Carcinoid Tumours of the Small Bowel Colon and Rectum

Carcinoid tumours originate from enterochromaffin cells within the diffuse endocrine system. Representing a confusing group of tumours displaying a wide range of behaviour, their clinical and histologic recognition was initially described in 1888 by Lubarsch. The term “carcinoid” was first applied to these tumours in 1907 by Obendorfer. In 1914, Gossett and Masson demonstrated the argentaffinreducing properties of appendiceal carcinoids and these tumours became known as “argentaffinomas”. The association between carcinoid tumours and serotonin production was first reported by Lembeck in 1953, while the first description of the carcinoid syndrome was published by Waldenstrom in 1954. The variable nature of carcinoids was first documented by Sandler and Snow. The amine precursor and decarboxylation abilities (APUD) of these tumours were recognized by Pearse in 1969 and carcinoid tumours were termed as APUDomas, now considered as part of a group of tumours known as neuroendocrine tumours (NET). As a result, the previously called “carcinoid tumours” were renamed “welldifferentiated neuroendocrine tumours”. With a reported prevalence of between 2.5 and 4.5 cases per 100,000 population in USA, the gastrointestinal tract is the most common site of carcinoids [1,2,3,4]. The increasing incidence observed in recent years has been attributed to various potential factors, including increased clinical awareness, a more thorough pathologic evaluation, including the use of immunostaining for specific molecular markers related to NETs such as synaptophysin and chromogranin A (CgA), and the widespread use of proton pump inhibitors [5,6] . In decreasing order of frequency, the locations of carcinoids include the appendix, ileum, rectum, colon and stomach [7].