The Mucosal Changes and Influencing Factors in Upper Gastrointestinal Anisakiasis: Analysis of 141 Cases / 대한소화기학회지

BACKGROUND/AIMS: Anisakiasis is a well known parasitosis resulted from eating raw seafoods and there were many reports of cases. However, its endoscopic and clinical characteristics have not been reviewed well. The aim of this study was to clarify the gastric mucosal changes and influencing factors of upper gastrointestinal (UGI) anisakiasis. METHODS: We analyzed retrospectively the endoscopic and clinical characteristics of 141 cases with UGI anisakiasis diagnosed during UGI endoscopy, based on the review of medical records. The patients' data were collected consecutively from October 1999 through September 2006. RESULTS: In the 141 patients with UGI anisakiasis, the peak age was the 40s (44.7%). The female to male ratio was 1.82:1. The most prevailed season was winter (41.1%). The most frequent symptom was acute epigastric pain and 76.6% of the patients developed symptoms within 12 hours after the ingestion of raw seafoods. The greater curvature of body was the most preferred site of anisakid larvae. The median time from meal to symptom onset was shortest in esophageal location and longest in fundus location (3 vs. 18.7 hours). The various mucosal changes were observed and the most frequent mucosal change was edema (90.8%). Submucosal tumor was also found in 31.9% of the patients. The severity of mucosal change was related inversely with the time interval from meal to endoscopy (p=0.048). CONCLUSIONS: Anisakiasis presented various mucosal changes depending on the time interval from ingestion of raw seafood to endoscopy. Delayed endoscopy may lead chronic mucosal change and cause difficulty in the detection of anisakiasis. Therefore, the prompt endoscopic examination is required for the patients presenting acute gastrointestinal symptoms after taking raw fish.

Effect of 17beta-estradiol on the Contraction to Endothelin-1 in Porcine Coronary Artery / 대한내과학회지

OBJECTIVES: It is widely accepted that estrogen has favorable effects on cardiovascular diseases, especially in the postmenopausal women. Endothelin-1(ET-I), released from the vascular endothelium, is a 21-amino acid peptide with strong vasoconstrictor activity. However, the effect of estrogen on the vasoconstriction to ET-1 has not been extensively studied. METHODS: To investigate the effect of estrogen (175beta-estradiol) on the vascular contraction to ET-1, porcine coronary artery(PCA) rings were suspended in organ chambers(37 degrees C, 95% O2/5% CO2) for measurement of isometric tension change. Endothelium was removed mechanically if necessary. In acute experiments, vascular rings were preincubated for 15minutes with 3different concentrations of 170beta-estradiol(10(-6), 10(-5), 10(-4)M) and concentration-contraction curves to cumulative doses of ET-1 were constructed. In the experiments after a longer exposure to 17beta-estradiol, the vessels with endothelium were exposed in the 5% CO2 incubator to 3different concentrations of 17beta-estradiol(10(-9), 10(-8), 10(-7)M) for 44-50 hours, and then concentrationcontraction curves to ET-1 were obtained. RESULTS: Incubation for 15minutes with 170beta-estradiol(10(-4)M) inhibited ET-1-induced contraction in the vessels with endothelium(area under the curve and maximal contraction, p<0.05 compared with control). This effect persisted regardless of the sex and the presence or absence of the endotheliurn. Incubation of the vessels far a longer time with 170beta-estradiol(44-50 hours) resulted in the inhibition of maximal contraction to ET-1(p<0.05) by a lower concentration of 175beta-estradiol(10(-7)M) than in acute experiments in male PCA rings, but an enhanced contraction to ET-1(area under the curve; p<0.05) by 10M of 175beta-estradiol was observed in female PCA rings. CONCLUSION: Short-time incubation with 17Pbeta-estradiol has an inhibitory effect on the contraction to ET-1 in PCA rings. This effect is independent of the presence of the endothelium and the sex of the pigs. A longer incubation with 17beta-estradiol results in a similar inhibitory effect on male(but not female) PCA rings, suggesting that a sex-related difference may exist concerning the effect of 17beta-estradiol on ET-1-induced contraction.