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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.
Hyperthyroidism as a Cause of Autonomic Dysreflexia
Chang, Jae Hyeok,Han, Ji Eui,Sohn, Hyun Joo,Shin, Yong Beom,Ko, Hyun-Yoon Lippincott Williams Wilkins, Inc. 2008 AMERICAN JOURNAL OF PHYSICAL MEDICINE & REHABILITA Vol.87 No.9
Chang JH, Han JE, Sohn HJ, Shin YB, Ko H-Y: Hyperthyroidism as a cause of autonomic dysreflexia. Am J Phys Med Rehabil 2008;87:768–772.A 25-yr-old female tetraplegic patient experienced autonomic dysreflexia episodes involving hypertension, headache, facial flushing, and tachycardia. The symptoms were not related to the bladder or bowel. The episodes did not seem to be linked to any mechanical cause. The patient was incidentally diagnosed with hyperthyroidism. Treatment with antithyroid medication resulted in resolution of the autonomic dysreflexia. This case suggests that hyperthyroidism may trigger autonomic dysreflexia in tetraplegic patients.