Antineutrophil Cytoplasmic Antibodies (ANCA)-Associated Crescentic Glomerulonephritis and Propylthiouracil Therapy

Yuasa, Shigekazu; Hashimoto, Mayuko; Yura, Takafumi; Sumikura, Tohru; Takahashi, Norihiro; Shoji, Tetsuo; Uchida, Koichi; Fujioka, Hikaru; Kihara, Minoru; Matsuo, Hirohíde

doi:10.1159/000189164

Cited by 40 publications

(24 citation statements)

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“…Numerous articles have appeared on ANCA positivity arising from administration of propylthiouracil (PTU) for anti-thyroid treatment in patients with Graves disease, hyperthyroidism, and thyrotoxicosis (13, [207][208][209]. The majority of these patients had ANCA directed against MPO, although ANCA that were simultaneously directed against other antigens such as human leukocyte elastase, lactoferrin, and even PR3 were also described (210,211).…”

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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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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“…Concerning small vessel vasculitis in patients with Graves' disease including that induced by anti-thyroid drugs, immune-complex vasculitis [2] and cutaneous vasculitis [3] have been reported. Recently, ANCA-associated vasculitis has also been described based on pathological findings and the clinical course [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] . However, there has not been any detailed discussion concerning drug dose and duration of anti-thyroid drug use, or titers of myeloperoxidase (MPO)-ANCA, anti-nuclear antibody (ANA) and anti-thyroid antibodies.…”

mentioning

confidence: 99%

Anti-Thyroid Drug-Induced ANCA-Associated Vasculitis. A Case Report and Review of the Literature.

2000

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Abstract.We report a case of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis induced by propylthiouracil (PTU), and review the literature concerning to anti-thyroid drug-induced ANCA-associated vasculitis.A 45-year-old man treated with PTU developed fever and arthralgia without pulmonary, skin or eye involvement. These symptoms persisted for a long period without specific symptom, sign or laboratory data of other arthritis. Laboratory findings of urine and blood were normal, except for positive MPO-ANCA (191EU) and PR3-ANCA (37EU) findings. After PTU was discontinued without steroids or immune modulating drugs, both symptoms disappeared.Our patient had a high titer of MPO-ANCA. Moreover, titers of ANCA fell in correlation with the course of symptoms after the cessation of PTU, and we diagnosed PTU-induced ANCA-associated vasculitis. Most patients with pulmonary renal syndrome receive anti-thyroid drugs over a prolonged period, but the duration of our case was shorter than those of these patients.It is suggested that our patient was diagnosed at an early stage of ANCA-associated vasculitis before the start of pulmonary or renal involvement.

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“…However, although true ANCA-related vasculitis is described in a few cases, most of these incidences are not associated with signi¢cant clinical features. 44 ANCAs are reported in the majority of ulcerative colitis and almost one-third of patients with Crohn's disease, almost 90% of patients with primary sclerosing cholangitis 45 and a similar percentage in Felty's syndrome. 46 They are also described in a minority of SLE 47 and RA patients, especially if they are a¡ected by rheumatoid vasculitis.…”

Section: Does a Positive Anca Always Mean Systemic Vasculitis?mentioning

confidence: 99%

“…[41][42][43] Drug induced syndromes Propylthiouracil, minocycline and hydralazine among many others are associated with a P-ANCA, although only a minority go on to develop and ANCA-related vasculitis. 44 Anti-GBM antibody disease 10-40% of GBM antibody disease are also ANCA positive, most are MPO-ANCA. 52 Autoimmune gastrointestinal disease ANCA reported in the majority of ulcerative colitis and primary sclerosing cholangitis; very few are MPO or PR3 positive however.…”

mentioning

confidence: 99%

Role of antineutrophil cytoplasmic antibodies and glomerular basement membrane antibodies in the diagnosis and monitoring of systemic vasculitides

Sinclair

Stevens

2007

Ann Clin Biochem

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This article was prepared at the invitation of the Clinical Sciences Reviews Committee of the Association for Clinical Biochemistry Systemic vasculitis, although rare, is often diagnosed late and long after the onset of symptoms. The small vessel vasculitides are recognized clinically by their multisystem presentation, markers of inflammation and evidence for an acute glomerulonephritis (GN), with the most apparent organ involved directing referral to secondary care. Routine laboratory tests are usually non-specific in systemic vasculitis but the use of anti-neutrophil cytoplasmic antibodies (ANCAs) and glomerular basement membrane (GBM) antibodies can aid diagnosis, treatment and monitoring decisions. These antibodies are detected and quantified by indirect immunofluorescence (IIF) and antigen-specific enzyme-linked immunosorbent assay (ELISA), usually in combination for ANCA, and ELISA systems (or direct IIF on kidney biopsy) for GBM antibodies. The presence or absence of ANCA does not confirm or exclude the diagnosis of systemic vasculitis but negative and positive predictive values will be strongly influenced by clinical presentation. Various large studies have been unable to conclude that following serial ANCA titres has great clinical utility in each case but each patient must be considered on its own merits; for example the reappearance of ANCA in a patient who was rendered ANCA negative following treatment is more likely to indicate relapse. The adoption of consensus guidelines that direct testing towards patients with rapidly progressive GN, pulmonary haemorrhage, persistent and destructive ear, nose and upper airways problems, such as subglottic tracheal stenosis, a retro-orbital mass and cutaneous vasculitis with systemic features or peripheral neuropathy, will greatly increase the clinical utility and positive predictive value of these tests.

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Antineutrophil Cytoplasmic Antibodies (ANCA)-Associated Crescentic Glomerulonephritis and Propylthiouracil Therapy

Cited by 40 publications

References 13 publications

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

Anti-Thyroid Drug-Induced ANCA-Associated Vasculitis. A Case Report and Review of the Literature.

Role of antineutrophil cytoplasmic antibodies and glomerular basement membrane antibodies in the diagnosis and monitoring of systemic vasculitides

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