Autoantibodies to Myeloperoxidase in Idiopathic and Drug-Induced Systemic Lupus Erythematosus and Vasculitis

Cambridge, G; Wallace, HA; Bernstein, Robert; Leaker, Brian

doi:10.1093/rheumatology/33.2.109

Cited by 93 publications

(59 citation statements)

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“…In LN, the prevalence of ANCA is reported to be about 46% (45/99 cases) [1,13]. In our study, the prevalence of ANCA in LN was similar to the previous reports.…”

Section: Discussionsupporting

confidence: 91%

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Clinical Implications of Antineutrophil Cytoplasmic Antibody Test in Lupus Nephritis

et al. 2000

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To elucidate the prevalence and clinical implications of antineutrophil cytoplasmic antibody (ANCA) in lupus nephritis (LN), we examined ANCA by indirect immunofluorescence and by ELISA against antilactoferrin (anti-LF) and antimyeloperoxidase (anti-MPO) antibody. To discriminate perinuclear ANCA (pANCA) with antinuclear antibody (ANA), all the ANCA-positive sera were tested again after incubating patients’ sera with single-stranded (SS) and double-stranded (ds) DNA. These results were compared with clinicopathologic manifestations and clinical courses of LN. ANCA was positive in 19 (37.3%) of 51 LN patients. Among these LN patients, 3 had cytoplasmic ANCA (cANCA) and 16 had pANCA. ANCA was not found in 8 SLE patients without nephritis and 30 normal controls. The presence of ANCA, particularly pANCA, was associated with the presence of nephritis (18/51 cases vs. 0/8 cases, p < 0.05), especially with diffuse proliferative lupus nephritis, WHO class IV (17/18 cases vs. 21/31 cases, p < 0.05) as well as the presence of anti-dsDNA antibody (17/19 cases vs. 18/30 cases, p < 0.05). Patients with ANCA frequently had deterioration of renal function (3/16 vs. 0/26 cases). Anti-LF antibody was positive in 13 patients. Among those, 12 patients had nephritis. Five patients with anti-LF antibody did not have ANCA, but 7 had pANCA, and 1 had cANCA. Patients with anti-LF antibody had lower initial creatinine levels than those without it [serum creatinine (mg/dl): 0.78 (0.6–1.0) vs. 1.43 (0.5–5.0), p < 0.05]. Anti-MPO antibody was positive in only 1 patient, suggesting that MPO is a rare antigen for ANCA in LN.

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“…In LN, the prevalence of ANCA is reported to be about 46% (45/99 cases) [1,13]. In our study, the prevalence of ANCA in LN was similar to the previous reports.…”

Section: Discussionsupporting

confidence: 91%

“…It is highly associated with drug-induced SLE [5,13], serositis [3] or dermal vasculitis [17]. But until now, its relationship to renal involvement is not clear.…”

Section: Clinical Implications Of Antineutrophil Cytoplasmic Antibodymentioning

confidence: 99%

Clinical Implications of Antineutrophil Cytoplasmic Antibody Test in Lupus Nephritis

et al. 2000

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“…Of note, the presence of p-ANCA is suggested to be a marker for lupus symptoms in genetically susceptible individuals treated with minocycline for acne in relation with certain major histocompatibility complex class II genes including HLA-DR4, HLA-DR2 and HLA-DQB1, as observed in our patient [4]. Indeed, p-ANCA antibodies have been reported in druginduced autoimmune disorders such as hydralazine-induced lupus, and vasculitis and propylthiouracil-associated vasculitis [5][6][7]. The role of HLA-DR4 has been implicated in the development of hydralazine-induced lupus [8].…”

supporting

confidence: 63%

Minocycline-Induced Lupus and Autoimmune Hepatitis: Family Autoimmune Disorders as Possible Risk Factors

Bachmeyer

Cadranel

2002

Dermatology

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“…The occurrence of ANCA-associated vasculitis and glomerulonephritis has also been associated with hydralazine treatment (227)(228)(229), administered for hypertension. Again, MPO is the most important antigen that ANCA target in these patients (230,231). Some case reports suggested that, next to PTU and hydralazine, a variety of other medications, such as penicillamine, minocycline, allopurinol, sulfasalazine, levamisole, and thioridazine, were associated with ANCA-associated vasculitis (232-236); however, in larger studies, these hypotheses could not be confirmed (237).…”

Section: Pharmacologic Inductionmentioning

confidence: 99%

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

Wijngaarden¹,

Rijn²,

Hagen³

et al. 2008

Clinical Journal of the American Society of Nephrology

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The first description of what is now known as antineutrophil cytoplasmic autoantibody-associated necrotizing vasculitis appeared more than 140 yr ago. Since then, many aspects of the pathogenic pathway have been elucidated, indicating the involvement of antineutrophil cytoplasmic autoantibodies, but why antineutrophil cytoplasmic autoantibodies are produced in the first place remains unknown. Over the years, many hypotheses have emerged addressing the etiology of antineutrophil cytoplasmic antibody production, but no exclusive factor or set of factors can so far be held responsible. Herein is reviewed the most influential hypotheses regarding the causes of antineutrophil cytoplasmic antibody-associated vasculitis with the aim of placing in an epidemiologic background the different hypotheses that are centered on environmental and genetic influences.Clin J Am Soc Nephrol 3: 237-252, 2008237-252, . doi: 10.2215 A ntineutrophil cytoplasmic autoantibody (ANCA)-associated necrotizing vasculitis was probably first described in 1866 by Kussmaul and Maier (1) as "polyarteritis nodosa." It was not until the early 1930s when the first case of what was later named Wegener's granulomatosis (WG) was described (2). The disease was named after Friedrich Wegener, who described it as an entity in 1939 (3). In 1985, antibodies associated with the disease were detected and later became known as ANCA (4). WG is a systemic autoimmune disease that can cause damage in various organs. Later, microscopic polyangiitis (MPA) was distinguished as a separate ANCA-associated vasculitis. The disease-or its immunosuppressive treatment-can cause high levels of morbidity and death, especially in patients with renal involvement. Animal experiments have shown that ANCA directed against myeloperoxidase (MPO) can cause vasculitis that resembles human vasculitic disease (5,6); however, the cause of ANCA production remains unresolved.Theories have been developed to explain how ANCA could interact with neutrophils, along with monocytes and most probably T lymphocytes, to form the lesions that are characteristic of ANCA-associated vasculitis, such as fibrinoid necrosis and granulomas (7). A recent theory of interest has been postulated by Pendergraft et al. (8), stating that an antibody against the complementary peptide of proteinase-3 (PR3) in an idiotypic/anti-idiotypic network is essential to the development of ANCA and to the development of clinical vasculitis, but why and how these ANCA are produced in the first place remains unanswered. Nonetheless, many hypotheses have been developed about the initiating factor for ANCA production. Many factors, either directly or indirectly, have been considered important in the development of ANCA: Silica exposure (9); genetic predisposition (10); bacterial infection by Staphylococcus aureus (11); viral infection by, for instance, parvovirus B19 (12); and thyroid drugs (13) all have been correlated with and held to contribute to the incidence of ANCA-associated vasculitis. Some of these hypotheses are still th...

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Autoantibodies to Myeloperoxidase in Idiopathic and Drug-Induced Systemic Lupus Erythematosus and Vasculitis

Cited by 93 publications

References 0 publications

Clinical Implications of Antineutrophil Cytoplasmic Antibody Test in Lupus Nephritis

Clinical Implications of Antineutrophil Cytoplasmic Antibody Test in Lupus Nephritis

Minocycline-Induced Lupus and Autoimmune Hepatitis: Family Autoimmune Disorders as Possible Risk Factors

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

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