and cancer or the demonstration of mutations such as KRAS in colorectal cancer or HER2 amplification in oesophageal and gastric cancer.[1, 2].These applications can have important therapeutic consequences. It has been shown for instance that activating mutations of the KRAS gene are associated with poor response to anti-EGFR therapies and that patients