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The incidence and prevalence of inflammatory bowel disease (IBD) in Asia has witnessed a rapid increase within a few decades. The genetic susceptibility and epidemiologic backgrounds in the Asian population have been found to be different from that of Western populations. There is an extensive crosstalk between gut microbiota and human hosts, with evidence of reciprocal interactions. It is well known that gut microbiota can affect the host immune system and in turn, host genetic backgrounds can affect gut microbiota reciprocally. Evidences have implicated gut microbes in the development of IBD, but no causative microorganisms have been identified. Recent advances in sequencing technology and computational analysis have now made identification of complex gut microbiomes accessible. Further research targeting gut microbiota could help in identifying biomarkers to predict clinical response, and therapeutic modalities that might affect their resilience.

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The extensive study of genetic alterations in colorectal cancer (CRC) has led to molecular diagnostics playing an increasingly important role in CRC diagnosis and treatment. Currently, it is believed that CRC is a consequence of the accumulation of both genetic and epigenetic genomic alterations. It is known that there are at least 3 major pathways that lead to colorectal carcinogenesis: (1) the chromosomal instability pathway, (2) the microsatellite instability pathway, and (3) the cytosine-phospho-guanine island methylator phenotype pathway. With recent advances in CRC genetics, the identification of specific molecular alterations responsible for CRC pathogenesis has directly influences clinical care. Patients at high risk for developing CRC can be identified by genetic testing for specific molecular alterations, and the use of molecular biomarkers for predictive and prognostic purposes is also increasing. This is clearly supported by the recent advances in genetic testing for CRC whereby specific molecular alterations are identified for the purpose of guiding treatment with targeting therapies such as anti-endothelial growth factor receptor monoclonal antibodies.

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Patients with inflammatory bowel disease (IBD) are at an increased risk of developing colorectal cancer (CRC), and key contributing factors include chronic colonic inflammation and the extent and duration of disease. This increase in risk is more likely to result from chronic inflammation of the colonic mucosa than from any clearly defined genetic predisposition. However, globally, the true magnitude of this risk is debatable, since results from different studies are heterogeneous in terms of geographical and methodological variables. The prevalence of IBD-related CRC in the Asia-Pacific region ranges from 0.3% to 1.8% and a recent study found that the cumulative incidence of IBD-related CRC is comparable to that in Western countries. However, the CRC mortality rate in the Asia-Pacific region is on the rise compared with that in Western countries, and a few Asian countries show particularly rapid upward trends in CRC incidence. Although our understanding of the molecular and clinical basis for IBD-related CRC has improved substantially, our means of prevention, endoscopic surveillance, chemoprevention, and prophylactic surgery remain modest at best. Furthermore, published data on IBD-related CRC in the Asia-Pacific region is lacking, and this review addresses many aspects including epidemiology, natural history, etiopathogenesis, morphology, and biological behaviors of IBD-related CRC and sporadic CRC in the Asia-Pacific region. In this review, we will also discuss the risk factors for CRC in IBD patients, endoscopic technology screening, and surveillance programs and management strategies for IBD-related CRC.

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Amyloidosis is characterized by the abnormal deposition of extracellular amyloid fibrils. Cases involving amyloid light-chain amyloidosis in the small intestine have been reported infrequently in Korea. Here, we report a case of localized light chain protein amyloidosis in the small intestine. Esophagogastroduodenoscopy, push enteroscopy, and capsule endoscopy revealed submucosal tumor-like lesions, multiple shallow ulcers, and several erosions in the distal duodenum and jejunum. An endoscopic biopsy established the diagnosis of amyloidosis. In through an immunohistochemical analysis, the presence of lambda light chain protein was detected. The patient had no evidence of an underlying clonal plasma cell disorder or additional organ involvement. Therefore, we concluded that the patient had localized amyloidosis of the small intestine.

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Gastrocolocutaneous fistula is a rare complication of the percutaneous endoscopic gastrostomy (PEG) procedure. Typical symptoms usually occur in the first few months. We recently encountered 2 patients with 8- and 33-month asymptomatic periods. A 74-year-old man presented with watery diarrhea for 1 month. He had undergone PEG 9 months earlier. During workup, an upper endoscopy and abdominal CT scan revealed the migration of the feeding tube into the transverse colon. He was discharged with a nasogastric tube after treatment. A 77-year-old man presented with sudden loosening of his PEG tube with a duration over 3 days. He had undergone PEG procedure three times until that time. During workup, a gastrocolocutaneous fistula was diagnosed. However, when previous studies were reviewed, an abdominal CT scan, which was done 6 months ago before the third PEG, showed the fistula already existed at that time, suggesting that it was created about 33 months earlier when he underwent the second PEG procedure. The patient died of pneumonia aggravation despite conservative treatment. Both a high index of suspicion and the careful inspection of the upper endoscopy are very important for early diagnosis regardless of symptoms.

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• Author's Reply
  Kang-Moon Lee
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