Kyu Choi

Role of Hyperinsulinemia and Glucose Intolerance in the Pathogenesis of Nonalcoholic Fatty Liver in Patients with Normal Body Weight

Objectives The pathogenesis of nonalcoholic fatty liver in non-obese persons is poorly understood. We aimed to elucidate whether hyperinsulinemia and glucose intolerance are associated with development of fatty liver in patients with normal body weight Methods Forty-seven patients with fatty liver were divided into non-obese (n=25) and obese groups (n=22) according to age adjusted body mass index. Inclusion criteria were as follows: (1) elevated transaminase levels during more than 3 months of follow up period, (2) no detectable HBsAg or anti-HCV in the serum, (3) alcohol consumption less than 40 gm/week, (4) no use of potential hepatotoxic drugs within 3 months and (4) sonographic evidence of fatty liver(moderate to severe degree). Baseline insulin levels and oral glucose tolerance test using 75gm of glucose were performed and the results were compared in each group of patients. Results Mean baseline insulin levels were elevated in both groups above the reference value, 9.3±3.5 μU/L in non-obese group and 9.9±3.5 μU/L in obese group (p=0.26). Seventeen of non-obese patients (68%) had elevated basal insulin level and 16 of obese patients (73%) had elevated basal insulin level (p=0.39). In oral glucose tolerance test, there was no difference in glucose level between non-obese and obese groups from O minute to 180 minutes (p > 0.05). Eleven patients from the non-obese group (44%) and 8 patients from the obese group (36%) had either impaired glucose tolerance or diabetes (p=0.29). Conclusion Our data suggest that hyperinsulinemia and glucose intolerance may play a role in the pathogenesis of fatty liver in patients with normal body weight as well as in patients with obesity.

Impaired Esophageal Mucosal Integrity May Play a Causative Role in Patients With Nongastroesophageal Reflux Disease–Related Noncardiac Chest Pain

AbstractBaseline impedance (BI) measurement can be used to evaluate the status of the esophageal mucosa integrity. We hypothesized that impaired esophageal mucosal integrity may play a causative role in patients with nongastroesophageal reflux disease (non-GERD)–related noncardiac chest pain (NCCP). This retrospective study analyzed 24-hour multichannel intraluminal impedance-pH testing data from 77 patients with NCCP and 5 healthy volunteers. BI was calculated at 3u200acm (distal esophagus) and 17u200acm (proximal esophagus) above the lower esophageal sphincter. GERD was defined by the presence of pathologic acid exposure or reflux esophagitis. Among the 77 patients with NCCP, 16 (20.8%) were classified into the GERD-related NCCP group and 61 (79.2%) into the non-GERD-related NCCP group. BI (median, interquartile range) of the non-GERD-related NCCP group was lower than the control group at the proximal esophagus (2507u200a&OHgr;, 2156–3217 vs 3855u200a&OHgr;, 3238–4182, Pu200a=u200a0.001) but was similar at the distal esophagus. The GERD-related NCCP group showed lower BI than the control group at both the distal and proximal esophagus (2024u200a&OHgr;, 1619–2308 vs 3203u200a&OHgr;, 2366–3774, Pu200a=u200a0.007 and 2272u200a&OHgr;, 1896–2908 vs 3855u200a&OHgr;, 3238–4182, Pu200a=u200a0.003, respectively). At the distal esophagus, BI was lower in the GERD-related NCCP group than the non-GERD-related NCCP group (Pu200a=u200a0.002), whereas it did not differ between the 2 groups at the proximal esophagus. In conclusion, the mucosal integrity is impaired at the proximal esophagus in patients with non-GERD-related NCCP, which might be the pathogenic mechanism of NCCP.

A Case of Riata® Dual Coil Defibrillator Lead Failure in a Patient with Ventricular Fibrillation

A 50-year-old man, who underwent a procedure for an implantable cardioverter defibrillator (ICD), visited the outpatient department of our clinic after suffering multiple ICD shocks. The ICD interrogation revealed recurrent shock due to a high frequency of noise that is sensed by the device as ventricular fibrillation. Chest radiography revealed a significant split in the insulation of the lead allowing the inner wire to protrude. We considered the removal of the failed lead, but the removal of ICD lead is potentially a high risk procedure, so we cut and capped a proximal part of the failed lead and inserted a new lead. This is the first report of a St. Jude Riata® dual coil defibrillator lead failure with clinical and radiologic evidence of a defect in lead insulation in Korea.

Comparison of 22-gauge standard fine needle versus core biopsy needle for endoscopic ultrasound-guided sampling of suspected pancreatic cancer: a randomized crossover trial

Abstract Background: Endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) is effective for tissue diagnosis of pancreatic mass. To improve diagnostic yield and drawbacks, 22-gauge (G) core biopsy (FNB) needle has been developed. This study aims to compare 22G FNA and FNB needles for EUS-guided sampling of suspected pancreatic cancer. Methods: This is a randomized controlled crossover trial. A total of 60 patients with suspected unresectable pancreatic cancer referred for EUS-guided sampling were randomly assigned to two groups. Both groups had 22G FNA and FNB needles performed in a randomized order. The primary endpoint was the cytological, histological and overall diagnostic accuracy of pancreatic cancer. Results: FNA and FNB needles reported similar level of diagnostic accuracy (FNA needle 95% vs. FNB needle 93.3%; pu2009=u2009.564), and it was not statistically different. However, cytological cellularity was significantly higher in the FNB needles compared to FNA needles (odds ratio 2.75, 95% confidence interval (CI)). There were no procedure-related complications in both needles. Conclusions: The diagnostic accuracy of EUS-guided sampling for pancreatic cancer using 22G FNA is comparable to FNB needles. The cytological quality of specimen is better in the FNB needle.

Tu1975 The Impairment of Proximal Esophageal Mucosal Integrity May Play a Causative Role in Patients With Noncardiac Chest Pain

OBJECTIVES: Noncardiac chest pain (NCCP) is defined as recurrent chest pain which does not originate from cardiac cause. Gastroesophageal reflux disease (GERD) is themost common cause of NCCP. However, there are patients presenting NCCP whose symptom is not related with GERD. This study aims to evaluate novel mechanism of non-GERD-related NCCP using high-resolution impedance manometry (HRIM) and 24-hour multichannel intraluminal impedance-pH (MII-pH) testing. PATIENTS AND METHODS: This retrospective study was conducted at Samsung Medical Center between June 2011 and December 2012. A total of 77 NCCP patients and 14 healthy volunteers (control group) were included. The subjects underwent upper endoscopy, esophageal HRIM and 24-hr MII-pH testing. According to the presence of erosive esophagitis and/or pathologic acid exposure, patients were divided into GERD-related group and non-GERD-related group. We measured mean esophageal baseline intraluminal impedances and investigated esophageal motility disorders and/or peristaltic abnormalities. The mean baseline intraluminal impedance was measured at distal and proximal esophagus, 3 cm and 17 cm above the lower esophageal sphincter. The esophageal motility disorders and peristaltic abnormalities were determined by Chicago classification. RESULTS: Among 77 NCCP patients, 16 (11.7%) were included in GERD-related group and 61 (88.3%) were included in non-GERD-related group. The distal mean baseline intraluminal impedance did not differ between NCCP patients and control group. However, the proximal mean baseline intraluminal impedance was lower in NCCP patients than in control group (2463±631 vs. 3739±486 V, P<0.001). In subgroup analysis, the distal mean baseline intraluminal impedance was lower only in GERD-related group than in non-GERD-related NCCP group (1924±802 vs. 2666±804 V, P<0.001) and control group (1924±802 vs. 3739±486 V, P=0.02). There was no difference in distal mean baseline intraluminal impedance between non-GERD-related group and control group. On the contrary, the proximal mean baseline intraluminal impedance was lower both in GERD-related (2391±711 vs. 3739±486V, P<0.001) and non-GERD-related group (2482±614 vs. 3739±486V, P<0.001) than in control group. The proximal mean baseline intraluminal impedance did not differ between GERD-related and non-GERD-related group. There was no difference in esophageal motility disorders, peristaltic abnormalities or impaired bolus transit among these groups. CONCLUSIONS: The proximal esophageal mucosal integrity impairment may play a causative role in patients with non-GERD-related NCCP. The proximal mucosal integrity seems to be impaired by another mechanism rather than esophageal hypomotility and impaired bolus transit.

Static and dynamic prognostic factors for hepatitis-B-related acute-on-chronic liver failure.

Background/Aims Hepatitis-B-related acute-on-chronic liver failure has a poor prognosis. However, the advent of potent oral antiviral agents means that some patients can now recover with medical treatment. We aimed to identify the prognostic factors for hepatitis-B-related acute-on-chronic liver failure including the initial as well as the dynamically changing clinical parameters during admission. Methods Sixty-seven patients were retrospectively enrolled from 2003 to 2012 at Samsung Medical Center. The patients were classified into three categories: Recovery group (n=23), Liver transplantation group (n=28), and Death group (n=16). The Liver transplantation and Death groups were combined into an Unfavorable prognosis group. We analyzed the prognostic factors including the Model for End-Stage Liver Disease (MELD) scores determined at 3-day intervals. Results A multivariable analysis showed that the unfavorable prognostic factors were a high initial MELD score (≥28) (odds ratio [OR] =6.64, p=0.015), moderate-to-severe ascites at admission (OR=6.71, P=0.012), and the aggravation of hepatic encephalopathy during hospitalization (≥grade III) (OR=15.41, P=0.013). Compared with the baseline level, significant reductions in the MELD scores were observed on the 7th day after admission in the Recovery group (P=0.016). Conclusions Dynamic changes in clinical parameters during admission are useful prognostic factors for hepatitis-B-related acute-on-chronic liver failure.

Sa2065 Purinergic Pathway Is the Major Mechanism of Inhibitory Effect of Motilitone on the Rat Gastric Fundus Relaxation

Previous studies found that mechanical stretch in bowel obstruction markedly induced gene expression of COX-2, but not COX-1, in colonic smooth muscle cells (SMCs). The aims of the present study were to determine whether genes encoding individual prostaglandin synthases are mechanically responsive, and whether the composition of prostaglandins resulting from obstruction differs from that in inflammation. Methods: Partial colon obstruction was induced with a silicon band implanted surgically in the distal colon of male SpragueDawley rats. Static mechanical stretch (18% elongation) was mimicked in vitro in the culture of rat colonic circular SMCs with a Flexercell FX-4000 System. Rat colon inflammation was induced by manipulation of the colonic surface with wet cotton applicators. Results: 1. Quantitative RT-PCR found that the expression of PGDS and PGIS genes was not significantly changed on day 3 of obstruction. However, the membrane bound PGES-1 (mPGES-1) mRNA was significantly up-regulated in the obstructed segment, whereas mRNAs for other two types of PGES, cytosolic PGES and mPGES-2, were not changed. On the contrary, the PGFS mRNA was down-regulated in the obstructed colon. 2. PGE2, but not PGF2 α, was significantly increased in the colonic muscularis externae in obstruction. The PGE2 level increased to 4577±1249 pg/mg at day 3 of obstruction, compared to 1264±259 in sham (n=6, p,0.05). The PGF2α level was 5718±910 pg /mg in obstruction compared to 6550±2178 pg/mg in the sham (n=5, p.0.05). 3. Direct stretch of rat colonic circular SMCs in vitro significantly up-regulated the mPGES-1 mRNA, but down-regulated that of PGFS. After stretch for 3 hrs, the mRNA levels of PGES and PGFS changed by 2.61±0.42 fold and 0.82±0.03 fold, respectively (n = 4 or 5, p,0.05). 4. In colonic inflammation, both PGE2 and PGF2α were significantly increased in the colonic smooth muscle (5.2(±1.5)-fold and 4.7(±1.3)-fold of control, respectively, p,0.05, n = 3). 5. Rat colonic circular muscle contractility was inhibited by exogenous PGE2 (10-9 ~10-6 M), but enhanced by PGF2 α (10-9 ~10-6 M) in a concentration-dependent manner (n = 4). Conclusions: Genes involved in the COX pathway of arachidonic acid metabolism are highly mechanosensitive in colonic SMCs, and play a critical role in motility function. Mechano-regulation of prostaglandin synthases accounts for increased PGE2 and unchanged PGF2 α in bowel obstruction, a pathological feature different from inflammation in which both PGE2 and PGF2 α are increased.