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고혁재 ( Hyeok Jae Ko ),박성환 ( Sung Hwan Park ) 대한류마티스학회 2009 대한류마티스학회지 Vol.16 No.3
Tumor necrosis factor (TNF) inhibitors are now established as therapeutic agents for treating active rheumatoid arthritis (RA) that is resistant to conventional drug treatment. However, TNF Inhibitors decrease resistance to infection, including unusual infections such as tuberculosis, and they have been shown to impair wound healing in an experimental setting. To date, there is limited data on patients with RA regarding their infections or the complications of surgery performed while taking TNF inhibitors and there is no professional consensus about this. This problem emphasizes a need for awareness and communication between patients, the rheumatologist and the surgeon when treating patients with RA. We reviewed the effects of TNF inhibitors on the incidence of surgical site infection (SSI) and the risk factors for SSIs after performing elective surgery in patients with RA. TNF inhibitors should not be used during the perioperative period until conclusive evidence to the contrary is available.
고혁재 ( Hyeok Jae Ko ),유승아 ( Seung Ah Yoo ),우성용 ( Seong Yong Woo ),김해림 ( Hae Rim Kim ),조철수 ( Chul Soo Cho ),김완욱 ( Wan Uk Kim ) 대한류마티스학회 2004 대한류마티스학회지 Vol.11 No.2
Objective: Vascular endothelial growth factor (VEGF), an angiogenic factor, has been suggested to play a critical role in the pathogenesis of rheumatoid arthritis (RA). In this study, we investigated whether VEGF would directly regulate the activation of mononuclear cells of RA patients. Methods: Mononuclear cells and/or synoviocytes of RA patients were cultured in the presence of VEGF, and the levels of TNF-α and IL-6 were determined in the culture supernatants by ELISA. The TNF-α-or IL-6-producing cells were also assessed by flow cytometry analysis. Blocking experiments were performed by adding anti-VEGF receptor (anti-Flt-1) mAb to the cells, stimulated with VEGF. Results: VEGF directly increased the productions of TNF-α and IL-6 from peripheral blood mononuclear cells (PBMC) from healthy controls. Treatment of PBMC with anti-VEGF receptor (anti-Flt-1) mAb blocked the VEGF-induced productions of TNF-α and IL-6, suggesting that VEGF activates the PBMC via a receptor (Flt-1) coupling event. Synovial fluid mononuclear cells (SFMC) of RA patients showed a greater response to VEGF stimulation than the PBMC of healthy controls. The major cell types responding to VEGF were monocytes and synoviocytes. In addition, dexamethasone completely abrogated VEGF- stimulated productions of TNF-α and IL-6 from adherent cells, isolated from SFMC. Conclusion: Our data suggest that VEGF may directly activate RA monocytes and synoviocytes to produce TNF-α and IL-6.
류마티스 관절염에서 제2형 콜라겐 반응 T세포와 활막 섬유 모세포의 상호 활성화
윤종현 ( Chong Hyeon Yoon ),박미경 ( Mi Kyung Park ),조미라 ( Mi La Cho ),고혁재 ( Hyeok Jae Ko ),박경수 ( Kyung Soo Park ),김완욱 ( Wan Uk Kim ),민준기 ( Jun Ki Min ),이상헌 ( Sang Heon Lee ),홍연식 ( Yeon Sik Hong ),박성환 ( Sun 대한류마티스학회 2004 대한류마티스학회지 Vol.11 No.1
Objective: To investigate the interaction between type II collagen (CII)-reactive T cell and fibroblast-like synoviocyte in rheumatoid arthritis (RA). Methods: Peripheral blood T cells from RA patients were cultured with bovine CII and analyzed by flow cytometry. After co-culture with CII-reactive T cells and fibroblast-like synoviocytes (FLS), the expression of cytokines (IL-15 and TNF-α from FLS, IFN-γ and IL-17 from CII-reactive T cells) were determined by ELISA and RT-PCR. Results: CII-reactive T cells expressed CD69, one of the early activation markers, and produced significant amount of IFN-γ, and proliferated. IL-15 and TNF-α expression from FLS were significantly elevated when co-culture with CII-reactive T cells and inhibited by physical interruption of cell-to-cell contact or anti-CD40 antibody. IFN-γ and IL-17 expression from CII-reactive T cells were also significantly elevated when co-culture with FLS and inhibited by anti-IL-15 monoclonal antibody. Conclusion: CII-reactive T cells can activate FLS to secret proinflammatoy cytokines and interactions between these two cells drive further activation of each other. These data suggest that CII-reactive T cell may play a important role in pathogenesis of RA.
Leflunomide로 치료중인 류마티스 관절염 환자에서 발생한 간질성 폐렴
신아영 ( Ah Young Shin ),김승수 ( Seung Soo Kim ),김경희 ( Kyung Hee Kim ),주일남 ( Il Nam Ju ),고혁재 ( Hyeok Jae Ko ) 대한결핵 및 호흡기학회 2009 Tuberculosis and Respiratory Diseases Vol.66 No.6
Leflunomide, a disease-modifying antirheumatic drug (DMARD) for the treatment of rheumatoid arthritis has been available in Korea since 2003. Leflunomide-associated interstitial pneumonitis has been appearing recently. A 25-year-old woman with a 12-month history of seronegative rheumatoid arthritis (RA) presented with acute respiratory insufficiency. She developed fever, dyspnea, and non-productive cough. Her medication history included methotrexate (15 mg/week. commencing 1 year prior) and leflunomide (20 mg/day, no loading dose, commencing 4 months prior). She was diagnosed with leflunomide-associated interstitial pneumonitis based on history, physical examination, laboratory and radiologic findings. She recovered quickly after leflunomide was withdrawn and steroids and cholestyramine were initiated quickly. We report a case of leflunomide-associated interstitial pneumonitis treated successfully with intravenous high-dose steroid and cholestyramine.
전신성 홍반성 루푸스 환자와 신장이식 환자에서 발생한 결핵의 임상적 특징 비교
김충현 ( Choong Hyun Kim ),김완욱 ( Wan Uk Kim ),양철우 ( Chul Woo Yang ),정영옥 ( Young Ok Jung ),도주호 ( Ju Ho Do ),고혁재 ( Hyeok Jae Ko ),김해림 ( Hae Rim Kim ),윤종현 ( Chong Hyeon Youn ),이상헌 ( Sang Heon Lee ),박성환 ( Su 대한류마티스학회 2003 대한류마티스학회지 Vol.10 No.3
Objective: To compare the incidence and clinical characteristics of tuberculosis (tbc) between patients with systemic lupus erythematosus (SLE) and kidney transplantation (KT) recipients. Methods: Six hundreds and twenty-two patients who were diagnosed as SLE from 1990 to 2001 in Kang-Nam St. Mary`s hospital were reviewed, retrospectively. As a control group, 347 kidney transplant recipients in the same center were evaluated. The extent of tbc was categorized into two groups: (1) limited disease (2) extensive disease. Cumulative steroid dosage and disease activity index including SLEDAI, serum complement levels, and anti-dsDNA titers were compared between the two groups. Results: The cumulative incidence rate of tbc was similar in both groups (37 cases and 5.7% in SLE versus 17 cases and 4.9% in KT). Mean interval from SLE diagnosis or KT to tbc development was not different between the two groups. The most common site of tbc was lung/pleura, and the others included lymph nodes (2 cases), knee joint (1), bone marrow (1), critecentral nervous system (1), kidney (1), colon (1), liver (1), and skin (1) in SLE. In contrast, most of tbc (16/17) developed exclusively in the lung and pleura in KT recipients. Cumulative doses of prednisolone 1 or 6 months before tbc diagnosis were not different between the two groups. Interestingly, extensive disease tended to be more frequent in SLE patients than in KT recipients although immuno-suppressants such as cyclosporine and azathioprine were more frequently administered in KT recipients. There were no differences in disease activity index including SLEDAI, complement levels, and anti-ds DNA titers at the time of tbc diagnosis as well as in the cumulative doses of steroid between extensive and limited diseases of tbc in SLE. Conclusion: The cumulative incidence rate of tbc was higher in SLE patients than in general population. The patterns of tbc tended to be more extensive in SLE compared to KT recipients in whom a stronger immuno-suppression was required, suggesting that immune dysfunction implicated by SLE itself may play an important role in determining the incidence and patterns of tbc infection.