Colon Polyp Detection in Primary Health Care Institutions of Korea: Detection Rate and Issues with Following the Guidelines.

Background/Aims: There have been few multicenter studies on colonic polyps conducted by primary medical institutions. This study examined the detection rate of colonic polyps in primary health care institutions and the related factors while following the guidelines. Methods: The medical records of 14,029 patients who underwent colonoscopy between January-June 2020 at 40 primary medical institutions in Korea were analyzed. High-risk adenoma was defined as advanced adenoma, carcinoma, or ≥3 adenomas. Results: Most patients (71.2%) aged ≥50 years underwent re-colonoscopy within 5 years (51.3%) for diagnostic purposes (61.3%) in Korean primary medical institutions. The detection rates of colon polyps, adenoma, advanced adenoma, high-risk adenoma, and carcinoma was 59.9%, 38.9%, 5.9%, 11.4%, and 0.3% in all subjects and 59.8%, 37.5%, 8.5%, 12.9%, and 0.3% in average-risk patients, respectively. The incidences of adenoma in average-risk patients increased significantly with age (30s/40s/50s: 20.1%/29.4%/43% for adenoma, 4.4%/6.7%/10.3% for advanced adenoma, and 5.6%/9.5%/14.6% for high-risk adenoma; p<0.05). Before 50 years of age, high-risk adenoma was detected in 9.1% of patients in the first-time screening group, and the significant risk factors were being male and ≥40 years of age. The detection rate of high-risk adenoma in the normal index colonoscopy group within 5 years was 9.0%. The significant risk factors included older age, male sex, positive fecal occult blood test, stool form changes, and nonspecific symptoms (gas and indigestion). Conclusions: More colonic adenoma studies targeting real-world clinical practice will be needed to revise the Korean guidelines for colorectal cancer screening and surveillance.

[Prevalence of erosive esophagitis in patients with subtotal gastrectomy: case-control study].

BACKGROUND/AIMS: Enterogastric bile reflux has been implicated as a definite causative factor for the development of postoperative bile reflux gastritis. However, little is known about the role of bile reflux into the stomach in gastro-esophageal reflux disease in patients with subtotal gastrectomy. In this study, we tried to prove that the bile reflux gastritis does increase the development of erosive esophagitis in patients who underwent subtotal gastrectomy. METHODS: From January 1997 to December 2001, 222 patients with previous subtotal gastrectomy were enrolled. We also reviewed the endoscopic findings in 1,633 age and sex-matched healthy controls who had visited our hospital for routine check-up without significant gastrointestinal symptoms. RESULTS: The prevalence of erosive esophagitis is 5% (LA A 2.7%, LA B 2.3%) in gastrectomized patients and 4.9% (LA A 3.2%, LA B 1.7%, LA C 0.0%) in healthy controls. There was no significant difference in the prevalence and the degree of esophagitis between the two groups. CONCLUSIONS: These results suggest that subtotal gastrectomy may not be a risk factor for developing the erosive reflux esophagitis.

[Inhibitory effect of angiotensin II receptor antagonist on the contraction and growth of hepatic stellate cells].

BACKGROUND/AIMS: This study aimed to investigate the effects of angiotensin II (ANG II) and its receptor antagonist (losartan) on the contraction and growth of HSCs. METHODS: HSCs were isolated from Sprague Dawley rat and cultured at various conditions as follows: control, pretreatment of 10(-5) M ANG II, pretreatment of 10(-5) M endothelin, and pretreatment of 10(-5) M ANG II and 10(-6) M losartan. We conducted morphologic analysis with cellular area and length by image analysis system to estimate cell growth in each group. In addition, we measured the change of intracellular calcium currents via electrophysiological methods to evaluate the contractile effect of ANG II and losartan on HSCs. RESULTS: At the fifth day of incubation, the mean cellular area of ANG II-pretreated group and ANG II with losartan-pretreated group were 704.68+/-22.6 micro m2 and 332.90+/-32.6 micro m2, respectively. This difference was statistically significant (p<0.05). ANG II induced an increase in the intracellular calcium current by 22.0+/-3.0% compared with basal current level (p<0.05). However, when losartan was pretreated, ANG II did not cause a significant increase in calcium current (3.1+/-0.8%, p>0.05). CONCLUSION: ANG II accelerates the contraction and growth of HSCs, while its receptor blocker, losartan, inhibits the contraction and growth of HSCs.

Endoscopic sonographic evaluation of the thickened gallbladder wall in patients with acute hepatitis.

PURPOSE: Thickening of the gallbladder wall is often observed during abdominal sonographic examination in patients with acute hepatitis. However, there is rarely an opportunity for a histopathologic analysis of these structural changes. Endoscopic sonography (EUS) can accurately delineate the structure of the gallbladder wall and therefore may be useful for visualizing changes in the gallbladder wall in patients with acute hepatitis. Hence, we prospectively studied the ability of EUS to detect specific structural changes in the gallbladder wall in patients with acute hepatitis and examined the effect of high elevation of serum liver enzyme levels on the gallbladder wall. METHODS: A study group of patients diagnosed with acute hepatitis who had gallbladder wall thickening and a control group of patients without acute hepatitis or gallbladder disease underwent EUS between May 1, 1999, and June 1, 2002. EUS was used to measure the thickness of the gallbladder wall and to visualize each of its layers. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels of the patients with acute hepatitis were measured at the time of the EUS examination. Statistically significant differences were determined using an independent t test and the chi-squared test. A p value of less than 0.05 was considered statistically significant. RESULTS: The acute hepatitis group comprised 28 men and 24 women with a mean age of 40.8 years. The control group comprised 25 men and 25 women with a mean age of 45.1 years. The mean gallbladder wall thickness +/- standard deviation in the acute hepatitis group (6.3 +/- 2.6 mm) was significantly greater than that in the control group (1.6 +/- 0.4 mm; p < 0.01). The mean thickness of the gallbladder wall for patients in whom both the AST and the ALT levels were 500 U/l or higher (7.0 +/- 2.6 mm) was significantly greater than that for patients with levels below 500 U/l (5.4 +/- 2.3 mm; p < 0.05). In the acute hepatitis group, EUS showed thickened, well-defined muscular and serosal layers of the gallbladder wall in 24 of the patients and a diffusely thickened gallbladder wall, in which each layer was ill defined, in the other 28 patients. The mean thickness of the gallbladder wall for patients with the pattern of ill-defined layers was significantly greater than that for the patients with the pattern of well-defined layers (p < 0.05). The pattern of ill-defined layers was more common among patients in whom the serum AST and ALT levels were at least 500 U/l than among patients with levels below 500 U/l (p < 0.05). CONCLUSIONS: We propose that gallbladder wall thickening in patients with acute hepatitis is associated with prominent changes in the muscular and serosal layers. Patients with highly elevated serum liver enzyme levels are more likely to have gallbladder wall thickening and disruption of planes between the muscular and serosal layers than are patients with normal liver enzyme levels.

Comparison of Doppler ultrasonography and the hepatic venous pressure gradient in assessing portal hypertension in liver cirrhosis.

BACKGROUND AND AIM: This prospective study aimed to determine whether Doppler ultrasonography can represent the hepatic venous pressure gradient (HVPG) as an assessment of the severity of portal hypertension and the response to terlipressin, which reduces the portal pressure in liver cirrhosis. METHODS: The HVPG and the Doppler ultrasonographic parameters, such as the portal venous velocity and the splenic venous velocity, the pulsatility and the resistive index of the hepatic, splenic and renal arteries were measured in 138 patients with liver cirrhosis. The changes in the HVPG and the portal venous velocity after administering terlipressin were evaluated in 43 of the 138 patients. The patients who showed a reduction in the HVPG of more than 20% of the baseline were defined as responders to terlipressin. RESULTS: None of the Doppler ultrasonographic parameters correlated with the HVPG. Both the HVPG (28.0 +/- 19.8%) and the portal venous velocity (29.7 +/- 13.2%) showed a significant reduction after terlipressin administration. However, the portal venous velocity decreased significantly, not only in the responders (31.0 +/- 12.0%) but also in the non-responders (25.2 +/- 16.4%). CONCLUSIONS: Doppler ultrasonography does not represent the HVPG, and is therefore not suitable for replacing HVPG as a means of assessing the severity of portal hypertension and the response to drugs which reduce the portal pressure in liver cirrhosis.

Captopril reduces portal pressure effectively in portal hypertensive patients with low portal venous velocity.

BACKGROUND: The effect of an angiotensin II blockade in lowering the portal pressure in patients with liver cirrhosis and portal hypertension is controversial. This prospective study was undertaken to evaluate the portal hypotensive effect of captopril compared to that of propranolol, and to determine the factors that contribute to a successful reduction in the portal pressure after longterm captopril administration in patients with liver cirrhosis. METHODS: The hepatic venous pressure gradient (HVPG) and portal venous velocity (PVV) were measured both before and 3 months after initiation of the administration of captopril (n = 29) or propranolol (n = 29) in cirrhotic patients with a variceal bleeding episode. Patients who showed a reduction in the HVPG of more than 20% of the baseline were defined as being responders. RESULTS: At 3 months, the mean reduction in the HVPG after captopril was less than that after propranolol (-3.0 +/- 9.3% vs -28.5% +/- 4.1%; P < 0.05). However, of the 29 patients receiving captopril, 9 were classified as being responders. On multivariate analysis with parameters including age, cause, Child-Pugh score, HVPG, and PVV, only low PVV was found to be a significant independent factor for responders (PVV < 12 cm/s; odds ratio [OR], 12.2; 95% confidence interval [CI], 1.47-102.40) in the captopril group. CONCLUSIONS: Longterm captopril administration reduces the portal pressure effectively in cirrhotic patients with a low PVV. This suggests that the reduction in portal pressure after captopril administration is a result of improved portal venous outflow brought about by a decrease in the intrahepatic vascular resistance. When the PVV is below 12 cm/s, a captopril trial might be useful in preventing variceal bleeding in portal hypertensive patients.

[Comparison of Doppler ultrasonography and hepatic venous pressure gradient in assessing portal hypertension in liver cirrhosis].

BACKGROUND/AIMS: This prospective study aimed to determine if Doppler ultrasonography can be representative of hepatic venous pressure gradient (HVPG) in assessing the severity of portal hypertension and response to drug reducing portal pressure. METHODS: The HVPG and the parameters of Doppler ultrasonography including portal venous velocity (PVV) and splenic venous velocity, the pulsatility and resistive index of hepatic, splenic and renal arteries were measured in 105 patients with liver cirrhosis. In 31 patients the changes of hepatic venous pressure gradient and portal venous velocity after administration of terlipressin were evaluated. The patients who showed a reduction in HVPG of more than 20% of the baseline were defined as responders to terlipressin. RESULTS: Any Doppler ultrasonographic parameters did not correlate with HVPG. Both HVPG and PVV showed a highly significant reduction after the administration of terlipressin(-28.3 +/- 3.9%, -31.2 +/- 2.2% respectively). However, PVV decreased significantly not only in responders(31.7 +/- 2.4%) but also in nonresponders(29.5 +/- 6.1%). CONCLUSION: Doppler ultrasonography can not be representative of HVPG in assessing the severity of portal hypertension and response to drug reducing portal pressure in liver cirrhosis.