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최신 연구 소개 : 총담관 담석증의 치료를 위한 내시경적 괄약근절개술 후의 Wait-and-See 정책과 복강경담낭절제술의 비교: 무작위 조사
김호각 ( Kim Ho Gak ) 대한소화기학회 2003 대한소화기학회지 Vol.42 No.1
요약: 내시경적 역행성 췌담관조영술(endoscopic retrograde choledochopancreaticography, ERCP)과 괄약근절개술 (sphincterotomy) 후에 담낭에 담석이 있는 환자들에서 후향적, 무작위, 다기관 공동연구로 내시경적 괄약근절개술로 성공적으로 총담관 담석증을 치료한 후 복강경담낭절제술(laparoscopic cholecystectomy)을 시행할 것인지, 기다려 볼것인지(wait-and-see 정책)를 비교 연구하였다. 저자들은 복부초음파검사에서 담낭담석을 확인한 108명의 환자에서 ERCP를 통한 괄약근절개술로 총담관의 담석을 모두 제거하고, 이들을 무작위로 두 군으로 분류하여 49명에서 선택적으로 6주 내에 복강경담낭절제술을 시행하였고(담낭절제 술군) 59명에서는 경과관찰만 시행하였다(wait-and-see군). 2년 간 경과관찰 중 한번이상 담도관련 경과, 즉 Rome 기준의 담관의 통증, 급성담낭염, 담관염, 췌장염, 폐쇄성 황달, 담석 일레우스, 그리고 담낭암이 나타나는 경우를 1차 결과로 하였고 담낭절제술의 합병증, 삶의 질을 2차 결과로 하였다. 이들의 성적에 의하면 평균 30개월의 추적기간 동안 담낭절제술군에서 49명 중 1명(2%), wait-and-see군에서 59명 중 27명(47%)에서 적어도 한번 이상의 담도관련 경과가 있어서 wait-and-see군에서 의미 있게 더 빈번히 나타났다(p<0.0001). Wait-and-see군에서의 나타난 담도관련 경과 로는 통증이 18명(31%), 담낭염이 7명(12%)이었다. 담낭절제술군에서는 담도관련 경과로 1명(2%)에서만 담낭암이 발견되었다. 한편 wait-and-see군 27명 중 22명(81%)에서 추적 기간동안 담낭절제술을 시행했으며, 복강경담낭절제술 도중 여러 가지 이유로 12명(55%)에서 개복담낭절제술로 전환하였으나 처음부터 담낭절제술을 계획한 군에서는 44명 중 9명(20%)에서만 복강경담낭절제술에서 개복술로 전환하였다(p=0.0104). 수술 후의 합병증은 wait-and-see 후에 담낭절제를 한 경우는 22예 중 7예(32%)에서 있었으나 담낭절제술을 처음부터 시행한 군에서는 44예 중 6예(14%)에서 볼 수 있었다(p=0.1048). 치료 3개월 후에 MOS-24 설문지를 이용한 삶의 질의 조사에서는 두 군 모두에서 정상인과의 비교에서 차이는 없었다. 단변량 분석에서 추적기간동안 담도관련 경과가 한번이상 재발한 환자들은 그렇지않은 환자에 비해 젊은 나이였으나(p=0.0344), 당뇨병, 적은 크기의 담석, 담낭관의 개폐유무 등은 위험인자가 아니었다.
김호각 ( Ho Gak Kim ) 대한내과학회 2010 대한내과학회지 Vol.78 No.3
Cystic diseases of pancreas are increasingly detected because of high quality of imaging modality. Most of pancreatic cysts are discovered incidentally. Differential diagnosis of pancreatic cysts is very important because they include wide range of pathologic disease such as inflammation, benign neoplasm, borderline and malignant neoplasm. The most common cystic disease of pancreas is post-inflammatory pseudocyst, but in recent decades the incidence of neoplastic cysts, such as serous cyst neoplasm, mucinous cyst neoplasm, intraductal papillary mucinous neoplasm has increased. Among the cystic neoplasms, mucinous cystic neoplasm, intraductal papillary mucinous neoplasm are premalignant, and serous cystadenoma has no malignant potential. Patient`s age, symptoms and a possible history of acute or chronic pancreatitis together with cross-sectional imaging modalities are mainstay for differential diagnosis of cystic diseases of pancreas. Cystic fluid cytology and analysis for CEA, mucin stain, and viscosity are providing additional information for differentiation. But cross-sectional images have overlapping findings in various cystic diseases and cystic fluid aspiration has still lack of sensitivity. The purpose of this review article is to provide the overview of the differentiation of pancreatic cystic lesions. (Korean J Med 78:279-288, 2010)
만성 (慢性) 활동성 (活動性) 간염에서 (肝炎) 근섬유아세포의 (筋纖維芽細胞) 동태 (動態)
김호각(Ho Gak Kim),정준모(J.Mo Chung),손윤경(Yoon Kyung Shon),곽정식(Jyung Sik Kwak),손태중(Tae Joong Sohn) 대한소화기학회 1988 대한소화기학회지 Vol.20 No.3
N/A This study has been carried out to investigate the behavior and histologic origin of myofibroblasts, which are able to be found in the liver tissue of chronic active hepatitis. The biopsied liver tissues of patient were examined under the light and electron microscopes and studied through the immunohistochemical method. Through light microscopic examination, the cases were devided into four mild ones, eight moderate ones and four severe ones. On immunohistochemical study, all mild cases show negative findings to antibody to antiactin and positive findings were demonstrated in all moderate and severe ones. On electron microscopic study, myofibroblasts were found in each three cases of moderate and severe ones and they exhibit intermediate forms between smooth muscle cells and myofibroblasts having the hundles of microfilaments, wrinkled nuclei and basement membrane. Most of them are located in nearby areas of portal veins and in the periphery of these areas, proliferation of Ito cells and transformation of them into similar forms of myofibroblasts were noted. These findings suggest that the myofibroblasts are noted in the moderate and more severe cases of chrrniic active hepatitis showing marked fibrosis and they contribute to the fibrosis of portal areas. Besides, it is presumed that myofibroblasts of chronic active hepatitis are originated from Ito cells.
김호각 ( Ho Gak Kim ),한지민 ( Ji Min Han ) 대한소화기학회 2012 대한소화기학회지 Vol.59 No.1
Obesity is defined as BMI (calculated as weight in kg divided by height in m2) more than 30, and overweight is defined as BMI of 25-29.9. Obesity has been considered as a risk factor for pancreatic diseases, including pancreatitis and pancreatic cancer. Severe acute pancreatitis is significantly more frequent in obese patients. Furthermore, obese patients develop systemic and local complications of acute pancreatitis more frequently. The underlying mechanisms are increased inflammation and necrosis from increased amount of intra- and peri-pancreatic fat. In addition, obesity is a poor prognostic factor in acute pancreatitis, and overweight before disease onset appears to be a risk factor for chronic pancreatitis. Overweight and/or obesity are associated with greater risk of pancreatic cancer and younger age of onset. Physical activity appears to decrease the risk of pancreatic cancer, especially among those who are overweight. Long-standing diabetes increases the risk of pancreatic cancer. The pathogenic mechanism is that obesity and physical inactivity increase insulin resistance. In a state of hypersinulinemia, increased circulating level of insulin-like growth factor-1 induces cellular proliferation of pancreatic cancer. Obesity is associated with negative prognostic factor and increased mortality in pancreatic cancer. However, there are controversies regarding the effects of obesity on long-term post-operative results in the patient with pancreatic cancer. (Korean J Gastroenterol 2012;59:35-39).
상부위장관질환 환자에서 H . pylori 감염에 의한 위점막의 조직학적 변화와 혈청 Gastrin 및 혈청 IgG항체가의 상관관계
손호상(Ho Sang Shon),최정윤(Jung Yoon Choe),김지희(Chi Hui Kim),김태석(Tae Sug Kim),김채기(Chae Gi Kim),김이근(Ih Geun Kim),안기성(Ki Sung Ahn),김호각(Ho Gak Kim),오훈규(Hoon Kyu Oh),김용진(Yong Jin Kim),배정동(Jung Dong Bae) 대한소화기학회 1996 대한소화기학회지 Vol.28 No.3
N/A Background/Aims: This study was performed to investigate the relationship between Helicobacter pylori infection and degree of gastric mucosal inflammation, IgG antibody titer against H. pylori, and fasting serum gastrin level. Methods: Patients were divided into 2 groups(H. pylori positive and negative) by identification of H. pylori in biopsied specimens with special staining. In H. pylori positive group, the density of gastric K. pylori colonization was further graded semiquantitatively from 1 to 3. The severity of gastritis in each group was scored according to the Sydney system from 0 to 3. Serum IgG antibody titer against H. pylori was detected by second-generation antigen based enzyme immunoassay(Cobas Core Anti-Helicobacter pylori EIA). Fasting serum gastrin level was measured by standard radioimmunoassay technique. Results: The severity of gastritis in H. pylori positive group was significantly higher than H. pylori negative group in mononuclear cell infiltration(pC0.001), activity of PMNL(pC0.001), and glandular atrophy(pC0.01). In H. pylori positive group, the density of H. pylori colonization was significantly correlated with mononuclear cell infiltration(r=0.67, p0.001), activity of PMNL(r=0.70, p0.001), and grandular atrophy (r=0.38, pC0.001). Neither density of H. pylori colonization nor severity of gastritis was correlated with fasting gastrin level and IgG antibody titer against H. pylori. Conclusions: H. pylori infection results in localized inflammatory reaction in gastric mucosa with relation to density of H. pylori colonization, but serum H. pylori IgG antibody titer does not reflect the severity of gastritis. Fasting serum gastrin level also has no relation with the density of H. pylori colonization and severity of gastritis. These findings suggest that the factor which cause inflammation in gastric mucosa may be different from that cause gastrin secretion or formation of IgG antibody. (Korean J Gastroenterol 1996; 28:311 - 319)