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이창돈(Chang Don Lee),서정민(Chong Min Seo),조현미(Hyun Mi Cho),한남익(Nam Ik Han),최상욱(Sang Wook Choi),정진우(Jin Wu Jeong),박두호(Doo Ho Park),김부성(Boo Sung Kim) 대한내과학회 1989 대한내과학회지 Vol.36 No.6
N/A Previously, we reported that subcutaneous daily injections of 3 MU recobinant interferon alpha-2b (INTRON A®) for 28 days (short-term therapy) was safe and effective in the decrement of serum hepatitis B viral (HBV) replication markers and transaminase levels transiently in patients with chronic active hepatitis (CAH) type B. Therefore, to evaluate the safety and efficacy of INTRON A® in patients with CAH type B on the loss of HBV replication markers according to the duration of administration, we followed up (9~24 months) and compared patient, who were divided into two random long-term and short-term therapy groups (previously they were transient on each group). Negative conversion of DNA polymerase activities and HBV DNA, and normalization of ALT levels were observed in similar proportions in each group, but these changes were found to be transient in the short-term compared to the long-term group proportionally. In comparison of the characteristics between responders (10 cases) and nonresponders (12 cases) to INTRON A® just before treatment, 5 out of 6 females responded, compared to a male response of 5 out of 6; the younger patients (31.9±5.9 years) responded significantly better than the older (39.9±12.1 years), (p<0.05); but changes in serum ALT and AST levels, DNA polymerase activities and peripheral blood mono-lymphocyte counts were not significantly reported in the short-term group. (12 cases) and long-term therapy group (3 MU, thrice weekly for 12 weeks, 7 patients; or 24 weeks, 3 patients). On entry into the trial, there was no significant difference between each group in respect ot several clinical, biochemical and HBV replication markers and histology. With respect to changes in HBV replication makers during or after INTRON A® treatment, HBsAg negative conversion cases were absent on each group. However, HBeAg negative conversion cases were observed in only 3 of 12 cases on the short-term group but in 7 of 10 cases in the long-term group (2 cases in HBeAg negative conversion defference). We did not observe serious complication during and after the INTRON A® treatment. We concluded that subcutaneous injection of 3 MU of INTRON A® was safe and effective in decreasing the level of HBV replication markers and tran-saminase activities in patients with CAH type B, but long-term therapy rather than short-term therapy was necessary for the eradication of HBe antigenemia and clinical improvment for an extended period of time.
선희식(Hee Sik Sun),김부성(Boo Sung Kim),이창돈(Chang Don Lee),김인식(In Sik Kim),민창기(Chang Gi Min),최정현(Jung Hyun Choi),서정민(Chong Min Seo),정인식(In Shik Chung) 대한소화기학회 1990 대한소화기학회지 Vol.22 No.2
Mucosal bridge, endoscopically observed, is a cord-like mucosal connection across the lumen, looking very much like a bridge. Mucosal bridges have been infrequently reported in the esophagus, stomach and colon. Recently we experienced a 41-year-old male patient who had multiple esophageal mucosal bridges with duodenal ulcer. We report this case with a review of relevant literatures.
문맥압 항진과 식도 정맥류 출혈을 동반한 Agnogenic Myeloid Metaplasia 1예
장지정,오기원,김정아,최종영,문찬수,서정민,한석원,심규식,백남종,김부성 대한내과학회 1993 대한내과학회지 Vol.44 No.5
저자들은 식도정맥류 파열에 의한 위장관 출혈로 입원한 70세 여자환자에서 간경변과 문맥 혈전증 소견없이, 문맥압 항진과 심한 간, 비종대가 있으며, 골수 검사 및 비장 절제술 후 조직 검사결과 AMM으로 진단된 환자를 경험하였기에 문헌고찰과 함께 보고하는 바이다. Agnogenic myeloid metaplasia is a syndrome in which the excessive fibroblast proliferation and collagen deposition in the bone marrow is accompanied by myeloid metaplasia of organ such as the liver, spleen, and lymph nodes. Typically, there is progressive splenomegaly, the gradual replacement of marrow elements by fibrosis, progressive anemla, variable changes in the number of granulocytes and platelets, and leukoerythroblastic peripheral blood picture. Here we report on a case of AMM associated with gastrointestinal bleeding due to ruptured esophageal varices. The portal vein was patent and the cause of portal hypertension was infiltration of liver by immature myeloid and erythroid cells and megakaryocytes.