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Lee, Soo Teik,Kim, Chung Hun 의과학연구소 1997 全北醫大論文集 Vol.21 No.1
Gastroparesis는 섭취된 음식물의 위내에서 지연배출로 인한, 미심, 구토, 식욕저하, 복, 조기포만감 및 팽만감 등의 위장증상을 주로 동반하는 소화기질환으로 당뇨병, 위부분절제술, 약물투여, 바이러스 감염 후에 발생될 수 있다. 위 내용물의 위내에서 배출속도는 내용물의 물리적 성격에 따라 좌우되고 위장증상을 악화시킬 수 있기 때문에 만성 gastroparesis환자들은 섭취하는 음식의 양과 질면에서 영양장애등의 여러 문제들을 일으킬 수 있지만 증상완화를 위한 식이요법과 영양학적인 접근에 대한 보고는 드물다. 이에 gastroparesis환자들의 식이의 문제점과 중요영양소의 결핍 유 뮤, 식단의 변화가 우장증상변화에 대한 효과를 평가하고자 하였다. 검사대상은 위장증상에 대한 점수 합계가 6점 이상 환자 중 6개월 이상된 8명 환자(평균나이 38.3세, 2명 postviral gastroparesis, 6명 idopathic gastroparesis)를 대상으로 하였다. 위장증상과 식이습관은 환자에 직접 설문조사에 의해, 영양상태는 Creatinie arm index(CAI), serumvitamin과 mineral, 혈액생화학검사를 통해 평가하였다. 칼로리가 비슷한 두 종류의 다른 음식[음식A(저지방, 정상 섬유소) 1067Kcal, 170g 탄수화물, 59g 단백, 53g 지방, 3g 섬유소]를 각각 5일씩 연2주간 영양사에 의해 제공된 뒤 각각의 음식섭취 전후의 증상의 변화에 대해 기록 비교 분석하였다. 식이습관:8명의 전체환경중 5명(72.5%)에소 고기, 어류, 과일들을 2명(25%)에서 우유제품, 모든 환자(8명, 100%)에서 알코올제품을 제한하고 있었으며 5명(72.5%)에서는 보조적인 vitamine/mineral제재를 투여받고 있었다. 영양상태 : 혈청내 vitamine B6(6명, 75%), vitamine B1(4명, 50%), 철분(3명, 37.5%)에 대한 검사결과는 정상이하의 수치를 보였으나 다른 혈청내 vitamins, minerals, CAI(107+17%)들은 정상범위에 있었다. 위장증상에 대한 식이의 효과 : Gastroparesis와 연관된 각각의 위장증상들에 음식제공전과 음식A와B 섭취기간동안에 증상변화의 정도에 따라 0점(무증상)에서 3점(정상생활 장해)까지 점수를 주어 비교분석하였다. 증상합계의 총점수는 음식B (4.3±0.9)에서 음식제공전(9.3±1.0)과 음식A에 비해 의미있게 개선되었다. 결론 : Gastroparesis환자들은 흔히 스스로 증상완화를 위해 음식제한을 하고 있으며 이로 인한 영양결핍이 발생할 위험을 가지고 있다. 정상지방과 저섬유소의 음식이 저지방과 정상섬유소의 음식에 비해 증상의 완화효과를 보였다. 본 연구결과 음식내 섬유소의 양이 위장증상의 발생에 중요한 역할을 하며, 식이요법이 gastroparesis환자의 효과적인 치료임을 제시한다.
만성 B 형 간염 환자와 B 형 간염에 의한 간경변 환자에서의 Lamivudine 1 년 치료 효과
김승수,이승옥,안득수,김대곤,이수택,김용성,진흥용,마명신 대한간학회 2001 Clinical and Molecular Hepatology(대한간학회지) Vol.7 No.2
Background/Aims: Lamivudine is highly effective in suppressing hepatitis B virus replication and hepatitis B induced necroinflammatory activity. The objective of this study was to evaluate the virological and biochemical responses to lamivudine by patients with HBV associated chronic liver disease. In particular we stressed the importance of lamivudine therapy by patients with decompensated liver cirrhosis. Methods - We conducted a one - year trial of lamivudine in 80 patients with HBV associated chronic liver disease (chronic hepatitis 44, cirrhosis 36). We classified these patients according to the severity of hepatic dysfunction as chronic B hepatitis (Group A) or liver cirrhosis (Group B). These patients were treated for 12 months with 100 mg daily doses of lamivudine. Results: The seroconversion rate of HBeAg was 23.5% in group A patients and 26.7% in group B patients. The negative conversion of HBV - DNA was sustained for one year in 79.5% of patients in group A and 86.1% in group B. The normalization rates of serum ALT were 90.99% in group A and 88.9% in group B patients. No serious side effect after discontinuance of the treatment was found. There were 12 ALT breakthrough cases and all of them showed mutation of YMDD motif. However, they did not deteriorate clinically in spite of ALT elevation and HBV - DNA reappearance. The Child - Pugh scores improved even in patients with decompensated liver cirrhosis. Conclusion: One - year lamivudine treatment resulted in excellent virological and biochemical improvements and was well tolerated in the patients with HBV associated chronic liver disease, even in decompensated cirrhosis. We conclude that lamivudine is relatively safe in chronic hepatitis B and liver cirrhosis treatment..(Korean J Hepatol 2001;7:171-180)
( Jeong Ho Kim ),( A Soo Heon Park ),( Chul Soo Cho ),( Soo Teik Lee ),( Wan Hee Yoo ),( Sung Kook Kim ),( Young Mo Kang ),( Jong Sun Rew ),( Yong Wook Park ),( Soo Kon Lee ),( Yong Chan Lee ),( Won P 대한소화기학회 2014 Gut and Liver Vol.8 No.4
Background/Aims: The use of proton pump inhibitors or misoprostol is known to prevent the gastrointestinal complications of nonsteroidal anti-inflammatory drugs (NSAIDs). Rebamipide is known to increase the mucosal generation of prostaglandins and to eliminate free oxygen radicals, thus enhancing the protective function of the gastric mucosa. However, it is unknown whether rebamipide plays a role in preventing NSAID-induced gastropathy. The aim of this study was to determine the effectiveness of rebamipide compared to misoprostol in preventing NSAID-induced gastrointestinal complications in patients requiring continuous NSAID treatment. Methods: We studied 479 patients who required continuous NSAID treatment. The patients were randomly assigned to groups that received 100 mg of rebamipide three times per day or 200 μg of misoprostol three times per day for 12 weeks. The primary endpoint of the analysis was the occurrence rate of gastric ulcers, as determined by endoscopy after 12 weeks of therapy. Results: Of the 479 patients in the study, 242 received rebamipide, and 237 received misoprostol. Ultimately, 44 patients (18.6%) withdrew from the misoprostol group and 25 patients (10.3%) withdrew from the rebamipide group. There was a significant difference in withdrawal rate between the two groups (p=0.0103). The per protocol analysis set was not valid because of the dropout rate of the misoprostol group; thus, the intention to treat (ITT) analysis set is the main set for the efficacy analysis in this study. After 12 weeks, the occurrence rate of gastric ulcers was similar in the rebamipide and misoprostol groups (20.3% vs 21.9%, p=0.6497) according to ITT analysis. In addition, the therapeutic failure rate was similar in the rebamipide and misoprostol groups (13.6% vs 13.1%, p=0.8580). The total severity score of the gastrointestinal symptoms was significantly lower in the rebamipide group than in the misoprostol group (p=0.0002). The amount of antacid used was significantly lower in the rebamipide group than in the misoprostol group (p=0.0258). Conclusions: Rebamipide can prevent gastric ulcers when used with NSAIDs and can decrease the gastrointestinal symptoms associated with NSAID administration. When the possibility of poor compliance and the potential adverse effects of misoprostol are considered, rebamipide appears to be a clinically effective and safe alternative. (Gut Liver 2014;8:371-379)
문병식,안혁수,김광훈,이승옥,김인희,이수택,김대곤,안득수 의과학연구소 1997 全北醫大論文集 Vol.21 No.1
Acute pancreatitis in the patient of tuberculous lymphadenitis is rare disorder, little reported in the literature. It may not develop primarily within the pancreas and may occur secondary to a focus elsewhere in the body. But, there was no evidence of disseminated tuberculosis or immuno-deficiency. A 21-year-Korean women revealed epigastric pain, nausea, vomiting and fever. An ultrasound and computed tomographic scan of abdomen revealed multiple heterogenous mesenteric lymphadenopathy. Gradually, the patient suffered from aggrevated symptom. For purpose of diagonsis, exploratory laparotomy was done and lymph node was obtained for biopsy and it resulted in tuberculous lymphadenitis. The patient started on antituberculous chemotherapy, so she has been improved rapidly and has remained well after 6 months follow-up. In epidemic area of tuberculosis, development of pancreatitis and pacreatic mass or retroperitoneal lymphadenitis of unknown origin may be high probablity of tuberculosis and is recommended percutaneous tissue diagnosis and early anti-tuberculous treatment. (Key Word : Pancreatitis, Tuberculous lymphadenitis, Pancreatic mass)
만성 간질환 환자들의 간 기능 정도에 따른 내당능 장애(Glucose Intolerance)의 비교
이승옥,안득수,김대곤,이수택,안혁수 대한소화기학회 1999 대한소화기학회지 Vol.33 No.5
Background/Aims: We investigated correlation between the severity of liver disease and glucose intolerance. Additionally, we compared the rate of glucose intolerance between the patients with pure liver cirrhosis and non-insulin-dependent diabetes mellitus (NIDDM) preceded cirrhosis. Methods: We classified eighty patients with chronic liver disease from L1 to L3 according to the severity liver injury by biochemical factors and the patients with NIDDM preceded cirrhosis were classified into L3-D group. We measured HbA1C, serum insulin and C-peptide and carried out 100 g ora glucose tolerance tests (OGTT). Results: The rate of glucose intolerance was 35% in L2 group and 89% in L3 group, and the rate of diabetic range was 5% and 41%, respectively. In L3 group, fastin blood sugar and HbA1C were in normal range, but the increment of serum insulin, C-peptide and blood glucose in OGTT were higher than in L1 or L2 group. In L3-D group, fasting blood sugar and HbA1C were higher than normal and more increment of blood glucose after oral glucose load was observed than in L3. Significant difference in insulin or C-peptide level was not observed between L3 and L3-D. Conclusions: Glucose intolerance appears to be proportional to the severity of live injury in chronic liver disease. It suggests that OGTT can be an indicator of hepatic injury. We should carefully interpret the glucose intolerance in liver cirrhosis because it shows different pattern from NIDDM preceded cirrhosis.