Jin Heon Hong

Yonsei University, Sŏul, Seoul, South Korea

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Publications (7)30.99 Total impact

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    ABSTRACT: The clinical impact and complications of hepatogenous diabetes (HD) on cirrhosis have not been elucidated. This study aimed to evaluate the relationship of HD with portal hypertension (PHT) and variceal hemorrhage and to assess the prevalence of HD. From July 2007 to December 2009, 75-g oral glucose tolerance test and insulin resistance (IR) were evaluated for 195 consecutive cirrhotic liver patients (M:F = 164:1, 53.0 ± 10.2 years) who had no history of diabetes mellitus. IR was calculated using the homeostasis model of assessment-insulin resistance (HOMA-IR) formula. Endoscopy for varices, hepatic venous pressure gradient (HVPG), and serologic tests were also conducted. HD was observed in 55.4 % (108/194) of the patients. Among them, 62.0 % required OGTT for diagnosis because they did not show an abnormal fasting plasma glucose level. The presence of HD showed a significant correlation with high Child-Pugh's score, variceal hemorrhage, and HVPG (p = 0.004, 0.002, and 0.019, respectively). In multivariate analysis, Child-Pugh's score (OR 1.43, 95 % CI 1.005-2.038) and HVPG (OR 1.15, 95 % CI 1.003-2.547) had significant relationships with HD. Patients with recent variceal hemorrhages (within 6 months) exhibited significantly higher glucose levels at 120 min in OGTT compared to patients without hemorrhages (p = 0.042). However, there was no difference in fasting glucose levels. The 120-min glucose level and HOMA-IR score were significantly and linearly correlated with HVPG (r (2) = 0.189, p < 0.001 and r (2) = 0.033, p = 0.011, respectively). HD and IR have significant relationships with PHT and variceal hemorrhage. Postprandial hyperglycemia in particular had a significant relationship with variceal hemorrhage.
    Digestive Diseases and Sciences 08/2013; 58(11). DOI:10.1007/s10620-013-2802-y · 2.55 Impact Factor
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    ABSTRACT: BACKGROUND: Although endoscopic submucosal dissection (ESD)-induced ulcers heal faster and recur less often than non-iatrogenic gastric ulcers, the optimal dosage and duration of proton pump inhibitor treatment for ESD-induced ulcers remain unclear. AIMS: To evaluate the efficacy of half-dose rabeprazole on endoscopic submucosal dissection-induced ulcer compared with standard dose rabeprazole. METHODS: The study was a prospective randomized controlled double-blind trial at a single tertiary hospital. A total of 80 patients who underwent ESD for gastric neoplasia were enrolled. Of these patients, 10 were not followed to completion. Final analysis included the remaining 70 patients. Rabeprazole 20 or 10 mg, depending on randomization, was given orally for 4 weeks after ESD. RESULTS: Of the 70 patients, 45 (64 %) were men, and the median age was 65.2 ± 9.7 years. The mean ESD-induced ulcer area was 673 mm(2). No significant differences in ulcer area reduction ratio (p = 0.49) or ulcer-related symptoms (p = 0.91) were observed between the two groups at 4 weeks after ESD. CONCLUSION: For ESD-induced ulcers, treatment with 10 mg of rabeprazole daily produces a similar outcome as 20 mg of rabeprazole with regard to healing efficacy and symptom resolution.
    Digestive Diseases and Sciences 10/2012; 58(4). DOI:10.1007/s10620-012-2436-5 · 2.55 Impact Factor
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    ABSTRACT: The measurement of the hepatic venous pressure gradient (HVPG) for the estimation of portal hypertension (PH) in cirrhosis has some limitations, including its invasiveness. Hepatic vein arrival time (HVAT), as assessed by microbubble contrast-enhanced ultrasonography (CEUS), is negatively correlated with the histological grade of liver fibrosis because of the associated hemodynamic abnormalities. Anatomical and pathophysiological changes in liver microcirculation are the initial events leading to PH. However, the direct relationship between HVAT and PH has not been evaluated. The present study measured both HVPG and HVAT in 71 consecutive patients with compensated cirrhosis and analyzed the relationship between the two parameters (i.e., the derivation set). Results were validated in 35 compensated patients with cirrhosis at another medical center (i.e., the validation set). The derivation set had HVPG and HVAT values of 11.4 ± 5.0 mmHg (mean ± standard deviation; range, 2-23) and 14.1 ± 3.4 seconds (range, 8.4-24.2), respectively; there was a statistically significant negative correlation between HVPG and HVAT (r(2) = 0.545; P < 0.001). The area under the receiver operating characteristic curve (AUROC) was 0.973 for clinically significant PH (CSPH; HVPG, ≥ 10 mmHg), and the sensitivity, specificity, positive predictive value, negative predictive value, and positive and negative likelihood ratios for CSPH for an HVAT cut-off value of 14 seconds were 92.7%, 86.7%, 90.5%, 89.7%, 6.95, and 0.08, respectively. In addition, a shorter HVAT was associated with worse Child-Pugh score (P < 0.001) and esophageal varices (P = 0.018). In the validation set, there was also a significant negative correlation between HVAT and HVPG (r(2) = 0.538; P < 0.001), and AUROC = 0.953 for CSPH. HVAT was significantly correlated with PH. These results indicate that measuring HVAT is useful for the noninvasive prediction of CSPH in patients with compensated cirrhosis.
    Hepatology 09/2012; 56(3):1053-62. DOI:10.1002/hep.25752 · 11.19 Impact Factor
  • Gastrointestinal Endoscopy 04/2012; 75(4):AB138. DOI:10.1016/j.gie.2012.04.058 · 4.90 Impact Factor
  • Gastrointestinal Endoscopy 04/2012; 75(4):AB373. DOI:10.1016/j.gie.2012.03.982 · 4.90 Impact Factor
  • Jin Heon Hong, Hyun-Soo Kim
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    ABSTRACT: The incidence of adenocarcinoma of esophagogastric junction (AEG) has increased rapidly over the past three decades in Western countries, but data from Asian populations are conflicting. The most commonly used classification is that described by Siewert and Stein, which defines AEG as tumors that have their center within 5 cm proximal or distal to the anatomic cardia. However, there is lack of consensus in definition and classification of AEG, which has resulted in difficulties in comparing the various studies on the epidemiology of AEG. The cause of changing pattern of AEG is not clear. Known risk factors for AEG are Barrett's esophagus, gastroesophageal reflux, obesity, smoking, and medications that relax the lower esophageal sphincter. On the other hand, non-steroidal anti-inflammatory drugs (NSAIDs), Helicobacter pylori infection, fruits and vegetables, and antioxidants might reduce the risk. Currently, there is no evidence that strongly supports any strategy for surveillance of population at high risk of AEG. In Asian countries, the incidence of AEG still low, however, some countries report the increasing trend of adenocarcinoma of lower esophagus and cardia.
    01/2012; 12(3):133. DOI:10.7704/kjhugr.2012.12.3.133
  • Gastrointestinal Endoscopy 04/2006; 63(5). DOI:10.1016/j.gie.2006.03.530 · 4.90 Impact Factor