MPA/WG 2 7 CY/AZ. J Jpn Coll Angiol, 2009, 49: compromized host, immunosuppressive therapy, ANCA associated vasculitis, infection control

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1 Online publication June 24, 2009 ANCA MPA WG ANCA CRP PSL CY / AZ MPA/WG 2 7 QOL PSL CY/AZ 3 CMV J Jpn Coll Angiol, 2009, 49: compromized host, immunosuppressive therapy, ANCA associated vasculitis, infection control antineutrophil cytoplasmic antibodies: ANCA renal limited vasculitis: RLV Wegener s granulomatosis: WG microscopic polyangiitis: MPA allergic granulomatous angiitis: AGA ANCA ANCA-associated vasculitis: AAV 1 CS IS AAV MPO-ANCA JMAAV AAV AAV 266 1: C PR-3 AAV P MPO AAV 1:3 MPA WG AGA 121 RLV 104 RA PSS SSc 33 [ rapidly progressive glomerulonephritis: RPGN ] [ WG ] ANCA CRP THE JOURNAL of JAPANESE COLLEGE of ANGIOLOGY Vol. 49,

2 Table 1 Clinical findings in dead AAV cases (n = 41) I: Infection death (n = 19) II: Vasculitis death (n = 22) Fisher s test Age > 65 y.o. 12/19 (63%) 16/22 (73%) Male/Female 18/19 (95%) 14/22 (64%) RPGN 17/19 (89%) 19/22 (86%) Dyspnea 14/19 (74%) 17/22 (77%) Lung bleeding 3/18 (16%) 14/22 (64%) *p < 0.01 GI. bleeding 0/19 (0%) 6/22 (27%) *p < 0.02 CNS sym 1/18 (5.6%) 8/22 (36.4%) *p < 0.02 Anemia 4/19 (21%) 16/22 (73%) Leukocytosis 14/19 (74%) 19/22 (86%) Thrombocytosis 4/19 (21%) 6/22 (27%) High CRP 19/19 (100%) 22/22 (100%) High LDH 10/19 (53%) 16/22 (73%) PSL < 60mg/day 8/16 (50%) 13/15 (87%) *p < 0.05 Pulse steroid therapy 12/17 (71%) 19/20 (95%) Immunosuppressant 11/19 (58%) 10/22 (46%) Plasmapheresis 5/18 (28%) 7/21 (33%) γ 1, 2 AAV ANCA CRP ANCA CRP 1, 2 AAV CS CY IS RLV AAV MRSA 3 Table AAV 41 3 I 19 II 22 RPGN I II p < 0.01 CS PSL 60mg/ I II p < 0.05 AAV CS PSL 60mg/ Keller 5 WG 155 CY WG 3 6 PSL 5 10mg/ Fig JMAAV MPO-ANCA CY CY β AAV β CSBG ELISA 7 CSBG β β-6 β Fig. 2 CSBG 22 2,677 ± 1,686U 94 Vol. 49, 2009

3 Figure 1 Infection events periods in MAAV (n = 50)(2008). 6 Figure 2 Comparison of Anti-CSBG titer in AAV patients. 9 AAV ± 522U AAV ± 416U CSBG CSBG Fig. 3 MPO-ANCA 68U AAV RPGN β 300U CSBG 100U AAV CS 2 MPO-ANCA CSBG 800U 2 CS [1, /mm 3 ] /mm 3 CSBG 1,400U 700U AAV CSBG β AAV 7, 8, 13, 14 Fig. 4 AAV 2 IS CS Vol. 49,

4 Figure 3 A 67-year-old woman with AAV + Aspergillus pneumonia. 9 Figure 4 Hypothesis of opportunistic infections in compromised AAV. compromised host Fig. 3 T 1 2 AZ CY 9 10 Fig. 3 CD4 200 /µl IgG 600mg/dl 600 /µl 96 Vol. 49, 2009

Figure 5 Strategy of prevention of infections in AAV. AAV 2002 9 Fig.

5 Figure 5 Strategy of prevention of infections in AAV. AAV Fig. 5 8 AAV ANCA CRP LDH 1 AAV AAV 37 3 CRP [ 2, /mm 3 ] [CD4 200 /µl] IgG 600mg/dl WG AAV ST 13, / / 2,400mg/ 500ml ITCZ mg/ AAV CS PSL 1.2mg/kg/ PSL 0.8mg/kg/ IS PSL 0.4mg/kg IS PSL 0.8mg/kg/ 500 /µl PSL 0.4mg/kg/ 500 /µl 2 ST TMP/SMX 1 1g 1g/ 4g/ 2g/ 8g 4g/ 1A 300mg 300mg/ 300mg/2 3 1,000/µl 500 /µl Fig. 5 Vol. 49,

6 AAV AAV ANCA ANCA JMAAV JMAAV 1 ANCA ANCA ANCA Axel A, Brakhage, Bernhard J, Axel S eds. Aspergillus fumigatus. Biology, Clinical Aspects and Molecular Approaches to Pathogenesity (Contributions to Microbiology, Vol. 2). Tokyo: Karger, 1999, Reinhold-Keller E, Beuge N, Latza U et al: An interdisciplinary approach to the care of patients with Wegener s granulomatosis: long-term outcome in 155 patients. Arthritis Rheum, 2000, 43: ANCA Masuzawa S, Yoshida M, Ishibashi K et al: Solubilized Candida Cell Wall β-glucan, CSBG, Is an epitope of Natural Human Antibody. Drug Devel Res, 2003, 58: Ishibashi K, Yoshida M, Nakabayashi I et al: Role of anti-β-glucan antibody in host defense against fungi. FEMS Immunol Med Microbiol, 2005, 44: Yoshida M, Ishibashi K, Hida S et al: Rapid decrease of anti-β-glucan antibody as an indicator for early diagnosis of carinii pneumonitis and deep mycotic infections following immunosuppressive therapy in antineutrophil cytoplasmic antibody-associated vasculitis. Clin Rheumatol, 2008, 28: ANCA β Stegeman CA, Tervaert JW, de Jong PE et al: Trimethoprim-sulfamethoxazole (co-trimoxazole) for the prevention of relapses of Wegener s granulomatosis. N Engl J Med, 1996, 335: Hida S, Yoshida M, Nakabayashi I et al: Anti-fungal activity of sulfamethoxazole toward Aspergillus species. Biol Pharm Bull, 2005, 28: , Vol. 49, 2009

7 Strategy of Infection Control in Immunosuppressive Therapy for ANCA-Associated Vasculitis Masaharu Yoshida Renal Unit of Internal Medicine, Hachioji Medical Center of Tokyo Medical University, Tokyo, Japan compromized host, immunosuppressive therapy, ANCA associated vasculitis, infection control Antineutrophil cytoplasmic antibodies (ANCA) are well known to be associated with small vessel vasculitic diseases such as microscopic polyangiitis (MPA), allergic granulomatous angiitis (AGA), and Wegener s granulomatosis (WG). Disease assessment by 1) vasculitic activity, 2) damage resulting from vasculitis, and 3) patient function, were the required endpoints for the therapeutic trials in ANCA-associated vasculitis (AAV). Harmonized steroids and cyclophosphamide or azathiopurine are effective for active AAV. In evaluating tools for monitoring disease, titers of ANCA and the levels of CRP were found useful in AAV. However, it will be important for clinicians to observe AAV patients more closely and reduce immunosuppressive drug doses more cautiously, especially to prevent several infections (i.e., deep mycosis, pneumocystis jirovecii pneumonia and cytomegalovirus). We indicated that strategy of infection control in immunosuppressive therapy for AAV. (J Jpn Coll Angiol, 2009, 49: 93 99) Vol. 49, 2009 Online publication June 24,

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