Ok-Jae Lee

Indirect evidence of ectopic pancreatic fascioliasis in a human

Fascioliasis is not common in humans and, furthermore, its ectopic migration into the pancreas is extremely rare. A definitive diagnosis of ectopic fascioliasis is based on the demonstration of flukes in the affected organ. If the flukes invade the parenchyma, however, imaging studies are limited in the detection of worms and surgical identification is required. We encountered a clinical case of probable ectopic pancreatic fascioliasis diagnosed through indirect evidence. A 46‐year‐old Korean woman was admitted with left upper quadrant pain. She had taken praziquantel for hepatic fascioliasis, which had been diagnosed at another hospital, and then developed abdominal pain. Peripheral eosinophilia, hyperamylasemia and hyperlipasemia were documented. Abdominal computed tomography (CT) revealed multiple, hypodense foci which had coalesced, forming irregular nodules in the medial and lateral segments of the left lobe of the liver, and similar 2‐ to 3‐cm sized, hypodense lesions in the body and isthmus of the pancreas. IgG antibody against Fasciola hepatica was positive. Bithionol was given orally, and the patient’s symptoms and biochemistry then improved, with reversal of eosinophilia. Radiological studies showed normalization of the liver and pancreas at the 10th week, and the serology for Fasciola hepatica was negative at the fifth month.

Esophageal anthracosis complicated by mediastinal tuberculous lymphadenitis presenting as submucosal tumor

Anthracosis is a black pigment discoloration located mainly in the bronchi because of inhalation of dust or particulates. 1 Extrapulmonary anthracosis that includes the esophagus is very rare, and its etiology is not well established. 2,3 We present a case of esophageal anthracosis presenting as a submucosal tumor (SMT) complicated by mediastinal tuberculous lymphadenitis.

Clinical features of hepatitis B and C virus infections, with high α-fetoprotein levels but not hepatocellular carcinoma

Abstract The appropriate &agr;-fetoprotein (AFP) level to confirm hepatocellular carcinoma (HCC) could be 100 ng/mL; however, the clinical significance of falsely elevated AFP in patients without HCC has not been fully studied. We investigated the clinical features and outcome of patients without HCC but with high AFP levels (100 ng/mL), especially with chronic hepatitis B (CHB) or C (CHC). The sample included 124 consecutive patients with CHB (n = 97) or CHC (n = 27), with AFP levels >100 ng/mL and without HCC at baseline. Multivariate Cox proportional regression analysis was performed to determine the factors associated with AFP normalization and HCC development. During the mean 52-month follow-up, the proportion of patients with CHB with AFP normalization (90.7%) was significantly higher than the proportion of patients with CHC (59.3%, P < 0.001). Initial aspartate aminotransferase levels (hazard ratio [HR] = 1.02 per 10 U/L increase, P = 0.021) and antiviral therapy (HR = 2.89, P < 0.001) were significantly associated with AFP normalization. Of the 16 (12.9%) patients who developed HCC, hepatitis B virus infection (HR = 10.82, P = 0.001), initiation of antiviral treatment postenrollment (HR = 0.23, P = 0.030), and AFP normalization within 12 months (HR = 0.13, P = 0.011) were associated with HCC development. CHB and CHC were the most common causes of falsely elevated AFP (>100 ng/mL). With either CHB or CHC, persistent AFP elevation (>12 months), regardless of antiviral treatment, might be an important marker of HCC development.

Unusual gastrointestinal metastases from an alveolar soft part sarcoma.

Alveolar soft part sarcoma (ASPS) is a rare subtype of soft tissue sarcoma that occurs predominantly in young patients. Despite its relatively indolent course, it generally has a poor prognosis with widespread metastases. The common metastatic sites from an ASPS include the lung, brain and bone. However, metastasis of an ASPS to the gastrointestinal tract is extremely rare. Here, we report a rare case of upper gastrointestinal bleeding and jejunal intussusception due to gastrointestinal metastases from an ASPS.

Clinical Features and Outcomes of Patients With Genotype 3 Hepatitis C Virus Infection in Korea: A Retrospective Observational Study

AbstractHepatitis C virus (HCV) genotype 3 infection is very rare in high-income Asia Pacific. The aim of our retrospective observational study was to evaluate the incidence, clinical features, and treatment outcomes of patients with a genotype 3 HCV infection in the Gyeongnam Province of Korea. Ninety-eight consecutive patients diagnosed with a genotype 3 HCV infection at Gyeongsang National University Hospital, between January 2005 and December 2014, were enrolled into the study. Relevant characteristics of the study group included: 80.6% men, mean age of 41.8 years, and including 69 patients with chronic hepatitis, 25 with liver cirrhosis, and 4 with hepatocellular carcinoma (HCC). Risk factors for HCV infection, sustained virologic response rate, development of HCC, and mortality in patients with genotype 3 were retrospectively analyzed.Among all patients diagnosed with a HCV infection during the study period, the prevalence of genotype 3 was 7.3%. The incidence of genotype 3 was higher in young patients with a risk factor of IVDU (54.0%) and tattooing (62.3%). Among 45 treatment-naive genotype 3 patients, sustained virologic response was achieved with a combination of pegylated-interferon alpha and ribavirin in 75.6%. The cumulative 5-year incidence of HCC was 13.6%, and 8.9% for overall mortality. Liver cirrhosis at enrollment was an independent risk factor for HCC development.This is the first study to elucidate the clinical features and outcomes among the patients with HCV genotype 3 infection in Korea. Further prospective studies are needed to investigate transmission routes and outcomes for HCV genotype 3 infections.

Tu1119 A Randomized, Double Blinded, Multicenter Clinical Trial to Assess the Efficacy and Safety of Lafutidine in the Management of Reflux Esophagitis

Background. The use of patient reported outcome (PRO)measures for evaluation of functional diseases is frequent and is based on the concept that healthcare personnel cannot appropriately evaluate patients perception of symptom severity. Previously, we described that output scores from both, patient (using ReQuest in PracticeTM questionnaire) and physician (Likert scale), had enough sensitivity to detect changes on GERD symptoms severity.1 The aim of this analysis was to evaluate the effect of exogenous latent factors, like patient characteristics (BMI, age), physician evaluation (clinical specialty, Likert symptoms score) and PROmeasures (ReQuest in PracticeTM on basal evaluation) over endogen factors (ReQuest in PracticeTM results 2nd and 4thweek of treatment) in a cohort of patients withGERD receivingMagnesium pantoprazole (Mg-Pa). Material and Methods. A total of 3665 patients with clinical diagnostic of GERD were enrolled by 1306 practitioners in a nationwide, prospective, observational study. They were treated with Mg-Pa 40mg for 28 days. To evaluate the severity of GERD symptoms, patients answered ReQuest-in-PracticeTM, a PRO instrument, every week. Physicians also assessed symptom severity with a 4-point Likert scale. Lineal combination and data transformation to Z-scores (structural equation model) was performed to assess the effect size of each factor over symptom severity progression. Endogenous variables were ReQuest in PracticeTM results at 2nd and 4th weeks. Results. A total of 2345 patients were included in the analysis (mean age 36 ± 8 years old, 54% females). Patient characteristics did not show influence upon ReQuest in PracticeTM results (2nd week of treatment, b= 0.05; 4th week, b=0.03; p-value > 0.1 for both). ReQuest in PracticeTM questionnaire showed median influence (week 2, b= 0.34; week 4, b= 0.12; p<0.05). In contrast, physician effect was of relevance (2nd week b= 0.89; 4th week b=0.78; p<0.05). Conclusion. Physicians can have a valid subjective impression about the symptoms severity percibed by the patient. The evaluation of a clinical response to GERD treatment can be supported by clinicians appreciation and not only by PRO instruments. 1.Lopez-Alvarenga et al. J Neurogastroenterol Motil 2011;17:381-6

Mo1832 The Frequency and Risk Factors of Anti-Tuberculosis Therapy-Induced Hepatotoxicity

isms by which IFNγ affects AQP1 expression in the mouse intestinal epithelium. Methods: 1. CMT93 cells (mouse cecal epithelial cell line that constitutively expresses AQP1) grown to confluence on Transwell membranes were pre-treated with a PI3K inhibitor (LY294002, 20 μM, 2 hrs) or a NFκB inhibitor (BAY-11-7082, 10 μM, 2 hrs) prior to IFNγ (10 ng/mL, 24 hrs) treatment. Protein levels for pAKT or NFκB-p65 respectively and AQP1 were determined by Western blot. 2. Further studies were performed involving CMT93 cells pretreated with either a JAK1 inhibitor (20 μM, 2 hrs) or siRNA to knock down STAT1 or STAT3 (both at 80 nM, 24 hrs), and then treated with IFNγ (10 ng/mL, 24 hrs) in serum free media. Cells were then lysed and protein levels for AQP1, as well as phosphorylated and total STAT3 were assessed by Western blot. Results: 1. CMT93 cells demonstrated a significant suppression in AQP1 protein expression after treatment with IFNγ at 24 hours. Inhibition of either PI3K or NFκB did not affect the suppression of AQP1 exerted by IFNγ, nor did siRNA knockdown of STAT1. 2. However, pre-treatment with either the JAK1 inhibitor or STAT3 siRNA, prior to IFNγ administration resulted in the amelioration of the IFNγ-induced suppression of AQP1 protein expression. Conclusions: Inflammatory cytokines present during IBD are able to influence AQP1 levels and may contribute to the water transport deficiencies associated with these diseases. In this study, the results suggest that epithelial AQP1 expression is reduced by IFNγ in CMT93 cells through unique JAK1 and STAT3 dependent, STAT1/PI3K/NFκB independent mechanisms.

Su1784 The Clinical Features and Risk Factors of Nonvariceal Bleeding in the Patients With Liver Cirrhosis

gluten was added to the cultures. As indexes of DC activation, surface expression of HLADR, CD80, CD83, CD86, cytokine production and CD4+ T cell stimulatory capacity were measured. Results: We found that PT-gluten induces phenotypic and functional DC maturation. In particular, PT-gluten up-regulates the expression on immature DC of surface molecules known to be critical for their APC function. These molecules include HLA-DR, CD83, CD80 and CD86. The functional consequence of PT-gluten treatment of immature DC is an increase in cytokine (IL-12, TNF-α) production as well as in their stimulatory capacity. Interestingly, we found that pre-treatment of immature DC with pDAV significantly prevents the functional maturation of immature DC induced by PT-gluten. On the other hand, pDAV does not revert the PT-gluten-induced phenotypic maturation of DC. Conclusion: Here we report, for the first time, that naturally occurring peptides are able to prevent the gliadindependent DC activation. This finding could have implication for CD, raising the perspective of a therapeutic strategy alternative to a gluten free diet, consisting in the oral administration of small peptides naturally occurring in wheat.