Byoung Hwan Lee

Change in antibiotic resistance of Helicobacter pylori strains and the effect of A2143G point mutation of 23S rRNA on the eradication of H. pylori in a single center of Korea.

Background The current prevalence of primary antibiotic resistance of H. pylori is not known in Korea. This study was done to evaluate the prevalence of primary antibiotic resistance of H. pylori, and to evaluate the effect of point mutations of 23S rRNA on the rate of eradication of H. pylori. Methods H. pylori were isolated from gastric mucosal biopsy specimens obtained from 222 Koreans. The susceptibilities of the H. pylori isolates to amoxicillin, clarithromycin, metronidazole, tetracycline, ciprofloxacin, and levofloxacin were examined using the agar dilution method. DNA sequencing was carried out to detect H. pylori 23S rRNA mutations. Results The resistance to clarithromycin, tetracycline, ciprofloxacin, and levofloxacin increased during the period of 2007 to 2009 compared with 2003 to 2005 (P<0.05). However, amoxicillin and metronidazole resistance slightly decreased. The rates of eradication were 95.5% for the clarithromycin-sensitive strains, which was higher than the 67.9% for the clarithromycin-resistant strains (P=0.001). By contrast, the eradication rate was 100% in patients with amoxicillin-resistant H. pylori. Among 26 clarithromyin-resistant strains, 6 (23%) had A2143G mutations, and all of the cases in which these mutations were present were not eradicated by proton pump inhibitor-based triple therapy (P=0.0004). By contrast, none of the 26 clarithromyin-sensitive strains had A2143G mutations. The T2183C and A2223G mutations were frequently found in the sensitive strains and in the resistant strains. Conclusions Clarithromycin resistance of H. pylori, which determined the efficacy of H. pylori eradication of proton pump inhibitor triple regimen, was found to be increased in a single center study. A2143G was an important 23S rRNA mutation associated with clarithromycin resistance and affected the H. pylori eradication efficacy.

Bismuth‐Containing Quadruple Therapy as Second‐Line Treatment for Helicobacter pylori Infection: Effect of Treatment Duration and Antibiotic Resistance on the Eradication Rate in Korea

Background:  The eradication rate of first‐line Helicobacter pylori treatment is only 70–85% and has been decreasing due to the increase in antibiotic resistance. The aim of this study was to evaluate the efficacy of bismuth‐containing quadruple therapy as second‐line treatment for H. pylori infection based on treatment duration.

Moxifloxacin-Containing Triple Therapy as Second-Line Treatment for Helicobacter pylori Infection: Effect of Treatment Duration and Antibiotic Resistance on the Eradication Rate

Background and Aim:  The aim of this study was to evaluate the efficacy of a moxifloxacin‐containing triple therapy as second‐line treatment for Helicobacter pylori infection. We also investigated the effect of treatment duration and antibiotic resistance on the eradication rate of this therapy.

Effect of aging on gastric mucosal defense mechanisms: ROS, apoptosis, angiogenesis, and sensory neurons.

Aging changes in the stomach lead to a decreased capacity for tissue repair in response to gastric acid. The aim of this study was to determine the mechanism associated with the increased susceptibility to injury of aging mucosa including reactive oxygen species (5), apoptosis, angiogenesis, and sensory neuron activity. Fischer 344 rats at four different ages (6, 31, 74 wk, and 2 yr of age) were studied. The connective tissue indicators [salt-soluble collagen and sulfated glycosaminoglycan (sGAG)], lipid hydroperoxide (LPO), myeloperoxidase (MPO), and hexosamine were assessed. We also evaluated the expression of early growth response-1 (Egr-1), phosphatase and tension homologue deleted on chromosome 10 (PTEN), caspase-9 (index of apoptosis), VEGF (index of angiogenesis), calcitonin gene-related peptide (CGRP, index of sensory neurons), and neuronal nitric oxide synthase (nNOS). The histological connective tissue area in the lower part of rat gastric mucosa increased with aging, with increase of salt-soluble collagen and sGAG. LPO and MPO in old rats were significantly greater than in the young rats, whereas hexosamine was significantly reduced. The old gastric mucosa had increased expression of Egr-1, PTEN, and caspase-9, whereas the VEGF, CGRP, and nNOS expression were significantly reduced. These results indicate that the lower part of rat gastric mucosa was found to be replaced by connective tissue with accumulation of oxidative products with aging. In addition, impairment of apoptosis, angiogenesis, and sensory neuron activity via the activation of Egr-1 and PTEN might increase the susceptibility of gastric mucosa to injury during aging.

CDX1 and CDX2 Expression in Intestinal Metaplasia, Dysplasia and Gastric Cancer

Intestinal metaplasia (IM) has been regarded as a premalignant condition. However, the pathogenesis of IM is not fully understood. The aim of this study was to evaluate the role of CDX1 and CDX2 in the formation of IM and the progression to dysplasia and gastric cancer (GC). A total of 270 subjects included 90 with GC, dysplasia and age- and sex-matched controls. Real-time PCR (RT-PCR) was performed with body specimens for CDX1 and CDX2. The expression of CDX2 was significantly higher in H. pylori positive group than H. pylori negative group (P = 0.045). CDX1 and CDX2 expression increased proportional to the IM grade of the body (P < 0.001). CDX2 expression was significantly higher in incomplete type of IM than in complete type (P = 0.045). The expression of CDX1 in dysplasia group was significantly higher than in the control group (P = 0.001); in addition, CDX1 and CDX2 in cancer group was significantly higher than control group (P < 0.001, and P < 0.001, respectively). Aberrant expression of CDX1 and CDX2 correlated with H. pylori infection and grade of IM in the body. Furthermore, the results suggest that CDX1 and CDX2 play a role in the progression to GC and dysplasia.

The Long-term Clinical Efficacy of Biofeedback Therapy for Patients With Constipation or Fecal Incontinence

Background/Aims There has been a controversy regarding the usefulness of biofeedback therapy for functional constipation or fecal incontinence. This study was performed to investigate the long-term clinical efficacy of biofeedback therapy. Methods Sixty-four patients with constipation or fecal incontinence received biofeedback therapy for 4 weeks. Symptom improvements were evaluated immediately after the completion of biofeedback therapy and during the follow-up period of about 12 to 64 months. Results Twenty-five patients in the constipation group [mean age of 52.1 years, 16 men (64.0%)] received 6.2 sessions of biofeedback therapy. Improvement of constipation after the completion of biofeedback therapy was as follows: major response (or improvement) in 3 patients (12.0%), fair in 6 (24.0%), minor in 11 (44.0%) and none in 5 (20.0%). Among 9 patients who showed major or fair improvement, 8 patients (88.9%) maintained the symptom improvement through the long term follow-up periods. Thirty-nine patients in the fecal incontinence group [59.7 years old, 15 men (38.5%)] received 6.8 sessions of biofeedback therapy. Improvement of incontinence after the completion of biofeedback therapy was as follows: major improvement in 6 patients (15.4%), fair in 14 (35.9%), minor in 14 (35.9%), and none in 5 (12.8%). All 11 patients with major or fair improvement maintained the symptom improvement to the end of follow-up periods. Conclusions Symptom improvements after biofeedback therapy were disappointing in both the constipation and incontinence group. However, when the symptom improvements were classified as major or fair, the improvements continued for at least a year.

Risk factors for peptic ulcer bleeding in terms of Helicobacter pylori, NSAIDs, and antiplatelet agents

Abstract Objectives. The role of the Helicobacter pylori, nonsteroidal anti-inflammatory drugs (NSAIDs), and antiplatelet agents in the risk of peptic ulcer bleeding has not yet been established. This study was performed to identify the risk factors for peptic ulcer bleeding compared with non-bleeding peptic ulcer disease (PUD). Material and methods. A total of 475 patients, 265 with bleeding PUD and 210 with non-bleeding PUD were consecutively recruited. H. pylori status was determined by histology, rapid urease test, and culture. Exposure to NSAIDs, aspirin, and antiplatelet agents (clopidogrel and ticlopidine) within 4 weeks was obtained. Results. Compared with non-bleeding PUD, bleeding PUD had a higher proportion of male gender and current smoking, alcohol drinking, history of aspirin/antiplatelet use, and history of PUD. Whereas the proportion of H. pylori infection and history of H. pylori eradication in bleeding PUD were significantly lower than that in non-bleeding PUD. In multivariate analysis, male gender (OR 1.78, 95% CI 1.10–2.89), drinking alcohol (OR 2.08, 95% CI 1.29–3.14), aspirin/antiplatelet use (OR 2.35, 95% CI 1.45–3.82), and history of PUD (OR 2.46, 95% CI 1.36–4.46) remained independent risk factors for bleeding PUD. When H. pylori status and aspirin/antiplatelet agent use were combined, highest risk of bleeding peptic ulcers was found among H. pylori-negative patients with a history of aspirin/antiplatelet agent use (OR 3.03 95% CI 1.48–6.18) compared with H. pylori-positive patients with no history of aspirin/antiplatelet agent use. Conclusions. Patients with H. pylori-negative peptic ulcers who continuously took aspirin or antiplatelet agents had the highest peptic ulcer bleeding risk.

Comparison of Indomethacin, Diclofenac and Aspirin-Induced Gastric Damage according to Age in Rats

Background/Aims Aging gastric mucosa is known to have decreased mucosal defenses and increased susceptibility to injury by nonsteroidal anti-inflammatory drugs. Depending on the type of nonsteroidal anti-inflammatory drug (NSAID), the underlying mechanisms and the extent of damage to the stomach or intestine may differ. This study was performed to evaluate the acute gastric damage caused by different doses of indomethacin, diclofenac and aspirin in rats of various ages. Methods For the acute models, indomethacin (10, 20 or 40 mg/kg), diclofenac (40 or 80 mg/kg) or aspirin (100 mg/kg) was given to 7- and 25-week-old and 1-year-old Sprague-Dawley rats by intragastric gavage. The gross ulcer index, damage area as assessed by imaging, histological index, myeloperoxidase (MPO) activity, and cytosolic phospholipase A2 (cPLA2) levels were measured after 24 hours. Results The gross ulcer index and damage area increased with age in the presence of three NSAIDs (p<0.05). The increases in MPO levels induced by diclofenac and aspirin were significantly higher in 1-year-old than 7-week-old rats (p<0.05). cPLA2 expression induced by indomethacin (10 and 40 mg/kg) was greater in the 1-year-old rats, compared with 7-week-old rats (p<0.05). Conclusions NSAID-induced acute gastric damage increased in a dose- and age-dependent manner.

Analysis of direct medical care costs of peptic ulcer disease in a Korean tertiary medical center

Abstract Objectives. There have been no reported data on the medical care cost of idiopathic peptic ulcer disease (PUD) compared with H. pylori (+) and/or NSAID (+) cases although H. pylori-negative idiopathic ulcers are increasing. The aim of this study was to investigate the direct medical care costs of PUD based on whether it was H. pylori infection/from NSAIDs or idiopathic. Material and methods. One hundred and seventy three patients with PUD comprising H. pylori and/or NSAID use-associated PUD (n = 145) and idiopathic PUD (n = 28) were prospectively enrolled in this study. The direct medical care costs were analyzed retrospectively for the patients with PUD during a one-year follow-up period. Results. The recurrence rate within one year was significantly higher in idiopathic PUD than H. pylori and/or NSAID-associated PUD (p = 0.002). Direct medical care costs of idiopathic PUD (

Gastroprotective effect of Cochinchina momordica seed extract in nonsteroidal anti-inflammatory drug-induced acute gastric damage in a rat model.

2483.8) were higher than in patients with H. pylori and/or NSAID-associated PUD (