Taking More Gastroscopy Images Increases the Detection Rate of Clinically Significant Gastric Lesions: Validation of a Systematic Screening Protocol for the Stomach

Background/Aims@#For systematic screening protocol for the stomach (SSS), 22 gastroscopy images are considered sufficient to avoid blind spots during gastroscopy. The aim of this study was to investigate the relationship between the number of gastroscopy images taken during the gastroscopy procedure and the detection rate of clinically significant gastric lesions (CSGLs). @*Materials and Methods@#We retrospectively reviewed the data obtained from a cohort of consecutive subjects at a health promotion center. The primary outcome measure was the detection rate of CSGLs per endoscopist, according to the number of gastroscopy images. We also analyzed whether all the CSGLs were detected via SSS. @*Results@#The mean number of gastroscopy images obtained by eight endoscopists was 27.6±10.5 in 2,912 subjects without CSGLs and without biopsies. Among the 5,970 subjects who underwent gastroscopy by the eight endoscopists, 712 CSGLs were detected in 551 subjects. Fifty-six CSGLs (7.9%) in 55 subjects (10.0%) were not detected during the SSS. Photo-endoscopists who took more images achieved a higher detection rate of CSGLs than those who took fewer images (adjusted OR 2.07, 95% CI 1.41~3.05; P<0.0001). @*Conclusions@#The modified SSS, which included 22 SSS images, the fundus, and the saddle area, detected significantly more CSGLs. This modified SSS should be validated with further prospective studies.

A Case of Amyloidosis Presenting as Lymphadenopathy at the Porta Hepatis

We report a rare case of systemic amyloidosis with gastrointestinal and lymph node involvement. A 64-year-old woman was admitted to our hospital with dyspepsia and weight loss. Initial esophagogastroduodenoscopy (EGD) revealed nonspecific findings, and abdominal computed tomography showed necrotizing lymphadenopathy at the porta hepatis. Laparoscopic lymph node biopsy was performed under suspicion of tuberculous lymphadenopathy, but a definite diagnosis was not established. Follow-up EGD performed 6 months later revealed multiple telangiectasia-like lesions at the gastric body, and endoscopic biopsy revealed amyloid deposition. Through additional blood and urine protein electrophoresis, the patient was finally diagnosed with systemic amyloidosis associated with multiple myeloma. She was treated with dexamethasone, thalidomide, and bortezomib; however, she died 3 months after diagnosis because of pneumonia and multiple organ failure.

A Case of Severe Chronic Active Epstein-Barr Virus Infection with Aplastic Anemia and Hepatitis / 대한소화기학회지

Epstein-Barr virus (EBV) causes various acute and chronic diseases. Chronic active EBV infection (CAEBV) is characterized by infectious mononucleosis-like symptoms that persist for more than 6 months with high viral loads in peripheral blood and/or an unusual pattern of anti-EBV antibodies. Severe CAEBV is associated with poor prognosis with severe symptoms, an extremely high EBV-related antibody titer, and hematologic complications that often include hemophagocytic lymphohistiocytosis. However, CAEBV which led to the development of aplastic anemia (AA) has not been reported yet. A 73-year-old woman was admitted to our hospital with intermittent fever, general weakness and elevated liver enzymes. In the serologic test, EBV-related antibody titer was elevated, and real-time quantitative-PCR in peripheral blood showed viral loads exceeding 10(4) copies/microg DNA. Liver biopsy showed characteristic histopathological changes of EBV hepatitis and in situ hybridization with EBV-encoded RNA-1 was positive for EBV. Pancytopenia was detected in peripheral blood, and the bone marrow aspiration biopsy showed hypocellularity with replacement by adipocytes. AA progressed and the patient was treated with prednisolone but deceased 8 months after the diagnosis due to multiple organ failure and opportunistic infection. Herein, we report a rare case of severe CAEBV in an adult patient accompanied by AA and persistent hepatitis.

Case of Atypical Wernicke's Encephalopathy in a GB Cancer Patient / 대한내과학회지

Wernicke's encephalopathy (WE) is an acute neuropsychiatric syndrome resulting from thiamine deficiency. Traditionally, diagnosis of WE rests on a clinical symptom triad consisting of ocular signs, altered consciousness, and ataxia. However, the complete triad is only present in a fraction of cases, which means that WE tends to be under-diagnosed, especially in nonalcoholic patients. Brain MRI of WE patients usually shows symmetrical signal intensity alterations in the thalami, mammillary bodies, and periaqueductal area, because of cytotoxic edema in the same region. These typical findings are useful diagnostic leads in WE patients with atypical symptoms. However, atypical findings can occasionally be seen in the vermis of cerebellum and cerebellar nuclei. Notably, alterations of signal intensity in the cerebellar dentate nuclei, which is a typical finding of metronidazole-induced encephalopathy (MIE), need to be distinguished according to medication history and response to thiamine.