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Biomedical subjects

Ming-Shiang Wu

Publications and source records attributed to Ming-Shiang Wu.

At least 37 records · Page 2Linked to original sources

Circadian change of cardiac autonomic function in correlation with intra-esophageal pH.

BACKGROUND AND AIM: Although autonomic alterations are observed in patients with gastroesophageal reflux disease (GERD), the influence of visceral receptor responses on the dynamics of autonomic function remains unknown. The aim of this study was to investigate the autonomic functional changes in association with intra-esophageal pH under ambulation. METHODS: Thirty patients referred for 48 h ambulatory pH monitoring underwent simultaneous 24 h cardiac monitoring for heart rate variability (HRV). We used linear mixed-effects models to estimate the relationship between esophageal acid exposure and power spectral analysis of HRV, including low-frequency power (0.04 < LF < 0.15 Hz), high-frequency power (0.15 < or = HF < 0.4 Hz), and LF/HF power ratio. RESULTS: Over the 24-h period, patients with pathological reflux had lower average LF and HF powers than patients with functional heartburn, but the LF/HF power ratios were similar for the two patient groups. As we stratified the data according to waking and sleeping times, a significantly higher HF power but lower LF/HF power ratio was found during sleeping time regardless of diagnosis. In the regression analysis, esophageal pH was positively associated with change (not basal tone) of both LF and HF powers during waking, but only with change of HF power during sleeping time. The significant associations between pH values and changes in HRV decreased gradually with time. The LF/HF power ratio did not alter significantly with pH. CONCLUSION: Esophageal acid exposure is generally associated with decreases in autonomic tone. A predominant parasympathetic fluctuation during sleeping and a superimposed sympathetic interaction during waking dictate diurnal characteristics of autonomic regulation.

Adult↗

A community-based study of Helicobacter pylori therapy using the strategy of test, treat, retest, and re-treat initial treatment failures.

BACKGROUND: Although eradication of Helicobacter pylori infection can decrease the risk of gastric cancer, the optimal regimen for treating the general population remains unclear. We report the eradication rate (intention-to-treat and per protocol) of a community-based H. pylori therapy using the strategy of test, treat, retest, and re-treat initial treatment failures. MATERIALS AND METHODS: In 2004, a total of 2658 residents were recruited for 13C-urea breath testing. Participants with positive results for infection received a standard 7-day triple therapy (esomeprazole 40 mg once daily, amoxicillin 1 g twice daily, and clarithromycin 500 mg twice daily), and a 10-day re-treatment (esomeprazole 40 mg once daily, amoxicillin 1 g twice daily, and levofloxacin 500 mg once daily) if the follow-up tests remained positive. Both H. pylori status and side-effects were assessed 6 weeks after treatment. RESULTS: Among 886 valid reporters, eradication rates with initial therapy were 86.9% (95% confidence interval [CI]: 84.7-89.1%) and 88.7% (95%CI: 86.5-90.9%) by intention-to-treat and per protocol analysis, respectively. Re-treatment eradicated infection in 91.4% (95%CI: 86-96.8%) of 105 nonresponders. Adequate compliance was achieved in 798 (90.1%) of 886 subjects receiving the initial treatment and in all 105 re-treated subjects. Mild side-effects occurred in 24% of subjects. Overall intention-to-treat and per protocol eradication rates were 97.7% (95%CI: 96.7-98.7%) and 98.8% (95%CI: 98.5-99.3%), respectively, which were only affected by poor compliance (odds ratio, 3.3; 95%CI, 1.99-5.48; p < .0001). CONCLUSIONS: A comprehensive plan using drugs in which the resistance rate is low in a population combined with the strategy of test, treat, retest, and re-treat of needed can result in virtual eradication of H. pylori from a population. This provides a model for planning country- or region-wide eradication programs.

Anti-Bacterial Agents↗

The influence of Helicobacter pylori infection and corpus gastritis on the postoperative outcomes of laparoscopic vertical banded gastroplasty.

BACKGROUND: Helicobacter pylori (HP) infection is linked to weight control through gastric inflammation-induced deregulation of satiety-related hormone, and eradication of HP before a weight reduction operation has been advocated. We aimed to examine the impact of HP infection and corpus gastritis on preoperative patient characteristics, postoperative complications and weight loss following laparoscopic vertical banded gastroplasty (LVBG). METHODS: A prospective cohort of 152 patients undergoing LVBG was enrolled. Gastric specimens at the corpus were obtained during LVBG operation and scored histologically according to the Sydney classification of gastritis. Excess weight loss, and early and late complications following LVBG, were recorded and correlated. RESULTS: 63 and 89 patients were identified as HP positive and negative groups respectively. The prevalence of individual components of the metabolic syndrome was comparable in both groups except hypertension. The occurrence of early and late complications, either minor or major, in both groups was similar. The severity of gastritis was correlated positively with age and negatively with preoperative BMI and excess weight. Patients with higher neutrophil activity, chronic inflammation, and HP density experienced less excess weight loss at 24 to 48 months follow-up. The impact of gastritis on weight loss became less recognizable after 48 months follow-up. CONCLUSIONS: HP infection and gastric inflammation play a significant role in the amount of weight loss after LVBG. Further prospective studies should examine possible mechanisms and long-term effects on weight loss to determine the utility of preventive eradication of HP in different types of bariatric surgery.

Adolescent↗

The influence of Helicobacter pylori infection on the development of gastric ulcer in symptomatic patients after bariatric surgery.

BACKGROUND: There are few data relating to the role of H. pylori infection and surgical procedures on the occurrence of gastric ulcer following bariatric surgery. METHODS: Subjects with upper gastrointestinal symptoms after bariatric surgery and receiving gastroscopic examinations were prospectively enrolled. All clinical data including age, sex, BMI before surgery, and surgical method were recorded. IgG antibodies against H. pylori were measured in preoperative serum by enzyme-linked immunosorbent assay (ELISA). RESULTS: A cohort of 636 patients undergoing laparoscopic vertical banded gastroplasty (LVBG) or Roux-en-Y gastric bypass (LRYGBP) was recruited. The seropositivity of H. pylori in symptomatic and asymptomatic patients after surgery was 39% (32/82) and 39.7% (220/554) respectively. Endoscopic examinations revealed that 22 (26.8%) of 82 symptomatic patients had a gastric ulcer. Comparison of demographic characteristics between patients with ulcer (n=22) and patients without ulcer (n=60) showed no difference in distribution of gender, age, BMI, and seroprevalence of H. pylori (27.3%, 6/22 vs 43.3%, 26/60, P=0.212). Patients undergoing LRYGBP showed a higher rate of gastric ulcer (45.5%, 10/22) when compared to patients undergoing LVBG (20%, 12/60; P=0.027). CONCLUSION: Gastric ulcers in symptomatic patients following laparoscopic bariatric surgery are related to surgical procedures rather than exposure to H. pylori infection.

Adult↗

Spectrum of endoscopic findings and therapy in patients with upper gastrointestinal symptoms after laparoscopic bariatric surgery.

BACKGROUND: More should be known about the spectrum of endoscopic abnormalities and treatments in patients with upper gastrointestinal (UGI) symptoms after laparoscopic bariatric surgery. METHODS: Patients referred for endoscopic evaluation of UGI symptoms after laparoscopic bariatric surgery were studied. Clinical manifestations, endoscopic findings and therapy were recorded and correlated. RESULTS: 76 patients who had undergone laparoscopic vertical banded gastroplasty (LVBG) and 28 who had undergone laparoscopic Roux-en-Y gastric bypass (LRYGBP) underwent 160 instances of upper endoscopy. The symptoms included nausea or vomiting (n=47, 29.4%), epigastric discomfort (n=44, 27.5%), UGI bleeding (n=26, 16.3%), heartburn or acid regurgitation (n=26, 16.3%), dysphagia (n=10, 6.3%) and anemia with dizziness (n=7, 4.4%). The endoscopic diagnosis consisted of normal findings (n=57, 35.6%), marginal ulcer (n=39, 24.4%), erosive esophagitis or esophageal ulcer (n=21, 13.1%), food impaction (n=21, 13.1%), stenosis or stricture (n=14, 8.8%), gastric ulcer (n=7, 4.4%), and duodenal ulcer (n=1, 0.6%). Patients with UGI bleeding, dysphagia and LRYGBP tended to have endoscopic abnormalities (P<0.001, P=0.09 and P=0.021, respectively). Endoscopic therapy was successful in resolving the complications including stenosis, UGI bleeding and food impaction. CONCLUSIONS: Endoscopy is an essential method of combining relevant endoscopic findings and therapeutic intervention in symptomatic patients following laparoscopic bariatric surgery.

Adult↗

Gene expression profiling of gastric cancer by microarray combined with laser capture microdissection.

AIM: To examine the gene expression profile of gastric cancer (GC) by combination of laser capture microdissection (LCM) and microarray and to correlate the profiling with histological subtypes. METHODS: Using LCM, pure cancer cells were procured from 45 cancerous tissues. After procurement of about 5000 cells, total RNA was extracted and the quality of RNA was determined before further amplification and hybridization. One microgram of amplified RNA was converted to cDNA and hybridized to cDNA microarray. RESULTS: Among 45 cases, only 21 were qualified for their RNAs. A total of 62 arrays were performed. These included 42 arrays for cancer (21 cases with dye-swab duplication) and 20 arrays for non-tumorous cells (10 cases with dye-swab duplication) with universal reference. Analyzed data showed 504 genes were differentially expressed and could distinguish cancerous and non-cancerous groups with more than 99% accuracy. Of the 504 genes, trefoil factors 1, 2, and 3 were in the list and their expression patterns were consistent with previous reports. Immunohistochemical staining of trefoil factor 1 was also consistent with the array data. Analyses of the tumor group with these 504 genes showed that there were 3 subgroups of GC that did not correspond to any current classification system, including Lauren's classification. CONCLUSION: By using LCM, linear amplification of RNA, and cDNA microarray, we have identified a panel of genes that have the power to discriminate between GC and non-cancer groups. The new molecular classification and the identified novel genes in gastric carcinogenesis deserve further investigations to elucidate their clinicopathological significance.

Gene Expression Profiling↗

Helicobacter pylori-Induced invasion and angiogenesis of gastric cells is mediated by cyclooxygenase-2 induction through TLR2/TLR9 and promoter regulation.

Cyclooxygenase-2 (COX-2) plays a crucial role in Helicobacter pylori-associated gastric cancer. In this study, we report that H. pylori-induced COX-2 expression enhances the cancer cell invasion and angiogenesis via TLR2 and TLR9, which can be attenuated by the specific COX-2 inhibitor NS398 or celecoxib. The cAMP response element (CRE) and AP1 sites, but not kappaB on the COX-2 promoter, are involved in MAPKs-regulated COX-2 expression. Differential bindings of the CREB-1, ATF-2, c-jun to the CRE site, and the c-fos, c-jun, ATF-2 to the AP1 site are demonstrated by DNA affinity protein-binding, supershift, and chromatin immunoprecipitation assays. Activations of these transcription factors were attenuated by different MAPKs inhibitors. The mutants of TLR2, TLR9, or MAPKs inhibited H. pylori-induced COX-2 promoter, CRE, and AP-1 activities. MAPKs inhibitors attenuated the H. pylori-induced COX-2 mRNA and protein expressions. These results indicate that H. pylori acts through TLR2 and TLR9 to activate MAPKs, especially p38, and their downstream transcription factors (CREB-1, ATF-2, c-jun, and c-fos), resulting in the activations of CRE and AP-1 on the COX-2 promoter. These intracellular networks drive the COX-2-dependent PGE2 release and contribute to cell invasion and angiogenesis.

Cell Line, Tumor↗

Prevalence of advanced colonic polyps in asymptomatic Chinese.

AIM: To investigate the prevalence of advanced polyps in asymptomatic Chinese and to determine the risk of proximal advanced colonic polyps in subjects with and without polyps in the distal colon. METHODS: Data were collected prospectively during colonoscopic examinations performed in 5 973 subjects as part of health evaluation at our unit from December 1997 to December 2003. Polyps were considered advanced, if they were larger than 10 mm or were tubovillous, villous or malignant. Proximal colon was defined as the splenic flexure and more proximal portions of the colon. RESULTS: Colon polyps were detected in 971 (16.3%) subjects (613 males and 358 females) with their mean age being 56.6+/-10.7 years. Advanced polyps were noted in 199 (3.3%) individuals. Subjects were sub-classified according to the location of polyps into three groups: distal (569, 58.6%), proximal (284, 29.2%), and combined proximal and distal (118, 12.2%) groups. Subjects with advanced polyps in these three groups were 95 (9.8%), 56 (5.8%), and 48 (4.9%) respectively. In the 48 subjects with advanced combined polyps, 13 advanced polyps were distributed at the distal colon, 17 at the proximal colon, and 18 at both. Eighteen colon cancers including 12 at sigmoid and 6 at ascending colon were confirmed by final pathology. The relative risk for advanced proximal polyp according to distal findings was 3.1 (95%CI: 1.3-7.4) for hyperplastic polyp, 2.7 (95%CI: 1.4-5.3) for tubular polyp and 13.5 (95%CI: 5.1-35.4) for advanced polyp as compared to that for no polyp. However, 56 (28.2%) of 199 subjects with advanced polyps had no index polyps at the distal colon and might go undetected under sigmoidoscopic screening. CONCLUSION: Although distal lesions can predict the risk of advanced proximal polyps, a substantial portion of Chinese with advanced proximal polyps is not associated with any distal sentinel lesions. These data have implications for screening policy of colon cancers in Taiwanese Chinese.

Adult↗

Expression of CD86 and increased infiltration of NK cells are associated with Helicobacter pylori-dependent state of early stage high-grade gastric MALT lymphoma.

AIM: A high percentage of early-stage high-grade gastric mucosa-associated lymphoid tissue (MALT) lymphomas remain Helicobacter pylori (H pylori)-dependent. However, unlike their low-grade counterparts, high-grade gastric MALT lymphomas may progress rapidly if unresponsive to H pylori eradication. It is mandatory to identify markers that may predict the H pylori-dependent status of these tumors. Proliferation of MALT lymphoma cells depends on cognate help and cell-to-cell contact of H pylori-specific intratumoral T-cells. To examine whether the expression of co-stimulatory marker CD86 (B7.2) and the infiltration of CD56 (+) natural killer (NK) cells can be useful markers to predict H pylori-dependent status of high-grade gastric MALT lymphoma. METHODS: Lymphoma biopsies from 26 patients who had participated in a prospective study of H pylori-eradication for stage I(E) high-grade gastric MALT lymphomas were evaluated. Tumors that resolved to Wotherspoon grade II or less after H pylori eradication were classified as H pylori-dependent; others were classified as H pylori-independent. The infiltration of NK cells and the expression of CD86 in pre-treatment paraffin-embedded lymphoma tissues were determined by immunohistochemistry. RESULTS: There were 16 H pylori-dependent and 10 H pylori-independent cases. CD86 expression was detected in 11 (68.8%) of 16 H pylori-dependent cases but in none of 10 H pylori-independent cases (P = 0.001). H pylori-dependent high-grade gastric MALT lymphomas contained significantly higher numbers of CD56 (+) NK cells than H pylori-independent cases (2.8+/-1.4% vs 1.1+/-0.8%; P = 0.003). CD86 positive MALT lymphomas also showed significantly increased infiltration of CD56 (+) NK cells compared to CD86-negative cases (2.9+/-1.1% vs 1.4+/-1.3%; P = 0.005). CONCLUSION: These results suggest that the expression of co-stimulatory marker CD86 and the increased infiltration of NK cells are associated with H pylori-dependent state of early-stage high-grade gastric MALT lymphomas.

Adult↗

A case-control study of association of Helicobacter pylori infection with morbid obesity in Taiwan.

BACKGROUND: Obesity is an increasing health problem in developed countries, where the prevalence of Helicobacter pylori infection is decreasing. Recent studies suggested colonization of the stomach by H pylori might affect gastric expression of appetite- and satiety-related hormone and patients cured of H pylori infection gained weight. It was hypothesized that H pylori could be a contributing pathogenic factor in childhood and adult obesity. METHODS: To determine whether H pylori infection is linked to obesity, a case-control study composed of 414 patients with morbid obesity (a body mass index [calculated as weight in kilograms divided by the square of height in meters] of > or = 35 with serious comorbidity or a body mass index of > or = 40) and 683 control subjects (a body mass index of <25) with a comparable socioeconomic status was conducted. Immunoglobulin G antibodies against H pylori were measured from frozen serum samples by an enzyme-linked immunosorbent assay. Logistic regression was used to calculate the odds ratio (OR) and 95% confidence interval (CI). RESULTS: The overall seropositivity was significantly lower in obese patients (181 [43.7%] of 414) than controls (410 [60.0%] of 683) (OR, 0.50; 95% CI, 0.39-0.65; P<.001). Differences in the estimated risk of the presence of H pylori were more pronounced in younger age groups, with ORs of 0.32 (95% CI, 0.10-1.00; P = .05) in those aged 10 to 19 years, 0.55 (95% CI, 0.34-0.89; P = .01) in those aged 20 to 29 years, 0.49 (95% CI, 0.30-0.80; P = .007) in those aged 30 to 39 years, and 0.58 (95% CI, 0.33-1.00; P = .05) in those aged 40 years or older. CONCLUSIONS: Our data indicated an inverse relationship between morbid obesity and H pylori seropositivity. These findings raise the hypothesis that a lack of H pylori infection, especially during childhood, might enhance the risk of the development of morbid obesity.

Adult↗

Expression of macrophage migration inhibitory factor is associated with enhanced angiogenesis and advanced stage in gastric carcinomas.

AIM: Macrophage migration inhibitory factor (MIF) was reported to inactivate p53 and play an essential role in the growth and angiogenesis of tumors that arise at sites of chronic inflammation. Gastric inflammation is a prerequisite for the development of gastric carcinoma (GC), which has recently been linked to Helicobacter pylori (H pylori) infection. This study aimed to investigate clinicopathological significance of MIF expression in GCs. METHODS: We selected 90 consecutive patients with GCs for investigation of the relation among MIF status, clinicopathological parameters, p53 expression and angiogenesis. MIF and p53 expression was assessed by immunohistochemistry as positive and negative groups. Tumor vascularity was evaluated by counting microvessel density on anti-CD34 stained sections. Expression status of MIF was correlated with determined clinicopathological data, p53 immunoreactivity and microvessel counts. RESULTS: Strong immunostainings of MIF were observed in the cytoplasm of cancerous cells in 40% (36/90) of cases but not in normal or metaplastic epithelia. There was no statistically significant correlation between MIF expression and age, gender, H pylori infection, tumor location, histological subtypes, lymph node metastasis or p53 expression. Early GC less frequently overexpressed MIF as compared to advanced GCs (4/20 vs 32/70, P = 0.04). A remarkably increased microvessel count was noted in GCs with MIF expression than those without MIF expression (55.1+/-30.1 vs 31.3+/-28.8, P = 0.0001). CONCLUSION: Our results suggest that expression of MIF may contribute to the progression and enhanced angiogenesis in a substantial portion of GCs.

Adult↗

Nuclear expression of BCL10 or nuclear factor kappa B helps predict Helicobacter pylori-independent status of low-grade gastric mucosa-associated lymphoid tissue lymphomas with or without t(11;18)(q21;q21).

The t(11;18)(q21;q21) translocation is a specific marker for Helicobacter pylori-independent status of low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma. However, there are no reliable markers to predict tumor response to H pylori eradication in patients without t(11;18)(q21;q21). Nuclear expression of BCL10 and nuclear factor kappa B (NF-kappaB) was recently found to be closely associated with H pylori-independent status of the high-grade counterpart of gastric MALT lymphoma, which usually lacks t(11;18)(q21;q21). This study examined whether these 2 markers can also predict H pylori-independent status of low-grade gastric MALT lymphomas without t(11; 18)(q21;q21). Sixty patients who underwent successful H pylori eradication for low-grade gastric MALT lymphomas were included. Forty-seven (78.3%) patients were negative for t(11;18)(q21;q21); among them, 36 (76.6%) were H pylori dependent and 11 (23.4%) were H pylori independent. Nuclear expression of BCL10 was significantly higher in H pylori-independent than in H pylori-dependent tumors (8 of 11 [72.7%] vs 3 of 36 [8.3%]; P < .001). Nuclear expression of NF-kappaB was also significantly higher in H pylori-independent than in H pylori-dependent tumors (7 of 11 [63.6%] vs 3 of 36 [8.3%]; P < .001). Further, nuclear translocation of BCL10 and NF-kappaB was observed in 12 of the 13 patients with t(11;18)(q21;q21), and all these 12 patients were H pylori independent. In summary, nuclear expression of BCL10 or NF-kappaB is predictive of H pylori-independent status of low-grade gastric MALT lymphoma with or without t(11;18)(q21; q21).

Active Transport, Cell Nucleus↗

Proteomic analysis of proteins expressed by Helicobacter pylori under oxidative stress.

Helicobacter pylori is a spiral, slow growing gram-negative microaerophilic bacterium. It has been shown to be the etiological agent of gastroduodenal diseases, such as chronic gastritis, gastric and duodenal ulcers, and gastric cancer. To address the influence of oxidative stress and its underlying mechanisms, we have compared proliferation, urease activity and protein expression profile of H. pylori incubated under normal microaerophilic (5% O2) and aerobic stress (20% O2) conditions. Oxidative-stress cells displayed coccoid morphology and time-dependent decrease in proliferation. The urease activity was completely abrogated after 32 h. We have further compared the protein expression profiles of H. pylori under normal growing and oxidative-stress conditions by a global proteomic analysis, which includes high-resolution 2-DE followed by MALDI-TOF-MS and bioinformatic databases search/peptide-mass comparison. The results revealed that more than ten proteins were differentially expressed under oxidative stress. Most notably, the protein expression levels of urease accessory protein E (UreE, an essential metallochaperone for urease activity) and alkylhydroperoxide reductase (AhpC) with antioxidant potential are greatly decreased under stress conditions. Measurements of messenger RNA transcription level by performing RT-PCR on total mRNA also confirmed that gene expressions for these two proteins are consistently repressed under oxygen tension. These changes form a firm basis to account for the loss of urease activity and anti-oxidative ability of H. pylori after long-term exposure to reactive oxygen. Conceivably, UreE and AhpC may thus be listed as potential targets for the development of therapeutic drugs against H. pylori.

Animals↗

Cyclooxygenase-2 increases hypoxia-inducible factor-1 and vascular endothelial growth factor to promote angiogenesis in gastric carcinoma.

Cyclooxygenase-2 (COX-2) is an inducible enzyme important in inflammation and which is overexpressed in a variety of cancers. This study investigated its role in angiogenesis of gastric carcinoma (GC). Immunohistochemical examination of surgical specimens showed a positive correlation among COX-2, vascular endothelial growth factor (VEGF), and vasculature in GC. After transfection with a COX-2-expressing vector, the AGS GC cell line showed increases in both proliferation and tube formation of human umbilical vein endothelial cells (HUVECs). These in vitro angiogenic effects on HUVECs were reduced either by blocking VEGF or NS-398, a COX-2 inhibitor. To elucidate the mechanism by which COX-2 increases angiogenesis, we established a COX-2-expressing clone, AGS/COX-2, and its vector control clone, AGS/pcDNA3, and verified their functions by determining prostaglandin E2 (PGE2). Among 6 angiogenesis-associated factors, VEGF was considerably expressed in AGS/COX-2. After reducing hypoxia-inducible factor-1alpha (HIF-1alpha) protein by antisense HIF-1alpha transfection, VEGF production was reduced in AGS/COX-2 cells in a dose-dependent manner. We found that HIF-1alpha increased concomitantly with VEGF after exogenous PGE2 stimulation to wild-type AGS cells, but this effect was blocked by SC19220, a PGE2 receptor antagonist. In addition, pretreatment with NS-398 to reduce PGE2 also effectively suppressed HIF-1alpha protein accumulation and achieved a similar inhibitory effect on VEGF production as did antisense HIF-1alpha transfection. Our work supports the COX-2/PGE2/HIF-1alpha/VEGF pathway possibly contributing to tumor angiogenesis in GC.

Adult↗

A prospective study of the frequency and the topographical distribution of colon neoplasia in asymptomatic average-risk Chinese adults as determined by colonoscopic screening.

BACKGROUND: The goal of this study was to determine the frequency of colorectal neoplasia in an asymptomatic Taiwanese population and the topographic distribution of lesions relative to age and gender. METHODS: Colonoscopy was performed in 1846 consecutive asymptomatic adults undergoing a health evaluation in 2003. Neoplastic lesions were considered advanced if they exceeded 10 mm in size, had a villous component, or contained moderately or severely dysplastic tissue or invasive cancer. Lesions at and proximal to the splenic flexure were considered proximal in location; those distal to the splenic flexure were classified as distal in location. RESULTS: Of 1741 (94.3%) patients (1041 men, 700 women; mean 52.5 years) enrolled, 1708 (98.1%) underwent total colonoscopy. Of these patients, 263 (15.4%) had colorectal neoplasia; 51 (3.0%) had advanced lesions. A total of 331 lesions were detected; 125 (37.8%) were proximal in location. Two thirds of patients with proximal advanced lesions (66.7%, 10/15) had no distal lesion. The proportion of patients with proximal or proximal plus distal lesions increased with age ( p = 0.027). CONCLUSIONS: Colonoscopy is an effective primary screening modality for colorectal neoplasia in asymptomatic Chinese patients. Many lesions would be missed, especially in the elderly, if only sigmoidoscopy was used for initial screening.

Adult↗