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임홍일, 손병관

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Sun-053

CMV colitis in initially diagnosed with ulcerative colitis ; A Case report

을지대학교 을지병원 내과

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임홍일, 손병관

CMV infection in ulcerative colitis patient is well recognized and frequently reported in patient with steroid refractory colitis. Treatment of UC, where us- ing high dose of immunosuppressive agents is mainstream, can increase risk of CMV infection. However, we report a case of 55-year-old im- munocompetent woman who can be initially diagnosed with UC and CMV colitis at the same time A 55-year-old female visited to hospital complaining of intermittent hematochezia and constipation for 2 months ago. Colonofibroscopy revealed diffuse edema and friability throughout sigmoid colon and rectum. Pathology confirmed Chronic inflammatory infiltrate with acute inflammatory cells. She was diagnosed ulcerative colitis and treated with mesala- zine for 8 weeks. The patient continued to report hematochezia, abdominal pain and was admitted to hospital. On physical examination, lower abdominal tenderness was found.Her initial blood pressure was 110/70 mmHg, heart rate was 83 beats/min, and temperature was 38.1℃. Initial laboratory data were as follows: white blood cell count, 16.54 × 10³/mm3 ; hemoglobin, 12.7 g/dL; platelet count, 384 × 10³/mm3; C-reactive protein, 9.41 mg/dL.. Maintaining mesalazine, Treatment with prednisolone was started after follow-up colonoscopy, which revealed erythema, edema and ulcerative lesions from transverse colon to rectum. Repeat colonoscopy performed after initiating steroid for 1 week, and revealed worsened progression of the previous findings. Biopsy specimen obtained from the ulcers, showed positive for immunostaining of the CMV antigen. Ganciclovir was administered for 2 weeks and follow up co- lonoscopy showed resolved ulcerative lesions. Additional 1 week use of ganciclovir improved her symptoms clearly and discharged with mesalazine and prednisolone. She has been regular monitored at an outpatient clinic for 5 months since discharge, and remission state was maintained. CMV colitis is prone to occur in immunocompromised patient, especially taking steroids high dose in UC. This case demonstrate that even in newly diagnosed UC patient, CMV infection need to be ruled out before using immunosuppressive drug aggressively.

Sun-054

A case of primary hemochromatosis in patient with aplastic anemia

1을지대학교 의과대학 을지대학병원 내과, 2을지대학교 의과대학 을지대학병원 소화기내과

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장재혁

1

, 김지혜

2

, 전제혁

2

, 장지웅

2

, 김새희

2

, 백일현

2

, 정성희

2

, 도영석

2

Hemochromatosis is an iron storage disease characterized by iron deposition and tissue injury in multiple organs. In Korea, primary hemochromatosis caused by gene mutation is extremely rare while secondary hemochromatosis associated with parenteral iron overload including transfusion have been re- ported frequently. Here, we reported a case of patient who was suspected as primary hemochromatosis in spite of several transfusions. A 38-year-old male had red cell aplasia and had been administered frequent transfusion for 7 years. In addition, he was diagnosed diabetes mellitus and cardiomyopathy. The computed tomography(CT) showed an increased liver parenchymal attenuation suggesting hemochromatosis and splenomegaly. Because of transfusion his- tory, it was not assumed primary hemochromatosis during the 2-year

treatment. But sustained elevation of AST and ALT was observed without transfusion for 2 months. Serum ferritin was over 1650 ng/ml and transferrin saturation was 98.12%. Magnetic resonance imaging(MRI), liver biopsy and hemochromatosis protein (HFE) mutation study were performed to evaluate the nature of hemochromatosis and hepatic injury. In the MRI, liver and pan- creas showed dark SI in T1, T2WI while spleen, kidney, bone marrow did not show abnormal SI. In the liver biopsy, diffuse scattered hemosiderin pigments in periportal hepatocytes and adjacent parenchymal cells were observed in- cluding cirrhosis. In secondary hemochromatosis, iron is deposited in Kupffer cells in the liver and phagocyte in the spleen, bone marrow, lymph node. On the other hand, primary hemochromatosis shows increased intestinal iron ab- sorption and iron deposition in the hepatocytes and other parenchymal tissues. By the results, we supposed primary hemochromatosis in this case.

Most common HFE mutation, C282Y and H63D, were negative. So, it is sup- posed to be non-HFE-associated primary hemochromatosis in this patient.

Because of red cell aplasia, we could not apply phlebotomy. We administered iron chelator, deferoxamine to the patient so that his laboratory findings had improved to be normal. It could be better to investigate the nature of hemo- chromatosis more actively by MRI and biopsy.

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