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Biomedical subjects

Jaw-Town Lin

Publications and source records attributed to Jaw-Town Lin.

At least 55 records · Page 3Linked to original sources

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↗

Bedside colonoscopy for critically ill patients with acute lower gastrointestinal bleeding.

OBJECTIVE: To determine the clinical impact of bedside colonoscopy for critically ill patients with acute lower gastrointestinal (GI) bleeding. DESIGN AND SETTING: A 3-year retrospective analysis (chart review). Medical intensive care unit (ICU) of a 1,312-bed tertiary-care center in Taiwan. PATIENTS AND PARTICIPANTS: Fifty-five people undergoing bedside colonoscopy for lower GI bleeding that developed while in the ICU. INTERVENTIONS: Bedside colonoscopy. MEASUREMENTS AND RESULTS: Colonoscopy was successful in diagnosing the source of bleeding in 37 patients. Among them, colitis (15 patients, including ischemic, pseudomembranous, or radiation-induced) and acute hemorrhagic rectal ulcer (nine patients) were the most frequent confirmed causes. In seven patients, fresh blood was noticed above the colonoscopically accessible area and considered to originate from the small bowel. No adverse event was associated with colonoscopy. Spontaneous cessation of bleeding was noted in 29 (29/55, 53%) patients, whereas 16 (16/55, 29%) achieved endoscopic hemostasis. Ten (10/55, 18%) patients failed primary hemostasis or localization. Overall in-hospital mortality was 53% (29/55); however, hemorrhage-related death occurred in only two patients. CONCLUSIONS: ICU patients with acute lower GI bleeding have distinctive causes. Bedside colonoscopy is effective for diagnosis in two-thirds of patients, but only a minority of them needs endoscopic hemostasis.

Acute Disease↗

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↗

Patients with functional heartburn are more likely to report retrosternal discomfort during wireless pH monitoring.

BACKGROUND: Although the wireless Bravo pH system is effective, some patients experience retrosternal sensations possibly caused by esophageal sensitivity that may complicate clinical application. METHODS: Ambulatory pH of 40 consecutive patients with GERD who had erosive esophagitis or nonerosive reflux disease, were monitored for 2 days with the Bravo system. Results were stratified and compared on the basis of self-awareness of the intraesophageal capsule. RESULTS: Pathologic acid reflux was diagnosed in 20 patients and normal reflux was diagnosed in 20 patients. Seventeen patients (42.5%) reported retrosternal discomfort, and 12 of them (70.6%) had normal reflux. Patients with retrosternal discomfort were less likely to have moderate endoscopic esophagitis, i.e., Los Angeles classification grades B, C, and D endoscopic esophagitis (p = 0.006), and were less likely to have significantly elevated esophageal acid exposure (p = 0.0036) than those who did not perceive the discomfort. Reported discomfort was not associated with age, gender, or the presence of endoscopic esophagitis. CONCLUSIONS: The negative correlation between Bravo-capsule-induced retrosternal discomfort and esophageal-acid exposure indicates modified mechanical afferent nerve function after long-term acid stimulation. Capsule-induced retrosternal discomfort in the presence of normal acid exposure suggests functional heartburn.

Adult↗

The optimal age threshold for screening upper endoscopy for uninvestigated dyspepsia in Taiwan, an area with a higher prevalence of gastric cancer in young adults.

BACKGROUND: It is estimated that 1% to 2% of patients with dyspepsia are associated with gastric cancer. To avoid missing gastric cancer, most guidelines recommend that patients over 45 years old should undergo EGD for uninvestigated dyspepsia. In Taiwan, however, the prevalence of gastric cancer in younger patients is higher than that of Western countries. The optimal age threshold for endoscopy in patients with uninvestigated dyspepsia in Taiwan remains controversial. Therefore, we aimed to determine an optimal age threshold for screening endoscopy in patients with uninvestigated dyspepsia to avoid missing gastric cancer in Taiwan. METHODS: We reviewed the findings in all adult patients who underwent upper endoscopy because of uninvestigated dyspepsia at the National Taiwan University Hospital. In those patients with confirmed gastric cancer histology, further analysis was performed. Cumulative age frequency distributions for gastric cancer were calculated according to gender and to the presence or the absence of alarm features. The stages of gastric cancer also were analyzed according to the presence or the absence of alarm symptoms. RESULTS: During the 5-year period, a total of 17,894 patients received upper endoscopy caused by uninvestigated dyspepsia. Gastric cancer was found in 225 (12.6 cases per 1000 EGDs) patients who presented with uninvestigated dyspepsia, 135 men and 90 women. Thirty-one (13.7%) and 17 (7.6%) patients were aged less than 45 and 40 years old, respectively. Among these 225 patients with gastric cancer, 114 (50.7%) patients did not have alarm symptoms (simple dyspepsia), whereas 111 (49.3%) had alarm symptoms. About 5.3% (12/225) of gastric cancer cases would have been missed if endoscopy had been omitted in patients without alarm symptoms and aged less than 45 years. The cumulative age relative frequencies of patients with gastric cancer who presented with simple dyspepsia were 1.8 (12/6720), 1.02 (5/4920), and 0.59 (2/3411) cases per 1000 EGDs for uninvestigated dyspepsia in patients aged less than 45, 40, and 35 years, respectively. When the frequencies of gastric cancer were stratified by age and gender, we found a trend of male predominance in older patients but not in younger patients. The cutoff age was 60 years old ( p < 0.05). Early gastric cancer was detected in 9.9% (11/111) and 26.3% (30/114) of patients with and without alarm symptoms, respectively (p = 0.002). CONCLUSIONS: Gastric cancer is not uncommon in patients with dyspepsia aged less than 45 years in Taiwan. The age threshold of screening endoscopy for uninvestigated dyspepsia should be the same for both genders in view of comparable frequencies of gastric cancer in a young age population. Because more than 5% of gastric cancer cases would be missed in Taiwan if endoscopy was omitted in simple dyspeptic patients who were aged less than 45 years, we recommend that 40 years old might be an optimal age threshold for screening endoscopy for uninvestigated dyspepsia in Taiwan, in both men and women patients.

Adult↗

Host-environment interactions: their impact on progression from gastric inflammation to carcinogenesis and on development of new approaches to prevent and treat gastric cancer.

Revelation of the connection between Helicobacter pylori infection and gastric adenocarcinoma has prompted new investigations pertaining to its basic and clinical aspects. H. pylori-induced persistent and uncontrolled gastric inflammation nearly always precedes the development of cancer and is instrumental in initiating a multistep process leading to carcinogenesis. Despite initial optimism about the potential of combination anti-H. pylori therapy to ultimately eradicate gastric adenocarcinoma, recent investigations suggest its use should be targeted and tailored to a selected patient group considering the multifaceted role of H. pylori in disease and the disease heterogeneity of gastric adenocarcinoma. The clinical spectrum of H. pylori infection ranges from asymptomatic gastritis and peptic ulcer to gastric malignancies. The occurrence of one versus another is the result of differences in the magnitude of gastritis, and the current disease paradigm suggests gastric inflammation is common to all H. pylori-associated gastroduodenal diseases. Therefore, the host inflammatory responses to environmental triggers, rather than to bacteria or environmental factors per se, would dictate the variable outcomes of H. pylori infection. Putative factors that are expected to play an important role in stimulating inflammatory pathways and modulating the cross-talk between host and environment are age at the time of infection, environmental cofactors, H. pylori virulence, and host genetics. Elucidation of the intimate relationship between host-environment interaction and gastric inflammation, although currently a formidable task, is essential in the development of new prevention and treatment strategies. Such knowledge might provide clues that allow more accurate prediction of variable outcomes of gastric inflammation and appropriate adjustment of treatment strategies, and might open up novel areas for studying gastric carcinogenesis. The evolving new technologies, such as microarray, proteomic, and functional genomic analyses, promise to shed new light on the immense complexity of the presumed host-environment interactions and will reveal more useful markers for the diagnosis and prognosis of gastric adenocarcinoma.

Adenocarcinoma↗

The interaction of H. pylori infection and NSAIDs in cyclooxygenase-2 mRNA expression in gastric antral, corpus mucosa, and gastric ulcer.

BACKGROUND: Although Helicobacter pylori infection and use of nonsteroidal anti-inflammatory drugs (NSAIDs) are the two major causes of gastric ulcer, their interaction remains controversial. We constructed a prospective cohort study to evaluate how these two factors influence the expression of COX-2 mRNA in gastric antral, corpus mucosa, and gastric ulcer. METHODS: Tissues were obtained by endoscopic biopsy of gastric antral, corpus mucosa, and gastric ulcer. The presence of H. pylori was determined by culture or histology using Giemsa stain. NSAID use was assessed by structured questionnaire and medical record review. The expression of COX-2 mRNA was detected by the TaqMan quantitative RT-PCR system. RESULTS: H. pylori infection was associated with increased COX-2 expression only in antral mucosa (0.77 +/- 0.13 vs. 0.31 +/- 0.07, P < 0.01). NSAID use was significantly associated with decreased COX-2 expression in ulcer (4.49 +/- 1.50 vs. 9.82 +/- 2.48, P < 0.05) but not in antral or corpus mucosa. Regarding the interaction between H. pylori and NSAID, we found that H. pylori infection was associated with increased COX-2 expression in antral mucosa for both NSAID users and nonusers. In NSAID users, H. pylori infection was not associated with increased COX-2 expression in ulcer edge. CONCLUSION: H. pylori infection was associated with increased COX-2 expression in gastric antral mucosa for both NSAID users and nonusers, but not in gastric ulcer, where the effect of NSAID inhibition plays a major role. With these observations, we can interpret indirectly that H. pylori eradication does not interfere with gastric ulcer healing in NSAID users.

Adult↗

Distinct chromosomal aberrations of ampulla of Vater and pancreatic head cancers detected by laser capture microdissection and comparative genomic hybridization.

Despite the continuous progress in molecular methodology, the genetic events involved in the carcinogenesis of pancreatic head ductal carcinomas (PHDCs) and ampulla of Vater cancer (AVC) remain largely unknown. Their proximity within the confined region lends them to very similar clinical presentations and operative approaches. However, it is unclear why AVC has a significantly better outcome than PHDCs. The drastic difference may arise from the distinct tumor origins. Therefore, the study of genetic alterations within these two neighboring tumors may elucidate their mechanisms. However, previous genetic analysis of PHDCs may have been influenced by contamination of excessive stromal and inflammatory cells in the background. To date, most comparative genomic hybridization (CGH) studies of pancreatic cancer are based in cell lines or specimens that were not microdissected. Even AVC has a paucity of data. To determine the differences of the genetic alterations of PHDCs and AVC, we used laser capture microdissection combined with degenerated oligonucleotide polymerase chain reaction and CGH to identify the chromosomal aberrations. Frequent gains were found on 5p, 13q, 3q, 8q, 1p, 2p, 2q, 3q, 7p, 8p, 9p, 13q, and 21q, while frequent losses were located on 7p, 18q, 1p, 11q, 16q, 19q, 1q, 2q, 3p, 19p, and 17p in PHDCs. In AVC, chromosomal gains occurred frequently in 7p, 8q, 1q, 2q, 3p, 4p, 7p, 3q, 5p, 20p, 20q, 4q, 5q, 7q, 11p, 12p, 13q, 14q, 18p, 18q, 21q, 9p, 10p, and 15q, and losses frequently in 17q, 1p, 18q, 19p, 5q, 10p, and 10q. This is the first report on the CGH profiles of AVC. These data provide evidence that chromosomal gains/amplifications of AVC differ from those of PHDCs. Among them, chromosomal gains on 1q25, 7p15, 8q23, and 3p21, and losses on 17q24, were statistically higher in AVC than PHDCs (P<0.05). The gains and losses suggest possible putative tumor suppressors and oncogenes that may be involved in the different carcinogenic pathways of AVC.

Adult↗

Heart rate variability in patients with different manifestations of gastroesophageal reflux disease.

BACKGROUND: Autonomic nervous dysfunction has frequently been observed in patients with gastroesophageal reflux diseases (GERD) and impacts the pathogenesis of GERD. However, the characteristics that distinguish between GERD patients with different manifestations remain unknown. AIM: To investigate the autonomic nervous function in subgroups of GERD patients. PATIENTS: Of the 164 participants in this study, 57 were healthy controls, 34 had non-erosive reflux disease (NERD), 40 had symptomatic esophagitis (SE), and 33 asymptomatic esophagitis (AE). METHODS: Resting autonomic activity was assessed by measuring the 5-min heart rate variability (HRV) and HRV indices including time-domain parameters (standard deviation of normal-to-normal intervals [SDNN] and root mean square of successive differences [RMSSD]) and frequency-domain parameters (low-frequency power [LF; 0.04-0.15 Hz], high-frequency power [HF; 0.15-0.4 Hz], and LF/HF power ratio). Mental stress was assessed by use of a self-reported questionnaire (Brief Symptom Rating Scale [BSRS]). RESULTS: HF power was (ANOVA, p=0.041) but time-domain parameters, LF power, LF/HF power ratio, and BSRS parameters were not significantly different between the four groups. A higher HF power was found in examinees with NERD than in those with SE and AE (LSD methods: both p=0.02). When split into two groups (erosive vs. non-erosive), nearly all measures of autonomic tonus were significantly lower in the erosive than non-erosive group. Age and the presence of endoscopic esophagitis influenced the RMSSD and HF power results in the regression analysis. Mental stress or gender did not correlate with any HRV index. CONCLUSION: In comparison with NERD subjects, autonomic tonus in patients with endoscopically confirmed esophagitis (even without symptom) is lower. This finding may suggest that the structural state of esophagus but not symptomatology dictates autonomic function status.

Adult↗

Nuclear expression of BCL10 or nuclear factor kappa B predicts Helicobacter pylori-independent status of early-stage, high-grade gastric mucosa-associated lymphoid tissue lymphomas.

PURPOSE: A high percentage of early-stage, high-grade gastric mucosa-associated lymphoid tissue (MALT) lymphomas remain Helicobacter pylori dependent. t(11;18)(q21;q21), a genetic aberration highly predictive of H. pylori-independent status in low-grade gastric MALT lymphoma, is rarely detected in its high-grade counterpart. This study examined whether nuclear expression of BCL10 or nuclear factor kappa B (NF-kappaB) is useful in predicting H. pylori-independent status in patients with stage IE high-grade gastric MALT lymphomas. PATIENTS AND METHODS: Twenty-two patients who had participated in a prospective study of H. pylori eradication for stage IE high-grade gastric MALT lymphomas were studied. The expression of BCL10 and NF-kappaB in pretreatment paraffin-embedded lymphoma tissues was evaluated by immunohistochemistry and confocal immunofluorescence microscopy. The presence of t(11;18)(q21;q21) was identified by a multiplex reverse transcriptase polymerase chain reaction of the API2-MALT1 chimeric transcript. RESULTS: Aberrant nuclear expression of BCL10 was detected in seven (87.5%) of eight H. pylori-independent and in none of 14 H. pylori-dependent high-grade gastric MALT lymphomas (P <.001). All seven patients with nuclear BCL10 expression had nuclear expression of NF-kappaB, compared with only two of 15 patients without nuclear BCL10 expression (P =.002). As a single variable, the frequency of nuclear expression of NF-kappaB was also significantly higher in H. pylori-independent tumors than in H. pylori-dependent tumors (seven of eight [87.5%] v two of 15 [12.3%]; P =.002). The API2-MALT1 fusion transcript was detected in only one (12.5%) of eight H. pylori-independent lymphomas. CONCLUSION: Nuclear expression of BCL10 or NF-kappaB is highly predictive of H. pylori-independent status in high-grade gastric MALT lymphoma, and coexpression of these two markers in the nuclei is frequent.

Adaptor Proteins, Signal Transducing↗

Promoter polymorphisms of tumor necrosis factor-alpha are associated with risk of gastric mucosa-associated lymphoid tissue lymphoma.

Genes involved in regulating antimicrobial immunity and inflammation may modulate the risk of Helicobacter pylori-associated diseases. IL-1 and TNF-alpha are major cytokines detected in H. pylori-infected tissues. We aimed to determine the role of gene polymorphisms for these cytokines and their receptors in 2 distinct H. pylori-related gastric malignancies, adenocarcinoma (GAC) and maltoma. Genotyping for IL-1beta (-31 C/T, -511 C/T), TNF-alpha (-238 G/A, -308 G/A, -857 C/T, -863 C/A, -1031 T/C), TNFR1 (-383 A/C) and TNFR2 (196 G/T) was undertaken for 70 patients with maltoma and 204 patients with noncardia GAC and compared to 210 unrelated healthy controls. Genotype frequencies showed no differences among patients with GAC or maltoma and controls for IL-1beta, TNFR1 or TNFR2. The TNF-alpha -857 T variant was significantly underrepresented in maltoma compared to controls (6.4% vs. 14.3%, p = 0.018), conferring a 3-fold decrease in risk (OR = 0.33, 95% CI 0.15-0.75). Comparison of allele frequencies between GAC and controls failed to show any statistical significance for TNF-alpha polymorphisms. We concluded that TNF-alpha -857 T itself or a neighboring gene may modify the risk of maltoma. The differences in genetic background as well as divergent clinicopathologic features between GAC and maltoma support the notion that fundamental mechanistic differences exist in these 2 well-defined H. pylori-related malignancies.

Adenocarcinoma↗

Modification effects of GSTM1, GSTT1 and CYP2E1 polymorphisms on associations between raw salted food and incomplete intestinal metaplasia in a high-risk area of stomach cancer.

Incomplete intestinal metaplasia (IM) is a precursor of stomach cancer. To identify risk factors of incomplete IM, a 2-stage survey was carried out in 1995 among 1,485 residents in Matzu, an area with highest mortality from stomach cancer in Taiwan. There were 312 study subjects including 174 men and 138 women sampled for the gastroendoscopic examination of IM. Information on personal and familial history of stomach cancer, cigarette smoking, alcohol consumption and intake frequency of various salted food items were obtained by personal interview based on a structured questionnaire. Blood samples were collected from each participant. Four biopsies per subject were taken from all subjects at gastroendoscopic examination to diagnose the status of IM pathologically. The Helicobacter pylori in biopsies was detected by the histomorphological or immunochemistry method, and antibodies against H. pylori in serum by the enzyme-linked immunosorbent assay. Plasma level of selenium was determined by atomic absorption spectrometry, plasma level of retinol, alpha-tocopherol, alpha-carotene, and beta-carotene by high performance liquid chromatography, genotypes of glutathione S-transferase (GST) M1 and T1 and cytochrome P450 (CYP) 2E1 by polymerase chain reaction. The significant association between history of stomach cancer among first-degree relatives and incomplete IM was found (odds ratio [OR] = 2.50; 95% confidence interval [CI] = 1.15-5.43). There was no association between H. pylori infection and incomplete IM. Alcohol drinkers for >20 years had an elevated risk compared to non-drinkers (OR = 3.34; 95% CI = 1.19-9.39). No associations between incomplete IM and plasma levels of selenium, retinol, alpha-tocopherol, alpha-carotene and beta-carotene were found. Salted food including salted meat, dehydrated salted vegetables and raw salted seafood consumed at ages of </=15 and 16-30 years old was associated with an increased IM risk with OR ranging from 2-3. More striking associations between incomplete IM and salted food intake were observed among subjects with genotypes of GSTM1 null, GSTT1 non-null and CYP2E1 c1/c1. Our study suggests the importance of gene-environment interaction on the development of incomplete IM.

Adolescent↗

Unusual sonographic appearance of a gastrointestinal stromal tumor presenting as a large multilocular cystic mass.

Cystic change is uncommon in gastrointestinal stromal tumor, (GISTs). This report describes 1 case in which a GIST presented as a large multilocular cystic mass. Sonography of the abdomen showed a huge cystic lesion with multiple septa in the left upper quadrant of the abdomen, compressing the left lobe of the liver. Esophagogastroscopy showed only a small submucosal tumor at the anterior wall of the mid portion of the gastric body. Endoscopic sonography revealed a hypoechoic mass, measuring 0.9 x 0.7 cm, arising from the fourth layer of the anterior wall of the mid portion of the gastric body. A huge cystic tumor, containing multiple septa and continuous with the small submucosal lesion, was found. Doppler signals were detected within the septa. Laparotomy revealed a huge exophytic cystic tumor arising from the stomach. Immunohistochemical analysis confirmed that the lesion was a GIST by detecting expression of the c-kit and CD34 proteins. GIST that has undergone cystic change must be differentiated from other cystic lesions to guide the treatment approach. Imatinib mesylate is a new therapeutic alternative for patients who have advanced GIST, but surgery remains the therapy of choice for resectable disease.

Cysts↗

Sonographic demonstration of duodenobiliary reflux with soda enhancement.

Cholangitis rarely occurs after sphincteroplasty if there is no biliary obstruction. We report the case of a patient who developed recurrent cholangitis despite having a patent biliary tract after sphincteroplasty. Duodenobiliary reflux was demonstrated on sonography after enhancement of the reflux flow with a novel oral contrast agent, a carbonated soda beverage. Sonography with contrast enhancement provided by soda solution may prove satisfactory to detect duodenobiliary reflux after sphincteroplasty safely, effectively, and economically.

Abdominal Pain↗